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2015v1.0
Macleod’s
Clinical Examination
John Macleod (1915–2006)
John Macleod was appointed consultant physician at the Western General Hospital,
Edinburgh, in 1950. He had major interests in rheumatology and medical education.
Medical students who attended his clinical teaching sessions remember him as
an inspirational teacher with the ability to present complex problems with great
clarity. He was invariably courteous to his patients and students alike. He had an
uncanny knack of involving all students equally in clinical discussions and used
praise rather than criticism. He paid great attention to the value of history taking
and, from this, expected students to identify what particular aspects of the physical
examination should help to narrow the diagnostic options.
His consultant colleagues at the Western welcomed the opportunity of contributing
when he suggested writing a textbook on clinical examination. The book was first
published in 1964 and John Macleod edited seven editions. With characteristic
modesty he was very embarrassed when the eighth edition was renamed Macleod’s
Clinical Examination. This, however, was a small way of recognising his enormous
contribution to medical education.
He possessed the essential quality of a successful editor – the skill of changing
disparate contributions from individual contributors into a uniform style and format
without causing offence; everybody accepted his authority. He avoided being
dogmatic or condescending. He was generous in teaching others his editorial
skills and these attributes were recognised when he was invited to edit Davidson’s
Principles and Practice of Medicine.
Examination
Clinical
Edited by
J Alastair Innes
BSc PhD FRCP(Ed)
Consultant Physician, Respiratory Unit, Western General
Hospital, Edinburgh; Honorary Reader in Respiratory Medicine,
University of Edinburgh, UK
Anna R Dover
PhD FRCP(Ed)
Consultant in Diabetes, Endocrinology and General Medicine,
Edinburgh Centre for Endocrinology and Diabetes, Royal
Infirmary of Edinburgh; Honorary Clinical Senior Lecturer,
University of Edinburgh, UK
Karen Fairhurst
PhD FRCGP
General Practitioner, Mackenzie Medical Centre, Edinburgh;
Clinical Senior Lecturer, Centre for Population Health Sciences,
University of Edinburgh, UK
ISBN 978-0-7020-6993-2
International ISBN 978-0-7020-6992-5
Notices
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any
information, methods, compounds or experiments described herein. Because of rapid advances in the medical
sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent
of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to
persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.
The
publisher’s
policy is to use
paper manufactured
from sustainable forests
Printed in Europe
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Contents
Preface vii
Acknowledgements ix
How to make the most of this book xi
Clinical skills videos xiii
Contributors xv
Index 375
Preface
Despite the wealth of diagnostic tools available to the modern to the use of pattern recognition to identify spot diagnoses.
physician, the acquisition of information by direct interaction Section 2 deals with symptoms and signs in specific systems
with the patient through history taking and clinical examination and Section 3 illustrates the application of these skills to specific
remains the bedrock of the physician’s art. These time-honoured clinical situations. Section 4 covers preparation for assessments
skills can often allow clinicians to reach a clear diagnosis without of clinical skills and for the use of these skills in everyday practice.
recourse to expensive and potentially harmful tests. An expertly performed history and examination of a patient
This book aims to assist clinicians in developing the consultation allows the doctor to detect disease and predict prognosis, and is
skills required to elicit a clear history, and the practical skills crucial to the principle of making the patient and their concerns
needed to detect clinical signs of disease. Where possible, the central to the care process, and also to the avoidance of harm
physical basis of clinical signs is explained to aid understanding. from unnecessary or unjustified tests.
Formulation of a differential diagnosis from the information gained We hope that if young clinicians are encouraged to adopt
is introduced, and the logical initial investigations are included for and adapt these skills, they not only will serve their patients
each system. Macleod’s Clinical Examination is designed to be as diagnosticians but also will themselves continue to develop
used in conjunction with more detailed texts on pathophysiology, clinical examination techniques and a better understanding of
differential diagnosis and clinical medicine, illustrating specifically their mechanisms and diagnostic use.
how the history and examination can inform the diagnostic The 14th edition of Macleod’s Clinical Examination has an
process. accompanying set of videos available in the online Student
In this edition the contents have been restructured and the Consult electronic library. This book is closely integrated with
text comprehensively updated by a team of existing and new Davidson’s Principles and Practice of Medicine and is best read
authors, with the aim of creating an accessible and user-friendly in conjunction with that text.
text relevant to the practice of medicine in the 21st century.
Section 1 addresses the general principles of good interaction JAI, ARD, KF
with patients, from the basics of taking a history and examining, Edinburgh, 2018
Acknowledgements
The editors would like acknowledge the immense contribution McDonald, Jon Harvey, Alexandra Hawker, Raja K Haynes, Emma
made by Graham Douglas, Fiona Nicol and Colin Robertson Hendry, Malik Hina, Bianca Honnekeri, Justina Igwe, Chisom
who edited the three previous editions of Macleod’s Clinical Ikeji, Sushrut Ingawale, Mohammad Yousuf ul Islam, Sneha Jain,
Examination. Together they re-shaped the format of this textbook Maria Javed, Ravin Jegathnathan, Helge Leander B Jensen,
and their efforts were rewarded by a substantial growth in both Li Jie, Ali Al Joboory, Asia Joseph, Christopher Teow Kang
its sales and international reputation. Jun, Janpreet Kainth, Ayush Karmacharya, JS Karthik, Aneesh
The editors would like to acknowledge and offer grateful thanks Karwande, Adhishesh Kaul, Alper Kaymak, Ali Kenawi, Abdullah
for the input of all previous editions’ contributors, without whom Al Arefin Khadem, Haania Khan, Muhammad Hassan Khan,
this new edition would not have been possible. In particular, we Sehrish Khan, Shrayash Khare, Laith Khweir, Ankit Kumar, Vinay
are indebted to those former authors who step down with the Kumar, Ibrahim Lafi, Armeen Lakhani, Christopher Lee, David Lee,
arrival of this new edition. They include: Elaine Anderson, John Benjamin Leeves, Soo Ting Joyce Lim, Chun Hin Lo, Lai Hing Loi,
Bevan, Andrew Bradbury, Nicki Colledge, Allan Cumming, Graham Chathura Mihiran Maddumabandara, Joana Sousa Magalhães,
Devereux, Jamie Douglas, Rebecca Ford, David Gawkrodger, Aditya Mahajan, Mahabubul Islam Majumder, Aaditya Mallik,
Neil Grubb, James Huntley, John Iredale, Robert Laing, Andrew Mithilesh Chandra Malviya, Santosh Banadahally Manjegowda,
Longmate, Alastair MacGilchrist, Dilip Nathwani, Jane Norman, Jill Marshall, Balanuj Mazumdar, Alan David McCrorie, Paras
John Olson, Paul O’Neill, Stephen Payne, Laura Robertson, Mehmood, Kartik Mittal, Mahmood Kazi Mohammed, Amber
David Snadden, James C Spratt, Kum-Ying Tham, Steve Turner Moorcroft, Jayne Murphy, Sana Mustafa, Arvi Nahar, Akshay
and Janet Wilson. Prakash Narad, Shehzina Nawal, Namia Nazir, Viswanathan
We are particularly grateful to the following medical students, Neelakantan, Albero Nieto, Angelina Choong Kin Ning, Faizul
who undertook detailed reviews of the book and gave us a wealth Nordin, Mairead O’Donoghue, Joey O’Halloran, Amit Kumar Ojha,
of ideas to implement in this latest edition. We trust we have listed Ifeolu James Oyedele, Anik Pal, Vidit Panchal, Asha Pandu, Bishal
all those who contributed, and apologise if any names have been Panthi, Jacob Parker, Ujjawal Paudel, Tanmoy Kumar Paul, Kate
accidentally omitted: Layla Raad Abd Al-Majeed, Ali Adel Ne’ma Perry, Daniel Pisaru, David Potter, Dipesh Poudel, Arijalu Syaram
Abdullah, Aanchal Agarwal, Hend Almazroa, Alhan Alqinai, Amjed Putra, Janine Qasim, Muhammad Qaunayn Qays, Mohammad
Alyasseen, Chidatma Arampady, Christian Børde Arkteg, Maha Qudah, Jacqueline Quinn, Varun MS Venkat Raghavan, Md.
Arnaout, Rashmi Arora, Daniel Ashrafi, Herry Asnawi, Hemant Atri, Rahmatullah, Ankit Raj, Jerin Joseph Raju, Prasanna A Ramana,
Ahmed Ayyad, Kainath N Azad, Sadaf Azam, Arghya Bandhu, Ashwini Dhanraj Rangari, Anurag Ramesh Rathi, Anam Raza,
Jamie Barclay, Prithiv Siddarth Saravana Bavan, Rajarshi Bera, Rakesh Reddy, Sudip Regmi, Amgad Riad, Patel Riya, Emily
Craig Betton, Apoorva Bhagat, Prachi Bhageria, Geethanjali Robins, Grace Robinson, Muhammad’Azam Paku Rozi, Cosmin
Bhas, Navin Bhatt, Shahzadi Nisar Bhutto, Abhishek Ghosh Rusneac, Ahmed Sabra, Anupama Sahu, Mohammad Saleh,
Biswas, Tamoghna Biswas, Debbie Bolton, Claude Borg, Daniel Manjiri Saoji, Saumyadip Sarkar, Rakesh Kumar Shah, Basil Al
Buxton, Anup Chalise, Amitesh Kumar Chatterjee, Subhankar Shammaa, Sazzad Sharhiar, Anmol Sharma, Homdutt Sharma,
Chatterjee, Farhan Ashraf Chaudhary, Aalia Chaudhry, Jessalynn Shivani Sharma, Shobhit Sharma, Johannes Iikuyu Shilongo,
Chia, Bhaswati Chowdhury, Robin Chowdhury, Marshall Colin, Dhan Bahadur Shrestha, Pratima Shrestha, Anurag Singh,
Michael Collins, Margaret Cooper, Barbara Corke, Andrea Culmer, Kareshma Kaur Ranjit Singh, Nishansh Singh, Aparna Sinha,
Gowtham Varma Dantuluri, Abhishek Das, Sonali Das, Aziz Dauti, Liam Skoda, Ethan-Dean Smith, Prithviraj Solanki, Meenakshi
Mark Davies, Adam Denton, Muinul Islam Dewan, Greg Dickman, Sonnilal, Soundarya Soundararajan, Morshedul Islam Sowrav,
Hengameh Ahmad Dokhtjavaherian, Amy Edwards, Muhammad Kayleigh Spellar, Siddharth Srinivasan, Pradeep Srivastava,
Eimaduddin, Laith Al Ejeilat, Divya G Eluru, Emmanuel Ernest, El Anthony Starr, Michael Suryadisastra, Louisa Sutton, Komal
Bushra El Fadil, Fathima Ashfa Mohamed Faleel, Malcolm Falzon, Ashok Tapadiya, Areeba Tariq, Imran Tariq, Jia Chyi Tay, Javaria
Emma Farrington, Noor Fazal, Sultana Ferdous, Matthew Formosa, Tehzeeb, Daniel Theron, Michele Tosi, Pagavathbharathi Sri Balaji
Brian Forsyth, David Fotheringham, Bhargav Gajula, Dariimaa Vidyapeeth, Amarjit Singh Vij, Cathrine Vincent, Ghassan Wadi,
Ganbat, Lauren Gault, Michaela Goodson, Mounika Gopalam, Amirah Abdul Wahab, James Warrington, Luke Watson, Federico
Ciaran Grafton-Clarke, Anthony Gunawan, Aditya Gupta, Digvijay Ivan Weckesser, Ben Williamson, Kevin Winston, Kyi Phyu Wint,
Gupta, Kshitij Gupta, Sonakshi Gupta, Md. Habibullah, Kareem Harsh Yadav, Saroj Kumar Yadav, Amelia Yong, Awais Zaka
Haloub, Akar Jamal Hamasalih, James Harper, Bruce Harper- and Nuzhat Zehra.
How to make
the most of this book
The purpose of this book is to document and explain how to:
Examination sequences
Patients
Abby Cooke
Omar Ali
Contributors
Anthony Bateman MD MRCP FRCA FFICM Kirsty Dundas DCH FRCOG
Consultant in Critical Care and Long Term Ventilation, Critical Consultant Obstetrician, Royal Infirmary of Edinburgh;
Care NHS Lothian, Edinburgh, UK Honorary Senior Lecturer and Associate Senior Tutor,
University of Edinburgh, UK
Shyamanga Borooah MRCP(UK) MRCS(Ed)
FRCOphth PhD Andrew Elder FRCP(Ed) FRCPSG FRCP FACP FICP(Hon)
Fulbright Fight for Sight Scholar, Shiley Eye Institute, Consultant in Acute Medicine for the Elderly, Western General
University of California, San Diego, USA Hospital, Edinburgh; Honorary Professor, University of
Edinburgh, UK
Kirsty Boyd PhD FRCP MMedSci
Consultant in Palliative Medicine, Royal Infirmary of Edinburgh; Karen Fairhurst PhD FRCGP
Honorary Clinical Senior Lecturer, Primary Palliative Care General Practitioner, Mackenzie Medical Centre, Edinburgh;
Research Group, University of Edinburgh, UK Clinical Senior Lecturer, Centre for Population Health
Sciences, University of Edinburgh, UK
Ivan Brenkel FRCS(Ed)
Consultant Orthopaedic Surgeon, Orthopaedics, NHS Fife, Jane Gibson MD FRCP(Ed) FSCP(Hon)
Kirkcaldy, UK Consultant Rheumatologist, Fife Rheumatic Diseases Unit,
NHS Fife, Kirkcaldy, Fife; Honorary Senior Lecturer, University
Gareth Clegg PhD MRCP FRCEM of St Andrews, UK
Senior Clinical Lecturer, University of Edinburgh; Honorary
Consultant in Emergency Medicine, Royal Infirmary of Iain Hathorn DOHNS PGCME FRCS(Ed) (ORL-HNS)
Edinburgh, UK Consultant ENT Surgeon, NHS Lothian, Edinburgh, UK;
Honorary Clinical Senior Lecturer, University of Edinburgh, UK
Steve Cunningham PhD
Consultant and Honorary Professor in Paediatric Respiratory Iain Hennessey FRCS MMIS
Medicine, Royal Hospital for Sick Children, Edinburgh, UK Clinical Director of Innovation, Consultant Paediatric and
Neonatal Surgeon, Alder Hey Children’s Hospital,
Richard Davenport DM FRCP(Ed) Liverpool, UK
Consultant Neurologist, Western General Hospital and Royal
Infirmary of Edinburgh; Honorary Senior Lecturer, University of J Alastair Innes BSc PhD FRCP(Ed)
Edinburgh, UK Consultant Physician, Respiratory Unit, Western General
Hospital, Edinburgh; Honorary Reader in Respiratory
Neeraj Dhaun PhD Medicine, University of Edinburgh, UK
Senior Lecturer and Honorary Consultant Nephrologist,
University of Edinburgh, UK Alan G Japp PhD MRCP
Consultant Cardiologist, Royal Infirmary of Edinburgh;
Anna R Dover PhD FRCP(Ed) Honorary Senior Lecturer, University of Edinburgh, UK
Consultant in Diabetes, Endocrinology and General Medicine,
Edinburgh Centre for Endocrinology and Diabetes, Royal David Kluth PhD FRCP
Infirmary of Edinburgh; Honorary Clinical Senior Lecturer, Reader in Nephrology, University of Edinburgh, UK
University of Edinburgh, UK
Alexander Laird PhD FRCS(Ed) (Urol)
Colin Duncan MD FRCOG Consultant Urological Surgeon, Western General Hospital,
Professor of Reproductive Medicine and Science, University Edinburgh, UK
of Edinburgh; Honorary Consultant Gynaecologist, Royal
Infirmary of Edinburgh, UK
xvi CONTRIBUTORS
which is about the doctor’s own feelings of compassion for or or to offer additional support. When using the telephone, it is
sorrow about the difficulties that the patient is experiencing. even more important to listen actively and to check your mutual
understanding frequently.
Showing cultural sensitivity Similarly, asynchronous communication with patients, using
email or web-based applications, has been adopted by some
Patients from a culture that is not your own may have different doctors. This is not yet widely seen as a viable alternative
social rules regarding eye contact, touch and personal space. to face-to-face consultation, or as a secure way to transmit
In some cultures, it is normal to maintain eye contact for confidential information. Despite the communication challenges
long periods; in most of the world, however, this is seen as that it can bring, telemedicine (using telecommunication and other
confrontational or rude. Shaking hands with the opposite sex information technologies) may be the only means of healthcare
is strictly forbidden in certain cultures. Death may be dealt with provision for patients living in remote and rural areas and its use is
differently in terms of what the family expectations of physicians likely to increase, as it has the advantage of having the facility to
may be, which family members will expect information to be incorporate the digital collection and transmission of medical data.
shared with them and what rites will be followed. Appreciate and
accept differences in your patients’ cultures and beliefs. When
in doubt, ask them. This lets them know that you are aware of, Professional responsibilities
and sensitive to, these issues.
Clinical encounters take place within a very specific context
Addressing the problem configured by the healthcare system within which they occur,
the legal, ethical and professional frameworks by which we are
Communicating your understanding of the patient’s problem bound, and by society as a whole.
to them is crucial. It is good practice to ensure privacy for this, From your first day as a student, you have professional
particularly if imparting bad news. Ask the patient who else they obligations placed on you by the public, the law and your
would like to be present – this may be a relative or partner – and colleagues, which continue throughout your working life. Patients
offer a nurse. Check patients’ current level of understanding and must be able to trust you with their lives and health, and you
try to establish what further information they would like. Information will be expected to demonstrate that your practice meets the
should be provided in small chunks and be tailored to the patient’s expected standards (Box 1.3). Furthermore, patients want more
needs. Try to acknowledge and address the patient’s ideas, from you than merely intellectual and technical proficiency; they
concerns and expectations. Check the patient’s understanding will value highly your ability to demonstrate kindness, empathy
and recall of what you have said and encourage questions. After and compassion.
this, you should agree a management plan together. This might
involve discussing and exploring the patient’s understanding of
the options for their treatment, including the evidence of benefit 1.3 The duties of a registered doctor
and risk for particular treatments and the uncertainties around
Knowledge, skills and performance
it, or offering recommendations for treatment.
Make the care of your patient your first concern
Provide a good standard of practice and care:
Concluding the encounter Keep your professional knowledge and skills up to date
Recognise and work within the limits of your competence
Closing the consultation usually involves summarising the
Safety and quality
important points that have been discussed during the consultation.
This aids patient recall and facilitates adherence to treatment. Take prompt action if you think that patient safety, dignity or
Any remaining questions that the patient may have should be comfort is being compromised
Protect and promote the health of patients and the public
addressed, and finally you should check that you have agreed
a plan of action together with the patient and confirmed Communication, partnership and teamwork
arrangements for follow-up. Treat patients as individuals and respect their dignity:
Treat patients politely and considerately
Respect patients’ right to confidentiality
Alternatives to face-to-face Work in partnership with patients:
Listen to, and respond to, their concerns and preferences
encounters Give patients the information they want or need in a way they
can understand
The use of telephone consultation as an alternative to face-to- Respect patients’ right to reach decisions with you about their
face consultation has become accepted practice in parts of treatment and care
some healthcare systems, such as general practice in the UK. Support patients in caring for themselves to improve and
maintain their health
However, research suggests that, compared to face-to-face
Work with colleagues in the ways that best serve patients’ interests
consultations, telephone consultations are shorter, cover fewer
problems and include less data gathering, counselling/advice Maintenance of trust
and rapport building. They are therefore considered to be most Be honest and open, and act with integrity
suitable for uncomplicated presentations. Telephone consultation Never discriminate unfairly against patients or colleagues
with patients increases the chance of miscommunication, as Never abuse your patients’ trust in you or the public’s trust in the
there are no visual cues regarding body language or demeanour. profession
The telephone should not be used to communicate bad news
Courtesy General Medical Council (UK).
or sensitive results, as there is no opportunity to gauge reaction
7
Fundamentally, patients want doctors who: between countries. In the UK, follow the guidelines issued by the
General Medical Council. There are exceptions to the general 1
rules governing patient confidentiality, where failure to disclose
information would put the patient or someone else at risk of
needed death or serious harm, or where disclosure might assist in the
prevention, detection or prosecution of a serious crime. If you find
to them carefully yourself in this situation, contact the senior doctor in charge of
the patient’s care immediately and inform them of the situation.
Always obtain consent before undertaking any examination or
investigation, or when providing treatment or involving patients
in teaching or research.
their health and healthcare
Social media
help people make the best possible choices when death
is close Through social media, we are able to create and share web-based
information. As such, social media has the potential to be a
healthcare team valuable tool in communicating with patients, particularly by
facilitating access to information about health and services, and
other health professionals, and are ready to learn from by providing invaluable peer support for patients. However, they
others, regardless of their age, role or status. also have the potential to expose doctors to risks, especially when
One way to reconcile these expectations with your inexperience there is a blurring of the boundaries between their professional
and incomplete knowledge or skills is to put yourself in the and personal lives. The obligations on doctors do not change
situation of the patient and/or relatives. Consider how you would because they are communicating through social media rather than
wish to be cared for in the patient’s situation, acknowledging that face to face or through other conventional media. Indeed, using
you are different and your preferences may not be the same. social media creates new circumstances in which the established
Most clinicians approach and care for patients differently once principles apply. If patients contact you about their care or other
they have had personal experience as a patient or as a relative professional matters through your private profile, you should
of a patient. Doctors, nurses and everyone involved in caring for indicate that you cannot mix social and professional relationships
patients can have profound influences on how patients experience and, where appropriate, direct them to your professional profile.
illness and their sense of dignity. When you are dealing with
patients, always consider your:
Personal responsibilities
respect.
You should always be aware that you are in a privileged
professional position that you must not abuse. Do not pursue
accompanies each illness.
an improper relationship with a patient, and do not give medical
care to anyone with whom you have a close personal relationship.
Finally, remember that, to be fit to take care of patients, you
Confidentiality and consent must first take care of yourself. If you think you have a medical
condition that you could pass on to patients, or if your judgement
As a student and as a healthcare professional, you will be or performance could be affected by a condition or its treatment,
given private and intimate information about patients and their consult your general practitioner. Examples might include serious
families. This information is confidential, even after a patient’s communicable disease, significant psychiatric disease, or drug
death. This is a general rule, although its legal application varies or alcohol addiction.
2
2
J Alastair Innes
Karen Fairhurst
Anna R Dover
General aspects of
history taking
The importance of a clear history 10 Difficult situations 16
Gathering information 10 Patients with communication difficulties 16
Beginning the history 10 Patients with cognitive difficulties 16
The history of the presenting symptoms 11 Sensitive situations 16
Past medical history 13 Emotional or angry patients 16
Drug history 13
Family history 14
Social history and lifestyle 14
Systematic enquiry 16
Closing the interview 16
10 GENERAL ASPECTS OF HISTORY TAKING
When did you first feel unwell, and what did you
feel? (Open questioning)
Well, I’ve been getting this funny feeling in my chest
Gathering information over the last few months. It’s been getting worse and
worse but it was really awful this morning. My husband
called 999. The ambulance came and the nurse said I
was having a heart attack. It was really scary.
Beginning the history
When you say a ‘funny feeling’, can you tell me
Preparation more about what it felt like? (Open questioning,
steering away from events and opinions back to
symptoms)
Well, it was here, across my chest. It was sort of tight,
Allowing sufficient time like something heavy sitting on my chest.
And did it go anywhere else? (Open but clarifying)
Well, maybe up here in my neck.
What were you doing when it came on? (Clarifying
precipitating event)
Just sitting in the kitchen, finishing my breakfast.
How long was the tightness there? (Closed)
About an hour altogether.
So, you felt a tightness in your chest this morning
that went on for about an hour and you also felt it
Starting your consultation in your neck? (Reflection)
Yes that’s right.
Did you feel anything else at the same time?
(Open, not overlooking secondary symptoms)
I felt a bit sick and sweaty.
Drug allergies/reactions
Drug history
Family history
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Fig. 2.1 Symbols used in constructing a pedigree chart, with an example. The terms ‘propositus’ and ‘proposita’ indicate the man or woman
identified as the index case, around whom the pedigree chart is constructed.
2
Alcohol problems
Alcohol
Difficult situations
Travel history
Sexual history
Sensitive situations
Systematic enquiry
2 3 4
8
Rub hands palm to palm Right palm over the back of the Palm to palm with
other hand with interlaced fingers interlaced
fingers and vice versa
5 6 7
9
Backs of fingers to opposing Rotational rubbing of left Rotational rubbing, backwards
palms with fingers interlocked thumb clasped in right and forwards with clasped
palm and vice versa fingers of right hand in left
palm and vice versa
Fig. 3.1 Techniques for hand hygiene. From WHO Guidelines on Hand Hygiene in Health Care First Global Patient Safety Challenge Clean Care is Safer
Care; http://www.who.int/gpsc/clean_hands_protection/en/ © World Health Organization 2009. All rights reserved.
Sequence for performing a system in this case) will be examined. In other circumstances,
however, a full integrated physical examination will be required
physical examination and this is described in detail on page 362.
There is no single correct way to perform a physical examination
The purpose of the physical examination is to look for the but standardised systematic approaches help to ensure that
presence, or absence, of physical signs that confirm or refute nothing is omitted. With experience, you will develop your own
the differential diagnoses you have obtained from the history. The style and sequence of physical examination. Broadly speaking,
extent of the examination will depend on the symptoms that you any systematic examination involves looking at the patient (for
are investigating and the circumstances of the encounter. Often, skin changes, scars, abnormal patterns of breathing or pulsation,
in a brief, focused consultation (such as a patient presenting to a for example), laying hands on the patient to palpate (feel) and
general practitioner with headache), a single system (the nervous percuss (tapping on the body), and finally using a stethoscope,
22 GENERAL ASPECTS OF EXAMINATION
Initial observations
The physical examination begins as soon as you see the patient.
Start with a rapid assessment of how unwell the patient is,
since the clinical assessment may have to be adjusted for a
Fig. 3.2 Tattoos can be revealing.
deteriorating or dying patient, and any abnormal physiology may
need to be addressed urgently before the actual diagnosis is found
(pp. 341 and 348). Early warning scoring systems (which include
assessment of vital signs: pulse, blood pressure, respiratory rate
and oxygen saturations, temperature, conscious level and pain
score) are used routinely to assess unwell patients and these
clinical measurements aid decisions about illness severity and
urgency of assessment (p. 340). If your patient is distressed
or in pain, giving effective analgesia may take priority before
undertaking a more structured evaluation, although a concurrent
evaluation for the cause of the pain is clearly important.
For the stable or generally well patient, a more measured
assessment can begin. Observe the patient before the consultation
begins. Do they look generally well or unwell? What is their
demeanour? Are they sitting up comfortably reading or on the
telephone to a relative, or do they seem withdrawn, distressed
or confused?
Notice the patient’s attire. Are they dressed appropriately?
Clothing gives clues about personality, state of mind and social
circumstances, as well as a patient’s physical state. Patients
with recent weight loss may be wearing clothes that look very
Fig. 3.3 The linear marks of intravenous injection at the right
baggy and loose. Are there signs of self-neglect (which may
antecubital fossa.
be underpinned by other factors such as cognitive impairment,
immobility or drug or alcohol dependence) or inappropriate
attire? For example, a patient with thyrotoxicosis may come
to see you dressed for summer in the depths of winter due to
heat intolerance.
Often there will be clues to the patient’s underlying medical
condition either about the person (for example, they may be
wearing a subcutaneous insulin pump to treat their type 1
diabetes, or carrying a portable oxygen cylinder if they have
significant pulmonary fibrosis) or by the bedside (look on the
bedside table for a hearing aid, peak flow meter or inhaler
device, and note any walking aid, commode and wheelchair,
which provide clues to the patient’s functional status). Patients
may be wearing a medical identity bracelet or other jewellery
alerting you to an underlying medical condition or life-sustaining
treatment. Note any tattoos or piercings; as well as there being
possible associated infection risks, these can provide important
background information (Fig. 3.2). Be sure to look for any
venepuncture marks of intravenous drug use or linear (usually
transverse) scars from recent or previous deliberate self-harm Fig. 3.4 Scars from deliberate self-harm (cutting).
(Figs 3.3 and 3.4).
normal or is there evidence of pain, immobility or weakness?
Gait and posture Abnormalities of gait can be pathognomonic signs of neurological
or musculoskeletal disease: for example, the hemiplegic gait
If patients are ambulant, watch how they rise from a chair and after stroke, the ataxic gait of cerebellar disease or the marche
walk towards you. Are they using a walking aid? Is the gait à petits pas (‘walk of little steps’) gait in a patient with diffuse
23
A B C
Fig. 3.7 Nail abnormalities in systemic disease. A Onycholysis with pitting in psoriasis. B Beau’s lines
seen after acute severe illness. C Leuconychia. D Koilonychia. (A) From Innes JA. Davidson’s Essentials of
D Medicine. 2nd edn. Edinburgh: Churchill Livingstone; 2016.
A B
Fig. 3.8 Clubbing. A Anterior view. B Lateral view.
Normal 3
1 2
Schamroth’s
window present
Clubbed
Clubbed 3
1 2
Schamroth’s
window absent
A B C
Fig. 3.9 Examining for finger clubbing. A Assessing interphalangeal depth at (1) interphalangeal joint and (2) nail bed, and nail-bed angle (3).
B Schamroth’s window sign. C Assessing nail-bed fluctuation.
26 GENERAL ASPECTS OF EXAMINATION
Skin Haemosiderin
This product of haemoglobin breakdown is deposited in the skin
A detailed approach to examination of the skin is described on of the lower legs following subcutaneous extravasation of blood
page 286. In everyday practice the skin can provide insights due to venous insufficiency. Local deposition of haemosiderin
into present and past medical disorders, as well as information (erythema ab igne or ‘granny’s tartan’) occurs with heat damage
about the patient’s social or mental status. to the skin from sitting too close to a fire or from applying local
The skin should be exposed where appropriate and inspected heat, such as a hot water bottle, to the site of pain (Fig. 3.12).
carefully for any abnormalities of pigmentation. Skin colour is
determined by pigments in the skin – melanin, an endogenous Easy bruising
brown pigment, and carotene, an exogenous yellow pigment Easy bruising can be a reflection of skin and connective tissue
(mainly derived from ingestion of carrots and other vegetables) fragility due to advancing age or glucocorticoid usage, or a more
– as well as by the amount of oxyhaemoglobin (red) and serious coagulopathy.
deoxyhaemoglobin (blue) circulating in the dermis.
Depigmentation occurs in the autoimmune condition vitiligo, in Hypercarotenaemia
which there is often bilateral symmetrical depigmentation, commonly
of the face, neck and extensor aspects of the limbs, resulting Hypercarotenaemia occurs due to excessive ingestion of
in irregular pale patches of skin (Fig. 3.10). It is associated with carotene-containing vegetables or in situations of impaired
other autoimmune diseases like diabetes mellitus, thyroid and metabolism such as hypothyroidism or anorexia nervosa. A
adrenal disorders, and pernicious anaemia. Hypopituitarism also yellowish discoloration is seen on the face, palms and soles
results in pale skin due to reduced production of melanotrophic but not the sclera or conjunctiva, and this distinguishes it from
peptides (see Fig. 10.10). Albinism is an inherited disorder in which jaundice (Fig. 3.13).
patients have little or no melanin in their skin or hair. The amount
of pigment in the iris varies; some individuals have reddish eyes Discoloration
but most have blue. Skin discoloration can also occur due to abnormal pigments such
Hyperpigmentation can be due to excess of the pituitary as the sallow yellow-brownish tinge in chronic kidney disease.
hormone adrenocorticotrophic hormone (ACTH), as in adrenal A bluish tinge is produced by abnormal haemoglobins, such as
insufficiency (or the very rare condition Nelson’s syndrome, sulphaemoglobin or methaemoglobin (see the section on cyanosis
in which there is ACTH overproduction following bilateral later), or by drugs such as dapsone. Some drug metabolites cause
adrenalectomy for pituitary Cushing’s disease). It produces brown
pigmentation, particularly in skin creases, recent scars, sites
overlying bony prominences, areas exposed to pressure such
as belts and bra straps, and the mucous membranes of the lips
and mouth, where it results in muddy brown patches (see Fig.
10.12B). Pregnancy and oral contraceptives may also cause
blotchy hyperpigmentation on the face, known as chloasma,
and pregnancy may increase pigmentation of the areolae, axillae,
genital skin and linea alba (producing a dark line in the midline
of the lower abdomen, called a ‘linea nigra’).
Haemochromatosis
This inherited condition of excessive iron absorption results in skin
hyperpigmentation due to iron deposition and increased melanin
production (Fig. 3.11). When iron deposition in the pancreas
Fig. 3.11 Haemochromatosis with increased skin pigmentation.
also causes diabetes mellitus, this is called ‘bronze diabetes’.
Fig. 3.16 Smooth red tongue (glossitis) and angular stomatitis of iron
deficiency.
B B
Fig. 3.17 Flushing due to carcinoid syndrome. A Acute carcinoid Fig. 3.19 Scurvy. A Bleeding gums. B Bruising and perifollicular
flush. B Chronic telangiectasia. haemorrhages.
disease resulting in chronic hypoxia or excess erythropoietin sufficient to raise the capillary deoxyhaemoglobin concentration
production. Plethora of the head and neck only may indicate above 50 g/L (5 g/dL). Since the detection of cyanosis relies on
superior vena cava obstruction (p. 86). the presence of an absolute concentration of deoxyhaemoglobin,
it may be absent in anaemic or hypovolaemic patients despite
Cyanosis the presence of hypoxia. Conversely, cyanosis may manifest
Cyanosis is a blue discoloration of the skin and mucous at relatively mild levels of hypoxia in polycythaemic patients.
membranes that occurs when the absolute concentration of
deoxygenated haemoglobin is increased. It can be difficult to Peripheral cyanosis
detect, particularly in black and Asian patients, but is most easily Peripheral cyanosis is seen in the distal extremities and may simply
seen where the subepidermal vessels are close to the skin surface, be a result of cold exposure, when prolonged peripheral capillary
as in the lips, mucous membranes, nose, cheeks, ears, hands flow allows greater oxygen extraction and hence increased levels
and feet. Rarely, cyanosis can be due to excessive circulating of deoxyhaemoglobin. As the patient is warmed and the circulation
methaemoglobin (which can be congenital or acquired, most improves, so does the cyanosis. Pathological causes of peripheral
often due to drug therapy) or sulphaemoglobin (usually due cyanosis include low cardiac output states, arterial disease and
to drug therapy), and typically does not resolve with oxygen venous stasis or obstruction.
administration.
both acute and chronic disease. The body mass index (BMI;
calculated from the formula weight(kg)/height(m)2) is more useful
than weight alone, as it allows for differing height. Normal values
for different ethnicities are available (Box 3.7).
Obesity
Obesity is associated with an increased risk of malignancy,
particularly oesophageal and renal cancer in both sexes, thyroid
and colon cancer in men, and endometrial and gallbladder cancer
Fig. 3.20 Neurofibromatosis. in women, as well as hypertension, hyperlipidaemia, type 2
diabetes mellitus, gastro-oesophageal reflux, gallbladder disease,
osteoarthritis and sleep apnoea. While it is usually the result of
excessive calorie intake relative to calories expended, it can
rarely be secondary to hypothyroidism, Cushing’s syndrome,
Tongue hypothalamic disease or drugs such as oral hypoglycaemic
agents, insulin and antipsychotics.
In addition to revealing central cyanosis, examination may uncover Note the distribution of fat, since central obesity (as judged
the smooth tongue of iron deficiency (see Fig. 3.16), enlargement by the waist circumference: the maximum abdominal girth at the
in acromegaly, or wasting and fasciculation in motor neurone midpoint between the lower costal margin and the iliac crest)
disease. correlates with increased visceral adiposity and has worse
health outcomes due to its association with hypertension, insulin
resistance, type 2 diabetes mellitus and coronary artery disease.
Odours Waist-to-hip ratio can also be a useful assessment of adipose
distribution: gluteal–femoral obesity or the ‘pear shape’ (waist : hip
Odours can provide clues to a patient’s social or behavioural ratio of ≤ 0.8 in females or < 0.9 in males) has a better prognosis,
habits; the smell of alcohol, tobacco or cannabis may be readily whereas ‘apple-shaped’ patients with a greater waist : hip ratio
apparent. Stale urine and anaerobic skin infections also produce have an increased risk of coronary artery disease and the
distinctive smells. Halitosis (bad breath) can be due to poor ‘metabolic syndrome’.
dental hygiene, gingivitis, stomatitis, atrophic rhinitis, tumours
of the nasal passages or suppurative lung conditions such as Weight loss
lung abscess or bronchiectasis. Weight loss or malnutrition (p. 94) may be due to inadequate
Other characteristic odours include: energy consumption or utilisation (such as malabsorption,
anorexia, glycosuria) or to conditions in which nutritional demand
acetone in diabetic ketoacidosis or starvation is increased (such as fever, infection, thyrotoxicosis, malignancy,
surgery). Psychiatric disease and alcohol or drug dependency
amine dimethylsulphide in patients with liver failure may also result in weight loss. Useful markers of malnutrition
include arm muscle circumference and grip strength. Malnutrition
uraemia may also be associated with biochemical and physical evidence
of hypoproteinaemia and/or vitamin deficiencies. Malnutrition
obstruction lengthens recovery time from illness and surgery, and delays
wound healing.
Stature
Body habitus and nutrition
Short stature
Weight Short stature may reflect general nutritional state or significant
illness during childhood, although it may be familial (ask about
Weight is an important indicator of general health and nutrition, the height of the patient’s parents and siblings; p. 310). Loss of
and serial weight measurements can be useful in monitoring height is part of normal ageing but is accentuated by compression
30 GENERAL ASPECTS OF EXAMINATION
A C
B D
Fig. 3.21 Marfan’s syndrome, an autosomal dominant condition. A Tall stature, with the torso shorter than the legs (note surgery for aortic
dissection). B Long fingers. C High-arched palate. D Dislocation of the lens in the eye. (A–D) From Forbes CD, Jackson WF. Color Atlas of Clinical
Medicine. 3rd edn. Edinburgh: Mosby; 2003.
31
Fig. 3.22 Swollen right leg, suggesting deep vein thrombosis or Size Pulsation, thrills and bruits
inflammation. Causes include soft tissue infection or a ruptured Position Inflammation:
Baker’s cyst. Attachments Redness
Consistency Tenderness
Edge Warmth
Surface and shape Transillumination
Inflammatory causes
Any cause of tissue inflammation, including infection or injury,
liberates mediators such as histamine, bradykinin and cytokines,
which cause vasodilatation and increase capillary permeability.
Inflammatory oedema is accompanied by the other features of
inflammation (redness, tenderness and warmth) and is therefore
painful.
Allergic causes
Increased capillary permeability occurs in acute allergic conditions:
for example, an insect bite in an allergic individual. The affected
area is usually red and pruritic (itchy) because of local release
of histamine and other inflammatory mediators but, in contrast
to inflammation, is not painful.
Angio-oedema is a severe form of allergic oedema affecting
the face, lips and mouth, most commonly caused by insect bites,
Fig. 3.23 Lymphoedema of the right arm following right-sided food allergy or drug reactions (Fig. 3.24). Swelling may develop
mastectomy and radiotherapy. rapidly and become life-threatening if the upper airway is involved.
Size Inflammation
Measure the size of any lump (preferably using callipers). Redness, tenderness and warmth suggest inflammation:
Position
lesions is usually red due to vasodilatation. In haematomas
The source of some lumps may be obvious from position, such the pigment from extravasated blood may produce the
as in the breast, thyroid or parotid gland; in other sites, such range of colours in a bruise (ecchymosis).
as the abdomen, this is less clear. Multiple lumps may occur in
neurofibromatosis (see Fig. 3.20), skin metastases, lipomatosis abscesses are usually tender or painful, while non-inflamed
and lymphomas. swellings such as lipomas, skin metastases and
Attachment neurofibromas are characteristically painless.
Malignant masses commonly infiltrate adjacent tissues, causing
especially if rapidly growing, may feel warm due to
them to feel fixed and immobile.
increased blood flow.
Lymphatic obstruction may cause skin swelling with fine
dimpling where the skin is tethered by hair follicles, giving it an
Transillumination
‘orange peel’ appearance (peau d’orange; see Fig. 11.5). This
is common in malignant disease when attachment to deeper In a darkened room, press the lighted end of a pen torch on to
structures, such as underlying muscle, may also occur. one side of the swelling. A cystic swelling, such as a testicular
hydrocoele, will light up if the fluid is translucent, providing the
Consistency covering tissues are not too thick (see Fig. 15.9).
The consistency of a lump can vary from soft to ‘stony’ hard.
Very hard swellings are usually malignant, calcified or dense
fibrous tissue. Fluctuation indicates the presence of fluid, as in Examination sequence
an abscess, cyst or blister (Fig. 3.25), or in soft, encapsulated
tumours, such as lipoma. Inspect the lump, noting any change in the colour or
texture of the overlying skin.
Edge Define the site and shape of the lump.
The margin may be well delineated or ill defined, regular or Measure its size and record the findings diagrammatically.
irregular, and sharp or rounded. The margins of enlarged organs, Gently palpate for tenderness or change in skin
such as the thyroid gland, liver, spleen or kidney, can usually temperature.
be defined more clearly than those of inflammatory or malignant Feel the lump for a few seconds to determine if it is
masses. An indefinite margin suggests infiltrating malignancy, in pulsatile.
contrast to the clearly defined edge of a benign tumour. Assess the consistency, surface texture and margins of
the lump.
Surface and shape
Try to pick up an overlying fold of skin to assess whether
The surface and shape of a swelling can be characteristic. In the lump is fixed to the skin.
the abdomen, examples include an enlarged spleen or liver, Try to move the lump in different planes relative to the
a distended bladder or the uterine fundus in pregnancy. The surrounding tissues to see if it is fixed to deeper
surface may be smooth or irregular: for example, the surface structures.
of the liver is smooth in acute hepatitis but is often nodular in Compress the lump on one side; see and feel if a bulge
metastatic disease. occurs on the opposite side (fluctuation). Confirm the
Pulsations, thrills and bruits fluctuation in two planes. Fluctuation usually indicates that
the lump contains fluid, although some soft lipomas can
Arterial swellings (aneurysms) and highly vascular tumours are
feel fluctuant.
pulsatile, expanding in time with the arterial pulse. Other swellings
Auscultate for vascular bruits.
may transmit pulsation if they lie over a major blood vessel. If the
Transilluminate.
blood flow through a lump is increased, a systolic murmur (bruit)
may be auscultated; occasionally, with sufficient flow, a thrill may Lymph nodes
be palpable. Bruits are also heard over arterial aneurysms and
arteriovenous malformations due to turbulent flow. Palpable lymphadenopathy (enlarged peripheral lymph nodes)
may be local or generalised, and is of diagnostic and prognostic
significance in the staging of lymphoproliferative and other
malignancies. Lymph nodes may also be palpable in normal
people, especially in the submandibular, axilla and groin regions
(Fig. 3.26).
As with any lump, note the size and position of the nodes
(normal nodes in adults are < 0.5 cm in diameter) and assess
fixation to deeper structures (lymph nodes fixed to deep structures
or skin suggest malignancy). Assess consistency: normal nodes
feel soft. In Hodgkin’s lymphoma, they are characteristically
‘rubbery’, in tuberculosis they may be ‘matted’, and in metastatic
cancer they feel hard. Acute viral or bacterial infection, including
infectious mononucleosis, dental sepsis and tonsillitis, causes
Fig. 3.25 Blister on a leg. tender, variably enlarged lymph nodes.
33
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/+1*.&#+&2%3&#,3$%&
0,,#)#*%$
4+51#$$%& !"#$$%&' 3
63).&#+&2,.&7#,%$
/+1*.&#+&2,.&7#,%$
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1*.&5+,$.#:+;%1*+#:< ()#*&+,-$.%&
63)&%,$%7#,3$%&
63=;%"#$$%&'
63=;.5*%$
>&+;2$+?.&2%=:+;.5
=.$+?23;=#$#,31
/+1*.&#+&27#.?2+E2@5..
>&+;2=3**+,@2%5:2=%,@
/+)$#*.%$
A+&#B+5*%$2C&+3)
D.&*#,%$2C&+3)
>&+;2$+?.&2$#;=
>&+;21@#52+E2).5#1F21,&+*3;F
)..3;F2$+?.&27%C#5%F
73$7%F2%531
Fig. 3.26 Distribution of palpable lymph glands.
A B C
Fig. 3.27 Palpation of the cervical glands. A Examine the glands of the anterior triangle from behind, using both hands. B Examine for the scalene
nodes from behind with your index finger in the angle between the sternocleidomastoid muscle and the clavicle. C Examine the glands in the posterior
triangle from the front.
A B C
Fig. 3.28 Palpation of the axillary, epitrochlear and inguinal glands. A Examination for right axillary lymphadenopathy. B Examination of the left
epitrochlear glands. C Examination of the left inguinal glands.
Spot diagnoses
Several disorders have characteristic physical or facial features
(Box 3.9) that allow a diagnosis to be made by observation
alone. These conditions, together with those that have a
more generalised distinctive physical phenotype, are often
over-represented in candidate assessments, where they are
referred to as ‘spot diagnoses’.
Osteogenesis imperfecta is an autosomal dominant condition
causing fragile and brittle bones; the sclerae (Fig. 3.30A) are blue
due to abnormal collagen formation. Hereditary haemorrhagic
telangiectasia is an autosomal dominant condition associated
with small, dilated capillaries or terminal arteries (telangiectasia),
most commonly on the lips and tongue (Fig. 3.30B). In systemic
Fig. 3.29 Petechiae. sclerosis the skin is thickened and tight, causing loss of the normal
wrinkles and skin folds, ‘beaking’ of the nose, and narrowing
and puckering of the mouth (Fig. 3.30C). Myotonic dystrophy,
the submandibular nodes are involved. If the lymphadenopathy is mentioned previously in the context of delayed relaxation of
non-tender, look for a malignant cause, tuberculosis or features grip after a handshake, is an autosomal dominant condition
of human immunodeficiency virus (HIV) infection. Generalised with characteristic features of frontal balding and bilateral ptosis
lymphadenopathy occurs in a number of conditions, including (Fig. 3.30D).
lymphoma, tuberculosis, HIV and systemic inflammatory disorders
such as sarcoidosis. Examine for enlargement of the liver and Major chromosomal abnormalities
spleen, and for other haematological features such as purpura
(bruising under the skin), which can be large (ecchymoses) or There are several genetic or chromosomal syndromes that are
pinpoint (petechiae; Fig. 3.29). easily identified on first contact with the patient.
35
A C
D
Fig. 3.30 Characteristic facial features of some disorders. A Blue sclerae of osteogenesis imperfecta. B Telangiectasia around the mouth, typical of
hereditary haemorrhagic telangiectasia. C Systemic sclerosis with ‘beaking’ of the nose and taut skin around the mouth. D Myotonic dystrophy with
frontal balding and bilateral ptosis.
36 GENERAL ASPECTS OF EXAMINATION
Fig. 3.32 Turner’s syndrome. From Henry M. Seidel, Jane Ball, Joyce
Dain, G. William Benedict. Growth and measurement. In: Mosby’s Guide to
Physical Examination, 6e; 2006.
Section 2
System-based examination
4 The cardiovascular system 39
5 The respiratory system 75
6 The gastrointestinal system 93
7 The nervous system 119
8 The visual system 151
9 The ear, nose and throat 171
10 The endocrine system 193
11 The reproductive system 211
12 The renal system 237
13 The musculoskeletal system 251
14 The skin, hair and nails 283
Nicholas L Mills
Alan G Japp
Jennifer Robson
4
The cardiovascular system
Heart 40 The history 64
Anatomy and physiology 40 Common presenting symptoms 64
Past medical history 67
The history 40
Drug history 67
Common presenting symptoms 40
Family history 67
Past medical history 44
Social history 67
Drug history 44
Family history 45 The physical examination 67
Social history 45 Investigations 69
The physical examination 45 Peripheral venous system 70
General examination 46 Anatomy and physiology 70
Arterial pulses 47
The history 70
Blood pressure 49
Common presenting symptoms 70
Jugular venous pressure and waveform 52
Precordium 53 The physical examination 72
Interpretation of the findings 61 Investigations 73
Investigations 61 OSCE example 1: Chest pain history 73
Peripheral arterial system 64 OSCE example 2: Cardiac examination 74
Anatomy and physiology 64 Integrated examination sequence for the cardiovascular system 74
40 THE CARDIOVASCULAR SYSTEM
HEART
ventricles. The pulmonary valve on the right side of the heart
Anatomy and physiology and the aortic valve on the left separate the ventricles from the
pulmonary and systemic arterial systems, respectively. Cardiac
The heart comprises two muscular pumps working in series, contraction is coordinated by specialised groups of cells. The
covered in a serous sac (pericardium) that allows free movement cells in the sinoatrial node normally act as the cardiac pacemaker.
with each heart beat and respiration (Fig. 4.1). The right heart Subsequent spread of impulses through the heart ensures that
(right atrium and ventricle) pumps deoxygenated blood returning atrial contraction is complete before ventricular contraction
from the systemic veins into the pulmonary circulation at relatively (systole) begins. At the end of systole the ventricles relax and
low pressures. The left heart (left atrium and ventricle) receives the atrioventricular valves open, allowing them to refill with blood
blood from the lungs and pumps it round the body to the tissues from the atria (diastole).
at higher pressures (Fig. 4.2). Atrioventricular valves (tricuspid
on the right side, mitral on the left) separate the atria from the
The history
90–140
60–90 4.1 Common symptoms of heart disease
70–105
Symptom Cardiovascular causes Other causes
15–30 Chest Myocardial infarction Oesophageal spasm
8–15 discomfort Angina Pneumothorax
10–20 Pericarditis Musculoskeletal pain
Aortic dissection
Breathlessness Heart failure Respiratory disease
Valvular disease Anaemia
0–8 Angina Obesity
Pulmonary embolism Anxiety
4–12
Pulmonary hypertension
Palpitation Tachyarrhythmias Anxiety
Ectopic beats Hyperthyroidism
Drugs
15–30 Syncope/ Arrhythmias Simple faints
0–5 presyncope Postural hypotension Epilepsy
90–140 Aortic stenosis Anxiety
4–12 Hypertrophic
cardiomyopathy
Atrial myxoma
Oedema Heart failure Nephrotic syndrome
Constrictive pericarditis Liver disease
Fig. 4.2 Normal resting pressures (mmHg) in the heart and great Venous stasis Drugs
vessels. dias., diastolic; LA, left atrium; LV, left ventricle; PA, pulmonary Lymphoedema Immobility
artery; RA, right atrium; RV, right ventricle; sys., systolic.
41
a large meal or while carrying a heavy load; the pain is promptly of chest pain episodes that may occur on minimal exertion or
relieved by rest and/or sublingual glyceryl nitrate (GTN) spray, and at rest. It may be difficult to distinguish between angina and
typically lasts for less than 10 minutes. The degree of physical non-cardiac causes of episodic chest pain, such as oesophageal
exertion required to precipitate symptoms is a better guide to pain or musculoskeletal problems (Box 4.3). The latter may occur
disease severity than the intensity of discomfort (Box 4.2). In at any site over the chest, often vary with posture or specific
unstable angina (caused by a sudden severe narrowing in a movements (such as twisting or turning), and may be associated
coronary artery), there is usually an abrupt onset or worsening with tenderness to palpation. 4
Ask about:
stabbing in character, exacerbated by inspiration or lying down, and arrhythmias. Patients with acute heart failure and pulmonary
and relieved by sitting forwards. It is caused by inflammation of oedema (accumulation of fluid in the alveoli) usually prefer to
the pericardium secondary to viral infection, connective tissue be upright, while patients with massive pulmonary embolism
disease or myocardial infarction, or after surgery, catheter ablation are often more comfortable lying flat and may faint (syncope) if
or radiotherapy. made to sit upright.
Aortic dissection (a tear in the intima of the aorta) is usually Exertional dyspnoea is the symptomatic hallmark of chronic
associated with abrupt onset of very severe, tearing chest pain heart failure. The New York Heart Association grading system is
that can radiate to the back (typically the interscapular region) used to assess the degree of symptomatic limitation caused by
and may be associated with profound autonomic stimulation. the exertional breathlessness of heart failure (Box 4.5). Dyspnoea
If the tear involves the cranial or upper limb arteries, there may caused by myocardial ischaemia is known as ‘angina equivalent’.
be associated syncope, stroke or upper limb pulse asymmetry. It may occur instead of, or with, chest discomfort, especially in
Predisposing factors include hypertension and connective tissue patients who are elderly or who have diabetes. It has identical
disorders, such as Marfan’s syndrome (see Fig. 3.21A–D). precipitants to angina and may be relieved by GTN.
As with intermittent chest pain, explore the characteristics of Orthopnoea, dyspnoea on lying flat, may occur in patients
the pain, and ask specifically about associated symptoms that with heart failure, where it signifies advanced disease or incipient
may guide you to a likely diagnosis, such as interscapular pain, decompensation. Lying flat increases venous return and in patients
sweating, nausea, vomiting, syncope or neurological features with left ventricular impairment may precipitate pulmonary oedema.
(Box 4.3). The severity can be graded by the number of pillows used
at night: ‘three-pillow orthopnoea’, for example. Paroxysmal
Dyspnoea (breathlessness) nocturnal dyspnoea is caused by the same mechanism, resulting
in sudden breathlessness that wakes the patient from sleep (Fig.
Heart failure is the most common cardiovascular cause of both
4.3). Patients may choke or gasp for air, sit on the edge of the
acute and chronic dyspnoea (Box 4.4). Other cardiovascular
bed and open windows in an attempt to relieve their distress. It
causes of acute breathlessness include pulmonary embolism
may be confused with asthma, which can also cause night-time
dyspnoea, chest tightness, cough and wheeze, but patients with
heart failure may also produce frothy white or blood-stained
sputum.
4.4 Some mechanisms and causes of heart failure
Mechanism Cause
4.5 New York Heart Association classification of heart
Reduced ventricular Myocardial infarction failure symptom severity
contractility (systolic Dilated cardiomyopathy, e.g. genetic,
dysfunction) idiopathic, alcohol excess, cytotoxic drugs, Class Description
peripartum cardiomyopathy I No limitations. Ordinary physical activity does not cause
Myocarditis undue fatigue, dyspnoea or palpitation (asymptomatic left
Impaired ventricular Left ventricular hypertrophy ventricular dysfunction)
filling (diastolic Constrictive pericarditis II Slight limitation of physical activity. Such patients are
dysfunction) Hypertrophic or restrictive cardiomyopathy comfortable at rest. Ordinary physical activity results in
Increased metabolic and Thyrotoxicosis fatigue, palpitation, dyspnoea or angina pectoris
cardiac demand (rare) Arteriovenous fistulae (symptomatically ‘mild’ heart failure)
Paget’s disease III Marked limitation of physical activity. Less than ordinary
Valvular or congenital Mitral and/or aortic valve disease physical activity will lead to symptoms (symptomatically
lesions Tricuspid and/or pulmonary valve disease ‘moderate’ heart failure)
(rare) IV Symptoms of congestive heart failure are present, even at
Ventricular septal defect rest. With any physical activity, increased discomfort is
Patent ductus arteriosus experienced (symptomatically ‘severe’ heart failure)
In acute dyspnoea, ask about: beats’, sometimes followed by a particularly strong heart beat
(‘jolt’ or ‘thump’).
Supraventricular tachycardia produces sudden paroxysms
exercise tolerance of rapid, regular palpitation that can sometimes be terminated
with vagal stimulation using Valsalva breathing manœuvres or
respiratory symptoms (such as cough, sputum, wheeze or carotid sinus pressure. It often affects young patients with no
haemoptysis; p. 79). other underlying cardiac disease. Ventricular tachycardia can 4
produce similar symptoms but is more commonly associated
In patients with chronic symptoms, ask about:
with presyncope or syncope, and tends to affect patients with
cardiomyopathy or previous myocardial infarction.
High-risk features that increase the likelihood of a life-threatening
on everyday activities
arrhythmia such as ventricular tachycardia include:
nocturnal breathlessness
sputum.
laid flat to aid cerebral circulation the individual wakes up, often infective endocarditis, such as skin infection, recent dental
flushing from vasodilatation and nauseated or even vomiting due work, intravenous drug use or penetrating trauma
to vagal overactivity. If the person is held upright by misguided
bystanders, continued cerebral hypoperfusion delays recovery as connective tissue diseases (pericarditis and Raynaud’s
and may lead to a seizure and a mistaken diagnosis of epilepsy. phenomenon), Marfan’s syndrome (aortic dissection) and
In patients with hypersensitive carotid sinus syndrome, pressure myotonic dystrophy (atrioventricular block).
over the carotid sinus may lead to reflex bradycardia and syncope.
Arrhythmias can cause syncope or presyncope. The most
common cause is bradyarrhythmia caused by sinoatrial disease Drug history
or atrioventricular block: Stokes–Adams attacks. Rate-limiting
drugs are a common cause of bradyarrhythmia. Supraventricular Drugs may cause or aggravate symptoms such as breathlessness,
tachyarrhythmias, like atrial fibrillation, rarely cause syncope chest pain, oedema, palpitation or syncope (see Box 4.7). Ask
whereas ventricular tachycardia often causes syncope or about ‘over-the-counter’ purchases, such as non-steroidal
presyncope, especially in patients with impaired left ventricular anti-inflammatory drugs (NSAIDs) and alternative and herbal
function. medicines, as these may have cardiovascular actions.
45
A B C
Fig. 4.4 Cardiac sources of systemic embolism: echocardiographic images. A A large apical thrombus in the left ventricle (arrow). B An atrial
myxoma attached to the interatrial septum (arrow). C A vegetation on the mitral valve (arrow) in infective endocarditis. Because all of these lesions are
located within the left side of the heart, emboli would flow to the systemic (or coronary) circulation. Conversely, emboli from the right side of the heart
would flow to the pulmonary circulation.
Hands
Examination sequence
Feel the temperature of the hands and measure capillary
refill time (p. 343).
Examine the hands for tobacco staining (see Fig. 5.8), skin
crease pallor (anaemia) or peripheral cyanosis.
Look at the nails for finger clubbing (p. 24) and for splinter
haemorrhages: linear, reddish-brown marks along the axis
of the fingernails and toenails (Fig. 4.5B).
C E
Fig. 4.5 Peripheral signs that may be present in infective
endocarditis. A Janeway lesions on the hypothenar eminence (arrows).
B Splinter haemorrhages. C Osler’s nodes. D Roth’s spot on
C
fundoscopy. E Petechial haemorrhages on the conjunctiva. (B and E)
From Walker BR, Colledge NR, Ralston SR, Penman ID, eds. Davidson’s Fig. 4.6 Features of hyperlipidaemia. A Xanthelasmata. B Tendon
Principles and Practice of Medicine. 22nd edn. Edinburgh: Churchill xanthomata. C Corneal arcus. (B) From Swartz M. Textbook of Physical
Livingstone; 2014. (D) From Forbes CD, Jackson WF. Color Atlas of Clinical Diagnosis. 6th edn. Philadelphia: Saunders; 2009. (C) From Kanski J.
Medicine. 3rd edn. Edinburgh: Mosby; 2003. Clinical Diagnosis in Ophthalmology. London: Mosby; 2006.
47
A B C D
Fig. 4.7 The radial, brachial and carotid pulses. A Locating and palpating the radial pulse. B Feeling for a collapsing radial pulse. C Assessing the
brachial pulse. D Locating the right carotid pulse with the fingers.
48 THE CARDIOVASCULAR SYSTEM
Sinus rhythm
4.9 Causes of abnormal pulse rate or rhythm
Abnormality Sinus rhythm Arrhythmia
Fast rate Exercise Atrial fibrillation
(tachycardia, Pain Atrial flutter
> 100 bpm) Excitement/anxiety Supraventricular
Fever tachycardia A
Hyperthyroidism Ventricular tachycardia Ventricular ectopic beat
Medication:
Sympathomimetics,
e.g. salbutamol
Vasodilators
Slow rate Sleep Carotid sinus
(bradycardia, Athletic training hypersensitivity
< 60 bpm) Hypothyroidism Sick sinus syndrome B
Medication: Second-degree heart block Atrial fibrillation
Beta-blockers Complete heart block
Digoxin
Verapamil, diltiazem
Irregular Sinus arrhythmia Atrial fibrillation
pulse Atrial extrasystoles Atrial flutter with variable
Ventricular response
extrasystoles Second-degree heart block C
with variable response Atrial flutter
E
4.11 Common causes of atrial fibrillation Fig. 4.8 Electrocardiogram rhythm strips. A Sinus rhythm.
B Ventricular ectopic beat. C Atrial fibrillation with ‘controlled’ ventricular
Hypertension Mitral valve disease response. D Atrial flutter: note the regular ‘saw-toothed’ atrial flutter
Heart failure Infection, e.g. respiratory, waves at about 300/min. E Ventricular tachycardia, with a ventricular rate
Myocardial infarction urinary of about 200/min.
Thyrotoxicosis Following surgery, especially
Alcohol-related heart disease cardiothoracic surgery
filling) explains why the pulse volume varies and there may be
a pulse deficit, with some cycles not felt at the radial artery.
The pulse deficit can be calculated by counting the radial pulse
The most common cause of tachycardia is sinus tachycardia
rate and subtracting this from the apical heart rate, assessed
(Box 4.9).
by auscultation.
The pulse may be regular or irregular (Box 4.9). Sinus rhythm
is regular (Fig. 4.8A) but heart rate varies with the respiratory
Volume and character
cycle, particularly in children, young adults or athletes (sinus
arrhythmia). During inspiration, parasympathetic tone falls and the The ventricles fill during diastole. Longer diastolic intervals are
heart rate increases; on expiration, the heart rate decreases (Box associated with increased stroke volume, which is reflected by
increased pulse volume on examination. Abnormalities of pulse
atrioventricular block, there may be an underlying regularity to volume and character are highly subjective, however, and tend
the pulse, interspersed with periods of irregularity (sometimes to have poor interobserver agreement.
referred to as ‘regularly irregular’). In atrial fibrillation the pulse A large pulse volume is a reflection of a large pulse pressure,
has no appreciable pattern and is often described as ‘irregularly which can be physiological or pathological (Box 4.12).
irregular’ (Fig. 4.8C and Box 4.11). The rate in atrial fibrillation Low pulse volume may result from severe heart failure and
depends on the number of beats conducted by the atrioventricular conditions associated with inadequate ventricular filling such as
node. Untreated, the ventricular rate may be very fast (up to hypovolaemia, cardiac tamponade and mitral stenosis. Asymmetric
200 bpm). The variability of the pulse rate (and therefore ventricular pulses may represent occlusive peripheral arterial disease or
49
200
Aortic regurgitation
Normal carotid pulse
Aortic stenosis
150
4
mmHg
100
50
Fig. 4.9 Coarctation of the aorta. Magnetic resonance image showing
the typical site of aortic coarctation, just distal to the origin of the left
subclavian artery (arrow). This explains why there is synchrony of the radial
pulses but radiofemoral delay. 0
0 100 200 300 400
Milliseconds
Fig. 4.10 Pulse waveforms.
4.12 Causes of increased pulse volume
Physiological
Exercise Increased environmental of these signs are rare, however, and of limited relevance in
Pregnancy temperature contemporary practice.
Advanced age Pulsus paradoxus is an exaggeration of the normal variability of
Pathological pulse volume with breathing. Pulse volume normally increases in
expiration and decreases during inspiration due to intrathoracic
Hypertension Aortic regurgitation
pressure changes affecting venous return to the heart. This
Fever Paget’s disease of bone
Thyrotoxicosis Peripheral atrioventricular variability is exaggerated when ventricular diastolic filling is
Anaemia shunt impeded by elevated intrapericardial pressure. This is usually
due to accumulation of pericardial fluid (cardiac tamponade; Fig.
4.11) but can occur to a lesser extent with pericardial constriction
and in acute severe asthma. If suspected, pulsus paradoxus
stenosis and, rarely, aortic dissection. Coarctation is a congenital can be confirmed using a blood pressure cuff (see later and Fig.
narrowing of the aorta, usually distal to the left subclavian artery 4.12); a fall of > 10 mmHg between the cuff pressure at which
(Fig. 4.9); it may produce reduced-volume lower limb pulses, which Korotkoff sounds appear in expiration only and the cuff pressure
are also delayed relative to the upper limb pulses (radiofemoral at which Korotkoff sounds persist throughout the respiratory
delay). In adults, coarctation usually presents with hypertension cycle is diagnostic.
and heart failure.
A slow-rising pulse has a gradual upstroke with a reduced Blood pressure
peak occurring late in systole, and is a feature of severe aortic
stenosis (Fig. 4.10). Blood pressure (BP) is a measure of the pressure that the
A collapsing pulse may occur with severe aortic regurgitation. circulating blood exerts against the arterial walls. Systolic pressure
The peak of the pulse wave arrives early and is followed by a is the maximal pressure that occurs during ventricular contraction
rapid fall in pressure (Fig. 4.10) as blood flows back into the left (systole). During ventricular filling (diastole), arterial pressure is
ventricle, resulting in a wide pulse pressure (systolic − diastolic maintained at a lower level by the elasticity and compliance of
blood pressure > 80 mmHg). This rapid fall imparts the ‘collapsing’ the vessel wall. The lowest value (diastolic pressure) occurs
sensation, and is exaggerated by raising the patient’s arm above immediately before the next cycle.
the level of the heart (see Fig. 4.7B). BP is usually measured using a sphygmomanometer (Fig.
Pulsus bisferiens, an increased pulse with a double systolic 4.12). In certain situations, such as the intensive care unit, it is
peak separated by a distinct mid-systolic dip, is classically measured invasively using an indwelling intra-arterial catheter
produced by concomitant aortic stenosis and regurgitation. connected to a pressure sensor.
Pulsus alternans, beat-to-beat variation in pulse volume with BP is measured in mmHg and recorded as systolic pressure/
a normal rhythm, may occur in advanced heart failure. Both diastolic pressure, together with a note of where and how the
50 THE CARDIOVASCULAR SYSTEM
B C
Fig. 4.11 Clinical and echocardiographic features of cardiac tamponade. A and B Echocardiographic images taken from the subcostal position at
the onset of systole (A) and in early diastole (B). The right ventricle (arrows) is collapsed in the early phase of diastole due to the elevated intrapericardial
pressure; this is an important echo finding in tamponade. In both images there is a large pericardial effusion adjacent to the right ventricle. C Clinical
features. JVP, jugular venous pressure.
Hypertension
reading was taken: for example, BP 146/92 mmHg, right arm,
supine. Although any threshold for distinguishing abnormal elevation of
BP provides vital information on the haemodynamic condition BP from normal BP is somewhat arbitrary, hypertension is widely
of acutely ill or injured patients. Over the longer term it is also defined as a systolic pressure of ≥140 mmHg and/or a diastolic
an important guide to cardiovascular risk. BP constantly varies pressure ≥90 mmHg (Box 4.13). Hypertension is associated with
significant morbidity and mortality from vascular disease (heart
coat hypertension’ refers to a transient increase in BP caused failure, coronary artery disease, cerebrovascular disease and
by the stress of being in a healthcare setting. Ambulatory chronic kidney disease). It is almost invariably asymptomatic,
51
Jugular
venous
pressure
A B C
Fig. 4.14 Jugular venous pressure in a healthy subject. A Supine: jugular vein distended, pulsation not visible. B Reclining at 45 degrees: the point
of transition between the distended and the collapsed vein can usually be seen to pulsate just above the clavicle. C Upright: the upper part of vein is
collapsed and the transition point obscured.
53
Precordium
The precordium is the anterior chest surface overlying the heart
and great vessels (Fig. 4.16).
Learn the surface anatomy and basic physiology of the heart
to understand the basis and timing of the heart sounds and
murmurs, and why they are heard best in different locations
and radiate in a particular direction (Figs 4.16 and 4.17). The
Fig. 4.15 Jugular venous pressure. A Inspecting the jugular venous optimal sites for auscultation (aortic, pulmonary, apex and left
pressure from the side (the internal jugular vein lies deep to the sternal border) do not correspond with the location of cardiac
sternocleidomastoid muscle). B Measuring the height of the jugular structures but are where the transmitted sounds and murmurs
venous pressure. C Form of the venous pulse wave tracing from the are best heard (Box 4.17). It is important to note that the heart
internal jugular vein: a, atrial systole; c, closure of the tricuspid valve; sounds and some murmurs can be heard widely across the
v, peak pressure in the right atrium immediately prior to opening of the precordium, but these sites represent the surface location where
tricuspid valve; a–x, descent, due to downward displacement of the the murmur is loudest or easiest to hear.
tricuspid ring during systole; v–y, descent at the commencement of
ventricular filling. Inspection
The JVP provides a guide to central venous pressure. It is Pectus excavatum (funnel chest; see Fig. 5.6D), a posterior
elevated in states of fluid overload, particularly heart failure. displacement of the lower sternum, and pectus carinatum (pigeon
Examine the patient for pulmonary oedema or pleural effusions chest; see Fig. 5.6C) may displace the heart and affect palpation
(p. 88), ascites (p. 109) and/or peripheral oedema (p. 245). It is and auscultation.
also elevated in any condition that leads to high right ventricular A midline sternotomy scar usually indicates previous valve
filling pressures, such as pulmonary embolism, chronic pulmonary replacement or coronary artery bypass surgery, in which case
54 THE CARDIOVASCULAR SYSTEM
Examination sequence
MCL Explain that you wish to examine the chest and ask the
patient to remove all clothing above the waist. Keep a
female patient’s chest covered with a sheet as far as
possible.
A P Inspect the precordium with the patient sitting at a
45-degree angle with shoulders horizontal. Look for
surgical scars, visible pulsations and chest deformity.
Place your right hand flat over the precordium to obtain a
T general impression of the cardiac impulse (Fig. 4.18A).
M Locate the apex beat by laying your fingers on the chest
parallel to the rib spaces; if you cannot feel it, ask the
patient to roll on to their left side (Fig. 4.18B).
Assess the character of the apex beat and note its
position.
Apply the heel of your right hand firmly to the left
Fig. 4.17 Sites for auscultation. Sites at which murmurs from the parasternal area and feel for a right ventricle heave. Ask
relevant valves are usually, but not preferentially, heard. A, aortic;
the patient to hold their breath in expiration (Fig. 4.18C).
M, mitral; MCL, mid-clavicular line; P, pulmonary; T, tricuspid.
Palpate for thrills at the apex and on both sides of the
sternum using the flat of your fingers.
A normal apical impulse briefly lifts your fingers and is localised.
it may be accompanied by saphenous vein or radial artery graft
There should be no parasternal heave or thrill. The apex beat
harvest scars. A left submammary scar is usually the result of mitral
may be impalpable in overweight or muscular people, or in
valvotomy or transapical transcatheter aortic valve implantation.
patients with asthma or emphysema because the lungs are
Infraclavicular scars are seen after pacemaker or defibrillator
hyperinflated. It may be diffusely displaced inferiorly and laterally
implantation, and the bulge of the device may be obvious.
in left ventricular dilatation, such as after myocardial infarction
or in dilated cardiomyopathy, severe aortic regurgitation or
Palpation
decompensated aortic stenosis. In dextrocardia the cardiac apex
The apex beat may be visible on inspection but is defined as the is palpable on the right side but this condition is uncommon,
most lateral and inferior position at which the cardiac impulse can with a prevalence of 1 : 10,000.
55
Left ventricular hypertrophy, as in hypertension or severe aortic Listen over the carotid arteries (ejection systolic murmur of
stenosis, produces a forceful but undisplaced apical impulse. This aortic stenosis and carotid bruits) and in the left axilla
thrusting apical ‘heave’ is quite different from the diffuse impulse (pansystolic murmur of mitral regurgitation).
of left ventricular dilatation. Pulsation over the left parasternal area At each site, identify the S1 and S2 sounds. Assess their
(right ventricular heave) indicates right ventricular hypertrophy or character and intensity; note any splitting of the S2.
dilatation, most often accompanying pulmonary hypertension. Palpate the carotid pulse to time any murmur. The S1
The ‘tapping’ apex beat in mitral stenosis represents a palpable barely precedes the upstroke of the carotid pulsation, 4
first heart sound and is not usually displaced. A double apical while the S2 is clearly out of phase with it.
impulse is characteristic of hypertrophic cardiomyopathy. Concentrate in turn on systole (the interval between S1
The most common thrill is that of aortic stenosis, which is and S2) and diastole (the interval between S2 and S1).
usually palpable over the upper right sternal border. The thrill Listen for added sounds and then for murmurs. Soft
caused by a ventricular septal defect is best felt at the left and diastolic murmurs are sometimes described as the
right sternal edges. Diastolic thrills are very rare. ‘absence of silence’.
Roll the patient on to their left side. Listen at the apex
Auscultation using light pressure with the bell, to detect the
mid-diastolic murmur of mitral stenosis (Fig. 4.19A).
Correct identification and characterisation of the heart sounds
Ask the patient to sit up and lean forwards, then to
and of any added sounds and/or murmurs require a careful,
breathe out fully and hold their breath (Fig. 4.19B). Listen
systematic approach to auscultation.
over the right second intercostal space and over the left
The diaphragm attenuates all frequencies equally, thus making
sternal edge with the diaphragm for the murmur of aortic
some low-frequency sounds less audible. Use the diaphragm
regurgitation.
to identify the first and second heart sounds, and high-pitched
Note the character and intensity of any murmur heard.
sounds such as the early diastolic murmur of aortic regurgitation.
Develop a routine for auscultation so that you do not
Listen with the diaphragm over the whole precordium for a
overlook subtle abnormalities. Identify and describe the
pericardial friction rub.
following:
The bell of the stethoscope transmits all sounds well, but in
the first and second heart sounds (S1 and S2)
patients with high-frequency murmurs additional low-frequency
extra heart sounds (S3 and S4)
sounds may be masked by the high-frequency murmur. The
additional sounds such as clicks and snaps
bell is particularly useful at the apex and left sternal edge to
murmurs in systole and/or diastole (timing,
listen for the diastolic murmur of mitral stenosis and third and
duration, character, pitch, intensity, location and
fourth heart sounds.
radiation)
pericardial rubs.
Examination sequence
Make sure the room is quiet when you auscultate. Your Heart sounds
stethoscope should fit comfortably with the earpieces angled Normal heart valves make a sound only when they close. The
slightly forwards. The tubing should be approximately 25 cm ‘lub-dub’ sounds are caused by closure of the atrioventricular
long and thick enough to reduce external sound. (mitral and tricuspid) valves followed by the outlet (aortic and
Listen with your stethoscope diaphragm at the: pulmonary) valves.
apex
lower left sternal border First heart sound
upper right and left sternal borders. The first heart sound (S1), ‘lub’, is caused by closure of the
Listen with your stethoscope bell at the: mitral and tricuspid valves at the onset of ventricular systole.
apex It is best heard at the apex. In mitral stenosis the intensity of
lower left sternal border. S1 is increased due to elevated left atrial pressure (Box 4.18).
! " #
Fig. 4.18 Palpating the heart. A Use your hand to palpate the cardiac impulse. B Localise the apex beat with your finger (if necessary, roll the patient
into the left lateral position). C Palpate from apex to sternum for parasternal pulsations.
56 THE CARDIOVASCULAR SYSTEM
"
n;
it
!
Fig. 4.19 Auscultating the heart. A Listen for the murmur of mitral
Fig. 4.20 Physiological and pathological splitting of the second heart
stenosis using the bell lightly applied with the patient in the left lateral
sound.
position. B Listen for the murmur of aortic regurgitation using the
diaphragm with the patient leaning forwards.
S1 A2P2
Ejection systolic murmur
Pulmonary valve
(pulmonary flow murmur) with 4
fixed splitting of second sound
LA
Atrial septal defect
RA
Tricuspid valve
S1 S2
Diastolic murmur (tricuspid
flow murmur) in children
Fig. 4.21 Atrial septal defect. LA, left atrium; RA, right atrium.
mechanism is similar to that of an opening snap. Ejection clicks do onset of ventricular systole. Determine whether the
not occur in calcific aortic stenosis because the cusps are rigid. murmur is systolic or diastolic:
Mid-systolic clicks are high-pitched and best heard at the Systole begins with S1 (mitral and tricuspid valve
apex with the diaphragm. They occur in mitral valve prolapse closure). This occurs when left and right ventricular
(Fig. 4.22C) and may be associated with a late systolic murmur. pressures exceed the corresponding atrial pressures.
Mechanical heart valves can make a sound when they close For a short period, all four heart valves are closed
or open. The closure sound is normally louder, especially with (pre-ejection period). Ventricular pressures continue to
modern valves. The sounds are high-pitched, ‘metallic’ and often rise until they exceed those of the aorta and pulmonary
palpable, and may even be heard without a stethoscope. A artery, causing the aortic and pulmonary valves to
mechanical mitral valve replacement makes a metallic S1 and open. Systole ends with the closure of these valves,
a sound like a loud opening snap early in diastole (Fig. 4.22D). producing S2.
Mechanical aortic valves have a loud, metallic S2 and an opening Diastole is the interval between S2 and S1.
sound like an ejection click at the start of systole (Fig. 4.22E). Physiologically, it is divided into three phases: early
They are normally associated with a flow murmur. diastole (isovolumic relaxation), the time from the
Pericardial rub (friction rub) is a coarse scratching sound, often closure of the aortic and pulmonary valves until the
with systolic and diastolic components. It is best heard using opening of the mitral and tricuspid valves; mid-diastole,
the diaphragm with the patient holding their breath in expiration. the early period of ventricular filling when atrial
It may be audible over any part of the precordium but is often pressures exceed ventricular pressures; and presystole,
localised, varying in intensity over time and with the position of coinciding with atrial systole.
the patient. It is most often heard in acute pericarditis or a few Murmurs of aortic and pulmonary regurgitation start in
days after an extensive myocardial infarction. A pleuropericardial early diastole and extend into mid-diastole. The murmurs
rub is a similar sound that occurs in time with the cardiac cycle, of mitral or tricuspid stenosis cannot start before
but is also influenced by respiration and is pleural in origin. mid-diastole. S3 occurs in mid-diastole and S4 in
Occasionally, a ‘crunching’ noise can be heard, caused by gas presystole.
in the pericardium (pneumopericardium).
Duration
Murmurs The murmurs of mitral and tricuspid regurgitation start with
Heart murmurs are produced by turbulent flow across an abnormal S1, sometimes muffling or obscuring it, and continue
valve, septal defect or outflow obstruction. ‘Innocent’ murmurs throughout systole (pansystolic; Fig. 4.23). The murmur
are caused by increased velocity of flow through a normal valve produced by mitral valve prolapse does not begin until the
and occur when stroke volume is increased, as in pregnant mitral valve leaflet has prolapsed during systole, producing
women, athletes with resting bradycardia or patients with fever. a late systolic murmur (Fig. 4.23). The ejection systolic
murmur of aortic or pulmonary stenosis begins after S1
reaches maximal intensity in mid-systole, then fades,
Examination sequence stopping before S2 (Fig. 4.24).
'Straight' left
heart border Apical pansystolic murmur
on chest X-ray radiates to axilla
S1 S2 S3
S1 MSC S2 S3
Fig. 4.23 Mitral regurgitation. Mitral regurgitation is caused by dilatation of the left ventricle and failure of leaflets to co-apt. The murmur begins at the
moment of valve closure and may obscure the first heart sound. It varies little in intensity throughout systole. In mitral valve prolapse the murmur begins in
mid- or late systole and there is often a mid-systolic click (MSC).
59
Aortic dilatation
S1 EC S2
Aortic valve
S4 S1 EC S2
Fig. 4.24 Aortic stenosis. There is a systolic pressure gradient across the stenosed aortic valve. The resultant high-velocity jet impinges on the wall of
the aorta (arrow), and is best heard with the diaphragm in the aortic area. Alternatively, the bell may be placed in the suprasternal notch. The ejection
systolic murmur follows an ejection click (EC).
valve prolapse, regurgitation begins in mid-systole, producing (Fig. 4.25), and is best heard at the left sternal edge with the
a late systolic murmur (see Fig. 4.23). The murmur of tricuspid patient leaning forwards in held expiration. The duration of the
regurgitation is heard at the lower left sternal edge; if significant, aortic regurgitation murmur is inversely proportional to severity.
it is associated with a prominent ‘v’ wave in the JVP and a Since the regurgitant blood must be ejected during the subsequent
pulsatile liver. systolic period, significant aortic regurgitation increases stroke
Ventricular septal defects also cause a pansystolic murmur. volume is usually associated with a systolic flow murmur.
Small congenital defects produce a loud murmur audible at the Pulmonary regurgitation is very uncommon. It may be caused
left sternal border, radiating to the right sternal border and often by pulmonary artery dilatation in pulmonary hypertension (Graham
associated with a thrill. Rupture of the interventricular septum can Steell murmur) or a congenital defect of the pulmonary valve.
complicate myocardial infarction, producing a harsh pansystolic Mid-diastolic murmurs are usually caused by mitral stenosis.
murmur. The differential diagnosis of a murmur heard after This is a low-pitched, rumbling sound that may follow an opening
myocardial infarction includes acute mitral regurgitation due to snap (Fig. 4.26). It is best heard with the bell at the apex and the
papillary muscle rupture, functional mitral regurgitation caused patient positioned on their left side. The murmur is accentuated
by left ventricular dilatation, and a pericardial rub. by exercise. The cadence sounds like ‘lup-ta-ta-rru’; ‘lup’ is the
loud S1, ‘ta-ta’ the S2 and opening snap, and ‘rru’ the mid-diastolic
Diastolic murmurs murmur. If the patient is in sinus rhythm, left atrial contraction
Early diastolic murmurs usually last throughout diastole but are increases the blood flow across the stenosed valve, leading to
loudest in early diastole, so the term ‘early diastolic murmur’ is presystolic accentuation of the murmur. The murmur of tricuspid
misleading. The murmur is typically caused by aortic regurgitation stenosis is similar but rare.
Uncoiled
aorta
Aortic valve
Fig. 4.25 Aortic regurgitation. The pulse pressure is usually increased. The jet from the aortic valve is directed inferiorly towards the left ventricular
outflow tract (arrow) during diastole, producing an early diastolic murmur, best heard with the diaphragm during held expiration with the patient leaning
forward. An associated systolic murmur is common because of the increased flow through the aortic valve in systole.
Left atrium
Mitral valve
S1 Continuous S2
murmur
Left-to-right shunt from 4
aorta to pulmonary artery
Pulmonary artery
shadow may be
enlarged on chest X-ray
Left ventricular
enlargement
Fig. 4.27 Persistent patent ductus arteriosus. A continuous ‘machinery’ murmur is heard because aortic pressure always exceeds pulmonary arterial
pressure, resulting in continuous ductal flow. The pressure difference is greatest in systole, producing a louder systolic component to the murmur.
An Austin Flint murmur is a mid-diastolic murmur that liver function tests performed prior to starting therapies that
accompanies aortic regurgitation. It is caused by the regurgitant may impact on renal function or cause hepatotoxicity. Blood
jet striking the anterior leaflet of the mitral valve, restricting inflow glucose and a lipid profile help identify patients with diabetes
to the left ventricle. mellitus and assess cardiovascular risk. In patients with acute
chest pain, cardiac troponin is measured to determine whether
Continuous murmurs there is myocardial injury or infarction.
Continuous murmurs are rare in adults. The most common cause
is a patent ductus arteriosus. In the fetus this connects the Electrocardiography
upper descending aorta and pulmonary artery, and normally
In performing standard 12-lead electrocardiography (ECG; Fig.
closes just after birth. The murmur is best heard at the upper left
4.28), the patient must be resting supine and relaxed to avoid
sternal border and radiates over the left scapula. Its continuous
muscle tremor. Good contact between the electrode and skin
character is ‘machinery-like’; as aortic pressure always exceeds
is important and it may be necessary to shave the chest. The
pulmonary pressure, there is continuous ductal flow, with the
electrodes must be positioned correctly to obtain recordings
greatest pressure difference in systole, resulting in a louder systolic
made from the six precordial electrodes (V1–V6) and six recordings
component (Fig. 4.27).
from the limb electrodes (left arm, right arm and left leg). The
right leg electrode is used as a reference. Confirm that the
Interpretation of the findings electrocardiograph is calibrated using a 1 mV signal prior to
recording.
Auscultation remains an important clinical skill, despite the Ambulatory ECG monitoring
availability of echocardiography. You must be able to detect Continuous ECG recording over 24–48 hours can be used to
abnormal signs to prompt appropriate investigation. Auscultatory identify symptomatic or asymptomatic rhythm disturbances in
signs, such as S3 or S4 and pericardial friction rubs, have no direct patients with palpitation or syncope. If symptoms are less frequent,
equivalent on echocardiography but do have diagnostic utility. In it may be necessary to use patient-activated recorders that record
addition, some patients, especially those with rheumatic heart the heart rhythm only when the patient is symptomatic; the
disease, have multiple heart valve defects, and the interpretation device is activated by the patient (Fig. 4.29).
of more subtle physical signs may be important. For example, a
patient with mixed mitral stenosis and regurgitation will probably Exercise ECG
have dominant stenosis if the S1 is loud but dominant regurgitation An exercise ECG is useful in the diagnosis and functional
if there is an S3. assessment of patients with suspected coronary artery disease.
Down-sloping ST segment depression, particularly when it occurs
during minor exertion, or ST segment elevation is of prognostic
Investigations significance and helps inform the need for invasive investigation
with coronary angiography.
Haematology and clinical chemistry
Ambulatory blood pressure monitoring
As anaemia can unmask angina or exacerbate heart failure, a full
blood count is useful and helps guide the safe use of antiplatelet A portable device can be worn by the patient at home that takes
therapies and anticoagulants. Measurement of the erythrocyte at least two BP measurements per hour. It is used to confirm the
sedimentation rate and serology are indicated if connective tissue diagnosis of hypertension and provide a more reliable assessment
disease is suspected. Urea and electrolytes are measured and of response to treatment.
62 THE CARDIOVASCULAR SYSTEM
aVR aVL
V6
V5
V1 V2 V3 V4
N aVF
T wave: ventricular
repolarisation
P wave: T
atrial activation
P Q S
* *
Fig. 4.29 Printout from a 24-hour ambulatory electrocardiogram recording, showing complete heart block. Arrows indicate visible P waves. At
times, these are masked by the QRS complex or T wave (*).
63
Chest X-ray of posterior structures such as the left atrium, mitral valve and
descending aorta, and is useful in detecting valvular vegetations
The maximum width of the heart divided by the maximum width in infective endocarditis.
of the thorax on a posteroanterior chest X-ray (the cardiothoracic
ratio) should normally be < 0.5. An increased cardiothoracic ratio Radionuclide studies
is common in valvular heart disease and heart failure. In heart
Technetium-99 is injected intravenously and detected using a
failure this is often accompanied by distension of the upper
lobe pulmonary veins, diffuse shadowing within the lungs due gamma camera to assess left ventricular function. Thallium and 4
to pulmonary oedema, and Kerley B lines (horizontal, engorged sestamibi are taken up by myocardial cells and indicate myocardial
lymphatics at the periphery of the lower lobes; Fig. 4.30A). A perfusion at rest and exercise.
widened mediastinum may indicate a thoracic aneurysm.
Cardiac catheterisation
Echocardiography
A fine catheter is introduced under local anaesthetic via a
Echocardiography uses high-frequency sound waves to evaluate peripheral artery (usually the radial or femoral) and advanced
valve abnormalities, ventricular function and blood flow (Doppler to the heart under X-ray guidance. Although measurements of
echocardiography). Most scans are performed through the intracardiac pressures, and therefore estimates of valvular and
anterior chest wall (transthoracic; Fig. 4.30B). Transoesophageal cardiac function, are possible, the primary application of this
echocardiography requires sedation but gives high resolution technique is imaging of the coronary circulation using contrast
LV
LA
A B
CX
LM
LAD
C D
Fig. 4.30 Cardiovascular imaging. A Chest X-ray in heart failure. This shows cardiomegaly with patchy alveolar shadowing of pulmonary oedema and
Kerley B lines (engorged lymphatics, arrow) at the periphery of both lungs. B Transthoracic echocardiogram in an apical two-chamber view, showing
thinning of the left ventricular apex. This is the site of a recent anterior myocardial infarct. LA, left atrium; LV, left ventricle. C Coronary angiography. The
arrow indicates an abrupt occlusion of the proximal left anterior descending artery. CX, circumflex; LAD, left anterior descending; LM, left main.
D Cardiac magnetic resonance imaging. Gadolinium enhancement image demonstrates regional uptake of gadolinium (white arrows) consistent with
myocardial fibrosis in the territory of the LAD.
64 THE CARDIOVASCULAR SYSTEM
medium. This is performed to inform and guide revascularisation, symptomatic patients at low to intermediate risk of coronary
either by coronary angioplasty or bypass grafting (Fig. 4.30C). artery disease. It can reduce the need for invasive investigation
in patients with a low probability of occlusive coronary disease
Computed tomography and magnetic who require valve surgery. Magnetic resonance imaging (MRI)
resonance imaging provides superior spatial resolution (Fig. 4.30D) and is the imaging
modality of choice for investigating the aetiology of heart muscle
Computed tomography (CT), with its superior temporal resolution
diseases (cardiomyopathy).
of the coronary arteries, is particularly useful for investigating
Popliteal artery
4.22 Fontaine classification of lower limb ischaemia
4.25 Acute limb ischaemia: embolus versus be present and the non-specific nature of symptoms may result in
thrombosis in situ misdiagnosis; the patient may have had numerous investigations,
including laparotomy, before the diagnosis is made.
Embolus Thrombosis
Acute mesenteric ischaemia is a surgical emergency. It is
Onset and Acute (seconds or Insidious (hours or most commonly caused by an embolus from the heart or by
severity minutes), ischaemia days), ischaemia less thrombosis in situ of a pre-existing atherosclerotic plaque in one
profound (no severe (pre-existing
of the mesenteric vessels. It is often hard to diagnose in the early
pre-existing collaterals) collaterals)
stages, as patients typically present initially with severe abdominal
Embolic source Present Absent pain that is out of proportion to often unimpressive abdominal
Previous Absent Present signs. Presentation with severe abdominal pain, shock, bloody
claudication diarrhoea and profound metabolic acidosis indicates infarction
Pulses in Present Often absent, reflecting of the bowel, which carries a high mortality rate. Rarely, renal
contralateral leg widespread peripheral angle pain occurs from renal infarction or ischaemia, and is
arterial disease associated with visible or non-visible haematuria.
Diagnosis Clinical Angiography Any patient suspected of having visceral ischaemia should
undergo urgent CT angiography.
Treatment Embolectomy and Medical, bypass
anticoagulation surgery, catheter- Abdominal aortic aneurysm
directed thrombolysis
Abdominal aortic aneurysm (AAA) is an abnormal focal dilatation
A
A
B
Fig. 4.33 Raynaud’s syndrome. A The acute phase, showing severe
blanching of the tip of one finger. B Raynaud’s syndrome occasionally
progresses to fingertip ulceration or even gangrene. (A and B) From Forbes
B CD, Jackson WF. Color Atlas of Clinical Medicine. 3rd edn. Edinburgh:
Mosby; 2003.
Drug history
Enquire about medication used for secondary prevention and
adherence to these: antiplatelet, lipid-lowering, antihypertensive
and diabetes therapies. Patients may be taking vasoactive drugs
C for claudication (naftidrofuryl or cilostazol, for example), although
their efficacy in this setting is not clear. Enquire about other
Fig. 4.32 Abdominal aortic aneurysm. A Abdominal X-ray showing
cardiac medications, as these may make symptoms of rest
calcification (arrow). B Computed tomogram of the abdomen showing an
abdominal aortic aneurysm (arrow). C At laparotomy the aorta is seen to pain worse through their BP-lowering or negatively inotropic
be grossly and irregularly dilated. effects.
Family history
Stroke Ask about a family history of premature coronary or other vascular
Stroke is a focal neurological deficit that has a vascular cause disease (p. 45). There is a strong familial association for AAAs
and is discussed on page 123. so, where relevant, a family history should be sought.
Buerger’s test
4
Examination sequence
superficial veins.
Ask the patient to sit up and hang their legs over the edge
A
of the bed.
The history
Dorsal
Common presenting symptoms venous arch
A B
Fig. 4.37 Lower limb venous disease. A Varicose veins and associated haemosiderin deposition. B Venous ulcer. (A) From Metcalfe M, Baker D.
Varicose veins. Surgery (Oxford) 2008; 26(1):4–7.
Obesity
Smoking
Recent bed rest or operations (especially to the leg, pelvis or
abdomen)
Recent travel, especially long flights
Previous trauma to the leg, especially long-bone fractures, plaster
of Paris splintage and immobilisation
Pregnancy or features suggesting pelvic disease
Malignant disease
Previous deep vein thrombosis
Family history of thrombosis
Inherited thrombophilia, e.g. factor V Leiden
Recent central venous catheterisation, injection of drug
Use of oral contraceptive or hormone replacement therapy
A
but is contraindicated unless there is documented evidence of
adequate arterial circulation, which is assessed by feeling the
pulses or by measuring the ABPI (see earlier).
Limb swelling
Swelling, or a feeling of swelling, even in the absence of visible
signs, may be associated with lower limb venous disease. Enquire
about risk factors for DVT (Box 4.29).
In upper limb DVT the arm is swollen and the skin is cyanosed
and mottled, especially when dependent. Look for superficial
distended veins (acting as collaterals) in the upper arm, over
the shoulder region and on the anterior chest wall (Fig. 4.38).
Symptoms are often exacerbated by activity, especially when
B
holding the arm overhead.
There may be a history of repetitive trauma at the thoracic Fig. 4.38 Axillary vein thrombosis. A Angiogram. Single arrow
outlet due to vigorous, repetitive exercise (swimming, weight shows site of thrombosis. Double arrows show dilated collateral vessels.
B Clinical appearance with swollen left arm and dilated superficial veins.
lifting, racquet sports). Upper limb DVT may also complicate
indwelling subclavian/jugular venous catheters.
Skin changes
usually associated with other skin changes of chronic venous
Chronic venous insufficiency is often associated with bluish insufficiency (varicose eczema, lipodermatosclerosis).
discoloration of the distal extremity. A range of skin changes
may be observed (see Fig. 4.37A). Varicose eczema leads to red, Superficial venous thrombophlebitis
itchy, dry areas of skin over the lower leg. Venous hypertension
causes extravasation of blood components into surrounding
veins and is more common during pregnancy. Recurrent superficial
tissues, leading to haemosiderin deposition, which is seen as
venous thrombophlebitis, especially that affecting different areas
a brown discoloration of the skin, primarily around the medial
sequentially and non-varicose veins, may be associated with
aspect of the lower third of the leg. Lipodermatosclerosis occurs
underlying malignancy. It may propagate into the deep system,
when there is an inflammatory response to the haemosiderin
leading to DVT and pulmonary embolism.
and causes red/purple discoloration and induration of the skin.
The thickened, fibrotic skin forms a tight band around the lower
leg, giving the appearance of an inverted champagne bottle. In Past history
atrophie blanche, there are multiple, small, white, scarred areas
within the affected skin. Enquire about previous varicose vein surgery and risk factors
for DVT (Box 4.29).
Chronic venous ulceration
primarily due to venous disease. Other causes include pyoderma The physical examination
gangrenosum, syphilis, tuberculosis, leprosy (Hansen’s disease),
sickle cell disease and tropical conditions. Chronic venous
ulceration (see Fig. 4.37B) usually affects the medial aspect
Examination sequence
of the calf. Ulcers are shallow and pink (granulation tissue) or Expose the patient’s legs and examine them with the patient
yellow/green (slough) in colour, with an irregular margin, and are standing and then lying supine.
73
Mr Munro, 82 years old, presents with progressive breathlessness and lightheadedness on exertion.
Please examine his cardiovascular system
Introduce yourself and clean your hands.
Carry out general observations. Is the patient tachypnoeic or distressed at rest? Are his hands cool?
Measure the pulse, blood pressure and jugular venous pressure. Are the pulse volume and systolic pressure reduced? Is the jugular venous
pressure elevated?
Palpate the precordium. Is the apex more forceful or displaced?
Auscultate over the apex and lower left, upper right and upper left sternal borders for the character of the first and second heart sounds, and the
presence and characteristics of any added sounds or murmurs. If a murmur is heard, is there any radiation?
Examine the chest, sacrum and lower limbs for signs of heart failure.
Thank the patient and clean your hands.
Summarise your findings
Mr Munro appears comfortable. His heart rate is 80 bpm with a low-volume, slow-rising pulse. His blood pressure is 110/60 mmHg. The jugular
venous pressure is not raised. There is an apical heave but the apex is not displaced. The first heart sound is normal but the second is diminished.
There is a grade 3 ejection systolic murmur, loudest over the aortic area but heard widely, radiating to the carotids. There are fine end-inspiratory
crackles at the lung bases.
Suggest a likely diagnosis
The likely diagnosis is aortic stenosis with left ventricular decompensation and heart failure.
Suggest initial investigations
Twelve-lead electrocardiogram, chest X-ray and transthoracic echocardiogram.
Position the patient: supine and reclined at 45 degrees, with the head resting on a pillow.
Examine the general appearance:
Is the patient breathless, cyanosed, sweating or distressed?
Note body habitus (overweight or cachectic), Marfanoid features and the presence of radial or saphenous vein harvest scars.
Check the hands, pulse and blood pressure, face and neck:
Hands: colour and temperature, tobacco staining, clubbing, splinter haemorrhages, Janeway lesions or Osler’s nodes, tendon xanthomata.
Pulse: rate, rhythm, character and synchronicity of radial pulse, collapsing pulse, volume and character of brachial or carotid pulse.
Blood pressure: systolic and diastolic pressure at the brachial artery.
Face: central cyanosis, xanthelasmata, corneal arcus, petechiae.
Neck: timing, waveform and abnormalities of the jugular venous pressure, carotid bruits.
Examine the precordium:
Inspection: look for midline sternotomy or left submammary scars, pacemaker site, visible pulsation.
Palpation: define the character and position of the apex beat, parasternal heave, thrills.
Auscultation: listen over the apex, lower left sternal border, upper right and left sternal borders, over the carotid arteries and left axilla. Listen
with the patient on their left side and leaning forward during expiration.
– Heart sounds: identify first and second heart sounds (S1 and S2), and any extra heart sounds (S3 or S4).
– Additional sounds: clicks and snaps.
– Murmurs in systole and/or diastole (timing, duration, character, pitch, intensity, location and radiation).
– Pericardial rub.
Other:
Listen for fine end-inspiratory crackles or pleural effusion at the lung bases.
Examine the abdomen for hepatomegaly or pulsatile liver.
Check for ankle and sacral oedema.
Peripheral arterial and venous system
Inspection of the lower limbs:
Check temperature and colour, capillary refill time, skin discoloration, ulceration, varicosities, scars.
Palpation:
Examine the abdomen for expansile aortic aneurysm.
Identify the femoral, popliteal, posterior tibial and dorsalis pedis pulses.
Identify pitting oedema.
Perform Buerger’s test.
Auscultation:
Listen for bruits over the abdomen and over the femoral arteries.
J Alastair Innes
James Tiernan
5
The respiratory system
Anatomy and physiology 76 Interpretation of the findings 89
The history 76 Investigations 89
Common presenting symptoms 77 OSCE example 1: Respiratory history 90
Past medical history 81
OSCE example 2: Respiratory examination 91
Drug and allergy history 81
Family history 81 Integrated examination sequence for the respiratory system 92
Social history 81
Systematic enquiry 82
The physical examination 82
Inspection 82
Palpation 87
Percussion 87
Auscultation 88
76 THE RESPIRATORY SYSTEM
the level of the anterior end of the fifth rib, slightly lower on the
Anatomy and physiology left. The lower anterior ribs therefore overlie the liver on the
right and the stomach and spleen on the left, with the parietal
An understanding of the surface anatomy of the lungs (Fig. 5.1) pleura extending lower than the lungs on the lateral chest wall.
and their relation to closely adjacent structures is essential for the Posteriorly, the lungs extend much lower, approaching the 12th
practice of respiratory medicine. At the end of tidal expiration the rib on full inspiration.
dome of the diaphragm extends high into the thorax to around The lung apex lies immediately beneath the brachial plexus, so
apical lung tumours commonly disrupt T1 root fibres, causing pain
and numbness in the inner aspect of the upper arm and wasting
of the small hand muscles. The upper thoracic sympathetic outflow
to the eye may also be compromised, leading to a constricted
pupil and ptosis. In the mid- and lower mediastinum, tumours can
invade and compromise the pericardium, atria and oesophagus.
In health, the lungs optimise gas exchange by close matching
of regional ventilation and perfusion. Airway and parenchymal lung
diseases disrupt this matching, causing hypoxia and cyanosis,
and commonly stimulate breathing through lung afferent nerves,
leading to a history of breathlessness, and tachypnoea on
examination.
The history
Patients use a wide range of terms to describe respiratory
symptoms (such as infection, phlegm, catarrh, pleurisy and
wheeze). These can be ambiguous and require careful definition to
avoid misunderstanding. ‘Wheeze’ may be used when describing
breathlessness, or ‘I had a chest infection’ may denote a
breathless episode actually due to pulmonary embolism.
As with other systems, the respiratory history should start
with open questions but should also specifically cover all the
areas outlined in Box 5.1.
on
78 THE RESPIRATORY SYSTEM
Signs of
consolidation, rigors Pneumonia
Hours/days Fever, cough, green
sputum
Wheeze Acute bronchitis
Bronchiectasis Daily purulent sputum for long periods patients with asthma (Fig. 5.3C), sometimes indicating
Pneumonia or whooping cough in underlying allergic bronchopulmonary aspergillosis.
childhood
Recurrent haemoptysis Haemoptysis
Lung cancer Persistent cough, especially in
smokers
Any haemoptysis tract. It can complicate any severe forceful cough but is most
Pneumonia that fails to clear in 4–6 commonly associated with acute or chronic respiratory tract
weeks
Rhinitis with postnasal drip Chronic sneezing, nasal blockage/ and lung cancer. Never assume haemoptysis has a benign cause
discharge until serious pathology has been considered and excluded.
Ask about how it appeared, how much blood there was,
Oesophageal reflux Heartburn or regurgitation of acid
whether there are associated features and over what time period
after eating, bending or lying
Nocturnal as well as daytime cough it came on:
MUCOID
MUCOPURULENT
PURULENT
1 cm
C
A
Fig. 5.3 Sputum appearance in disease. A Colour chart of sputum purulence used in bronchiectasis. B Rusty red sputum of pneumococcal
pneumonia. C Mucus plug from a patient with asthma. (A) Courtesy Medical Photography, NHS Lothian.
Chest pain
inflammation or adhesions with pleural traction on
Chest pain may originate from musculoskeletal, respiratory, respiratory movement
cardiovascular and gastro-oesophageal disease.
Establish: collapse
persist long after the rash has resolved, often with scarring in Ask about:
the dermatomal distribution.
Burning retrosternal pain may indicate oesophagitis but also
occurs with myocardial ischaemia. Alteration of discomfort after
eating or antacids helps to distinguish oesophageal pain; cardiac sleep patterns.
pain is described on page 40.
Central, constant, progressive, non-pleuritic chest pain may apnoea patients are exhausted in the morning.
5.4 Previous illness relevant to respiratory history 5.5 Respiratory problems caused by drugs
History Current implications Respiratory condition Drug
Eczema, hay fever Allergic tendency relevant to asthma Bronchoconstriction Beta-blockers
Childhood asthma Many wheezy children do not have Opioids
asthma as adults, yet many adults with Non-steroidal anti-inflammatory drugs
asthma had childhood wheeze Cough Angiotensin-converting enzyme
Whooping cough, measles, Recognised causes of bronchiectasis, inhibitors
inhaled foreign body especially if complicated by pneumonia Bronchiolitis obliterans Penicillamine
Pneumonia, pleurisy Recognised causes of bronchiectasis Diffuse parenchymal lung Cytotoxic agents: bleomycin,
Recurrent episodes may be a disease methotrexate
manifestation of bronchiectasis Anti-inflammatory agents:
Tuberculosis Reactivation if not previously treated sulfasalazine, penicillamine, gold salts,
effectively aspirin
Respiratory failure may complicate Cardiovascular drugs: amiodarone,
thoracoplasty hydralazine
Mycetoma in lung cavity may present Antibiotics: nitrofurantoin
with haemoptysis Intravenous drug misuse
Connective tissue disorders, Lung diseases are recognised Pulmonary thromboembolism Oestrogens
e.g. rheumatoid arthritis complications, e.g. pulmonary fibrosis, Pulmonary hypertension Oestrogens
effusions, bronchiectasis Dexfenfluramine, fenfluramine
Immunomodulatory treatments of these Pleural effusion Amiodarone
diseases may also cause pulmonary Nitrofurantoin
toxicity or render patients susceptible Phenytoin
to respiratory infection Methotrexate
Previous malignancy Recurrence, metastatic/pleural disease Pergolide
Chemotherapeutic agents recognised Respiratory depression Opioids
causes of pulmonary fibrosis Benzodiazepines
Radiotherapy-induced pulmonary
fibrosis
Cancer, recent travel, Pulmonary thromboembolism
surgery or immobility
Recent surgery, loss of Aspiration of foreign body, gastric Systematic enquiry
consciousness contents
Pneumonia, lung abscess Ask specifically about any risk factors, such as malignancy for
Neuromuscular disorders Respiratory failure thromboembolism. The remaining history may reveal previously
Aspiration unsuspected pathologies presenting with respiratory symptoms
or complicating respiratory illness, such as ovarian malignancy
presenting with pleural effusion.
Smoking Inspection
Obtaining an honest and accurate history of tobacco use is difficult
Much can be learned about the respiratory system by careful
and is covered on page 14. Ask if others smoke in the house;
inspection from the end of the bed. The normal shape and
this can be a major obstacle to smoking cessation. Remember
respiratory movements of the chest wall are significantly altered
also to enquire about the use of cannabis and e-cigarettes.
by the hyperinflation that accompanies chronic airflow obstruction
Occupational history
relative to inspiration, and sometimes ‘pursed-lip’ breathing
Many respiratory diseases are caused by occupational or on expiration. Forceful inspiration at these very high lung
domestic exposure to inhaled substances. Common examples volumes may cause indrawing of the intercostal spaces during
are summarised in Fig. 5.4. Ask the patient what work they have mid-inspiration and also the recruitment of muscles not normally
done, starting with their first job. Look out for the occupations involved in breathing (‘accessory muscles’). These include the
listed in Fig. 5.4, and also record the employers’ names, the sternocleidomastoid muscles lifting the sternum, and trapezius
dates and duration of exposure, and whether any protective and the scalenes lifting the shoulder girdle. Patients sometimes
masks were offered or used. sit forwards and brace their arms on a table, allowing them to
83
Demolition worker
Construction worker
5
Aspergillus in malt
Veterinarian
Laboratory worker
Normal
cricosternal
distance Upward, outward
rib movement
A Normal Heart causes
dullness at
left sternal edge
Outward movement
of lower ribs
Expiration Inspiration
Reduced cricosternal
distance (sternum high)
Reduced outward
movement
B Hyperinflated
Lingula overlies heart
– loss of cardiac dullness
Paradoxical inward
Low, flat diaphragm movement of lower ribs
due to flat diaphragm
Fig. 5.5 Respiratory movement of the ribs, sternum and diaphragm. A In normal adults. B In chronic hyperinflation due to obstructive lung disease.
Hyperinflation causes upward displacement of the sternum and clavicles, increased anteroposterior thoracic diameter, loss of cardiac dullness at the lower
left sternal edge, and a low flat diaphragm that pulls the lower ribs in during inspiration.
84 THE RESPIRATORY SYSTEM
A B
C D
Fig. 5.6 Abnormalities in the shape of the chest. A Hyperinflated chest with raised sternum and shoulder girdle. B Kyphoscoliosis. C Pectus
carinatum with Harrison’s sulcus (arrow). D Pectus excavatum.
use pectoralis major to pull the ribs outwards during inspiration. scars may be visible only on the lateral and posterior
In contrast to the hyperinflation of obstructive disease, interstitial aspects of the chest.
disease causes small, stiff lungs, diminishes thoracic volume and Quietly observe and time respiratory rate (for example,
raises resting respiratory rate. breaths in 15 seconds × 4) without drawing the patient’s
Chest deformity (Fig. 5.6) may be congenital, as in pectus attention to it, as this may cause it to change. Feeling the
excavatum, or acquired, as in pectus carinatum. The latter radial pulse, while timing breathing, is a common solution
is an inward displacement of the lower ribs with a prominent to this problem.
sternum, caused by severe airflow obstruction in early childhood, Inspect the remaining skin for relevant abnormalities.
when the rib cage is developing. Asymmetry of the chest may
be secondary to scoliosis, shrinkage of scarred lung following
tuberculous infection, or prior surgical resection of lung and/or ribs. over 20 breaths per minute is abnormal for an adult.
In healthy adults at altitude, elderly people and patients with
heart failure, a distinctive pattern of alternating periods of deep and
Examination sequence
Note the presence of nebulisers or inhalers (indicating respiration and is thought to represent abnormal feedback from
obstructive lung disease), oxygen therapy and cyanosis; the carotid chemoreceptors to the respiratory centre.
check sputum pots.
Look for asymmetry of the chest, deformities, operative be seen and offer the chance for rapid biopsy and diagnosis.
scars and chest drains, remembering that thoracotomy In the legs the painful dusky red lesions of erythema nodosum
85
B
Fig. 5.7 Skin lesions associated with respiratory conditions.
A Metastatic nodules of lung cancer. B Erythema nodosum on the shins
in sarcoidosis.
Ask the patient to hold their arms out straight with the
T1 root damage by an apical lung tumour wrists extended (Fig. 5.10).
Check the pulse while examining the hands.
syndrome (Fig. 5.9). Check for any tenderness in the distal forearm.
Fine tremor of the outstretched hands is common in respiratory
patients and usually due to the direct effect of high-dose
Examination sequence beta-agonist bronchodilators on skeletal muscle. A coarse
Examine the hands for finger clubbing (see Fig. 3.9), tar flapping tremor of the outstretched hands is seen in patients
staining, nail discoloration and cyanosis. with CO2 retention.
86 THE RESPIRATORY SYSTEM
Face Neck
Respiratory disease can cause important signs in the face.
pulmonary hypertension, and may be acutely raised in those with
of the head, neck and face (Fig. 5.11) with subconjunctival oedema tension pneumothorax or large pulmonary embolism. In superior
(looking like a tear inside the lower lid, but not mobile); this usually
indicates tumour invasion of the upper mediastinum. Tumour of the jaw, making pulsatility invisible. In those who are using
at the root of the neck may disrupt the sympathetic nerves to the sternocleidomastoids as accessory muscles (see earlier), it
the eye, which run from the upper thoracic spinal segments via
ganglia in the neck to join the carotid artery sheath. This causes vein lies deep to the active muscle.
Examination sequence
Examination sequence
Check the conjunctiva of one eye for anaemia, and the the neck, to facilitate relaxation of the sternocleidomastoid
colour of the tongue for central cyanosis (Fig. 5.12). muscles.
Check for ptosis and pupil asymmetry.
Remember that cyanosis becomes visible only when a sufficient Check for tracheal deviation by gently advancing a single
quantity of deoxyhaemoglobin is circulating, making it hard to finger resting in the sternal notch in the midline (Fig. 5.13).
detect in anaemia but obvious in polycythaemic patients with If the fingertip meets the centre of the trachea, it is not
only a mild percentage of desaturation. deviated.
Check the cricosternal distance (the vertical distance
between the sternal notch and the cricoid cartilage, the
first prominent ridge felt above the tracheal rings). In
health, three average fingers fit between the sternal notch
and the cricoid.
Examine the cervical lymph nodes from behind with the
patient sitting forward, as described in full on page 33.
Tracheal deviation away from the affected side is seen acutely
in tension pneumothorax. Chronic tracheal deviation towards
the affected side occurs with loss of lung volume in upper lobe
fibrosis or collapse, and following lobectomy or pneumonectomy.
Reduction in cricosternal distance is a sign of hyperinflation
and reflects upward displacement of the sternum (see Fig. 5.5B).
Upward movement of the sternum and downward movement
of the trachea on inspiration are normal, but may become more
obvious with forceful inspiratory efforts in respiratory disease.
Rarely, systolic downward movement of the trachea is felt in
patients with aortic aneurysm (sometimes called ‘tracheal tug’).
Cervical lymph nodes are frequently involved in lung neoplasms
Fig. 5.11 Superior vena cava obstruction. Dusky, swollen face and spreading via the mediastinum.
neck, and distended superficial collateral veins on the chest wall. From
Midthun DE, Jett JR. Clinical presentation of lung cancer. In Pass HI, Thorax
Mitchel JB, Johnson DH, et al. (eds). Lung Cancer: Principles and Practice.
Philadelphia: Lippincott–Raven; 1996, p. 421. First inspect the chest closely again, in case abnormalities have
been missed from the end of the bed. In patients with a thin
chest wall and increased respiratory drive (as in exacerbation of
Fig. 5.12 Central cyanosis of the tongue. Fig. 5.13 Examining for tracheal shift.
87
asthma or COPD), forced, rapid inspiration often causes visible (Fig. 5.15). This most commonly complicates pneumothorax with
indrawing of the skin in the intercostal spaces during inspiration, chest drainage or rib fracture, and feels like a palpable crackling
seen more easily with tangential light (see Fig. 5.6A). under the skin of the upper thorax and neck.
Palpation Percussion
Examination sequence Correctly performed, percussion can distinguish areas of the
chest wall over air-filled lung from those overlying consolidated
Locate the apex beat, the most inferior and lateral place lung or fluid. It generates a hollow, ringing sound accompanied by 5
where the finger is lifted by the twisting systolic movement a palpable resonance over air-filled lung, but a dull thud lacking
of the cardiac apex. This is normally in the fifth intercostal resonance over consolidation or fluid. The absolute quality and
space in the mid-clavicular line; count down the intercostal volume of the percussed sound vary widely between individuals
spaces from the second, which is just below the sternal with differing chest wall thickness, muscularity and subcutaneous
angle. fat, and is of little value. The value of percussion lies in detecting
Palpate for a right ventricular heave using a straight arm, asymmetry of resonance between mirror image positions on the
with the palm over the lower sternum (see Fig. 4.18C). right and left sides.
The apex beat is displaced laterally by dilatation of the ventricles
Examination sequence
obstructive lung disease causes the lingula of the left upper
lobe to come between the heart and the chest wall, making To percuss the chest, apply the middle finger of your
the apex beat impalpable and the heart sounds inaudible (see non-dominant hand firmly to an intercostal space, parallel
Fig. 5.5B; in this situation the heart sounds are best heard in to the ribs, and drum the middle phalanx with the flexed
the epigastrium). tip of your dominant index or middle finger (Fig. 5.16A).
In pulmonary hypertension the lower sternum is lifted by the Percuss in sequence, comparing areas on the right with
cardiac cycle (right ventricular heave). corresponding areas on the left before moving to the next
Next assess thoracic expansion in both the upper and lower level (Fig. 5.16B).
anterior chest wall. Posteriorly, the scapular and spinal muscles obstruct
percussion, so position the patient sitting forwards with
Examination sequence their arms folded in front to move the scapulae laterally.
Percuss a few centimetres lateral to the spinal muscles,
Cup your hands, with fingers spread, round the patient’s taking care to compare positions the same distance from
upper anterior chest wall, pressing the fingertips firmly in the midline on right and left (Fig. 5.16C).
the mid-axillary line. Pull your hands medially towards each In healthy people, anterior chest percussion is symmetrical
other to tighten any loose skin, and use your thumbs (off except for the area immediately lateral to the lower left sternal
the skin) as pointers to judge how much each hand moves edge, where the right ventricle causes dullness; this ‘cardiac
outwards when the patient is instructed to take a full dullness’ is lost in hyperinflated patients in whom the lingula
breath in (Fig. 5.14). In a healthy thorax, the ribs move out overlies the heart (see Fig. 5.5). Clear resonance is the usual
and up with inspiration. finding over a pneumothorax, although the difference between
Check for any asymmetry. This is more important than the normal lung and pneumothorax may be quite subtle because
absolute degree of expansion, which will vary between
individuals.
Repeat the process in the lower anterior chest wall.
In COPD with hyperinflation the normal outward movement of
the lower ribs on inspiration is replaced by paradoxical inward
movement, caused by contraction of the abnormally low flat
diaphragm (see Fig. 5.5). This striking sign (paradoxical rib cage
A B
Fig. 5.14 Assessing chest expansion from the front. A Expiration. Fig. 5.15 Subcutaneous air (surgical emphysema) seen in the neck
B Inspiration. and chest wall on chest X-ray (arrows).
88 THE RESPIRATORY SYSTEM
A B C
Fig. 5.16 Percussion of the chest. A Technique. B Anterior and lateral sites. C Posterior sites.
normal lung is almost all air. Resonance on percussion together are usually absent. These two causes of absent sounds are
with unilateral absent breath sounds indicates pneumothorax. readily distinguished by percussion, which will be resonant with
pneumothorax and completely dull over pleural fluid.
Auscultation
Use of the stethoscope
To understand chest auscultation it is necessary to understand Remember to wear the stethoscope with the ear pieces facing
the origin of breath sounds. The tracheobronchial tree branches forwards to align them with your auditory canal. Normal breath
23 times between the trachea and the alveoli. This results in an sounds are relatively quiet, so the greater area of contact offered
exponential rise in the number of airways and their combined by the diaphragm is usually well adapted to chest auscultation.
cross-sectional area moving towards the alveoli. During a maximal The two common exceptions are in patients with:
breath in and out, the same vital capacity (about 5 L of air in
healthy adults) passes through each generation of airway. In where it may be impossible to achieve flat skin contact
the larynx and trachea, this volume must all pass through a with the diaphragm.
cross-sectional area of only a few square centimetres and therefore
flow rate is fast, causing turbulence with vibration of the airway the diaphragm are easily mistaken for lung crackles. In
wall and generating sound. In the distal airway, the very large these situations, use the stethoscope bell instead to listen
total cross-sectional area of the multitude of bronchioles means to the breath sounds.
that 5 L can easily pass at slow flow rates, so flow is normally
virtually silent. The harsh ‘bronchial’ sound generated by the Breath sounds
major airways can be appreciated by listening with the diaphragm
of the stethoscope applied to the larynx (try this on yourself). As with percussion, the absolute volume and character of breath
Most of the sound heard when auscultating the chest wall sounds in individuals are greatly affected by the thickness,
originates in the large central airways but is muffled and deadened muscularity and fat content of the chest wall. The symmetry of
by passage through overlying air-filled alveolar tissue; this, together sounds is therefore the key feature.
with a small contribution from medium-sized airways, results in
‘normal’ breath sounds at the chest wall, sometimes termed
‘vesicular’. When healthy, air-filled lung becomes consolidated
Examination sequence
by pneumonia or thickened and stiffened by fibrosis, sound Auscultate the apices, comparing right with left, and
conduction is improved, and the centrally generated ‘bronchial’ changing to the bell if you cannot achieve flat skin contact
breath sounds appear clearly and loudly on the overlying chest with the diaphragm.
wall. In the same way, with soft speech (‘say one, one, one’), Ask the patient to take repeated slow, deep breaths in
the laryngeal sounds are muffled by healthy lung but heard and out through their open mouth. Auscultate the anterior
clearly and loudly at the chest wall overlying consolidation and chest wall from top to bottom, always comparing mirror
fibrosis, due to improved conduction of major airway sounds image positions on right and left before moving down.
through diseased lung. Use the same sequence of sites as for percussion (see
When there is lobar collapse caused by a proximal bronchial Fig. 5.16B and C). Do not waste time by listening to
obstruction, the signs are different from those in simple repeated breath cycles at each position, unless you
consolidation. The usual findings are diminished expansion, suspect an abnormality and wish to check.
sometimes with chest asymmetry due to loss of volume, dullness Note whether the breath sounds are soft and muffled,
to percussion over the collapsed lobe, and reduced breath sounds absent, or loud and harsh (bronchial, like those heard over
and vocal resonance.
When the lung tissue is physically separated from the chest sounds (see later), deciding which side is abnormal.
wall by intervening air (pneumothorax) or fluid (pleural effusion), Auscultate the lateral chest wall in the mid-axillary line,
sound conduction is greatly impaired and the breath sounds again comparing right with left before changing level.
89
Added sounds breath sounds). These signs can be confirmed by asking the
patient to generate laryngeal sounds deliberately (‘Please say “one,
There are three common added sounds: wheezes, crackles
one, one” each time I move my stethoscope on the skin’) and
and rubs. Wheeze is a musical whistling sound accompanying
listening on the chest wall in the same sequence of sites used
airflow and usually originates in narrowed small airways. It is
for breath sounds. The spoken sound is muffled and deadened
most commonly expiratory, due to dynamic airway narrowing
over healthy lung, but the spoken sound is heard loudly and
on expiration, but can also occur on inspiration. Usually, multiple
clearly through the stethoscope over consolidation or fibrotic
wheezing sounds are heard together (polyphonic wheeze); this
lung scarring. Consistent with absent breath sounds, vocal
sign is common in asthma, bronchitis and exacerbation of COPD.
A solitary wheeze that is present consistently with each breath and
resonance is absent or greatly diminished over pneumothorax 5
and pleural effusion.
does not clear with coughing suggests a possible fixed bronchial
‘Whispering pectoriloquy’ may be used to confirm the same
obstruction and can be an important sign of underlying cancer.
changes in sound conduction. Whispered speech is muffled to
Crackles accompanying deep breathing are thought to
silence by normal lung but may be heard over consolidated or
represent the sudden opening of small airways but sometimes
scarred lung.
may indicate secretions in the airways or underlying lung fibrosis.
In healthy people, gravitational compression of the dependent
lung bases often causes a few crackles on the first few deep
breaths; these are of no pathological significance. Crackles that
Interpretation of the findings
persist after several breaths and do not clear with a deliberate
cough are pathological. They are graded as ‘fine’, meaning soft, Review your findings and assemble the positive features you
multiple crackles, to ‘coarse’, indicating loud, scanty crackles have uncovered. On completion of the history and examination
you should have a broad idea of the category of respiratory
during inspiration, resembling the sound made by peeling a illness with which you are dealing. As with any system, consider
as you go the likely categories of disease and how these affect
and are most commonly heard at the lung bases posteriorly presentation. This approach is summarised in Box 5.6.
and laterally. Fine crackles also occur in pulmonary oedema and
some viral pneumonias. Coarse crackles are generally heard in
patients with significant purulent airway secretions such as those Investigations
with bronchopneumonia or bronchiectasis. Inspiratory crackles
are also often heard over the areas of incompletely inflated lung
immediately above a pleural effusion. revealed on history and examination. Investigations are costly
Pleural rub is a rasping, grating sound occurring with each and many carry risks, so choose tests capable of distinguishing
breath and sounding superficial, just under the stethoscope, like the likely diagnoses and prioritise the most decisive ones. In
two sheets of sandpaper rubbing together. It indicates pleural respiratory disease, imaging of the lungs is fundamental, but
inflammation, usually due to infection, and is often accompanied respiratory function testing is equally important to distinguish
by pleuritic chest pain. obstructive disease of the airways from the restrictive pattern
seen in many parenchymal diseases, and to quantify the degree
Vocal resonance of abnormality. A summary of the appropriate initial investigations
Breath sounds normally reveal the presence of consolidation or according to the type of respiratory presentation is included in
fibrosis (bronchial breath sounds) or pleural air or fluid (absent Box 5.7.
5.6 Categories of respiratory disease and associated features on history and examination
Category of problem Suggestive features on history Suggestive features on examination
Infection: Fever
Acute bronchitis Wheeze, cough, sputum Wheeze
Exacerbation of chronic obstructive Acute-on-chronic dyspnoea Hyperinflation
pulmonary disease
Pneumonia Pleuritic pain, rusty sputum, rigors If lobar, dull to percussion and bronchial breathing
Malignancy Insidious onset, weight loss, persisting pain Cervical lymphadenopathy, clubbing, signs of lobar/lung
or cough collapse ± effusion
Pulmonary fibrosis Progressive dyspnoea Tachypnoea, inspiratory fine crackles at bases, cyanosis
Pleural effusion Progressive dyspnoea Unilateral basal dullness and reduced breath sounds
Pulmonary embolism:
Large Sudden, severe dyspnoea Normal breath sounds
Medium Episodes of pleural pain, haemoptysis Pleural rub, swollen leg if deep vein thrombosis, crackles
if infarct
Multiple small Progressive dyspnoea Raised jugular venous pressure, right ventricular heave,
loud pulmonary second sound
Asthma Atopy, hay fever, pet ownership, variable Polyphonic expiratory wheeze, eczema
wheeze, disturbance of sleep
90 THE RESPIRATORY SYSTEM
ABG, arterial blood gas; COPD, chronic obstructive pulmonary disease; CRP, C-reactive protein; CT, computed tomography; FEV1, forced expiratory volume in 1 second;
IgE, immunoglobulin E; WCC, white cell count.
Mrs Walker, 55 years old, presents to the respiratory clinic with cough and wheeze.
Please take a history
Introduce yourself and clean your hands.
Ask an open question about why this person has come to the clinic.
Explore each presenting symptom:
Cough:
– Onset, duration?
– Productive? If so, characterise sputum volume and colour, and any blood.
– Triggers? Did it start with an upper respiratory tract infection? Is it provoked by exercise or environment?
– Time pattern – nocturnal (suggests asthma or reflux)?
– On angiotensin-converting enzyme inhibitors?
Wheeze:
– What exactly does the patient mean by ‘wheeze’?
– When does it occur – at night or during exercise?
– Provoking factors – infection, environment, contact with animals, dust, beta-blockers?
– Any relieving factors – inhalers?
– Associated respiratory symptoms – breathlessness, chest pain, fevers/rigors, weight loss.
Ask about past respiratory diagnoses, particularly childhood wheeze or asthma, rhinitis/hay fever and prior respiratory treatments/admissions.
Explore past non-respiratory illness: for example, eczema (suggests atopy), hypertension or angina (on beta-blockers?), other prior illnesses.
Take a drug history – prescribed medications, including inhalers/nebulisers and recreational drugs.
Ask about any known allergies.
Take a social history: smoking, occupation, contact with animals.
91
1
The history 3
2 4
Gastrointestinal symptoms are common and are often caused by
functional dyspepsia and irritable bowel syndrome. Symptoms
suggesting a serious alternative or coexistent diagnosis include
persistent vomiting, dysphagia, gastrointestinal bleeding, weight
loss, painless, watery, high-volume diarrhoea, nocturnal symptoms,
1 Liver 3 Spleen
fever and anaemia. The risk of serious disease increases with age.
2 Gallbladder 4 Pancreas
Always explore the patient’s ideas, concerns and expectations
about the symptoms (p. 5) to understand the clinical context.
B
Stomach
Gallbladder Pancreas
Intestines
Aorta
6
Spine
Rib
Liver
Left adrenal gland
Right kidney
Fig. 6.2 Normal computed tomogram of the abdomen at L1 level.
antacids)
premature satiety).
Often there is no structural cause and the dyspepsia is
functional. There is considerable overlap, however, and it is
peptic ulcer disease) impossible to diagnose functional dyspepsia on history alone
without investigation. Dyspepsia that is worse with an empty
regurgitation. stomach and eased by eating is typical of peptic ulceration. The
When heartburn is the principal symptom, GORD is the most patient may indicate a single localised point in the epigastrium
likely diagnosis. (pointing sign), and complain of nausea and abdominal fullness
96 THE GASTROINTESTINAL SYSTEM
Fig. 6.4 Abdominal pain. Perception of visceral pain is localised to the epigastric, umbilical or suprapubic region, according to the embryological origin of
the affected organ.
Abdominal pain
Characterise the pain using SOCRATES (see Box 2.2). Ask about
the characteristics described here. Gallbladder
Site
Ureter
Visceral abdominal pain from distension of hollow organs,
mesenteric traction or excessive smooth-muscle contraction is Inguinal canal
deep and poorly localised in the midline. The pain is conducted
via sympathetic splanchnic nerves. Somatic pain from the parietal
peritoneum and abdominal wall is lateralised and localised to the
Gallbladder pain
Pain arising from foregut structures (stomach, pancreas, liver
and biliary system) is localised above the umbilicus (Fig. 6.4). Diaphragmatic pain
Central abdominal pain arises from midgut structures, such as
Ureteric pain
the small bowel and appendix. Lower abdominal pain arises
Fig. 6.5 Characteristic radiation of pain from the gallbladder,
diaphragm and ureters.
cause localised pain: for example, left iliac fossa pain due to
diverticular disease of the sigmoid colon.
Pain from an unpaired structure, such as the pancreas, is
midline and radiates through to the back. Pain from paired Character
structures, such as renal colic, is felt on and radiates to the Colicky pain lasts for a short time (seconds or minutes), eases
affected side (Fig. 6.5). Torsion of the testis may present with off and then returns. It arises from hollow structures, as in small
abdominal pain (p. 232). In females, consider gynaecological or large bowel obstruction, or the uterus during labour.
Biliary and renal ‘colic’ are misnamed, as the pain is rarely
endometriosis or ectopic pregnancy (p. 218). colicky; pain rapidly increases to a peak and persists over several
hours before gradually resolving. Dull, constant, vague and poorly
Onset
Sudden onset of severe abdominal pain, rapidly progressing to infection, such as salpingitis, appendicitis or diverticulitis (Box 6.2).
become generalised and constant, suggests a hollow viscus
perforation (usually due to colorectal cancer, diverticular disease Radiation
or peptic ulceration), a ruptured abdominal aortic aneurysm or Pain radiating from the right hypochondrium to the shoulder or
mesenteric infarction.
Torsion of the caecum or sigmoid colon (volvulus) presents acute cholecystitis (see Fig. 6.5). Pain radiating from the loin
with sudden abdominal pain associated with acute intestinal to the groin and genitalia is typical of renal colic. Central upper
obstruction. abdominal pain radiating through to the back, partially relieved by
97
or diverticulitis.
98 THE GASTROINTESTINAL SYSTEM
Severity
Excruciating pain, poorly relieved by opioid analgesia, suggests
an ischaemic vascular event, such as bowel infarction or ruptured
abdominal aortic aneurysm. Severe pain rapidly eased by potent
analgesia is more typical of acute pancreatitis or peritonitis
secondary to a ruptured viscus. weight loss.
Features of the pain can help distinguish between possible
causes (Box 6.3). Do not confuse dysphagia with early satiety, the inability to
complete a full meal because of premature fullness, or with
The acute abdomen globus, which is a feeling of a lump in the throat. Globus does
The majority of general surgical emergencies are patients with not interfere with swallowing and is not related to eating.
sudden severe abdominal pain (an ‘acute abdomen’). Patients Neurological dysphagia resulting from bulbar or pseudobulbar
may be so occupied by recent and severe symptoms that they palsy (p. 129) is worse for liquids than solids, and may be
forget important details of the history unless asked directly. Seek
additional information from family or friends if severe pain, shock from the nose.
or altered consciousness makes it difficult to obtain a history Neuromuscular dysphagia, or oesophageal dysmotility, presents
from the patient. Note any relevant past history, such as acute in middle age, is worse for solids and may be helped by liquids and
perforation in a patient with known diverticular disease. Causes sitting upright. Achalasia, when the lower oesophageal sphincter
range from self-limiting to severe life-threatening diseases (Box fails to relax normally, leads to progressive oesophageal dilatation
6.4). Evaluate patients rapidly, and then resuscitate critically ill
patients immediately before undertaking further assessment respiratory tract may then occur, especially at night when the
and surgical intervention. Parenteral opioid analgesia to alleviate patient lies down, causing aspiration pneumonia. Oesophageal
severe abdominal pain will help, not hinder, clinical assessment. dysmotility can cause oesophageal spasm and central chest
In patients with undiagnosed acute abdominal pain, reassess pain, which may be confused with cardiac pain.
their clinical state regularly, undertake urgent investigations A pharyngeal pouch may cause food to stick or be regurgitated,
and consider surgical intervention before administering repeat and may lead to recurrent chest infections due to chronic silent
analgesia. aspiration.
‘Mechanical’ dysphagia is often due to oesophageal stricture It may indicate anxiety but sometimes occurs in an attempt to
but can be caused by external compression. With weight loss, relieve abdominal pain or discomfort, and accompanies GORD.
cancer. Longstanding dysphagia without weight loss but is a mixture of gases derived from swallowed air and from
accompanied by heartburn is more likely to be due to benign colonic bacterial fermentation of poorly absorbed carbohydrates.
peptic stricture. Record the site at which the patient feels the
food sticking; this is not a reliable guide to the site of oesophageal intestinal malabsorption.
obstruction, however.
bowel. Loud borborygmi, particularly if associated with colicky
Nausea and vomiting discomfort, suggest small bowel obstruction or dysmotility.
to air swallowing (aerophagy) and has no medical significance. Fig. 6.6 Abdominal distension due to ascites.
100 THE GASTROINTESTINAL SYSTEM
Ask about:
frequency
volume
colour
consistency: watery, unformed or semisolid
contents: red blood, mucus or pus
Reproduced from Rockall TA, Logan RF, Devlin HB, et al. Risk assessment after
acute upper gastrointestinal haemorrhage. Journal of the British Society of
Gastroenterology 1996; 38(3):316, with permission from BMJ Publishing
Group Ltd.
ischaemic colitis and colonic angioectasias.
Jaundice
Jaundice is a yellowish discoloration of the skin, sclerae (Fig. 6.8)
Melaena and mucous membranes caused by hyperbilirubinaemia (Box 6.6).
There is no absolute level at which jaundice is clinically detected
Melaena is the passage of tarry, shiny black stools with a
but, in good light, most clinicians will recognise jaundice when
characteristic odour and results from upper gastrointestinal
bilirubin levels exceed 50 μmol/L (2.92 mg/dL).
bleeding. Distinguish this from the matt black stools associated
Ask about:
with oral iron or bismuth therapy.
Peptic ulceration (gastric or duodenal) is the most common
itching
cause of upper gastrointestinal bleeding and can manifest with
melaena, haematemesis or both. Excessive alcohol ingestion
may cause haematemesis from erosive gastritis, Mallory–Weiss
tear or bleeding oesophagogastric varices in cirrhotic patients.
Oesophageal or gastric cancer and gastric angioectasias (Dieulafoy
lesion) are rare causes of upper gastrointestinal bleeding.
The Rockall and Blatchford scores are used to assess the
risk in gastrointestinal bleeding (Box 6.5). A profound upper
gastrointestinal bleed may lead to the passage of purple stool Unconjugated bilirubin is insoluble and binds to plasma albumin;
or, rarely, fresh blood. it is therefore not filtered by the renal glomeruli. In jaundice from
unconjugated hyperbilirubinaemia, the urine is a normal colour
Rectal bleeding (acholuric jaundice; Box 6.7).
Establish whether the blood is mixed with stool, coats the surface Bilirubin is conjugated to form bilirubin diglucuronide in the
of otherwise normal stool or is seen on the toilet paper or in the liver and excreted in bile, producing its characteristic green
pan. Fresh rectal bleeding (haematochezia) usually indicates a colour. In conjugated hyperbilirubinaemia, the urine is dark brown
disorder in the anal canal, rectum or colon. During severe upper due to the presence of bilirubin diglucuronide. In the colon,
gastrointestinal bleeding, however, blood may pass through the conjugated bilirubin is metabolised by bacteria to stercobilinogen
intestine unaltered, causing fresh rectal bleeding. Common causes and stercobilin, which contribute to the brown colour of stool.
of rectal bleeding include haemorrhoids, anal fissures (blood on Stercobilinogen is absorbed from the bowel and excreted in the
the toilet paper or in the pan), complicated diverticular disease, urine as urobilinogen, a colourless, water-soluble compound.
102 THE GASTROINTESTINAL SYSTEM
Symptom Drug and subcutaneous lumps and, less commonly, saphena varix
Weight gain Oral glucocorticoids (a varicosity of the long saphenous vein), hydrocoele of the
spermatic cord, undescended testis, femoral aneurysm and psoas
Dyspepsia and Aspirin
gastrointestinal bleeding Non-steroidal anti-inflammatory drugs abscess.
Eyes
Abdomen
vessels around
umbilicus
B Leuconychia
Genitalia
Hands
y
Legs
General
Skin pigmentation
Loss of body hair
Bruising
C Palmar erythema
Fig. 6.9 Features of chronic liver disease.
104 THE GASTROINTESTINAL SYSTEM
hepatic encephalopathy everted. Look tangentially across the abdomen and from the
foot of the bed for any asymmetry suggesting a localised mass.
sulphide on the breath, which is evidence of portosystemic
shunting (with or without encephalopathy) Abdominal scars and stomas
Note any surgical scars or stomas and clarify what operations
day/night pattern reversed, through confusion and have been undertaken (Figs 6.10 and 6.11). A small infraumbilical
disorientation, to unresponsive coma incision usually indicates a previous laparoscopy. Puncture scars
from laparoscopic surgical ports may be visible. An incisional
hernia at the site of a scar is palpable as a defect in the abdominal
105
Fig. 6.10 Some abdominal incisions. The midline and oblique incisions Tenderness
avoid damage to innervation of the abdominal musculature and later Discomfort during palpation may vary and may be accompanied
development of incisional hernias. These incisions have been widely by resistance to palpation. Consider the patient’s level of anxiety
superseded by laparoscopic surgery, however.
when assessing the severity of pain and degree of tenderness
elicited. Tenderness in several areas on minimal pressure may
be due to generalised peritonitis but is more often caused by
anxiety. Severe superficial pain with no tenderness on deep
palpation or pain that disappears if the patient is distracted also
suggests anxiety. With these exceptions, tenderness usefully
indicates underlying pathology.
Voluntary guarding is the voluntary contraction of the abdominal
muscles when palpation provokes pain. Involuntary guarding is
Epigastric mass v
ry
ysm
Hepatomegaly
Pa v wa v
wa
Pa e
Tender to palpation
Generalised distension
Fa
Fl
Fl
Fe
ve
Fig. 6.12 Palpable abnormalities in the abdomen.
Hepatomegaly
Examination sequence
Aorta Hard faeces
Liver edge Point your fingers upwards and your index and middle
Rectus abdominis fingers lateral to the rectus muscle, so that your fingertips
Lower pole of and its tendinous
right kidney insertions lie parallel to the rectus sheath (Fig. 6.14). Keep your hand
stationary.
Normal colon
Small lymph Ask the patient to breathe in deeply through the mouth.
nodes Distended Feel for the liver edge as it descends on inspiration.
bladder
Move your hand progressively up the abdomen,
1 cm at a time, between each breath the patient
Fig. 6.13 Palpable masses that may be physiological rather than takes, until you reach the costal margin or detect the
pathological. liver edge.
107
Costal margin
Costal margin
Liver edge
Tip enlargement
Mild enlargement
Moderate Moderate enlargement
enlargement
Marked Marked enlargement
enlargement
A B
Fig. 6.15 Patterns of progressive enlargement of liver and of spleen. A Direction of enlargement of the liver. B Direction of enlargement of the
spleen. The spleen moves downwards and medially during inspiration.
108 THE GASTROINTESTINAL SYSTEM
common reason for an audible bruit over the liver, however, is Splenomegaly
a transmitted heart murmur. Liver failure produces additional The spleen has to enlarge threefold before it becomes palpable,
symptoms of encephalopathy, which can be graded (Box 6.11). so a palpable spleen always indicates splenomegaly. It enlarges
Resonance below the fifth intercostal space suggests from under the left costal margin down and medially towards the
umbilicus (Fig. 6.15B). A characteristic notch may be palpable
transverse colon between the liver and the diaphragm (Chilaiditi’s midway along its leading edge, helping differentiate it from an
sign). enlarged left kidney (Box 6.12).
In a patient with right upper quadrant pain, test for Murphy’s
sign (see Box 6.9); a positive modestly increases the probability
of acute cholecystitis. Palpable distension of the gallbladder is
Examination sequence
rare and has a characteristic globular shape. It results from Place your hand over the patient’s umbilicus. With your
either obstruction of the cystic duct, as in mucocoele or hand stationary, ask the patient to inhale deeply through
empyema of the gallbladder, or obstruction of the common the mouth.
bile duct with a patent cystic duct, as in pancreatic cancer. In Feel for the splenic edge as it descends on inspiration.
a jaundiced patient a palpable gallbladder is likely to be due to Move your hand diagonally upwards towards the left
extrahepatic obstruction, such as from pancreatic cancer or, hypochondrium (Fig. 6.16A), 1 cm at a time between each
very rarely, gallstones (Courvoisier’s sign). In gallstone disease breath the patient takes.
the gallbladder may be tender but impalpable because of fibrosis Feel the costal margin along its length, as the position of
of the gallbladder wall. the spleen tip is variable.
If you cannot feel the splenic edge, palpate with your right
hand, placing your left hand behind the patient’s left lower
Fig. 6.16 Palpation of the spleen. A Initial palpation for the splenic edge moving diagonally from the umbilicus to the left hypochondrium. B If the
spleen is impalpable by the method shown in A, use your left hand to pull the ribcage forward and elevate the spleen, making it more likely to be palpable
by your right hand.
109
Fig. 6.17 Percussing for ascites. A and B Percuss towards the flank from resonant to dull. C Then ask the patient to roll on to their other side. In
ascites the note then becomes resonant.
Examination sequence
Examination sequence
With the patient supine, place your stethoscope diaphragm
Shifting dullness to the right of the umbilicus and do not move it.
With the patient supine, percuss from the midline out to Listen for up to 2 minutes before concluding that bowel
sounds are absent.
dull, along with areas of dullness and resonance. Listen above the umbilicus over the aorta for arterial bruits.
110 THE GASTROINTESTINAL SYSTEM
Anterior
6.14 Causes of ascites superior
iliac spine
Diagnosis Comment
Common
Hepatic cirrhosis with portal Transudate Internal
hypertension Inguinal inguinal ring
Intra-abdominal malignancy with Exudate, cytology may be ligament
External
peritoneal spread positive inguinal ring
Uncommon Pubic Spermatic
Hepatic vein occlusion (Budd–Chiari Transudate in acute phase tubercle cord
syndrome) Femoral
Constrictive pericarditis and right Check jugular venous pressure artery
heart failure and listen for pericardial rub
Femoral
Hypoproteinaemia (nephrotic Transudate vein
syndrome, protein-losing
enteropathy)
Tuberculous peritonitis Low glucose content
Pancreatitis, pancreatic duct Very high amylase content
disruption
Femoral canal
Fig. 6.19 Anatomy of the inguinal canal and femoral sheath.
Palpate systematically around the entire rectum; note any a ‘frozen pelvis’ with a hard, rigid feel to the pelvic organs due
abnormality and examine any mass (Fig. 6.24). Record the to extensive peritoneal disease, such as post-radiotherapy or
percentage of the rectal circumference involved by disease in metastatic cervical or ovarian cancer.
and its distance from the anus. Benign prostatic hyperplasia often produces palpable
Identify the uterine cervix in women and the prostate in symmetrical enlargement, but not if the hyperplasia is confined
men; assess the size, shape and consistency of the
prostate and note any tenderness.
If the rectum contains faeces and you are in doubt about 6.16 Causes of abnormal stool appearance
palpable masses, repeat the examination after the patient
has defecated. Stool appearance Cause
Slowly withdraw your finger. Examine it for stool colour Abnormally pale Biliary obstruction
and the presence of blood or mucus (Box 6.16). Pale and greasy Steatorrhoea
Haemorrhoids (‘piles’, congested venous plexuses around the
Black and tarry (melaena) Bleeding from the upper
anal canal) are usually palpable if thrombosed. In patients with
gastrointestinal tract
chronic constipation the rectum is often loaded with faeces.
Faecal masses are frequently palpable, should be movable and Grey/black Oral iron or bismuth therapy
can be indented. In women a retroverted uterus and the normal Silvery Steatorrhoea plus upper gastrointestinal
cervix are often palpable through the anterior rectal wall and a bleeding, e.g. pancreatic cancer
vaginal tampon may be confusing. Cancer of the lower rectum Fresh blood in or on stool Large bowel, rectal or anal bleeding
is palpable as a mucosal irregularity. Obstructing cancer of the
Stool mixed with pus Infective colitis or inflammatory bowel
upper rectum may produce ballooning of the empty rectal cavity disease
below. Metastases or colonic tumours within the pelvis may
Rice-water stool (watery Cholera
be mistaken for faeces and vice versa. Lateralised tenderness
with mucus and cell debris)
suggests pelvic peritonitis. Gynaecological malignancy may cause
Fig. 6.22 The correct position of the patient before a rectal Fig. 6.23 Rectal examination. The correct method for inserting your
examination. index finger in rectal examination.
! " # $
Fig. 6.24 Examination of the rectum. A and B Insert your finger, then rotate your hand. C The most prominent feature in the female is the cervix.
D The most prominent feature in the male is the prostate.
113
to the median lobe. A hard, irregular or asymmetrical gland with Remove the obturator and carefully examine the anal canal
no palpable median groove suggests prostate cancer. Tenderness under good illumination, noting any abnormality. Check for
accompanied by a change in the consistency of the gland may fissures, particularly if the patient reports pain during the
be caused by prostatitis or prostatic abscess. The prostate is procedure.
abnormally small in hypogonadism. Ask the patient to strain down as you slowly withdraw the
instrument to detect any degree of rectal prolapse and the
Proctoscopy presence and severity of any haemorrhoids.
Proctoscopic examination of the anus and lower rectum can
Proctoscopy is visual examination of the anal canal; it is an invasive confirm or exclude the presence of haemorrhoids, anal fissures
procedure and should only be practised after appropriate training. and rectal prolapse. Rectal mucosa looks like buccal mucosa,
Always undertake digital rectal examination first. If examination apart from the presence of prominent submucosal veins. During 6
straining, haemorrhoids distend with blood and may prolapse. If
rather than proctoscopy. the degree of protrusion is more than 3–4 cm, a rectal prolapse
may be present.
Examination sequence
Place the patient in the left lateral position, as for digital Investigations
rectal examination.
With gloved hands, separate the buttocks with the Selecting the relevant investigation depends on the clinical problem
forefinger and thumb of one hand. With your other hand, revealed on history and examination. Investigations are costly
gently insert a lubricated proctoscope with its obturator in and many carry risks, so choose tests capable of distinguishing
place into the anal canal and rectum in the direction of the the likely diagnoses and prioritise the most decisive ones (Box
umbilicus. 6.17 and Figs 6.26–30).
A B
Fig. 6.25 Acute pancreatitis. A Bruising over the flanks (Grey Turner’s sign). B Bruising round the umbilicus (Cullen’s sign).
Continued
114 THE GASTROINTESTINAL SYSTEM
A
B
C
Fig. 6.26 Radiography in gastrointestinal disease. A Air under the
diaphragm on chest X-ray due to a perforated duodenal ulcer. B Dilated B
small bowel due to acute intestinal obstruction. C Dilated loop of large Fig. 6.28 Gastrointestinal endoscopy. A Gastric ulcer. B Gastric
bowel due to sigmoid volvulus. varices.
116 THE GASTROINTESTINAL SYSTEM
Mr Reid, 29 years old, presents with a 6-month history of anorexia, 7 kg weight loss, abdominal pains and diarrhoea (liquid stool). He underwent
appendicectomy 4 months ago following severe right iliac fossa pain.
Please examine the gastrointestinal system
Introduce yourself and clean your hands.
Start with a general inspection: body habitus, signs of dehydration, fever and pallor.
Inspect the hands: palmar erythema, finger clubbing, leuconychia, koilonychia, nicotine stains and swollen finger or wrist joints.
Inspect the face: signs of anaemia (pallor, angular stomatitis), swollen lips and aphthous mouth ulcers.
Inspect the skin: erythema nodosum or pyoderma gangrenosum.
Inspect the abdomen: laparotomy scars or skin fistulae.
Palpate for right iliac fossa tenderness or the presence of a firm, non-tender mass.
Offer to examine the perianal area for the presence of dusky blue discoloration, oedematous skin tags and the presence of fissures, fistulae or
ulcerations.
Thank the patient and clean your hands.
Summarise your findings
This 29-year-old man with a history of weight loss and diarrhoea appears comfortable at rest but looks thin. He has a recently healed appendicectomy
scar, mild periumbilical and left iliac fossa tenderness, and normal bowel sounds.
Suggest a differential diagnosis
The differential diagnosis is Crohn’s disease and irritable bowel syndrome.
Suggest initial investigations
Full blood count, C-reactive protein, liver function tests, urea, creatinine and electrolytes, iron studies, vitamin B12 and folate levels, ileocolonoscopy and
small bowel magnetic resonance imaging, faecal calprotectin.
117
Mr MacDonald, a 61-year-old retired salesman, presents with increasing tiredness and loss of appetite over 4 months. Two weeks ago he noticed dark
urine and pale stools, and his friends have remarked that his eyes have become yellow. He has drunk a litre of whisky a day for the last 5 years,
although recently he has cut down to a bottle of whisky every 3 days.
Please examine this patient’s abdomen
Introduce yourself and clean your hands.
Unless prompted otherwise, proceed to peripheral examination prior to concentrating on the abdomen.
Carry out a general inspection: body habitus, evidence of malnutrition, pallor or jaundice, scratch marks on the forearm and back, bruising.
Examine the hands: palmar erythema, finger clubbing, leuconychia, Dupuytren’s contractures.
Check for flapping tremor.
6
Examine the face: telangiectasias, xanthelasmas, bilateral parotid enlargement and jaundice (yellow sclera of the eyes and skin).
Smell for alcohol or fetor hepaticus.
Inspect the neck and chest for spider naevi, gynaecomastia; look for axillary and chest hair loss.
Inspect the abdomen for distension, everted umbilicus, caput medusae or scars of recent drain insertion.
Palpate and percuss the abdomen for hepatomegaly and splenomegaly.
Percuss for shifting dullness.
Auscultate for hepatic bruits.
Look for peripheral oedema.
Thank the patient and your clean hands.
Summarise your findings
This patient is jaundiced with multiple spider naevi on the chest and abdomen. He has generalised abdominal swelling with shifting dullness and a firm
liver edge palpable 2 cm below the costal margin.
Suggest a differential diagnosis
The differential diagnosis is alcoholic cirrhosis, chronic hepatitis and hepatoma.
Suggested initial investigations
Liver function tests, ferritin, viral hepatitis screen, full blood count and prothrombin time, urea, creatinine and electrolytes, alpha-fetoprotein, abdominal
ultrasound scan and upper digestive endoscopy (to check for oesophagogastric varices).
Position the patient: supine and comfortable on the examination couch. Expose the abdomen from the xiphisternum to the pubic symphysis.
Inspection: start with general observation, then inspect the skin, face, neck and chest, and finally the abdomen.
Palpation:
Begin with light, superficial palpation away from any site of pain, then repeat with deeper palpation.
Describe any mass and decide whether there is an enlarged abdominal organ.
Palpation for hepatomegaly:
Ask the patient to breathe in deeply through the mouth and feel for descent of the liver edge on inspiration.
Move your hand progressively up the abdomen, between each breath, until you reach the costal margin or detect the liver edge.
Percussion to confirm hepatomegaly:
Ask the patient to hold their breath in full expiration.
Percuss for liver dullness and measure the distance in centimetres below the costal margin.
Palpation and percussion for splenomegaly:
Start with your hand over the umbilicus, moving diagonally up and left to feel for the splenic edge as it descends and moves towards the midline
on inspiration.
Check for ascites (shifting dullness):
Percuss from the midline out to the flanks for dullness.
Keep your finger on the site of dullness in the flank; ask the patient to turn on to their opposite side and then percuss again. If the area of
dullness is now resonant, shifting dullness is present.
Check for a fluid thrill:
Place the palm of your left hand flat against the left side of the patient’s abdomen and flick a finger of your right hand against the right side of
the abdomen. If you still feel a ripple against your left hand, a fluid thrill is present.
Auscultation:
Listen to the right of the umbilicus for bowel sounds, above the umbilicus over the aorta for arterial bruits, lateral to the umbilicus for bruits from
renal artery stenosis, and over the liver for hepatic bruits.
Check for peripheral oedema.
Consider a rectal examination (always with a chaperone).
Richard Davenport
Hadi Manji
7
The nervous system
Anatomy and physiology 120 Sensory system 142
The history 120 Anatomy 142
Common presenting symptoms 122 Common presenting symptoms 143
Past medical history 123 Sensory modalities 144
Drug history 124 Peripheral nerves 146
Family history 124 Median nerve 146
Social history 124 Radial nerve 146
The physical examination 124 Ulnar nerve 146
Assessment of conscious level 124 Common peroneal nerve 147
Meningeal irritation 124 Lateral cutaneous nerve of the thigh 147
Speech 125 Interpretation of the findings 147
Dysphasias 125 Investigations 147
Cortical function 126 Initial investigations 147
Cranial nerves 127 Specific investigations 149
Olfactory (I) nerve 127 OSCE example 1: Headache history 149
Optic (II), oculomotor (III), trochlear (IV) and abducens (VI) nerves 128
OSCE Example 2: Tremor 149
Trigeminal (V) nerve 128
Facial (VII) nerve 130 Integrated examination sequence for the nervous system 150
Vestibulocochlear (VIII) nerve 131
Glossopharyngeal (IX) and vagus (X) nerves 131
Accessory (XI) nerve 133
Hypoglossal (XII) nerve 133
Motor system 133
Anatomy 133
Stance and gait 134
Inspection and palpation of the muscles 136
Tone 137
Power 138
Deep tendon reflexes 139
Primitive reflexes 141
Coordination 141
120 THE NERVOUS SYSTEM
Cluster headache Rapid onset, often 30–120 mins, 1–4 attacks Orbital/retro-orbital; Autonomic features, including
waking patient from within 24 h, clusters usually always same side during conjunctival injection, tearing, nasal
sleep last weeks to months, with cluster, may switch stuffiness, ptosis, miosis, agitation
months to years of remission sides between clusters
Stabbing headache Abrupt, rarely from sleep Very brief, seconds or less Anywhere over head Common in migraineurs
Secondary syndromes
Meningitis Usually evolves over a Depends on cause and Global, including neck Fever, meningism, rash, false localising
day or two, can be treatment, usually days to stiffness signs, signs of raised intracranial
abrupt weeks pressure
Subarachnoid Abrupt, immediately May be fatal at onset, Anywhere, poor 20% isolated headache only; nausea/
haemorrhage maximal, rare from sleep usually days to weeks localising value vomiting, reduced consciousness, false
localising signs, III nerve palsies
Temporal arteritis Gradual onset of temple Continuous Temple and scalp Usually in those > 55 years; unwell, jaw
pain and scalp pain on chewing, visual symptoms, tender
tenderness temporal arteries, elevated erythrocyte
sedimentation rate and C-reactive protein
121
Central sulcus
Precentral gyrus
Postcentral gyrus (motor area)
(sensory area)
Parietal lobe
Temporal lobe 7
Cerebellum
Pons
Medulla oblongata
Mixed spinal
nerve Dendrites
Dura mater
Dural root
Anterior median sleeve
fissure Cell body
B Spinal Axon
motor neurone
Seizure
the patient remain symptom-free in between episodes?
An epileptic seizure is caused by paroxysmal electrical discharges
from either the whole brain (generalised seizure) or part of the
Precipitating, exacerbating or brain (focal seizure). A tonic–clonic seizure (convulsion) is the
most common form of generalised seizure, and typically follows a
relieving factors
stereotyped pattern with early loss of consciousness associated
with body stiffening (tonic phase) succeeded by rhythmical jerking
occurred? crescendoing and subsiding over 30–120 seconds (clonic phase);
this is followed by a period of unresponsiveness (often with
such as time of day, menstrual cycle, posture or heavy breathing, the patient appearing to be deeply asleep) and
medication? finally confusion as the patient reorientates (postictal phase).
The history from the patient and witnesses can help distinguish
Associated symptoms syncope from epilepsy (Box 7.2). Focal seizures may or may not
involve loss of awareness (complete loss of consciousness is less
Associated symptoms can aid diagnosis. For example, headache typical) and are characterised by whichever part of the brain is
may be associated with nausea, vomiting, photophobia (aversion involved: for example, a focal motor seizure arising from the motor
to light) and/or phonophobia (aversion to sound) in migraine; cortex, or temporal lobe seizures characterised by autonomic
headache with neck stiffness, fever and rash may be associated and/or psychic symptoms, often associated with automatisms
with meningitis (Box 7.1). such as lip smacking or swallowing. Functional dissociative
attacks (also known as non-epileptic or psychogenic attacks, or
pseudoseizures) are common, and may be difficult to distinguish
Common presenting symptoms from epileptic seizures. These attacks are often more frequent
than epilepsy, sometimes occurring multiple times in a day, and
Headache may last considerably longer, with symptoms waxing and waning.
Headache is the most common neurological symptom and Other features may include asynchronous movements, pelvic
may be either primary or secondary to other pathology. Primary thrusts, side-to-side rather than flexion/extension movements
(idiopathic) causes include: and absence of postictal confusion. The widespread availability
of videophones allows witnesses to capture such events and
may prove invaluable.
headache)
Stroke and transient ischaemic attack than ischaemia include use of anticoagulation, headache, vomiting,
seizures and early reduced consciousness. Haemorrhagic stroke
A stroke is a focal neurological deficit of rapid onset that is is much more frequent in Asian populations. Spinal strokes are
very rare; patients typically present with abrupt bilateral paralysis,
depending on the level of spinal cord affected. The anterior
important risk factor for impending stroke and demand urgent spinal artery syndrome is most common and causes loss of
assessment and treatment. Hemiplegia following middle cerebral motor function and pain/temperature sensation, with relative
artery occlusion is a typical example but symptoms are dictated by sparing of joint position and vibration sensation below the level
the vascular territory involved. Much of the cerebral hemispheres of the lesion.
are supplied by the anterior circulation (the anterior and middle
cerebral arteries are derived from the internal carotid artery), while Dizziness and vertigo
the occipital lobes and brainstem are supplied by the posterior
(vertebrobasilar) circulation (Fig. 7.2).
Patients use ‘dizziness’ to describe many sensations. Recurrent
‘dizzy spells’ affect approximately 30% of those over 65 years
7
A useful and simple clinical system for classifying stroke is
and can be due to postural hypotension, cerebrovascular disease,
shown in Box 7.3.
cardiac arrhythmia or hyperventilation induced by anxiety and
panic. Vertigo (the illusion of movement) specifically indicates a
problem in the vestibular apparatus (peripheral) or, much less
ischaemic, the remainder haemorrhagic. Factors in the history or
examination that increase the likelihood of haemorrhage rather
Dysphasias
2 Parietal lobe
Dominant side Non-dominant side
FUNCTION LESIONS FUNCTION LESIONS
Calculation Dyscalculia Spatial orientation Neglect of non-dominant side
Language Dysphasia Constructional skills Spatial disorientation
Planned movement Dyslexia Constructional apraxia
Appreciation of size, Apraxia Dressing apraxia
shape, weight Agnosia Homonymous hemianopia
and texture Homonymous hemianopia
1 Frontal lobe 3 Occipital lobe
FUNCTION FUNCTION
Personality Analysis of vision
Emotional response
Social behaviour LESIONS
1 2 Homonymous hemianopia
LESIONS Hemianopic scotomas
Disinhibition
Lack of initiative Visual agnosia
Antisocial behaviour Impaired face recognition
Impaired memory (prosopagnosia)
Incontinence 4 3 Visual hallucinations
Grasp reflexes (lights, lines and zigzags)
Anosmia
4 Temporal lobe
Dominant side Non-dominant side
FUNCTION LESIONS FUNCTION LESIONS
Auditory perception Dysphasia Auditory perception Poor non-verbal memory
Speech, language Dyslexia Music, tone sequences Loss of musical skills
Verbal memory Poor memory Non-verbal memory Complex hallucinations
Smell Complex hallucinations (faces, shapes, music) Homonymous hemianopia
(smell, sound, vision) Smell
Homonymous hemianopia
A
Trunk
Shoulder
Hip
Elbow
Wrist
Knee kle
d
Han
An
tle
To ng
Ri ddle x
Lit
es
Mi Inde b
um
Th eck
N ow
Br
Eye
Face
Lips
Vocalisation
Jaw
Ton
tion
Swa gue
llow
ing
liva
S ao n
i
at
c
sti
Ma
Examination sequence
Temporal lobe Bedside testing of smell is of limited clinical value, and rarely
performed, although objective ‘scratch and sniff’ test cards,
The temporal lobe contains the primary auditory cortex, Wernicke’s
area and parts of the limbic system. The latter is crucially important
in memory, emotion and smell appreciation. The temporal lobe their sense of smell is normal, although self-reporting can be
also contains the lower fibres of the optic radiation and the area surprisingly inaccurate.
of auditory perception.
Temporal lobe dysfunction may cause:
Olfactory nerves
Anterior cranial fossa (cribriform plate)
Hypoglossal nerve
(hypoglossal canal)
Posterior cranial fossa
Fig. 7.5 Base of the cranial cavity. The dura mater, with the cranial nerves and their exits from the skull. On the right side, part of the tentorium
cerebelli and the roof of the trigeminal cave have been removed.
C3
Optic (II), oculomotor (III), trochlear (IV)
and abducens (VI) nerves Fig. 7.6 The sensory distribution of the three divisions of the
trigeminal nerve. 1, Ophthalmic division. 2, Maxillary division.
3, Mandibular division.
Examination sequence
Four aspects need to be assessed: sensory, motor and two
reflexes.
Sensory
Ask the patient to close their eyes and say ‘yes’ each time
they feel a light touch (you use a cotton-wool tip for this
1, V2 and V3.
Repeat using a fresh neurological pin, such as a Neurotip,
to test superficial pain.
A B C
D
Fig. 7.9 Herpes zoster. A The ophthalmic division of the left trigeminal (V) nerve is involved. B The maxillary division of the left V nerve. C Cervical
spinal root left C5. D Thoracic spinal root right T8.
Sensory symptoms include facial numbness and pain. Unilateral from the lateral pontomedullary junction in close association with
loss of sensation in one or more branches of the V nerve may
result from direct injury in association with facial fractures
(particularly V2), local invasion by cancer or Sjögren’s syndrome. nerve continues in the facial canal within the temporal bone,
Lesions in the cavernous sinus often cause loss of the corneal exiting the skull via the stylomastoid foramen. Passing through
reflex and V1 or V2
in the facial canal it gives off branches to the stapedius muscle
causes severe, lancinating pain, typically in the distribution of V2 and its parasympathetic fibres, as well as being joined by the
or V3. Reactivation of herpes varicella zoster virus (chickenpox) taste fibres of the chorda tympani (see Fig. 7.10).
can affect any sensory nerve, but typically either V1 or a thoracic
1)
there is a risk of sight-threatening complications. Hutchinson’s
Examination sequence
sign, vesicles on the side or tip of the nose, may be present. Examination is usually confined to motor function; taste is
Clinically significant weakness of the muscles of mastication rarely tested.
is unusual but may occur in myasthenia gravis, with fatigable
chewing.
Motor function
eye closure on one side. Note that minor facial asymmetry
Facial (VII) nerve is common and rarely pathological.
Watch for spontaneous or involuntary movement.
The facial nerve supplies the muscles of facial expression (frontalis,
For the following actions it is often easiest to demonstrate
orbicularis oculi, buccinators, orbicularis oris and platysma) and
the actions yourself and ask the patient to copy you,
carries parasympathetic fibres to the lacrimal, submandibular and
observing for any asymmetry.
Ask the patient to raise their eyebrows and observe for
taste sensation from the anterior two-thirds of the tongue (via
symmetrical wrinkling of the forehead (frontalis muscle).
the chorda tympani; Fig. 7.10).
Ask the patient to screw their eyes tightly shut and resist
you opening them (orbicularis oculi).
Anatomy
Ask the patient to bare their teeth (orbicularis oris).
Ask the patient to blow out their cheeks with their mouth
closed (buccinators and orbicularis oris).
131
Superior salivatory
nucleus
Fig. 7.10 Component fibres of the facial nerve and their peripheral distribution.
Bell’s phenomenon
Loss of Loss of
nasolabial fold nasolabial fold
Anatomy 7
The spinal nuclei arise from the anterior horn cells of C1–5.
Fibres emerge from the spinal cord, ascend through the foramen
magnum and exit via the jugular foramen (see Fig. 7.5), passing
posteriorly.
Examination sequence
Face the patient and inspect the sternomastoid muscles Fig. 7.14 Left hypoglossal nerve lesion. From Epstein O, Perkin GD, de
for wasting or hypertrophy; palpate them to assess their Bono DP, et al. Clinical Examination. 2nd edn. London: Mosby; 1997.
bulk.
Stand behind the patient to inspect the trapezius muscle
for wasting or asymmetry.
Ask the patient to shrug their shoulders, then apply Ask the patient to put out their tongue. Look for deviation
downward pressure with your hands to assess the or involuntary movement.
power. Ask the patient to move their tongue quickly from side to
Test power in the left sternomastoid by asking the patient side.
to turn their head to the right while you provide resistance Test power by asking the patient to press their tongue
with your hand placed on the right side of the patient’s against the inside of each cheek in turn while you press
chin. Reverse the procedure to check the right from the outside with your finger.
sternomastoid. Assess speech by asking the patient to say ‘yellow lorry’.
Test both sternocleidomastoid muscles simultaneously by Assess swallowing with a water swallow test (p. 132).
asking the patient to flex their neck. Apply your palm to
the forehead as resistance. on the affected side and deviation to that side on protrusion (Fig.
7.14). Bilateral lower motor neurone damage results in global
be damaged during surgery in the posterior triangle of the neck, wasting, the tongue appears thin and shrunken and fasciculation
penetrating injuries or tumour invasion. Wasting of the upper fibres may be evident. Normal rippling or undulating movements may be
of trapezius may be associated with displacement (‘winging’) of the mistaken for fasciculation, especially if the tongue is protruded;
upper vertebral border of the scapula away from the spine, while these usually settle when the tongue is at rest in the mouth.
the lower border is displaced towards it. Wasting and weakness
of the sternomastoids are characteristic of myotonic dystrophy. in motor neurone disease, these features are termed bulbar
Weakness of neck flexion or extension, the latter causing head palsy (see Box 7.5).
drop, may occur in myasthenia gravis, motor neurone disease
lesions lead to a tongue with increased tone (spastic) and the
(neck flexed), retrocollis (neck extended) or torticollis (neck twisted patient has difficulty flicking the tongue from side to side. Bilateral
to one side) are not associated with weakness.
palsy (see Box 7.5). Tremor of the resting or protruded tongue
may occur in Parkinson’s disease, although jaw tremor is more
Hypoglossal (XII) nerve common. Other orolingual dyskinesias (involuntary movements
of the mouth and tongue) are often drug-induced and include
tardive dyskinesias due to neuroleptics.
in the dorsal medulla beneath the floor of the fourth ventricle.
A B
Thalamus Caudate
Caudate nucleus Striatum
nucleus Putamen
Putamen
positive result. Swaying is common and should not be stooped posture and impairment of postural reflexes can result
misinterpreted. in a festinant (rapid, short-stepped, hurrying) gait. As a doorway
The ‘pull test’ assesses postural stability. Ask the patient or other obstacle approaches, the patient may freeze. Turning
involves many short steps, with the risk of falls. Postural instability
are going to push them forwards or pull them backwards. on the pull test, especially backwards, occurs in Parkinsonian
They should maintain their position if possible. Standing syndromes. Proximal muscle weakness may lead to a waddling
136 THE NERVOUS SYSTEM
gait with bilateral Trendelenburg signs (see p. 259 and Fig. 13.37). such as professional sports players, may have physiological
Bizarre gaits, such as when patients drag a leg behind them, muscle hypertrophy. Pseudohypertrophy may occur in muscular
are often functional but some diseases, including Huntington’s dystrophy but the muscles are weak.
disease, produce unusual and chaotic gaits.
Fasciculation
Inspection and palpation of the muscles Fasciculations are visible irregular twitches of resting muscles
caused by individual motor units firing spontaneously. This occurs
Examination sequence in lower motor neurone disease, usually in wasted muscles.
Fasciculation is seen, not felt, and you may need to observe
Completely expose the patient while maintaining their
carefully for several minutes to be sure that it is not present.
comfort and dignity.
Physiological (benign) fasciculation is common, especially in the
Look for asymmetry, inspecting both proximally and
calves, but is not associated with weakness or wasting. Myokymia
distally. Note deformities, such as flexion deformities or
– fine, involuntary fascicular contractions – involves rapid bursts
pes cavus (high foot arches).
of repetitive motor unit activity that often affects orbicularis oculi
or the first dorsal interosseus, and is rarely pathological.
involuntary movement.
Abnormal movements
Muscle bulk
Lower motor neurone lesions may cause muscle wasting. This Myoclonic jerks
is not seen in acute upper motor neurone lesions, although These are sudden, shock-like contractions of one or more muscles
disuse atrophy may develop with longstanding lesions. A motor that may be focal or diffuse and occur singly or repetitively.
neurone lesion in childhood may impair growth (causing a smaller Healthy people commonly experience these when falling asleep
limb or hemiatrophy) or lead to limb deformity, such as pes (hypnic jerks). They may also occur pathologically in association
cavus. Muscle disorders usually result in proximal wasting (the with epilepsy, diffuse brain damage and some neurodegenerative
notable exception is myotonic dystrophy, in which it is distal, disorders such as prion diseases. Negative myoclonus (asterixis)
often with temporalis wasting). People in certain occupations, is seen most commonly in liver disease (liver flap).
137
rigidity.
Tone Spasticity is velocity-dependent resistance to passive
movement: it is detected with quick movements and is a feature
Tone is the resistance felt by the examiner when moving a joint
passively. weakness, hyper-reflexia, an extensor plantar response and
Examination sequence it limits the range of movement and may be associated with
Ask the patient to lie supine on the examination couch
and to relax and ‘go floppy’. Enquire about any pain or on attempted extension; in the legs it is more evident on
limitations of movement before proceeding. flexion.
THE NERVOUS SYSTEM
Assess individual muscles depending on the history. Ask weakness. This is helpful both diagnostically and therapeutically,
the patient to undertake a movement. First assess whether as you can show patients that their leg is not actually weak
they can overcome gravity. For example, give the using this sign.
instruction ‘Lift your right leg off the bed’ to test hip
flexion. Then apply resistance to this movement, testing
across a single joint; for instance, apply resistance to the Deep tendon reflexes
thigh in hip flexion, not the lower leg.
To test truncal strength, ask the patient to sit up from a Anatomy
lying position. A tendon reflex is the involuntary contraction of a muscle in
Upper motor neurone lesions produce weakness of a relatively
large group of muscles, such as a limb or more than one limb. of an afferent (sensory) and an efferent (motor) neurone with
Lower motor neurone damage can cause paresis of an individual
and specific muscle, so more detailed examination of individual
one synapse between (a monosynaptic reflex). Muscle stretch
activates the muscle spindles, which send a burst of afferent
7
muscles is required (Ch. 13). Look for patterns of weakness that signals that lead to direct efferent impulses, causing muscle
contraction. These stretch reflex arcs are served by a particular
for example – the extensors in the upper limbs are weaker than spinal cord segment that is modified by descending upper motor
the flexors, and vice versa in the lower limbs. Myopathies tend neurones. The most important reflexes are the deep tendon
to cause proximal weakness and neuropathies often give rise to and plantar responses, whereas others, such as abdominal and
more distal patterns, while mononeuropathies or radiculopathies cremasteric reflexes, are rarely tested and of questionable value.
lead to discrete focal weakness (such as a foot drop caused by
a common peroneal nerve palsy or L5 radiculopathy). example, pain going down one leg, with an absent ankle jerk
Patients may find it difficult to sustain maximum power for (S1) and sensory loss on the sole of the foot (S1 dermatome),
localises to the S1 root, most commonly due to a prolapsed
only show that the patient can achieve maximum power briefly intervertebral disc (sciatica).
to be satisfied that the weakness is not neurological. Very
few organic diseases cause power to fluctuate; the fatigable
weakness of myasthenia is the chief exception. Wildly fluctuating
Examination sequence
or sudden ‘give-way’ weakness suggests a functional explanation. Ask the patient to lie supine on the examination couch
with the limbs exposed. They should be as relaxed and
weak hip extension when it is tested at the same time as comfortable as possible, as anxiety and pain can cause an
contralateral hip flexion (as hip flexion is associated with reflex increased response.
contralateral hip extension), and is often present in functional leg Extend your wrist and allow the weight of the tendon
hammer head to determine the strength of the blow. Strike
your finger that is palpating the biceps and supinator
‘Push down with your right heel’ tendons (otherwise it is painful for the patient), or the
tendon itself for the triceps, knee and ankle jerks.
Weak hip extension Record the response as:
increased (+++)
normal (++)
decreased (+)
present only with reinforcement (+/-)
absent (0).
Principal (deep tendon) reflexes
Ensure that both limbs are positioned identically with the
same amount of stretch. This is especially important for
the ankle reflex, where the ankle is passively dorsiflexed
before striking the tendon.
Compare each reflex with the other side; check for
symmetry of response (Figs 7.19 and 7.20).
‘Lift your left leg’ Use reinforcement whenever a reflex appears to be absent.
Hip extension returns to normal For knee and ankle reflexes, ask the patient to interlock
their fingers and pull one hand against the other on
command (‘Have a tug of war with yourself’), immediately
before you strike the tendon (Jendrassik’s manœuvre).
To reinforce upper limb reflexes, ask the patient to make a
fist with the contralateral hand.
Hoffmann’s reflex
Place your right index finger under the distal
interphalangeal joint of the patient’s middle finger.
Use your right thumb to flick the patient’s finger
downwards.
Fig. 7.18 Hoover’s sign. Look for any reflex flexion of the patient’s thumb.
140 THE NERVOUS SYSTEM
A B C
Fig. 7.19 Testing the deep tendon reflexes of the upper limb. A Eliciting the biceps jerk, C5. B Triceps jerk, C7. C Supinator jerk, C6.
Fig. 7.20 Testing the deep tendon reflexes of the lower limb. A Eliciting the knee jerk (note that the patient’s legs should not be in contact with
each other), L3, L4. B Ankle jerk of the recumbent patient, S1.
mononeuropathy or radiculopathy, such as loss of ankle jerk with 7.10 Primitive reflexes
L5/S1 lumbosacral disc prolapse compressing the S1 nerve root.
Snout reflex
Reflex patterns are helpful in localising neurological lesions and
you should know the nerve roots that serve the commonly tested Lightly tap the lips. Lip pouting is an abnormal response
reflexes (Box 7.9). There are several reflex grading systems but Grasp reflex
interobserver agreement is poor; record reflexes as present (and, Firmly stroke the palm from the radial side. In an abnormal
if so, whether normal, increased or decreased) or absent. Never response, your finger is gripped by the patient’s hand
conclude that a reflex is absent until you have used reinforcement.
Palmomental reflex
An ‘inverted’ biceps reflex is caused by combined spinal cord
Apply firm pressure to the palm next to the thenar eminence with a
tongue depressor. An abnormal response is ipsilateral puckering of
common at the C5/6 level. When elicited, the biceps reflex is
absent or reduced but finger flexion occurs. This is because the
the chin
7
lesion at the C5/6 level affects the efferent arc of the biceps jerk Glabellar tap
(C5 nerve root), causing it to be reduced or lost, and also the Stand behind the patient and tap repeatedly between their eyebrows
spinal cord, increasing reflexes below this level (including the with the tip of your index finger. Normally, the blink response stops
after three or four taps
myeloradiculopathy.
A Hoffmann’s reflex and increased finger jerks suggest
hypertonia; they may occur in healthy individuals but can be
influence body equilibrium, while each hemisphere controls
be pendular and muscle contraction and relaxation tend to be ipsilateral coordination.
slow, but these are not sensitive or specific cerebellar signs.
An extensor plantar (Babinski) response is a sign of upper Examination sequence
motor neurone damage and is usually associated with other upper
motor neurone signs, such as spasticity, clonus and hyper-reflexia. Test cerebellar function by assessing stance and gait (p. 134),
Fanning of the toes is normal and not pathological. including tandem gait (walking in a straight line, heel to toe),
eye movements (looking for nystagmus; p. 164), speech
(dysarthria; p. 125) and limb coordination.
neurone lesions but are also affected by lower motor neurone
Finger-to-nose test
in the obese and the elderly or after abdominal surgery, and are Ask the patient to touch their nose with the tip of their
not part of the routine examination. index finger and then touch your fingertip. Hold your finger
The cremasteric reflex in males (L1, 2) may be absent on at the extreme of the patient’s reach (you should make the
the side of spinal cord or root lesions but this is of little clinical patient use the arm outstretched).
significance. Ask them to repeat the movement between nose and
target finger as quickly as possible.
Primitive reflexes Make the test more sensitive by changing the position of
your target finger. Timing is crucial; move your finger just
These are present in normal neonates and young infants but as the patient’s finger is about to leave their nose,
disappear as the nervous system matures (p. 305). People otherwise you will induce a false-positive finger-to-nose
with congenital or hereditary cerebral lesions and a few healthy ataxia.
individuals retain these reflexes, but their return after early Some patients are so ataxic that they may injure their eye/
childhood is often associated with brain damage or degeneration.
Although often referred to as frontal, the primitive reflexes (snout, targets or ask the patient to touch their chin rather than
grasp, palmomental and glabellar tap) have little localising value nose (Fig. 7.22).
and in isolation are of little significance, but in combination suggest Rapid alternating movements
diffuse or frontal cerebral damage (Box 7.10). Unilateral grasp and
palmomental reflexes may occur with contralateral frontal lobe with the palm and then the back of your opposite hand as
pathology. The glabellar tap is an unreliable sign of Parkinson’s quickly and regularly as possible.
disease. Ask the patient to copy your actions.
Repeat with the opposite hand.
Coordination Alternatively, ask the patient to tap a steady rhythm rapidly
with one hand on the other hand or table, and ‘listen to
Performing complex movements smoothly and efficiently depends the cerebellum’; ataxia makes this task difficult, producing
on intact sensory and motor function and an intact cerebellum. a slower, more irregular rhythm than normal.
2
1 2
A B
Fig. 7.22 Finger-to-nose test. A Ask the patient to touch the tip of their nose (1) and then your finger (2). B Move your finger from one position to
another, towards and away from the patient (1), as well as from side to side (2).
Examination sequence
Ask the patient to perform an imaginary act, such as
drinking a cup of tea, combing their hair, or folding a letter
and placing it in an envelope.
Ask the patient to copy movements you make with your
fingers, such as pointing or making a V sign.
Ask the patient to copy a geometric figure (interlocking
pentagons or cube).
Ask the patient to put on a pyjama top or dressing gown,
one sleeve of which has been pulled inside out.
Ask the patient to lie on the couch and perform cycling
movements with their legs.
The patient may be unable to initiate a task or may perform
Fig. 7.23 Performing the heel-to-shin test with the right leg. it in an odd or bizarre fashion. Constructional apraxia (difficulty
if the heel wavers away from the line of the shin. Weakness may Sensory system
produce false-positive finger-to-nose or heel-to-shin tests, so
demonstrate that power is normal first. The sensory system comprises the simple sensations of light
touch, pain, temperature and vibration, together with joint position
is evident as slowness, disorganisation and irregularity of sense (proprioception) and higher cortical sensations, which
include two-point discrimination, stereognosis (tactile recognition),
disease. Much less reliable signs of cerebellar disease include graphaesthesia (identification of letters or numbers traced on
the rebound phenomenon (when the displaced outstretched the skin) and localisation.
arm may fly up past the original position), pendular reflexes
and hypotonia. unnecessary unless the patient volunteers sensory symptoms
or you suspect a specific pathology, such as spinal cord
structures, such as tumours of the vermis and alcoholic cerebellar
damage, the tests described may be normal and truncal ataxia symptoms, assessing light touch of all four limbs as a screening
cases this may mean that the patient cannot sit unsupported. of the dermatomal distribution (a dermatome is an area of skin
Cerebellar dysfunction occurs in many conditions, and the innervated by a single nerve root) and sensory distribution of
differential diagnosis varies with age and speed of presentation. the more commonly entrapped peripheral nerves (see Figs 7.26
and 7.27 later).
Apraxia
Apraxia, or dyspraxia, is difficulty or inability to perform a task, Anatomy
cortical dysfunction, usually localising to the non-dominant frontal Proprioception and vibration are conveyed in large, myelinated
or parietal lobes. fast-conducting fibres in the peripheral nerves and in the posterior
143
Cerebral hemisphere the patient means lack of sensation rather than weakness or
clumsiness. Neuropathic pain (pain due to disease or dysfunction
of the PNS or CNS) is often severe and refractory to simple
Caudate nucleus analgesia. Reduced ability to feel pain may be accompanied by
scars from injuries or burns (trophic injuries). Sensory symptoms
are defined as follows:
Internal capsule
Lentiform
nucleus
Thalamus
V nerve sensory
nucleus Pons
stimulus 7
Medial lemniscus
and spinothalamic
tract
Examination sequence
The aim here is to focus the examination. Look for a sensory
Nucleus gracilis
Medulla level if the history and examination suggest spinal cord
Nucleus cuneatus pathology; a glove and stocking pattern usually starting
Medial lemniscus
distally, caused by a peripheral neuropathy; or sensory
Spinothalamic tract
Posterior columns disturbance in a specific nerve territory or dermatome. Be
(no relay) guided by the history and the examination findings from the
Vibration
Spinal cord map out their area(s) of sensory disturbance if they can.
Position
1/2 touch
Light touch
Pain Spinothalamic tract While the patient looks away or closes their eyes, use a
Temperature
1/2 touch wisp of cotton wool (or lightly apply your finger) and ask
the patient to say ‘yes’ to each touch.
A Time the stimuli irregularly and make a dabbing rather than
a stroking or tickling stimulus.
Start distally in the feet and hands; work proximally for a
neuropathy or focus on a specific nerve distribution or
dermatome.
C T
L S Superficial pain
Use a fresh neurological pin, such as a Neurotip, not a
side. Record the level at which vibration is detected by the Sensory inattention
patient. Only test if sensory pathways are otherwise intact.
Repeat the process in the upper limb. Start at the distal Ask the patient to close their eyes.
interphalangeal joint of the forefinger; if sensation is Touch their arms/legs in turn and ask which side has been
impaired, proceed proximally to the metacarpophalangeal touched.
joints, wrist, elbow, shoulder and finally clavicle. Now touch both sides simultaneously and ask
whether the left side, right side or both sides were
patient to close their eyes and to report when you stop touched.
the fork vibrating with your fingers.
Joint position sense (proprioception) Sensory modalities
With the patient’s eyes open, demonstrate the
procedure.
Lightly hold the distal phalanx of the patient’s great toe at pathways (touch, pain, temperature, vibration and joint position
the sides. Tell the patient you are going to move their toe sense), sensory examination includes tests of discriminative
up or down, demonstrating as you do so. aspects of sensation, which may be impaired by lesions of the
Ask the patient to close their eyes and to identify the sensory cortex. Assess these cortical sensory functions only if
direction of small movements in random order. the main pathway sensations are intact. Consider abnormalities
on sensory testing according to whether the lesion (or lesions)
ankle, knees and hips. Repeat for the other side. is in the peripheral nerve(s), dorsal root(s) or spinal cord, or is
Repeat for the upper limbs. Start with movements at the intracranial.
distal interphalangeal joint of the index finger; if the
movements are not accurately felt, move to the first Peripheral nerve and dorsal root
metacarpophalangeal joint, wrist, elbow and finally
Many diseases affect peripheral nerves, generally resulting
shoulder.
in peripheral neuropathies or polyneuropathies. Peripheral
Stereognosis and graphaesthesia neuropathies tend to affect the lower limbs, first starting in the
Ask the patient to close their eyes.
Place a familiar object, such as a coin or key, in their hand become involved once the symptoms extend above the knees.
and ask them to identify it (stereognosis). Symptoms first affecting the upper limbs suggest a demyelinating
Use the blunt end of a pencil or orange stick and trace rather than axonal neuropathy or a disease process in the nerve
letters or digits on the patient’s palm. Ask the patient to
identify the figure (graphaesthesia). are lost in a ‘stocking-and-glove’ distribution (Fig. 7.25A). There
Pyramidal weakness
Increased tendon reflexes in left
leg and extensor plantar response
A B
Fig. 7.25 Patterns of sensory loss. A Length-dependent peripheral neuropathy. B Brown–Séquard syndrome. Note the distribution of corticospinal,
posterior column and lateral spinothalamic tract signs. The cord lesion is in the left half of the cord.
145
T2
T2
T2
T1 T1
Fig. 7.26 Dermatomal and sensory peripheral map innervation. Points (shown in blue) for testing cutaneous sensation of the limbs. By applying
stimuli at the points marked, both the dermatomal and main peripheral nerve distributions are tested simultaneously. A Anterior view. B Posterior view.
146 THE NERVOUS SYSTEM
Fig. 7.27 Sensory and motor deficits in nerve lesions. A Median. B Radial. C Ulnar. D Common peroneal. E Lateral cutaneous of the thigh.
(for example, syncope versus seizure; see Box 7.2), and also
Examination sequence epidemiology (sudden-onset leg weakness in a 72-year-old man
Examine the medial elbow, palpating the nerve in the ulnar with diabetes and previous angina is unlikely to have the same
groove (the most common place of entrapment). Note any explanation as a new foot drop in a 20-year-old carpet fitter).
scars or other signs of trauma.
Look for wasting of the interossei (dorsal guttering). investigations are pertinent. Sometimes during the summarising
Test for weakness of finger abduction with the patient’s process it may become clear that there are aspects of the history
fingers on a flat surface, and ask them to spread the that have not been adequately addressed. Go back and resolve
fingers against resistance from your fingers. these areas. Time spent reviewing the history is never wasted;
Test adduction by asking them to grip a card placed undertaking unnecessary tests, on the other hand, is more than
between their fingers and pulling it out using your own just a waste of time.
fingers.
Assess for sensory loss on the ulnar side of the hand, to fit with the history, such as an apparently isolated extensor 7
splitting the ring finger (see Fig. 7.27C).
likely that this is a false-positive sign due to an inept examination/
interpretation of a ticklish patient rather than an indication of
Common peroneal nerve underlying pathology.
The nerve may be damaged by fractures as it winds around
the fibular head, or it may be compressed, particularly in thin,
immobile patients or as a result of repetitive kneeling, squatting Investigations
a foot drop.
Initial investigations
Examination sequence Not all patients require investigation. Most patients with headache,
Test for weakness of ankle dorsiflexion and eversion; for example, need no tests, but some do (such as a 75-year-
test for extension of the big toe (extensor hallucis old man with new-onset headache and temporal tenderness
on examination, who should have urgent measurement of
preserved. the erythrocyte sedimentation rate and C-reactive protein
Test for sensory loss over the dorsum of the foot (see and a temporal artery biopsy). Unfortunately, the increasing
availability of tests means that many patients are investigated
unnecessarily, which creates new problems (such as what to
do with the unexpected, and quite incidental, finding of an
Lateral cutaneous nerve of the thigh
unruptured intracranial aneurysm identified in a patient with
This purely sensory nerve may be compressed as it passes migraine). Avoid doing tests because you can or because you
under the inguinal ligament, producing paraesthesiae in the lateral do not know what else to do. Magnetic resonance imaging
thigh (meralgia paraesthetica, which means burning numbness)
(see Fig. 7.27E). relevance in up to 20%, depending on age, and there is an
irony – usually lost on your patient – in attempting reassurance
with a scan only to identify an incidental ‘abnormality’. Sometimes
Examination sequence a single carefully chosen test is all that is necessary to confirm a
Ask the patient to map out the area of disturbance. diagnosis. For example, a patient with chorea, whose father died
Test for disturbed sensation over the lateral aspect of the of Huntington’s disease, will almost certainly have the diagnosis
thigh. Palpate the abdomen and groin for masses or confirmed with genetic testing, without the need for imaging or
inguinal lymph nodes. other tests.
Consider your diagnosis and start with any necessary simple
blood tests (such as exclusion of metabolic disturbance, including
Interpretation of the findings what to image using which modality (computed tomography,
Having completed the history and examination, first decide sequences or techniques are necessary (like intravenous contrast;
whether the symptoms are due to neurological disease, a
functional neurological disorder or non-neurological causes. Try are unsure. For some PNS disorders, nerve conduction studies
to localise the lesion to a single area of the nervous system if and electromyography may be helpful. Electroencephalography
is perhaps the most misused test in neurology. Think carefully
about whether it will add anything to what you already know;
root, nerves or neuromuscular junction muscle?). Some conditions, it should not be used to diagnose epilepsy. The more invasive
like multiple sclerosis, may give rise to multiple symptoms and tests (lumbar puncture, nerve/muscle/brain biopsy) all require
signs because they involve several lesions; others, like migraine careful consideration and should be guided by specialists.
or functional disorders, do not follow strict neurological and Lastly, the worlds of antibody-mediated and genetic diseases
anatomical rules. are changing rapidly, and you may need to have a discussion with
Having localised the lesion, consider the likely underlying the relevant experts about which specialised test might be most
pathology (What is the lesion?). This will depend on the history appropriate.
THE NERVOUS SYSTEM
A B C
Fig. 7.28 Imaging of the head. A DaTscan showing uptake of tracer (dopamine receptors) in the basal ganglia on cross-section of the brain.
B Magnetic resonance scan showing ischaemic stroke. T2 imaging demonstrates bilateral occipital infarction and bilateral hemisphere lacunar infarction.
C Unenhanced computed tomogram showing subarachnoid blood in both Sylvian fissures (white arrows) and early hydrocephalus. The temporal horns of
the lateral ventricles are visible (black arrows).
A B C
Fig. 7.29 Imaging of the head. A Computed tomogram (CT) showing a cerebral abscess. B Magnetic resonance scan showing multiple sclerosis with
white demyelinating plaques. C CT scan showing a large meningioma arising from the olfactory groove.
A B
Fig. 7.30 T2 magnetic resonance images showing a large left paracentral L4–5 disc protrusion (arrowed) compressing the L5 nerve root.
A Sagittal section. B Axial section.
149
Miss Bolton, 32 years old, presents acutely with a severe global headache, associated with vomiting and feeling dreadful.
Please take a history from this patient
Confirm:
Onset – gradual or sudden.
Site – lateralised or global.
Severity.
Aggravating and relieving factors, such as bright light.
Associated symptoms, such as vomiting, photophobia, neck pain, visual disturbance.
Relevant family history.
Summarise your findings
This 32-year-old woman’s headache began gradually last night and is worse today; she has been in bed in a darkened room, trying to sleep. She has
vomited the analgesia she took. She often has headaches at the time of her period but this is the worst headache she has ever experienced. She
recalls having one or two migraines as a child, and her mother had migraine. She is otherwise well and takes no medication other than the oral
contraceptive. The examination is normal, although she looks tired and distressed.
Suggest a differential diagnosis
The most likely diagnosis is migraine; the headache evolved and worsened over a few hours, with no ‘red flags’, on a background of a predisposition
to migraine. The differential includes more sinister causes such as meningitis, cerebral venous sinus thrombosis or intracranial haemorrhage, but there
are no features to support these. The headache is likely to resolve in the next day or two.
Suggest initial investigations
She does not need any tests, as there are no features to suggest she needs brain imaging or lumbar puncture to exclude a subarachnoid haemorrhage
or meningitis.
Continued
150 THE NERVOUS SYSTEM
A complete neurological examination is demanding for both doctor and patient, and in many cases will not be necessary. The history will dictate a
more targeted examination, and time spent on the history is always more productive than an amateur neurological examination.
Cranial nerve examination
Ask about sense of smell and taste (I).
Assess visual acuity (using a Snellen chart) and visual fields (by confrontation) (II).
Observe pupils and test pupillary reactions bilaterally: direct and consensual (II).
Observe both eyes in the neutral position. Are they orthotropic (both pointing in the same direction)? Test eye movements, observing
for completeness of movement in pursuit and looking for nystagmus (III, IV, VI).
Test facial sensation (V) and corneal reflex (V and VII).
Observe for facial asymmetry and test facial muscles of the upper and lower parts of the face (VII).
Perform a bedside test of hearing (VIII).
Assess speech, swallow and palatal movement (IX, X, XI).
Inspect the tongue and assess movement (XII).
Neurological examination of the upper limb
Expose the upper limbs ensuring maintenance of dignity and privacy; request a chaperone if appropriate.
Inspect for wasting, fasciculations.
As a screening test ask the patient to hold the arms out (palms up) and close their eyes – watch for pronator drift.
Assess tone.
Test muscle power: shoulder abduction (axillary nerve C5), elbow flexion (musculocutaneous nerve, C5, C6) and extension (radial nerve, C7), finger
extension (posterior interosseus nerve, C7), index finger abduction (ulnar nerve, T1), little finger abduction (ulnar nerve, T1), thumb abduction
(median nerve, T1).
Assess reflexes at biceps (C5), triceps (C7) and supinator (brachioradialis, C6).
Test coordination with finger – nose test and look for dysdiodokinesia.
Test sensory modalities: pinprick, temperature, vibration sense, joint position sense.
Neurological examination of the lower limb
Undress the patient to expose both lower limbs fully, ensuring maintenance of dignity and privacy; request a chaperone if appropriate.
Carry out a general inspection, noting walking aids and other associated neurological signs, such as facial droop or ipsilateral arm flexion.
If the patient is able to do so, ask them to stand and walk so that you can assess stance and gait. Assess tandem gait.
Inspect both legs, noting any scars, muscle wasting or fasciculations, abnormal postures or movements.
Assess tone at the hip, knee and ankle. Test for ankle clonus.
Test muscle power. As a simple screen, assess hip flexion (iliofemoral nerve, L1, 2) and extension (sciatic, L5/S1), knee flexion (sciatic, S1) and
extension (femoral, L3, 4), and ankle plantar flexion (tibial, S1, 2) and dorsiflexion (deep peroneal, L4, 5).
Assess reflexes at the knee (L3) and ankle (S1), comparing sides. Test the plantar response.
Test coordination via heel-to-shin tests.
Test sensory modalities: pinprick, temperature, vibration and joint position sense. Map out any symptomatic areas of disturbed sensation.
Shyamanga Borooah
Naing Latt Tint
8
The visual system
Anatomy and physiology 152 The physical examination 160
Eye 152 General examination 160
Extraocular muscles 152 Visual acuity 160
Refractive elements of the eye 153 Orbit and periorbital examination 161
Visual pathway 153 Pupils 161
Pupillary pathways 153 Visual fields 162
The history 155 Ocular alignment and eye movements 163
Common presenting symptoms 155 Ophthalmoscopy 164
Past ocular history 159 Retinopathies 165
Past medical history 159 Investigations 165
Drug and allergy history 159 OSCE example 1: Gradual visual loss 168
Family history 159
OSCE example 2: Double vision 169
Social history 159
Integrated examination sequence for ophthalmology 169
152 THE VISUAL SYSTEM
elevated by the levator palpebrae superioris, innervated by cranial cornea. The cornea accounts for two-thirds of the
refractive power of the eye, focusing incident light on to
autonomic system. Eyelid closure is mediated by the orbicularis the retina.
The orbit also contains six extraocular muscles: the superior of the ciliary body and the iris, and posteriorly the choroid.
rectus, medial rectus, lateral rectus, inferior rectus, superior
responsible for converting light to neurological signals.
Extraocular muscles
fat, which is enclosed anteriorly by the orbital septum and the
eyelids (Fig. 8.1). The six extraocular muscles are responsible for eye movements
The conjunctiva is a thin mucous membrane lining the posterior
rectus, inferior oblique and inferior rectus muscles. Cranial nerve
fornices on to the surface of the globe. The conjunctiva is coated
innervates the lateral rectus muscle. The cranial nerves originate
Orbital fat
Septum
Ora serrata
Zonules
Orbicularis oculi muscle
Retina
Iris
Cornea Vitreous body
Pupil Lens Fovea centralis
Anterior chamber Central retina vein
Central retina artery
Meibomian glands Hyaloid canal Optic nerve
Inferior rectus muscle
Optic disc
Tarsal plate
Ciliary body
Sclera
Inferior oblique
Lateral Medial Lateral Fig. 8.2 Control of eye movements. The direction of
rectus rectus rectus displacement of the pupil by normal contraction of a particular
muscle can be used to work out which eye muscle is paretic. For
example, a patient whose diplopia is maximal on looking down and
Inferior Superior Superior Inferior to the right has either a weak right inferior rectus or a weak left
rectus oblique oblique rectus superior oblique muscle.
153
Oculomotor nerve
Trochlear nerve
Subarachnoid space
Arachnoid mater Temporal
Cavernous sinus lobe
Ophthalmic division
of trigeminal nerve
Maxillary division
of trigeminal nerve
8
in the midbrain and pons and then pass through the cavernous of Budge at the level of T1. Fibres then pass to, and synapse
sinus (Fig. 8.3). in, the superior cervical ganglion before joining the surface of
the internal carotid artery and passing to the pupil along the
nasociliary and the long ciliary nerves (Fig. 8.6B).
Refractive elements of the eye
cornea and the crystalline lens. The cornea possesses the greatest
refractive power and is the main refracting element of the eye; A
the lens provides additional controllable refraction, causing the
light to focus on to the retina. When light is precisely focused on
to the retina, refraction is called emmetropia (Fig. 8.4A). When
the focus point falls behind the retina, the result is hypermetropia
(Fig. 8.4B, long-sightedness). When rays focus in front of the
retina, the result is myopia (Fig. 8.4C, short-sightedness). These
refractive errors can be corrected with lenses or with a pinhole B
(Fig. 8.4D).
Visual pathway
The visual pathway consists of the retina, optic nerve, optic
chiasm, optic tracts, lateral geniculate bodies, optic radiations
C
Pupillary pathways
The pupil controls the amount of light entering the eye. The
intensity of light determines the pupillary aperture via autonomic
D
nerves, and pupillary dilatation is controlled by sympathetic
nerves.
For pupillary constriction, the afferent pathway is the optic
nerve, synapsing in the pretectal nucleus of the midbrain. Axons Fig. 8.4 Normal and abnormal refraction by the cornea and lens.
A Emmetropia (normal refraction). Cornea and lens focus light on the
retina. B Hypermetropia (long-sightedness). The eye is too short and the
passing along the inferior division of the oculomotor nerve to
image on the retina is not in focus. A convex (plus) lens focuses the image
synapse in the ciliary ganglion. The efferent postganglionic on the retina. C Myopia (short-sightedness). The eye is too long and the
image on the retina is not in focus. A concave (minus) lens focuses the
constriction (Fig. 8.6A). image on the retina. D Myopia corrected using a pinhole. This negates
For pupillary dilatation, the sympathetic pathway originates the effect of the lens, correcting refractive errors by allowing only rays from
in the hypothalamus, passing down to the ciliospinal centre directly in front to pass.
154 THE VISUAL SYSTEM
Fig. 8.5 Visual field defects. 1, Total loss of vision in one eye because of a lesion of the optic nerve. 2, Bitemporal hemianopia due to compression of
the optic chiasm. 3, Right homonymous hemianopia from a lesion of the optic tract. 4, Upper right quadrantanopia from a lesion of the lower fibres of the
optic radiation in the temporal lobe. 5, Lower quadrantanopia from a lesion of the upper fibres of the optic radiation in the anterior part of the parietal lobe.
6, Right homonymous hemianopia with sparing of the macula due to a lesion of the optic radiation in the occipital lobe.
A B Posterior
hypothalamus
Müller’s muscle
Light source
First-order neuron
Short ciliary nerve
Ciliary ganglion
Optic nerve
III nerve Long ciliary
Pupil dilator nerve
Edinger–Westphal nucleus Trigeminal nerve
Midbrain Carotid plexus
Lateral geniculate body
Superior
Posterior commissure colliculus
or itchiness
as red eye.
Pain There are many causes of eye discharge, and their clinical
Ask: features are summarised in Box 8.6.
Swollen eyes
The orbit is an enclosed structure, except anteriorly. Any swelling
inside the orbit can lead to proptosis or anterior displacement
of the globe.
Ask if:
The cornea is one of the most highly innervated regions of the
body. When the corneal nerves are activated, this leads to pain,
with these. Box 8.7 summarises the common causes of swollen eyes.
156 THE VISUAL SYSTEM
A B C
D E F
Fig. 8.7 Common causes of an acute change in vision. A Central retinal vein occlusion. B Retinal detachment. Elevation of the retina around
the ‘attached’ optic disc; the retina may even be visible on viewing the red reflex. C Central retinal arterial occlusion. D Herpes simplex virus keratitis.
E Wet age-related macular degeneration. F Swollen optic nerve head in acute optic neuritis.
A B
D E
Fig. 8.8 Common causes of a gradual loss of vision. A Cataract. B Altered red reflex in the presence of cataract. C Dry age-related macular
degeneration. D Compressive optic neuropathy. Optic nerve sheath meningioma causing optic disc pallor and increased disc cupping with sparing of the
outer optic nerve rim. E Retinitis pigmentosa, with a triad of optic atrophy, attenuated retinal vessels and pigmentary changes. The latter typically start
peripherally in association with a ring scotoma and symptoms of night blindness.
158 THE VISUAL SYSTEM
double vision
Fig. 8.9 Sixth nerve palsy causing weakness of the lateral rectus
muscle. The patient is attempting to look to the left.
peripheral vascular disease if starting glaucoma medication.
Family history
Several eye diseases have an inherited predisposition. Ask
8.6 Common causes of increased discharge from the eyes The physical examination
Causes Clinical features
Bacterial Red eye General examination
conjunctivitis Yellow or green sticky discharge
Vision usually unaffected Carefully and systematically examine:
Viral Red eye
conjunctivitis Clear, watery discharge
Possible itchy eye
Vision usually unaffected
Ocular examination: conjunctival chemosis and injection
Blocked White eye
tear duct Clear, colourless tearing
Possible occluded punctum Visual acuity
Possible malposition of the lid
Assessment of visual acuity is mandatory in all ophthalmic patients.
Trichiasis/ Foreign body sensation
foreign body Clear discharge Each eye must be tested separately. The most commonly used
Possible positive fluorescein staining method of testing distance visual acuity is using a Snellen chart,
which displays a random selection of letters at diminishing font
Allergic Possible red eyes
conjunctivitis Possible itchy eyes
Clear discharge
Possible history of hay fever or atopy, or recent start of should be worn only when testing reading vision.
eye medication
Blepharitis Mild injection of lids Examination sequence
Deposits on lashes
Use a backlit Snellen chart positioned at 6 metres and dim
Poor tear Constant tearing the room lighting.
film/dry Watering increased in the wind
Cover one eye and ask the patient to read the chart from
eyes Improvement with tear supplements
the top down until they cannot read any further. Repeat
Ocular examination: early break-up time (< 3 seconds)
with fluorescein staining of tear film for the other eye.
driving.
Assess near vision with a similar test using text of
masses.
Check eye movements (Fig. 8.11).
8
Use an ophthalmoscope (Fig. 8.12) to look for optic disc
swelling from compression. Fig. 8.11 Testing the six positions of gaze. Sit facing the patient, 1
metre away. Perform the test with both eyes open. Hold a pen torch or
target in front of the patient and ask them if they see the target as double.
Pupils Move the target to the six positions of gaze (blue arrows).
First inspect generally for squint and ptosis. Examine pupil shape
Anisocoria
The eyes should be assessed to determine which is the abnormal
pupil.
Examination sequence
there is a constricted pupil (loss of sympathetic dilator tone) and small white hatpin or a white Neurotip. With the patient
looking directly at your eye, bring the white target in from
in the upper eyelid. There may also be anhydrosis (loss of the periphery to the centre (again always in the plane
halfway between you and the patient). Ask the patient to
administering cocaine eye drops, which will cause pupil dilatation
in the unaffected pupil but no dilatation on the affected side. Undertake this for all four quadrants, testing each eye
separately.
Fig. 8.14 Testing the central visual field. Sit facing the patient, 1 metre
away. Present a red target at a point equidistant between yourself and the
Ocular alignment and eye movements patient in the periphery, starting when you can first see the target as red.
Bring the target inwards in the direction of the blue arrows, asking the
patient to alert you when they first see the target as red. Test each eye
for convergence. Any misalignment is referred to as a squint separately.
(strabismus). Squints are described as manifest (tropia) if present
with both eyes open, or latent (phoria) if revealed only by covering
Detection of squint is on the nasal aspect of the pupil in one eye, this
suggests that the eye is deviated outwards and is
described as an exotropia.
Examination sequence
Sit directly facing the patient, approximately 1 metre away uncover test:
and at a similar height. Ask the patient to look at the pen torch at all times and
Check visual acuity as part of the examination. then cover one eye.
Look for any abnormal head posture such as head tilts
be helpful to repeat this several times.
Hold a pen torch directly in front of the patient and instruct it was positioned abnormally outwards and is described
as an exotropia (divergent manifest squint).
164 THE VISUAL SYSTEM
Examination sequence as this will steady the head and improve your
proprioception when moving closer to the patient with the
ophthalmoscope.
target or pen-torch light about 50 cm away.
Rotate the ophthalmoscope lens to +10. This will allow
Ask them to say if and when they experience diplopia.
Starting from the primary position, move the target in the
able to examine the eyelid margins, conjunctiva, cornea
8
Fig. 8.15 Oculocephalic reflex. Move the head in the horizontal plane. Note that the eyes move in the opposite direction to head movement.
Retinopathies
Diabetes mellitus leads to a wide range of important abnormalities
in the retina, which are summarised on Fig. 8.17.
The eye also provides an opportunity to view the effects of
hypertension on the microvasculature. The retinal arteries are
effectively arterioles. Chronic arteriosclerosis with vessel-wall
thickening and hyalinisation appears as widening of the arterioles,
arteriovenous nicking where arterioles cross venules, and a ‘silver
irregularities.
Investigations
Appropriate initial tests for a variety of common presenting eye B
problems are summarised in Box 8.12. Fig. 8.16 The normal fundus. A Caucasian. B Asian.
166 THE VISUAL SYSTEM
8.10 Causes of optic disc swelling 8.11 Differential diagnosis of optic disc pallor
Unilateral Inherited
Optic neuritis Sarcoidosis Congenital optic atrophy, including Leber’s and Behr’s
Anterior ischaemic optic Leukaemia End-stage glaucoma
neuropathy Optic nerve glioma Trauma
Syphilis Secondary metastases
Lyme disease Compressive
Bartonella infection Orbital neoplasm Orbital cellulitis
Thyroid eye disease
Bilateral
Neurological
Papilloedema Pseudopapilloedema in End-stage papilloedema Devic’s disease
Optic disc drusen hypermetropes
Metabolic
Diabetic papillitis Hypertensive papillopathy
Nutritional deficiency Sulphonamide
Toxic amblyopia Diabetes mellitus
Ethambutol
Vascular
Central retinal artery occlusion Giant cell arteritis
Inflammatory
Meningitis Postoptic neuritis
A B
C D
E F
Fig. 8.17 Retinal abnormalities in diabetes mellitus. A Diabetic maculopathy. B Background diabetic retinopathy. C Severe non-proliferative
diabetic retinopathy. D Proliferative diabetic retinopathy. E Proliferative diabetic retinopathy with a vitreous haemorrhage. F Previous panretinal laser
photocoagulation in treated proliferative diabetic retinopathy.
167
A B
C D
Fig. 8.18 Hypertensive retinopathy. A Increased reflectance, giving a silver wiring appearance to the arteriole (arrow). B Focal arteriolar narrowing
(double arrows) seen in grade 2 disease. C Exudates and flame haemorrhages in grade 3 retinopathy. D Signs of malignant hypertension in grade 4
disease with a swollen optic disc and macular exudate.
168 THE VISUAL SYSTEM
8.12 Investigations
Investigation Indication
Clinic tests
Refraction Refractive error, cataract and corneal disorders
Fluorescein staining Corneal epithelial disease
Schirmer’s test Dry eyes, Sjögren’s syndrome
Nasolacrimal duct washout Watery eyes
Blood pressure Hypertensive retinopathy, retinal vein occlusion
Bacterial culture and sensitivity Bacterial conjunctivitis
Viral swab Viral conjunctivitis
Blood tests
Erythrocyte sedimentation rate, C-reactive protein Vasculitis, including giant cell arteritis
Antinuclear antibody Systemic lupus erythematosus
Rheumatoid factor Scleritis
Fasting glucose Diabetic retinopathy
Anti-acetylcholinesterase receptor antibody Myasthenia gravis
Quantiferon Uveitis
Serum angiotensin-converting enzyme Uveitis
Human immunodeficiency virus serology Vasculitis, uveitis
Syphilis serology Unexplained pathology and uveitis/vasculitis
Thyroid function tests Thyroid eye disease
Radiology
Chest X-ray Sarcoidosis/tuberculosis
Orbital ultrasound Incomplete fundal view
Optical coherence tomography Macular disease, glaucoma
Fundus fluorescein angiography Diabetic retinopathy, retinal vein occlusion
Computed tomography brain and sinuses Orbital cellulitis, thyroid eye disease, intracranial tumours, orbital compressive disease
Magnetic resonance imaging brain and orbits Pituitary tumour, compressive lesion
Carotid Doppler ultrasound Carotid artery stenosis in ocular ischaemic syndrome
Invasive tests
Lumbar puncture Idiopathic intracranial hypertension, inflammatory orbital neuropathies
Temporal artery biopsy Giant cell arteritis
Mrs Johnson, 55 years old, presents with a gradual reduction of vision over the last 6 months in both eyes. She says that she also has distortion in
her vision when she is looking at straight lines. In addition, she feels constantly thirsty and is passing urine frequently.
Please examine this patient’s eyes
Introduce yourself and clean your hands.
Perform a general inspection, looking for any signs of squint. Check the bedside for any clues that the patient wears glasses.
Assess visual acuity using a Snellen chart at the appropriate distance.
Examine the eyes, looking for any conjunctival injection, chemosis or swelling.
Dim the room lights.
Test the pupillary light reflexes.
Ideally, dilate the pupils at this stage.
Test the red reflex in each eye.
Dial the fundoscope to +10 and examine the anterior portion of the eye, including the lens.
Dial the fundoscope back to 0 and examine the fundus, looking at the disc and superior, nasal, inferior and temporal fundus.
Finally, inspect the macula.
Thank the patient and clean your hands.
Summarise your findings
Visual acuity is reduced to 6/18 in both eyes, and fundoscopy reveals multiple retinal haemorrhages and exudates, some close to the macula.
Suggest a diagnosis
The most likely diagnosis is diabetic maculopathy.
Suggest initial investigations
Urine dipstick, fasting blood glucose and blood pressure.
Advanced level comments
Diabetic macular oedema is the most common cause of reduced vision in diabetic patients. It may result in distortion of vision, making straight lines
appear bent.
169
Mr Penrose, 75 years old, presents with double vision that has increased rapidly over the last week. He says not only that objects appear side by side
but also that the two images are separated vertically. He feels that his eyelid is drooping on his left side. He constantly has to lift his eyelid to see out
of his left eye.
Please examine the patient’s eye movements
Introduce yourself and clean your hands.
Perform a general inspection: look for ptosis and squint, and examine the bedside for any spectacles that may contain a prism.
Inspect visual acuity for each eye.
Dim the room lights.
Test pupillary light reflexes.
Test all eye movements for ophthalmoplegia.
Examine the optic nerve using an ophthalmoscope.
Examine cranial nerves I, V, VI, VII, VIII, IX, X, XI and XII.
Thank the patient and clean your hands.
8
Summarise your findings
The patient has a partial ptosis on the left with a dilated pupil. Eye movements are diminished with impaired adduction and elevation of the eyeball.
Double vision is confirmed on testing of eye movements.
Suggest a diagnosis
The most likely diagnosis is left incomplete III nerve palsy (complete palsy would cause total ptosis with relief of double vision).
Suggested investigations
Fasting glucose and cholesterol, blood pressure, erythrocyte sedimentation rate, and a magnetic resonance angiogram to check for an underlying
cerebral artery aneurysm.
Advanced level comments
Palsies of the III nerve result in ptosis and diplopia. Microvascular damage to the III nerve usually spares the pupil. Compressive lesions such as
aneurysm cause a dilated pupil, which responds poorly or is completely unresponsive to light.
EAR
clearly. The outer portion of the canal has hair, and glands that
Anatomy and physiology produce ear wax, which forms a protective barrier.
The ear is the specialised sensory organ of hearing and balance. Middle ear
It is divided anatomically into the external, middle and inner ear.
The middle ear is an air-filled space that contains the three
External ear bony, articulated ossicles: the malleus, incus and stapes. The
Eustachian tube opens into the middle ear inferiorly and allows
The external ear consists of the cartilaginous pinna, the external equalisation of pressure and ventilation. Vibrations of the tympanic
auditory canal (cartilage in the lateral one-third, bone in the membrane are transmitted and amplified through the ossicular
medial two-thirds) and the lateral surface of the tympanic chain and focused on to the smaller oval window on which the
membrane (Fig. 9.1). Sound is collected and channelled by stapes sits (Fig. 9.1B). The malleus is attached to the tympanic
the pinna and transmitted via the external auditory canal to membrane and can be seen clearly on otoscopy (Fig. 9.2). The
the tympanic membrane. The external auditory canal has an long process of the incus can also be visible occasionally. The
elongated S-shaped curve; hence it is important to retract the tympanic membrane has a flaccid upper part (pars flaccida) and
pinna when examining the ear to see the tympanic membrane it is important to look carefully in this area, as this is where a
Auditory ossicles
Helix Malleus Incus Stapes
(on oval window)
Triangular fossa
Pinna Semicircular canal
Vestibular nerve
Antihelix Cochlear nerve
External Cochlea
auditory meatus
Tympanic cavity
Tympanic membrane
Tragus
Eustachian tube
Concha
A B
Fig. 9.2 Structures seen on otoscopic examination of the right ear. A Main structures. B Normal tympanic membrane.
173
Examination sequence
Inspection
Pinna skin, shape, size, position, scars from previous
Palpation
Gently pull on the pinna and push on the tragus to check
for pain.
Gently palpate over the mastoid bone behind the ear to
assess for pain or swelling. Fig. 9.3 Examination of the ear using an otoscope.
Fig. 9.5 Auditory canal abnormalities. A Otitis externa. B Exostosis of the external auditory meatus. C Cholesteatoma.
Fig. 9.6 Tympanic membrane abnormalities. A Tympanic membrane perforation (arrow). B Retraction pocket of the pars tensa (arrow). C Grommet
in situ.
Fig. 9.7 Otitis media. A With effusion. B Fluid level behind the tympanic membrane (arrow). C Acute otitis media.
If discharge is noted on otoscopy and the tympanic membrane an offensive discharge and erode the bony ossicles, resulting in
is intact, otitis externa is the likely cause (Fig. 9.5A). The canal a conductive hearing loss (Fig. 9.5C). Fluid behind the tympanic
can reveal exostoses, abnormal bone growth due to cold water membrane is called otitis media with effusion (OME or ‘glue
exposure, often seen in surfers (Fig. 9.5B). ear’, Fig. 9.7A), and a fluid level may be seen (Fig. 9.7B). This
Scarring on the tympanic membrane (tympanosclerosis) commonly affects children and can be treated surgically with
can be caused by previous grommet insertion or infections. insertion of a ventilation tube or grommet (see Fig. 9.6C). If
Tympanic membrane perforations can be central or marginal, persistent OME is seen in adults, the postnasal space needs
and the position and size of the perforation should be noted as to be examined by a specialist to exclude a lesion in that site.
a percentage (Fig. 9.6A). A severe retraction pocket of the pars Acute otitis media presents with pain; the tympanic membrane
tensa can mimic a perforation (Fig. 9.6B). A retraction of the can become inflamed (Fig. 9.7C), and may bulge and eventually
pars flaccida can contain a cholesteatoma, which may cause perforate.
177
Weber’s test
Examination sequence
Strike the prongs of the tuning fork against a hard surface
to make it vibrate.
Place the base of the vibrating tuning fork in the middle of
the patient’s forehead (Fig. 9.8).
Ask the patient, ‘Where do you hear the sound?’
central.
In a patient with normal hearing, the noise is heard in the
middle, or equally in both ears.
In conductive hearing loss the sound is heard louder in the
affected ear. In unilateral sensorineural hearing loss it is heard
louder in the unaffected ear. If there is symmetrical hearing loss
it will be heard in the middle. Fig. 9.8 Weber’s test.
A B
Fig. 9.9 Rinne’s test. A Testing bone conduction. B Testing air conduction.
178 THE EAR, NOSE AND THROAT
test is more sensitive and therefore the tuning fork will lateralise nystagmus may occur. This assesses for gaze nystagmus
and smooth pursuit.
test becomes abnormal (negative). In sensorineural hearing loss, If any oscillations are present, note:
whether they are horizontal, vertical or rotatory
bone conduction. which direction of gaze causes the most marked
Tuning fork test findings are summarised in Box 9.5. nystagmus
in which direction the fast phase of jerk nystagmus
Testing vestibular function occurs.
Discriminating characteristics of nystagmus are detailed in
Testing for nystagmus Box 9.4.
120 120
degrees degrees
A B C
Fig. 9.10 Dix–Hallpike position test. The examiner looks for nystagmus (usually accompanied by vertigo). Both nystagmus and vertigo typically decrease
(fatigue) on repeat testing. See text for details.
179
Unterberger’s test
Fig. 9.11 Magnetic resonance image showing a right acoustic
neuroma (arrow).
Examination sequence
Ask the patient to march on the spot with their eyes
If imbalance or vertigo with nystagmus is induced, it suggests an
closed. The patient will rotate to the side of the damaged
abnormal communication between the middle ear and vestibular
labyrinth.
system (such as erosion due to cholesteatoma).
Fistula test
Investigations
Examination sequence
Compress the tragus repeatedly against the external Initial investigations in ear disease are summarised in Box 9.6
auditory meatus to occlude it. and Figs 9.11–9.12.
40 40 40 40
50 50 50 50
60 60 60 60
70 70 70 70
80 80 80 80
90 90 90 90
100 100 100 100
110 110 110 110
120 120 120 120
130 130 130 130
140 140 140 140
Fig. 9.12 Hearing test (audiogram). A Normal-hearing right and left ears. B Right sensorineural loss. C Right conductive hearing loss. ( Right air
conduction, Left air conduction, Bone conduction)
The paranasal sinuses are air-filled spaces in the skull. There trauma. Bilateral obstruction can be due to rhinitis (allergic or
are paired frontal, sphenoid, maxillary and anterior and posterior non-allergic), or chronic rhinosinusitis with or without polyps.
ethmoid sinuses. The anterior nasal sinuses (frontal, maxillary
and anterior ethmoid) drain into the middle meatus (between Nasal discharge
the middle turbinate and lateral wall of the nose). The posterior
ethmoid and sphenoid sinuses drain into the sphenoethmoidal Ask about:
recess (between the superior turbinate and nasal septum).
Fig. 9.14 Nasal abnormalities. A Turbinate hypertrophy. B Nasal septum perforation post-surgery. C Nasal polyps.
182 THE EAR, NOSE AND THROAT
Drug history
Ask about:
rivaroxaban
Family history
A family history of atopy is relevant in rhinitis. In patients with
epistaxis it is important to establish a family history of hereditary
haemorrhagic telangiectasia or inherited bleeding disorders.
Social history
Fig. 9.15 Rhinophyma as a complication of rosacea.
Occupation is relevant because exposure to inhaled allergens,
occupational dusts and chemicals may exacerbate rhinitis.
Ask about: Exposure to hardwood dust is associated with an increased
risk of sinonasal cancers. Atopic patients should be asked
about pets.
stabbing, tight-band
Heavy alcohol intake, leading to liver disease, can affect
coagulation and is relevant for epistaxis. Smoking impedes
mucociliary clearance and can contribute to nasal problems.
The differential diagnosis of facial pain includes temporo- The physical examination
mandibular joint dysfunction, migraine, dental disease, chronic
rhinosinusitis, trigeminal neuralgia (severe, sharp pain in a
trigeminal distribution), tension headache (band-like, tight pain)
Examination sequence
and cluster headaches (unilateral nasal discharge, eye watering). Assess the external appearance of the nose, noting
swelling, bruising, skin changes and deformity.
Nasal deformity Stand above the seated patient to assess any external
deviation.
The most common cause of nasal deformity is trauma, resulting
Ask the patient to look straight ahead. Elevate the tip of
in swelling, bruising and deviation of the nose. The swelling
their nose using your non-dominant thumb to align the
following trauma will settle over a couple of weeks but residual
nostrils with the rest of the nasal cavity.
deviation may remain if the nasal bones were fractured and
Look into each nostril and assess the anterior nasal
displaced. It is important to establish the impact of the nasal
septum (Fig. 9.16); note the mucosal covering, visible
injury on function (nasal breathing, sense of smell) and cosmetic
vessels in Little’s area, crusting, ulceration and septal
appearance.
perforation. In trauma, a septal haematoma should be
Nasal septal destruction or perforation can result in ‘saddle
excluded.
deformity’ of the nasal bridge. Causes include granulomatosis
with polyangiitis, trauma, cocaine abuse, congenital syphilis and
assess the inferior turbinates. Note any hypertrophy and
iatrogenic factors (septal surgery, Fig. 9.14B).
swelling of the turbinate mucosa.
The nose can appear widened in acromegaly or with advanced
You may see large polyps on anterior rhinoscopy. To
distinguish between hypertrophied inferior turbinates and
chronic acne rosacea of the nasal skin (Fig. 9.15).
nasal polyps, you can lightly touch the swelling with a
cotton bud (polyps lack sensation).
Past medical history Palpate the nasal bones to assess for bony or
cartilaginous deformity.
Ask about:
In trauma, palpate the infraorbital ridges to exclude a step
deformity and also to check infraorbital sensation. Eye
movements should be assessed to rule out restriction of
have asthma) movement related to ‘orbital blowout’.
Place a metal spatula under the nostrils and look for
condensation marks to assess airway patency.
disorders may affect the nose and lower airways). Palpate for cervical lymphadenopathy (p. 32).
For patients with epistaxis it is important to identify any history Note that rigid nasendoscopy and tests of olfaction are
of bleeding diathesis or hypertension. confined to specialist clinics.
183
A B
Fig. 9.16 Nasal examination. A Elevation of the tip of the nose to give a clear view of the anterior nares. B Anterior rhinoscopy using an otoscope
with a large speculum.
9
A B
Fig. 9.17 Computed tomograms of the paranasal sinuses. A Normal scan. B Right-sided chronic sinusitis.
The mucosa of the inferior turbinate on anterior rhinoscopy is perforation and ‘saddle deformity’. It must therefore be identified
pale, moist and hypertrophied in allergic rhinitis (see Fig. 9.14A). and referred for early drainage.
In chronic rhinitis the mucosa is swollen and red. Large polyps Facial swelling is not usually seen in chronic sinusitis but can
occur with dental abscesses and cancer of the maxillary antrum.
(see Fig. 9.14C).
A septal haematoma will appear as a soft, red, fluctuant swelling
of the anterior septum. The septal cartilage receives its blood Investigations
supply from the overlying perichondrium; a septal haematoma
interrupts this supply and can result in cartilage necrosis, septal Initial investigations are summarised in Box 9.7 and Fig. 9.17.
184 THE EAR, NOSE AND THROAT
The mouth extends from the lips anteriorly to the anterior tonsillar Neck
pillar posteriorly and is divided into the vestibule, between the
buccal (cheek) mucosa and the teeth, and the oral cavity internal Anatomically the neck is divided into anterior and posterior
to the teeth. The oral cavity contains the anterior two-thirds of triangles (Fig. 9.21). The anterior triangle is bounded by the
the tongue, the floor of the mouth, the hard palate and the inner midline, the anterior border of the sternocleidomastoid muscle
surfaces of the gums and teeth (Fig. 9.18). The tongue anteriorly and the body of the mandible. The posterior triangle of the neck
has filiform papillae containing taste buds, giving the tongue its is bounded by the posterior border of sternocleidomastoid, the
velvet texture. The circumvallate papillae are groups of taste trapezius muscle and the clavicle. The cervical lymph nodes
buds marking the boundary between the anterior two-thirds drain the head and neck (see Fig. 3.26). Examination of these
and posterior third of the tongue. nodes is described on page 33 and shown in Fig. 3.27. Palpable
Saliva is secreted into the mouth from the parotid, submandibular
and sublingual salivary glands (Fig. 9.19). The parotid gland is caused by atypical infection, inflammation, lymphoma or metastatic
situated anterior to the ear and has a superficial and deep lobe malignancy. The neck can also be subdivided further into different
relative to the facial nerve that runs through it. The parotid duct levels that are used to describe the location of enlarged lymph
opens into the buccal mucosa opposite the second upper molar. nodes in the neck (Fig. 9.22).
The submandibular gland lies anterior and medial to the angle
of the mandible and its duct opens into the floor of the mouth
next to the frenulum of the tongue (see Fig. 9.18). The history
Throat
Common presenting symptoms
The pharynx is a shared upper aerodigestive channel that runs
from the anterior tonsillar pillar to the laryngeal inlet. The larynx Sore mouth
(‘voice box’) is responsible for phonation and also has a protective
Ask about:
function to prevent aspiration. It consists of two external cartilages,
the thyroid cartilage (Adam’s apple) and the cricoid cartilage
(prominence at the top of the trachea; see Fig. 10.1A). The
membrane between the two is called the cricothyroid membrane;
a cricothyroidotomy may be performed by an experienced
clinician at this site as an emergency procedure to obtain an
airway. The sensory supply to the larynx is via the superior and Aphthous ulcers are small, painful, superficial ulcers on the
recurrent laryngeal branches of cranial nerve X (vagus). The motor tongue, palate or buccal mucosa. They are common and usually
supply is mainly from the recurrent laryngeal nerve, which loops heal spontaneously within a few days. Oral ulcers can be caused
round the aortic arch on the left side and the subclavian artery by trauma, vitamin or mineral deficiency, cancer, lichen planus
on the right. or inflammatory bowel disease.
Hard palate
Uvula Opening of
Soft palate parotid duct
Undersurface
of tongue
Posterior Posterior pillar
pharyngeal wall
Tonsil
Vallate papillae Submandibular
Anterior pillar duct Buccal mucosa
Dorsum of tongue Opening of
submandibular Frenulum
duct
A B
Fig. 9.18 Anatomy of the mouth and throat. A Examination with the mouth open. B Examination with the tongue touching the roof of the mouth.
185
I II
III
VI
V
IV
Parotid
gland
Sublingual
gland
Incisors
Secondary dentition
Canine
9.8 The gums in systemic conditions
Premolars
Condition Description
Molars Phenytoin treatment Firm and hypertrophied
Scurvy Soft and haemorrhagic
Acute leukaemia Hypertrophied and haemorrhagic
Cyanotic congenital heart disease Spongy and haemorrhagic
Primary dentition
A sore mouth can also be due to conditions of the gums,
including inflammation (gingivitis) or systemic conditions (Box 9.8).
Infections, including candidiasis (caused by Candida albicans),
herpes simplex and herpes zoster, as well as dental sepsis,
can cause a painful mouth. Candidiasis may be secondary to
poorly fitted dentures, the use of inhaled glucocorticoids or
Fig. 9.20 Primary and secondary dentition. immunodeficiency. Herpes zoster of the maxillary division of
the trigeminal nerve (see Fig. 7.9B) can cause unilateral painful
vesicles on the palate.
Sore throat
Ask about:
jaw muscles)
Stridor
Stridor is a high-pitched noise produced by turbulent airflow
through a narrowed, partially obstructed upper airway and can
indicate laryngeal or tracheobronchial (p. 79) obstruction. It most
commonly occurs on inspiration but may also be expiratory or
biphasic. The level of obstruction determines the type of stridor.
Inspiratory stridor suggests narrowing at the level of the vocal
Dysphonia
Ask about:
Fig. 9.23 Sore throat. A Acute tonsillitis. The presence of pus strongly If hoarseness has been present continuously for more than
suggests a bacterial (streptococcal) aetiology. B Glandular fever showing 3 weeks, urgent laryngoscopy is indicated to exclude laryngeal
palatal petechiae. C A left peritonsillar abscess. (A) From Bull TR. Color cancer. If voice quality is breathy and associated with a weak
Atlas of ENT Diagnosis. 3rd edn. London: Mosby–Wolfe; 1995.
(bovine) cough (p. 78), a recurrent laryngeal nerve palsy
due to lung or oesophageal cancer should be considered.
Neurological disorder
Vocal fatigue
Weak, wet or dysarthric voice
Mouth and throat
Cancer of the larynx Rough voice, constant, progressive,
often affects smokers Examination sequence
Associated with dysphagia,
Listen to the patient’s voice (rough, breathy, wet, muffled,
odynophagia, otalgia
Functional cause nasal escape).
instruments.
Inspection
Ask the patient to remove any dentures.
Look at their lips. Ask them to half-open their mouth and
inspect the mucosa of the vestibule, buccal surfaces and
buccogingival sulci for discoloration, inflammation or
ulceration, then at bite closure. Inspect the parotid duct
opening opposite the second upper molar for any pus or
inflammation.
Ask the patient to open their mouth fully and put the tip of
their tongue behind their upper teeth. Check the mucosa
of the floor of the mouth and the submandibular duct
openings.
Ask them to stick their tongue straight out, noting any
deviation to either side (XII nerve dysfunction), mucosal
Fig. 9.24 Pus discharging from the parotid duct. change, ulceration, masses or fasciculation.
Sudden, painful, unilateral salivary gland swelling (sialadenopathy) Inspect the hard palate (Fig. 9.25) and note any cleft,
is due to a stone obstructing the duct (sialolithiasis). Other abnormal arched palate or telangiectasia.
causes of enlarged salivary glands are mumps (usually bilateral), Inspect the oropharynx. Ask the patient to say ‘Aaah’ and
sarcoidosis, human immunodeficiency virus-related cysts, bacterial use a tongue depressor to improve visualisation.
infection (suppurative parotitis; Fig. 9.24) and cancer. The clinical Assess the soft palate for any cleft, bifid uvula, swelling or
features of important neck lumps are summarised in Box 9.10. lesions.
188 THE EAR, NOSE AND THROAT
Cracking of the lips can be the result of cold exposure (‘chapped biopsy (Fig. 9.27B). Cancers (usually squamous) may occur at
lips’), riboflavin deficiency, chronic atrophic candidiasis or iron any site in the mouth. Any painless persistent mass in the mouth
deficiency (Fig. 9.26). Squamous and basal cell cancers occur should be assumed to be oral cancer and referred urgently for
on the lips and are associated with smoking and sun exposure. biopsy. Similarly, any mouth ulcer persisting for over 3 weeks
The normal tongue appearance includes areas of smooth requires biopsy to exclude cancer (Fig. 9.27C).
mucosa (‘geographic tongue’) or, conversely, excessive furring. A stone may be felt in the submandibular (or, rarely, the parotid)
A smooth red tongue with diffuse papillary atrophy occurs in
iron or vitamin B12 deficiency. Tongue protrusion may be limited poor oral hygiene (Fig. 9.27D).
by neurological disease, painful mouth or a tight frenulum.
Macroglossia (enlarged tongue) occurs in Down’s syndrome, Neck
acromegaly (see Fig. 10.9), hypothyroidism and amyloidosis.
Wasting and fasciculation of the tongue are features of motor The neck must be examined in all patients with mouth or throat
neurone disease. symptoms, or a neck mass.
White plaques of candidiasis on the tongue or mucosa (Fig.
9.27A) come away easily when scraped but leukoplakia (a Examination sequence
keratotic precancerous condition) does not and requires excision
With the patient sitting down and their neck fully exposed 9
(ties and scarves removed and shirt unbuttoned), look at
their neck from in front. Inspect for scars, masses or
pulsation.
From behind, palpate the neck. Work systematically
around the neck. Start in the midline and gently palpate
the submental, submandibular and preauricular areas,
assessing for the presence of any masses or swelling.
Then palpate down the anterior border of the
sternocleidomastoid muscle to the midline inferiorly.
Palpate the midline structures of the neck from inferior to
superior up to the submental area, noting any masses.
If a midline mass is present, ask the patient to swallow
(offer a glass of water if needed) and then instruct them to
stick out their tongue while you palpate the mass.
Fig. 9.26 Angular stomatitis. Movement superiorly on swallowing suggests a thyroid
Fig. 9.27 Disorders of the tongue and teeth. A Oral thrush. B Leukoplakia. C Aphthous stomatitis causing a deep ulcer in a patient with
inflammatory bowel disease. D Dental caries. (B) From Bull TR. Color Atlas of ENT Diagnosis. 3rd edn. London: Mosby–Wolfe; 1995.
190 THE EAR, NOSE AND THROAT
Mrs Lewis, 55 years old, presents with a lump just under her left ear at the angle of her jaw.
Please examine her neck lump
Introduce yourself and clean your hands.
Inspect the neck for scars or swelling. If a neck lump is visible, describe its size, shape and site, as well as any skin changes. If it is in the midline,
ask the patient to swallow and stick out their tongue.
Ask if the lump is painful and if the patient minds you examining it.
Palpate the lump to assess consistency, edge, fixation to deeper structures, tethering to the skin, warmth, fluctuance, pulsatility and
transillumination.
Palpate the anterior and posterior triangles of the neck, and the parotid region.
Examine the oral cavity, throat, nose and ears (as potential primary sites of infection or malignancy that might be causing the neck mass).
Assess facial nerve function if you suspect a parotid mass.
Thank the patient and clean your hands.
Summarise your findings
Examination confirms a firm, non-tender, mobile lump about 1 cm in diameter behind the angle of the jaw on the left. 9
Suggest a diagnosis
The most likely diagnosis is a pleomorphic salivary adenoma in the tail of the parotid.
Suggest investigations
Ultrasound scan with or without fine-needle aspiration.
Position the patient: on an examination couch with the upper body at 45 degrees and neck fully exposed.
Examine the ears:
Inspect: pinna skin, shape, size, position, deformity, scars.
Palpate: pinna, tragus, mastoid.
Otoscopy: external auditory canal (swelling, discharge), tympanic membrane (red, perforated).
If there is hearing loss: whispered voice test and tuning fork tests.
If there are balance symptoms: vestibular examination, including Dix–Hallpike.
Examine the nose:
Inspect:
– External nose (swelling, bruising, skin changes, deformity).
– Anterior nasal septum (swelling, visible vessels, crusting ulceration, septal perforation). Exclude septal haematoma in nasal trauma.
– Inferior turbinates (hypertrophy, swelling, polyps).
Palpate:
– Nasal bones (bony or cartilaginous deformity).
– Airway patency using metal spatula.
Examine the mouth and throat:
Listen to the voice (rough, breathy, wet, muffled, nasal escape).
Remove any dentures.
Inspect:
– Oral cavity, oropharynx.
– Mucosal discoloration, inflammation, ulceration, masses, opening of parotid and submandibular ducts.
– Hard palate for cleft, abnormal arched palate, telangiectasia.
– Soft palate for cleft, bifid uvula, swelling or lesions.
– Tonsils, noting size, symmetry, colour, pus or membrane.
Palpate:
– Any lesion, identifying characteristics.
– Base of tongue or tonsils if asymmetrical.
– Parotid and submandibular ducts, feeling for stones.
Examine the neck:
Inspect:
– Scars, skin changes.
– If there is midline swelling, ask the patient to swallow and stick out their tongue.
Palpate:
– Anterior and posterior triangles of the neck and parotid region.
– If there is a neck lump, note size, site, shape, consistency, edges, attachments, tenderness, warmth, pulsatility, transillumination.
– If there is a parotid lump, assess the facial nerve.
Anna R Dover
Nicola Zammitt
10
The endocrine system
The thyroid 194 The adrenals 201
Anatomy and physiology 194 Anatomy and physiology 201
The history 194 The history 201
Common presenting symptoms 194 Common presenting symptoms 201
Past medical, drug, family and social history 196 Past medical and drug history 202
The physical examination 197 The physical examination 202
General examination 197 The gonads 204
Thyroid gland 197
Anatomy and physiology 204
Eyes 198
The history 204
The parathyroids 198
Common presenting symptoms 204
Anatomy and physiology 198
Diabetes 205
The history 198
Anatomy and physiology 205
Common presenting symptoms 198
Past medical, drug, family and social history 199 The history 205
Common presenting symptoms 205
The physical examination 199
Past medical, drug, family and social history 205
The pituitary 200
The physical examination 206
Anatomy and physiology 200
OSCE example 1: Neck swelling 209
The history 200
OSCE Example 2: Diabetic feet 209
Common presenting symptoms 200
Family history 200
The physical examination 200
194 THE ENDOCRINE SYSTEM
Endocrine glands synthesise hormones that are released into Since hormones circulate throughout the body, symptoms and
the circulation and act at distant sites. Diseases may result signs of endocrine disease are frequently non-specific, affecting
from excessive or inadequate hormone production, or target many body systems (Box 10.1). Often, endocrine disease is
organ hypersensitivity or resistance to the hormone. The main picked up incidentally during biochemical testing or radiological
endocrine glands are the pituitary, thyroid, adrenals, gonads imaging. Careful history taking and examination are required to
(testes and ovaries), parathyroids and the endocrine pancreas. recognise characteristic patterns of disease. Thyroid disease and
With the notable exception of the pancreatic islet cells (which diabetes mellitus are common and frequently familial; establishing
release insulin) and the parathyroids, most endocrine glands a detailed family history is therefore important. Some less common
are themselves controlled by hormones released from the endocrine disorders (such as multiple endocrine neoplasia) show
pituitary. an autosomal dominant pattern of inheritance.
THE THYROID
is the most common cause (Fig. 10.2 and Box 10.2). It is an
Anatomy and physiology autoimmune disease with a familial component and is 5–10
times more common in women, usually presenting between 30
The thyroid is a butterfly-shaped gland that lies inferior to the and 50 years of age. Other causes include toxic multinodular
cricoid cartilage, approximately 4 cm below the superior notch goitre, solitary toxic nodule, thyroiditis and excessive thyroid
of the thyroid cartilage (Fig. 10.1A). The normal thyroid has a hormone ingestion.
volume of < 20 mL and is palpable in about 50% of women and Hypothyroidism is caused by reduced levels of thyroid
25% of men. It is comprised of a central isthmus approximately hormones, usually due to autoimmune Hashimoto’s thyroiditis,
1.5 cm wide, covering the second to fourth tracheal rings, and and affects women approximately six times more commonly
two lateral lobes that are usually no larger than the distal phalanx than men. Most other causes are iatrogenic and include previous
of the patient’s thumb. The gland may extend into the superior radioiodine therapy or surgery for Graves’ disease.
mediastinum and can be partly or entirely retrosternal. Rarely, it
can be located higher in the neck along the line of the thyroglossal
duct, an embryological remnant of the descent of the thyroid
from the base of the tongue to its final position. Thyroglossal
The history
cysts can also arise from the thyroglossal duct; they often occur
at the level of the hyoid bone (Fig. 10.1A) and characteristically
move upwards on tongue protrusion. The thyroid is attached to
Common presenting symptoms
the pretracheal fascia and thus moves superiorly on swallowing
Neck swelling
or neck extension.
Thyrotoxicosis is a clinical state of increased metabolism caused Goitre is enlargement of the thyroid gland (Fig. 10.3). It is not
by elevated circulating levels of thyroid hormones. Graves’ disease necessarily associated with thyroid dysfunction and most patients
195
Hyoid bone
Sternocleidomastoid
muscle
Thyroid cartilage
Cricothyroid membrane
Cricoid cartilage
Lobe of thyroid gland
Parathyroid
Isthmus of thyroid gland
Trachea
Manubrium of the sternum
A B
Fig. 10.1 The thyroid gland. A Anatomy of the gland and surrounding structures. B Palpating the thyroid gland from behind.
10
D
Fig. 10.2 Graves’ hyperthyroidism. A Typical facies. B Severe inflammatory thyroid eye disease. C Thyroid acropachy. D Pretibial myxoedema.
with goitre are euthyroid. Large or retrosternal goitres may cause occult nodules; thus many are found incidentally on neck or
compressive symptoms, including stridor, breathlessness or chest imaging.
dysphagia.
Thyroid nodules may be solitary (Fig. 10.3C) or may present as
Neck pain
a dominant nodule within a multinodular gland. Palpable nodules
(usually > 2 cm in diameter) occur in up to 5% of women and Neck pain is uncommon in thyroid disease and, if sudden in
less commonly in men, although up to 50% of patients have onset and associated with thyroid enlargement, may represent
196 THE ENDOCRINE SYSTEM
C D
Fig. 10.3 Thyroid enlargement. A 99m
Technetium radionuclide scan demonstrating diffuse goitre due to Graves’ disease. B Diffuse goitre due to
Graves’ disease. C Solitary toxic nodule. D 99mTechnetium radionuclide scan confirming multinodular goitre. (A and D) Courtesy of Dr Dilip Patel.
menses, respectively)
Past medical, drug, family and social history
pain, eyelid swelling or erythema, blurred vision or diplopia
(these symptoms of ophthalmopathy occur in the setting Ask about:
of autoimmune thyroid disease).
Husky voice
Graves’ disease)
Goitre
Bradycardia
Oligomenorrhoea
Carpal tunnel
syndrome
Menorrhagia
Constipation
(in Graves’ disease)
General
General
increased appetite
Fig. 10.4 Features of hyper- and hypothyroidism. Fig. 10.5 Typical facies in hypothyroidism.
198 THE ENDOCRINE SYSTEM
THE PARATHYROIDS
polyuria, polydipsia, renal stones, peptic ulceration, tender areas
Anatomy and physiology
and delirium or psychiatric symptoms. In hypoparathyroidism,
There are usually four parathyroid glands situated posterior to hypocalcaemia may cause hyper-reflexia or tetany (involuntary
the thyroid (see Fig. 10.1A). Each is about the size of a pea muscle contraction), most commonly in the hands or feet.
and produces parathyroid hormone, a peptide that increases Paraesthesiae of the hands and feet or around the mouth may
circulating calcium levels. occur. Hypoparathyroidism is most often caused by inadvertent
damage to the glands during thyroid surgery but may also be
caused by autoimmune disease. Patients with the rare autosomal
The history dominant condition pseudohypoparathyroidism have end-organ
resistance to parathyroid hormone and typically have short stature,
a round face and shortening of the fourth and fifth metacarpal
Common presenting symptoms bones (Fig. 10.6B,C).
10
C
Fig. 10.6 Parathyroid disease. A Well-defined lucent lesion with surrounding sclerosis within the shaft of the third metacarpal of the right hand (arrow),
in keeping with a Brown tumour. B Pseudohypoparathyroidism: short fourth and fifth metacarpals. C These are best seen when the patient makes a fist.
(A) Courtesy of Dr Dilip Patel.
Ask about:
(hypocalcaemia).
THE PITUITARY
or headache due to expansion of the sella. Adenomas may
Anatomy and physiology produce hormones such as prolactin, GH or ACTH; the resulting
symptoms and signs will depend on the excess hormone
The pituitary gland is enclosed in the sella turcica at the base of present.
the skull beneath the hypothalamus. It is bridged over by a fold of
dura mater (diaphragma sellae) with the sphenoidal sinus below Prolactinoma
and the optic chiasm above. Lateral to the pituitary fossa are the
Ask about:
cavernous sinuses, containing cranial nerves III, IV and VI and the
internal carotid arteries. The gland comprises anterior and posterior
lobes. The anterior lobe secretes adrenocorticotrophic hormone
(ACTH), prolactin, growth hormone (GH), thyroid-stimulating
hormone (TSH) and gonadotrophins (luteinising hormone (LH) frequency (in men).
and follicle-stimulating hormone (FSH)). The posterior lobe is
an extension of the hypothalamus, and secretes vasopressin Acromegaly
(antidiuretic hormone) and oxytocin. GH excess prior to puberty presents as gigantism; after puberty,
it causes acromegaly.
Ask about:
The history
Family history
Enquire about family history since pituitary disease can occur as
part of inherited multiple endocrine neoplasia or familial pituitary
syndromes.
Examination sequence
Look at the face for coarsening of features, thick, greasy
skin, prominent supraorbital ridges, enlargement of the
nose, prognathism (protrusion of the mandible) and
separation of the lower teeth (Fig. 10.9A,B).
Examine the hands and feet for soft-tissue enlargement
and tight-fitting rings or shoes, carpal tunnel syndrome
and arthropathy (Fig. 10.9C,D).
Assess the visual fields (p. 162).
Fig. 10.8 Pituitary macroadenoma. The tumour extends into the Check the blood pressure and perform urinalysis.
suprasellar cistern and is compressing the optic chiasm. Courtesy of Hypertension and diabetes mellitus are common
Dr Dilip Patel. associations.
201
10
D
Fig. 10.9 Acromegaly. A Typical facies. B Prognathism and separation of the lower teeth. C Large, fleshy hands. D Widening of the feet.
THE ADRENALS
A B
Fig. 10.10 Hypopituitarism. A Hypopituitarism caused by a pituitary adenoma (note the fine, pale skin). B Absent axillary hair.
distributed hump’).
Examine the skin for thinning and bruising (10.11D), striae
(especially abdominal; Fig. 10.11C), acne, hirsutism and
myopathy). signs of infection or poor wound healing.
Measure the blood pressure.
Addison’s disease Examine the legs for proximal muscle weakness and
oedema.
Ask about: Perform ophthalmoscopy for cataracts and hypertensive
retinal changes (see Fig. 8.18).
Perform urinalysis for glycosuria.
203
10
A B
C
Fig. 10.11 Cushing’s syndrome. A Cushingoid facies. B After curative pituitary surgery. C Typical features: facial rounding and plethora, central
obesity, proximal muscle wasting and violaceous skin striae. D Skin thinning: purpura caused by wristwatch pressure.
A
Fig. 10.12 Addison’s disease. A Hyperpigmentation in a patient with coexistent vitiligo. B Buccal pigmentation.
THE GONADS
failure). Klinefelter’s syndrome (47XXY) is the most common cause
Anatomy and physiology of primary hypogonadism in men (1 : 600 live male births; Fig.
10.13). Secondary hypogonadism may be caused by pituitary
The gonads (testes and ovaries) secrete sex hormones disease, extremes of weight, or drugs that suppress hypothalamic
(testosterone and oestrogen) in response to gonadotrophin gonadotrophin releasing hormone release (such as anabolic
(FSH and LH) release by the pituitary. The reproductive system steroids or opiates). Presenting symptoms in men include loss
is covered in Chapter 11. of libido, erectile dysfunction, loss of secondary sexual hair,
reduction in testicular size and gynaecomastia (p. 214).
Hyperandrogenism in women usually presents with hirsutism
The history (excessive male-pattern hair growth; Fig. 10.14), acne and/or
oligomenorrhoea, and is commonly due to polycystic ovarian
syndrome (PCOS; usually also associated with obesity).
Common presenting symptoms Other less common causes should be considered (such as
congenital adrenal hyperplasia). Virilisation is suggested by
Most commonly, men present with androgen deficiency, whereas male-pattern baldness, deepening of the voice, increased
women present with hyperandrogenism. muscle bulk and clitoromegaly; if present in women with a short
Hypogonadism can be primary (failure of the gonad itself) or history of severe hirsutism, consider a testosterone-secreting
secondary (where reduced gonadotrophin levels cause gonadal tumour.
205
10
DIABETES
insulin-resistant, although impaired beta-cell function is are risk factors for progression to type 2 diabetes.
also important. These patients may decompensate by
developing a hyperosmolar hyperglycaemic state. (increased incidence of type 1 diabetes).
Secondary causes of diabetes and the associated history and
examination features are described in Box 10.5. diabetes.
10.6 Routine history taking as part of the annual Assessment of a patient with newly
review in diabetes diagnosed diabetes
Glycaemic control
Ask about frequency of blood glucose testing and frequency and Examination sequence
awareness of symptoms of hypoglycaemia
When relevant, give guidance on driving and/or pre-pregnancy Look for evidence of weight loss and dehydration.
preparation Unintentional weight loss is suggestive of insulin deficiency.
Check for clinical features of acromegaly or Cushing’s
Injection sites
syndrome.
Enquire about any lumpiness (lipohypertrophy), bruising or Look for Kussmaul respiration (hyperventilation with a
discomfort deep, sighing respiratory pattern) or the sweet smell of
Symptoms of macrovascular disease ketones, both of which suggest insulin deficiency and
Ask whether there has been any angina, myocardial infarction, diabetic ketoacidosis.
claudication, stroke or transient ischaemic attack since the last Skin: look for signs of infection such as cellulitis, boils,
clinic review abscesses and fungal infections, paying particular attention
Symptoms of microvascular disease to the feet (see later). Look for signs of insulin resistance
such as acanthosis nigricans (Fig. 10.15A). Necrobiosis
Ask whether there has been any change in vision or any numbness
or altered sensation in the feet lipoidica, a yellow, indurated or ulcerated area surrounded
by a red margin indicating collagen degeneration (Fig.
Feet
10.15B), may occur on the shins in type 1 diabetes and
Ask about neuropathy and peripheral vascular symptoms as above often causes chronic ulceration.
Enquire about any breaks in the skin, infections or ulcers Look for xanthelasmata and xanthomata (Fig. 10.15C; see
Autonomic neuropathy Fig. 4.6); these are suggestive of dyslipidaemia, which may
Enquire about erectile dysfunction in men occur in type 2 diabetes.
Ask about postural hypotension, sweating, diarrhoea and vomiting in Measure the pulse and blood pressure, and examine the
all patients cardiovascular and peripheral vascular systems, with a
particular emphasis on arterial pulses in the feet (p. 69).
Examine the central nervous system, with a particular
focus on sensation in the lower limbs (p. 143).
Test visual acuity and perform fundoscopy (p. 164; see
In established diabetes, vital aspects of the history (Box Fig. 8.16).
10.6) and examination should be reviewed at least once Perform urinalysis for glycosuria.
a year. Microvascular, neuropathic and macrovascular complications
of hyperglycaemia can occur in patients with any type of diabetes
mellitus, and may be present at diagnosis in patients with
The physical examination slow-onset type 2 disease.
Glycosuria is in keeping with diabetes; the presence of urinary
The physical examination will differ, depending on whether this (or blood) ketones suggests insulin deficiency and the possibility
is a new presentation of diabetes or a patient with established of diabetic ketoacidosis. Other investigations to consider are
diabetes attending for their annual review. summarised in Box 10.7.
207
A B
A Fig. 10.17 Monofilament sensory testing of the diabetic foot.
A Apply sufficient force to allow the filament to bend. B Sites at highest
risk (toes and metatarsal heads).
and the best sites to test are shown in Fig. 10.17. Avoid
areas of untreated callus. Sensory loss typically occurs in
a stocking distribution.
Assess dorsal column function by testing vibration and
proprioception.
Undertake a foot risk assessment to guide management
(Box 10.8).
Hair loss and nail dystrophy occur with ischaemia. Feet are
warm in neuropathy and cold in ischaemia. Ischaemic ulcers are
B typically found distally: at the tips of toes (see Fig. 10.16B), for
Miss Duncan, 27 years old, presents with a 6-month history of palpitations, weight loss and neck swelling.
Please examine her thyroid status
Introduce yourself and clean your hands.
Carry out a general inspection, observing dress, body habitus, agitation, restlessness, diaphoresis, anxiety, exophthalmos, goitre and neck scars.
Inspect the hands for vitiligo, palmar erythema, thyroid acropachy and fine tremor (hands outstretched with paper over the dorsum).
Palpate the pulse for bounding pulse, tachycardia and atrial fibrillation.
Inspect the eyes for lid retraction (scleral show) and exophthalmos (look down from above and behind the patient).
Test eye movements for ophthalmoplegia and lid lag.
Examine the neck for scars, goitre, lymphadenopathy. Ask the patient to swallow to see the thyroid gland rise on swallowing.
Palpate the thyroid (again on swallowing) and cervical lymph nodes; percuss manubrium for retrosternal goitre.
Auscultate any goitre for bruit.
Assess the patient for proximal myopathy (ask them to stand from sitting, with their arms crossed).
Examine the shins for pretibial myxoedema and test for hyper-reflexia.
Thank the patient and clean your hands.
Summarise your findings
The patient is thin, with a fine tremor, tachycardia, exophthalmos and lid lag. In the neck there is a smooth, non-tender goitre. 10
Suggest a diagnosis
These findings suggest autoimmune thyrotoxicosis (Graves’ disease).
Suggest investigations
Thyroid function tests, thyroid receptor autoantibodies and thyroid scintigraphy.
Advanced level comments
Thyrotoxicosis may cause an elevated alkaline phosphatase and hypercalcaemia due to increased bone turnover and a normochromic normocytic
anaemia.
Mr Birnam, 67 years old, has type 2 diabetes and presents with pain in his lower limbs.
Please examine his feet
Introduce yourself and clean your hands.
Carry out a general inspection of the lower limbs, looking for hair loss, nail dystrophy or discoloration.
Inspect the skin for excessive callus, infections and ulcers.
Inspect the joints. Ask the patient to stand so that you can assess the foot arch and look for deformation of the joints of the feet.
Palpate the feet to assess the temperature of the skin.
Palpate the dorsalis pedis and posterior tibial pulses.
Test for peripheral neuropathy using a 10-g monofilament and tuning fork.
Thank the patient and clean your hands.
Summarise your findings
The patient has pale, cool feet with absent dorsalis pedis pulses bilaterally. The skin is intact but there is loss of sensation in a stocking distribution in
both feet.
Suggest a diagnosis
The most likely diagnosis is peripheral vascular disease and peripheral neuropathy secondary to diabetes.
Suggest investigations
Doppler studies to evaluate the ankle : brachial pressure index. Review of diabetes control.
Advanced level comments
With peripheral neuropathy, also take an alcohol history and check vitamin B12 levels to take other common causes of peripheral sensory loss into
account. Peripheral neuropathy can be confirmed on nerve conduction studies. Offer an examination for other microvascular complications, such as
retinopathy (fundoscopy) and nephropathy (test urine for microalbuminuria).
11
Oliver Young
Colin Duncan
Kirsty Dundas
Alexander Laird
Obstetric history and examination: the booking visit 225 OSCE example 1: Breast examination 236
BREAST
breast responds to fluctuations in oestrogen and progesterone
Anatomy and physiology levels. Swelling and tenderness are common in the premenstrual
phase. The glandular tissue reduces and fat increases with age,
The breasts are modified sweat glands. The openings of making the breasts softer and more pendulous. Lactating breasts
the lactiferous ducts are on the apex of the nipple, which is are swollen and engorged with milk, and are best examined
erectile tissue. The nipple is in the fourth intercostal space in after breastfeeding.
the mid-clavicular line, but accessory breast/nipple tissue may
develop anywhere down the nipple line (axilla to groin) (Figs 11.1
and 11.2). The adult breast is divided into the nipple, the areola The history
and four quadrants (upper outer to lower inner), with an axillary tail
(of Spence) projecting from the upper outer quadrant (Fig. 11.3). Benign and malignant conditions of the breast cause similar
The size and shape of the breasts are influenced by age, symptoms but benign changes are much more common. The
hereditary factors, sexual maturity, phase of the menstrual cycle, most common presenting symptoms are a breast lump, breast
parity, pregnancy, lactation and nutritional state. Fat and stroma pain, and skin and nipple changes. Men may present with
surrounding the glandular tissue determine the size of the breast, gynaecomastia (breast swelling). Women are often worried that
except during lactation, when enlargement is mostly glandular. The they have breast cancer, whatever breast symptom they have,
and it is important to explore these concerns.
The history of the presenting symptoms is crucial. Find out
the nature and duration of symptoms, any changes over time
and any relationship to the menstrual cycle.
Ask about risk factors for breast cancer, in particular:
those affected
Tail of Spence
Upper outer
Upper inner
Lower outer
Lower inner
Fig. 11.2 Cross-section of the female breast. Fig. 11.3 Adult right breast.
213
Fig. 11.4 Skin dimpling due to underlying malignancy. Fig. 11.6 Paget’s disease of the nipple.
Gynaecomastia patient declines, note this. Male doctors should always have a
chaperone. Ask the patient to undress to the waist and sit upright
on a well-illuminated chair or on the side of a bed.
A B C D
Fig. 11.9 Positions for inspecting the breasts. A Hands resting on the thighs. B Hands pressed on to the hips. C Arms above the head. D Leaning
forward with the breasts pendulous.
215
pectoral muscle contracts, note whether the mass moves This can be uncomfortable, so warn patients beforehand
with it and if it is separate when the muscle is relaxed. and check for any discomfort. Compress the contents of
Fixation suggests malignancy. the axilla against the chest wall. Assess any palpable
masses for:
Palpate the nipple by holding it gently between your index size
finger and thumb. Try to express any discharge. Massage consistency
the breast towards the nipple to uncover any discharge, fixation.
noting the colour and consistency, and the number and
position of the affected ducts. Test any discharge for abnormality. Palpate the neck from behind and
blood using urine-testing sticks. systematically review all cervical lymphatic chains (see
Palpate the regional lymph nodes, including the Figs 3.27 and 9.22).
supraclavicular group. Ask the patient to sit facing you, Cancers cause solid irregular masses. They are usually, but not
and support the full weight of her arm at the wrist with always, painless, firm and hard, in contrast with the surrounding
your opposite hand. Move the flat of your other hand high breast tissue. The cancer may extend directly into the overlying
into the axilla and upwards over the chest to the apex. skin, pectoral fascia or pectoral muscle, causing the lump to feel
fixed, or metastasise via regional lymph nodes or the systemic
circulation.
Fig. 11.11 Clinical examination of the breast. Palpating clockwise to cover all of the breast.
216 THE REPRODUCTIVE SYSTEM
Investigations
Accurate diagnosis of breast lesions depends on clinical malignant lesions require excision biopsy for the diagnosis to be
assessment, backed up by mammography and/or breast
ultrasound and pathological diagnosis; this should ideally be the extent of cancer in a mammographically dense breast, and
done by core biopsy, although fine-needle aspiration cytology for screening those with BRCA1 or BRCA2
can also be helpful in assessing axillary lymph nodes (‘triple
of patients with breast symptoms to specialist units.
(LMP) and whether it was normal; always consider that Unexpected bleeding suggests endometrial or cervical
these patients might be pregnant pathology. Ask when the bleeding occurs:
transmitted disease
35 days.
Prepuce
Clitoris
External urethral orifice
Frenulum of clitoris (meatus)
Labium majus Vaginal orifice
Labium minus
Hymen
Vestibule Posterior commissure
Fourchette
Anus
is required, particularly if the bleeding is associated with lower neurological in origin (p. 96). Psychological and social factors
abdominal pain.
To differentiate between the possible causes of lower abdominal
Lower abdominal pain pain, ask about:
Lower abdominal pain may arise from the reproductive organs
or the urinary or gastrointestinal tract, or be musculoskeletal or
or not).
Ovarian pain is often unilateral and can be physiological
Suspensory Fallopian (Mittelschmertz is discomfort associated with ovulation). Ovarian
ligament tube cyst accidents involving torsion (twisting on the vascular pedicle
of ovary Uterine Fundus
causing acute ischaemia), haemorrhage or rupture can lead to
cavity Ampulla acute severe pain.
Ovarian Primary dysmenorrhoea is pain arising from uterine contraction
ligament that is most intense just before and during peak menstruation.
Endometrium Secondary or progressive dysmenorrhoea, due to underlying
Myometrium pathology such as endometriosis or chronic infection, often
manifests as pain that lasts beyond the normal menstrual
Broad
ligament
generalised pain (Box 11.3).
Uterine body Internal os Dyspareunia is pain during intercourse. Ask if it is felt
Cervical canal External cervical os around the vaginal entrance (superficial) or within the pelvis
Vagina (deep). Pain due to involuntary spasm of muscles at the
Fig. 11.17 Section through the pear-shaped, muscular uterus. vaginal entrance (vaginismus) may make intercourse impossible.
The cervix, uterine body (corpus), fundus and Fallopian tubes, with the Persistent deep dyspareunia suggests underlying pelvic pathology.
ligamentous attachments of the ovary. The uterine mucosa is the Dyspareunia can be due to vaginal dryness following the
endometrium. The cervical canal has an internal and an external os. menopause.
a corpus luteum cyst of the ovary but may indicate a tubal ectopic
Posterior fornix pregnancy. Ruptured ectopic pregnancy results in generalised
Anterior fornix abdominal pain, peritonism, haemodynamic instability and referred
pain in the shoulder.
Sacral
promontory
Ureter
Sacro uterine
ligament Fallopian tube
Ovarian ligament
Pouch of Douglas Fundus of uterus
Body of uterus
Cervix Bladder
Vagina
Fornix of vagina
Symphysis pubis
Levator ani muscle Urethra
External Clitoris
anal sphincter
Labium minus
Anus Labium majus
Fig. 11.19 Lateral view of the female internal genitalia. The relationship to the rectum and bladder.
219
Vaginal discharge
This may be normal and variable during the menstrual cycle. 11
Prior to ovulation, it is clear and abundant, and stretches like
egg white; after ovulation, it is thicker, does not stretch and is
less abundant. Abnormal vaginal discharge occurs with infection.
Ask about:
Urinary incontinence
Prolapse
The top of the vagina (vault) can also prolapse after a previous Drug history
hysterectomy. More commonly the bulge relates to the vaginal
wall. A cystocoele is a bulge on the anterior wall containing Tamoxifen has oestrogenic effects in postmenopausal women,
the bladder (see Fig. 11.20) and a rectocoele is a bulge on the antibiotics can cause vaginal candidiasis, antipsychotic drugs can
posterior wall containing the rectum. An enterocoele is a bulge of cause hyperprolactinaemia, and antiepileptic or antituberculous
the distal wall posteriorly containing small bowel and peritoneum. drugs may reduce the effectiveness of oral contraceptives.
220 THE REPRODUCTIVE SYSTEM
Sometimes a sexual history is required but people often find it privacy to do this.
Examination sequence
11.4 Taking a sexual history
Look at the perineum for any deficiency associated with
Are you currently in a sexual relationship? childbirth; note abnormal hair distribution and clitoromegaly
How long have you been with your partner? (associated with hyperandrogenism). Note any skin
Have you had any (other) sexual partners in the last 12 months? abnormalities, discharge or swellings of the vulva, such
How many were male? How many female?
When did you last have sex with: (Fig. 11.23).
Your partner? Ask the woman to cough while you look for any prolapse
Anyone else? or incontinence.
Do you use barrier contraception – sometimes, always or never?
Have you ever had a sexually transmitted infection?
your right hand, gently insert a lightly lubricated bivalve
Are you concerned about any sexual issues?
speculum (Figs 11.25–11.26A), with the blades vertical,
PCOS, polycystic ovary syndrome; PMB, postmenopausal bleeding; STI, sexually transmitted infection.
221
11
Cytology
specimen jar
A B
Fig. 11.29 Coronal section. A Anteverted uterus. B Retroverted
uterus.
11
Fig. 11.31 Palpating an adnexal mass.
called an ectopy and looks red and friable; there may be small
cysts called Nabothian follicles. The normal uterus should feel
regular and be mobile and the size of a plum. The Fallopian
tubes cannot be felt and normal ovaries are palpable only in
very slim women.
Vulval changes include specific skin disease, infections such
as herpes or thrush, and malignancy. Visual abnormalities of the
cervix such as ulceration or bleeding suggest cervical pathology,
Fig. 11.30 Bimanual examination of the uterus. Use your vaginal
including polyps or malignancy. Tender nodules in the posterior
fingers to push the cervix back and upwards, and feel the fundus with your
fornix suggest endometriosis, and both endometriosis and pelvic
abdominal hand.
adhesions cause fixation of the uterus. Acute pain when touching
the cervix (cervical excitation) suggests an acute pelvic condition
such as infection, cyst accident or tubal rupture.
Fibroids can cause uterine irregularity and enlargement. The
Push your fingers into the posterior fornix and lift size is related to that of the uterus in pregnancy. A tangerine-sized
the uterus while pushing on the abdomen with your uterus is 6 weeks, apple 8 weeks, orange 10 weeks and
left hand. grapefruit 12 weeks. After 12 weeks the uterus can be palpated
Place your left hand above the umbilicus and bring suprapubically on abdominal palpation. A large midline mass
it down, palpating the uterus between both hands may be ovarian or uterine. Push the mass upwards with your
and note its size, regularity and any discomfort left hand and feel the cervix with your right hand; if the mass
(Fig. 11.30). moves without the cervix, this suggests it is ovarian.
Move your vaginal fingers into the anterior fornix and
palpate the anterior surface of the uterus, holding it in
position with your abdominal hand. Investigations
Move your fingers to the lateral fornix and, with your left
hand above and lateral to the umbilicus, bring it down to Common gynaecological investigations are summarised in Box
assess any adnexal masses between your hands on each 11.6. A woman of reproductive age should be considered
side (Fig. 11.31). potentially pregnant and a pregnancy test is routine. The mainstay
of gynaecological investigation is a pelvic ultrasound scan, which
lifting the anterior vaginal wall with your fingers and asking can be carried out abdominally or transvaginally (Fig. 11.32).
her to cough again. This stops genuine stress
incontinence. is performed during vaginal examination using a suction catheter
The normal cervix os may be a slit after childbirth. Vaginal (pipelle, Fig. 11.33). When a couple present with subfertility,
squamous epithelium and the endocervical columnar epithelium the key female investigations are serum progesterone 1 week
meet on the cervix. The position of this squamocolumnar junction before expected menses to confirm ovulation, and a test of
varies considerably, so the cervix can look very different in tubal patency (Fig. 11.34).
224 THE REPRODUCTIVE SYSTEM
CA-125, cancer antigen 125; CT, computed tomography; HCG, human chorionic gonadotrophin; MRI, magnetic resonance imaging; PCOS, polycystic ovary syndrome.
Bladder
Cervix
Endometrium
Myometrium
Fig. 11.33 Pipelle for endometrial biopsy.
Contrast spilling
Ampulla
Uterus
mm
53
50
mm
Uterus
Isthmus
visits; the visits may either be conducted by a midwife alone (some higher-risk women need a higher dose).
or be shared with an obstetrician. This plan is individualised
depending on the age, past medical history and general health Family history
of the woman, as well as any complications that develop as the
pregnancy proceeds. To explore possible inherited conditions, take a full family history
of both the pregnant woman and the father (Boxes 11.10
and 11.11).
(Box 11.9).
11.10 Examples of single-gene disorders that can be and liver (high vitamin A content). Domestic violence can start or
detected antenatally escalate in pregnancy and is associated with an increased risk
of maternal death. All women must be seen alone (without their
Autosomal dominant
partner) on at least one antenatal visit to allow this to be explored.
Huntington’s chorea Myotonic dystrophy
Autosomal recessive Occupational history
Cystic fibrosis Thalassaemia Ask the patient about her occupation and whether she plans to
Sickle cell disease continue it. Occupations involving exposure to ionising radiation
X-linked pose specific risks to the fetus or mother, so her job plan may
Duchenne muscular dystrophy Haemophilia require modification for safety reasons. There is no definitive
evidence of a link between heavy work and preterm labour or
pre-eclampsia.
during and after the pregnancy should have heart auscultation performed to exclude
pre-existing cardiac disease.
how she feels about it.
Lower socioeconomic status is linked with increased perinatal
and maternal mortality. Investigations
such as tuna (high mercury content), soft cheeses (risk of Listeria) Routine investigations are required at the booking visit (Box 11.12).
The history
from relaxation of the gastro-oesophageal sphincter and
Ask about: acid reflux.
always merits hospital review with a full history and examination. progresses and the expanding uterus makes palpation of other
Painless bleeding is more typical of local causes, such a cervical
polyp, or of a low-lying placenta, whereas painful bleeding is aid diagnosis.
to consider venous access and send blood for blood count Pre-eclampsia
and cross-matching in any pregnant woman presenting with
vaginal bleeding. Pre-eclampsia is a multifactorial syndrome comprised of high
blood pressure, proteinuria and placental compromise, and is
Abdominal pain
asymptomatic and detected by blood pressure monitoring and
urinalysis, although some women develop generalised headache
benign physiological issues such as constipation and is also a and rapidly worsening peripheral oedema. A history focused
common presenting feature of labour when women are contracting on headache, worsening oedema and upper abdominal pain
should be taken. The examination is that of a routine antenatal
caused by polyhydramnios or placental abruption. assessment but should also include a check for hyper-reflexia
Any condition causing abdominal pain can present coincidentally and ankle clonus.
in pregnancy, however. A common example is urinary tract
infection; less common causes include appendicitis, ovarian cyst
Pruritus
clear history in a pregnant woman with abdominal pain and to Pruritus (itching) affects one-quarter of pregnant women. Rarely, it
perform a full obstetric and abdominal examination, including is associated with liver cholestasis, in which case it is generalised
renal angle palpation. This becomes more difficult as pregnancy and there is no rash.
228 THE REPRODUCTIVE SYSTEM
A B C
Fig. 11.35 Abdominal examination. A Palpate the fundal area to identify which pole of the fetus (breech or head) is occupying the fundus. B Slip your
hands gently down the sides of the uterus to identify which side the firm back and knobbly limbs of the fetus are positioned on. C Turn to face the
patient’s feet and slide your hands gently on the lower part of the uterus.
Breathlessness
Mild breathlessness is physiological in pregnancy. Rarely, increased
breathlessness is due to pulmonary oedema in pre-eclampsia or
Level of
pelvic brim
Rectum
Bladder
Seminal vesicle
Symphysis pubis
Ejaculatory duct
Levator ani muscle Prostate gland
Urethra
Anus Hydatids of Morgagni
Epididymis
Bulbocavernosus
muscle Glans
Testis
Fig. 11.41 Anatomy of the male genitalia. The male genitalia include the external organs, seminal vesicles and prostate gland.
11
Spermatic cord
Glans penis
Urethra
Corpus cavernosum
Vas deferens
Corpus spongiosum
Pampiniform plexus
Epididymis
Testis
Crus penis
Scrotum
Ischial tuberosity
Fig. 11.42 The scrotum and its contents. Dorsal vein
Corpus cavernosum
There are many causes of scrotal swelling or pain but a patient of babies are born with a non-retractile prepuce but this usually
with sudden-onset unilateral scrotal pain should be considered to
have testicular torsion until proven otherwise. Testicular torsion a persistent phimosis. This may produce balanitis (recurrent
occurs most commonly between the ages of 10 and 30 years infection of the glans penis), posthitis (infection of the prepuce)
and is very rare over the age of 40. Pain is usually of acute or both (balanoposthitis).
associated with nausea and vomiting but not usually fever, lower and pain ensue, resulting in a paraphimosis due to the tight
urinary tract symptoms or urethral discharge. preputial band (Fig. 11.45).
Dermatological conditions and drug reactions may affect the
The pain of epididymo-orchitis is often more insidious in onset genital skin. Painful genital ulcers are usually caused by herpes
compared to testicular torsion and the patient may report a dull simplex; painless ulcers occur in reactive arthritis (p. 257), lichen
ache initially. There may be associated fevers, dysuria or urethral
as well as penile carcinoma.
The discomfort is often worse when standing or moving around
and may be relieved when lying still. On examination, it is usually Erectile dysfunction
possible to distinguish the tender, inflamed epididymis from the
attain and/or maintain a penile erection sufficient for penetrative
and examination, urgent testicular exploration is warranted, as
intercourse.
torsion will cause loss of a testis if not relieved within 4–6 hours.
Clarify from the history:
While an ultrasound examination may be used to confirm a
diagnosis of epididymo-orchitis, it should never be requested
painful erection, penile deformity on erection or a
to assess for torsion.
Other scrotal swellings include hernia, varicocoele, hydrocoele,
epididymal cyst and testicular tumour. These are usually painless,
although vague or constant dull ache may be described (Fig.
Drug history
Ask about previous urological drug treatments and obtain a full
prolonged erection
function.
Social history
Smoking, alcohol and recreational drugs can affect fertility and
sexual function. Smoking is a significant risk factor for urological
cancers.
11
The physical examination
Fig. 11.45 Paraphimosis. Oedema of the foreskin behind an encircling
constriction ring caused by the foreskin not being replaced – in this case,
after catheterisation.
offer is refused, record the fact. Apply alcohol gel and put on
gloves. Allow the patient privacy to undress.
Consider possible precipitating events: for example, relationship Ask the patient to stand and expose the area from his lower
difficulties or trauma. Assess cardiovascular, neurological and abdomen to the top of his thighs, unless you are examining the
psychiatric comorbidities as well as taking a drug history.
erection occurs in some but not all situations; early-morning Examination sequence
erections or erections with masturbation usually remain unaffected. Look in turn at the groin, skin creases, perineum and
scrotal skin for redness, swellings or ulcers. Note the hair
medical comorbidities, including diabetes mellitus, cardiovascular distribution.
disease, hypertension, peripheral vascular disease, endocrine
of metabolic syndrome and should precipitate screening for There may be alopecia or an infestation. Patients who shave
cardiovascular disease and diabetes. their pubic hair may have dermatitis or folliculitis (infection
around the base of the hairs), causing an irritating red rash.
penile shaft, of unknown aetiology, producing painful curvature, lymphadenopathy may stem from local or general causes.
narrowing or shortening of the corpora cavernosa with erection. Scrotal oedema can be caused by systemic or local disease.
duration and whether it is painful. Particular attention should be as may nephrotic syndrome and lymphoedema due to pelvic
paid to drug history, history of perineal trauma or past medical lymphadenopathy.
history of haematological, neurological or oncological disease.
Painful (low-flow or ischaemic) priapism is a urological emergency,
Penis
Examination sequence
Past medical history
Look at the shaft and check the position of the urethral
Ask about previous urological procedures, including neonatal opening to exclude hypospadias (urethra opening partway
surgery. Record relevant general surgical procedures, particularly along the shaft of the penis; see Fig. 15.11A).
pelvic operations that may contribute to lower urinary tract Palpate the shaft for fibrous plaques (usually on the
dorsum). Palpate any other lesions to define them.
and psychiatric disease may predispose or contribute to both Retract the prepuce and inspect the glans for red patches
or vesicles.
234 THE REPRODUCTIVE SYSTEM
Always draw the foreskin forward after examination to Place the bright end of a torch against a scrotal swelling
avoid a paraphimosis. (transillumination; see Fig. 15.9). Fluid-filled cysts allow
Take a urethral swab if your patient has a discharge or is light transmission and the scrotum glows bright red. This
having sexual health screening. is an inconsistent sign, which does not differentiate a
Normal enlarged follicles may mimic warts. Numerous uniform, hydrocoele from other causes of intrascrotal fluid such as
pearly penile papules around the corona of the glans are normal. a large epididymal cyst. With thick-walled cysts,
transillumination may be absent.
may occur on the shaft and phimosis, adhesions, inflammation The right testicle is usually closer to the inguinal canal than
or swellings on the foreskin or glans. the left but the testes may be highly mobile (retractile). A normal
testis is 5 cm long. The normal epididymis is barely palpable,
Scrotum except for its head (Fig. 11.48), which feels like a pea separate
from the superior pole of the body of the testicle.
pull the testis downward and place your fingers behind the
neck of the scrotum. Feel the spermatic cord and within it
the vas, like a thick piece of string.
Decide whether a swelling arises in the scrotum or from
A Fingers can ‘get above’ mass B Fingers cannot ‘get above’ mass
Epididymal cyst
Swellings of the epididymis that are felt to be completely separate
from the body of the testis are epididymal cysts. They are isolated Fig. 11.49 Left testicular torsion. There is shortening of the cord with
11
and adherent to the epididymis alone, they transilluminate and retraction of the testis and global swelling of the scrotal contents. Refer the
are never malignant. Painful swellings at the superior pole of patient urgently to a surgeon for scrotal exploration.
the testis, or adjacent to the head of the epididymis, are usually
due to torsion of a paramesonephric duct remnant, the hydatids
of Morgagni.
Testicular tumour
Note any tenderness.
Testicular tumours cause painless, hard swellings of the body
rete testis and may give rise to epididymal swelling and pain. Feel for any nodules.
urinary infection in the elderly. or sulcus, between the two lateral lobes. Sometimes the seminal
vesicles are felt above the prostate.
Testicular torsion
abscess.
A retracted or high-lying testicle, accompanied by acute pain
Prostate cancer may cause a discrete nodule, a craggy mass
and swelling, occurs in testicular torsion (Fig. 11.49).
or obliteration of the midline sulcus, and the prostate may feel
Single testis fixed to the lateral pelvic side wall.
testis through the inguinal canal or an ectopic testis in the groin. Investigations
Ask about previous surgery for a testicular tumour or testicular
maldescent. Unilateral testicular atrophy may result from mumps The relevant urological investigations depend on the clinical
infection, torsion, vascular compromise after inguinal hernia repair, problem revealed on history and examination. First-catch urine
or from a late orchidopexy for undescended testis. can be tested for both Chlamydia trachomatis and Neisseria
gonorrhoeae from a single specimen using nucleic acid
Bilateral testicular atrophy amplification tests, and this should be performed for all men
This suggests primary, or secondary, hypogonadism (p. 204) presenting with urethritis or acute scrotal pain suspected to be
or primary testicular failure. Look for hormonal abnormalities or due to epididymo-orchitis. Scrotal ultrasound is the gold standard
signs of anabolic steroid usage, and check the development of for confirming the clinical diagnosis of scrotal swelling or pain,
secondary sexual characteristics (see Fig. 15.19). with the exception of testicular torsion.
When prostate cancer is suspected a prostate-specific
Prostate antigen (PSA) blood test should be requested. PSA is raised in
prostate cancer but also increases with age, prostatic volume,
Ask the patient to lie in the left lateral position. following prostatic trauma and in seminal or urinary tract infection.
Ms McIntyre, 27 years old, presents with a 6-week history of a lump in her right breast.
Please examine her breast
Introduce yourself and clean your hands.
Obtain verbal consent for the examination from the patient.
Offer a chaperone.
Ask her to undress to the waist and sit on the edge of the bed.
Inspect for asymmetry, skin or nipple changes, or obvious lumps.
Ask her to put her hands on her hips and push in while you look for changes in the breast.
Ask her to lie on the couch with her upper body at 45 degrees. Palpate her breasts, noting the characteristics of any lumps.
Examine her axillae and supraclavicular fossae.
Thank the patient and clean your hands.
Summarise your findings
There is a firm, mobile, non-tender lump about 2 cm in diameter at 11 o’clock in the right breast, 5 cm from the nipple. There are no overlying skin
changes and the lump is not tethered. I could feel no lymphadenopathy in the neck or axilla.
Suggest a diagnosis
One possible diagnosis is breast cancer. The differential includes fibrocystic disease, a breast cyst or an abscess.
Suggest investigations
Triple assessment: clinical assessment, ultrasound scan and ultrasound-guided core biopsy.
Mr Atkins, 20 years old, presents to the emergency department with scrotal pain.
Please take a focused history
Introduce yourself and clean your hands.
Obtain verbal consent to take a history from the patient.
Ask an open question about why this person has come to the emergency department.
Explore the symptoms offered at presentation – in this case, scrotal pain:
time of onset and duration
severity of pain
exacerbating/relieving factors
constant or intermittent nature
radiation to groin or loin
any precipitating event such as trauma
associated urinary symptoms, urethral discharge, swelling, fever, nausea or weight loss
sexual history
past medical history, including undescended testes
drug history
social history.
Summarise your findings
The patient reports a gradual onset of aching testicular and scrotal pain with some associated urethral discharge and fever.
Suggest a differential diagnosis
This history is most suggestive of epididymo-orchitis. The differential includes testicular torsion and testicular cancer.
Suggest initial investigations
Ultrasound may confirm epididymo-orchitis, but if testicular torsion cannot be excluded on history and examination, urgent testicular exploration is
required.
Neeraj Dhaun
David Kluth
12
The renal system
Anatomy and physiology 238 Interpretation of the findings 246
The history 239 Investigations 246
Common presenting symptoms 239 Urinalysis 246
Past medical history 243 Investigation of renal function 247
Drug history 243 OSCE example 1: Renal history 249
Family history 243
OSCE example 2: Renal examination 250
Social history 243
Integrated examination sequence for renal disease 250
The physical examination 243
General appearance 243
Assessment of fluid balance 244
Abdominal examination 245
Targeted examination of other systems 246
238 THE RENAL SYSTEM
system
Costovertebral angle
11th rib
12th rib
Kidney
Fig. 12.1 The surface anatomy of the kidneys from the back. Kidney
Fibrous capsule
Renal papilla
Afferent Glomerulus Renal Minor calyx
arteriole pyramids
Major calyx
Renal Renal pelvis
columns
Efferent Collecting
Cortex
arteriole tubule
Ureter
Peritoneum
Detrusor muscle
Rugae
Ureteric orifices
Bladder neck
Internal urethral sphincter
External urethral sphincter
Urogenital diaphragm
Urethra
The history
Voiding symptoms
Common presenting symptoms
Dysuria
(>
Loin pain
THE RENAL SYSTEM
Haematuria
>
Visible haematuria
Non-visible haematuria
Acute kidney injury
+
Prerenal AKI
Intrinsic AKI
THE RENAL SYSTEM
}
1 ≥ 90 Kidney damage with normal or ↑ GFR
2 60–89 Kidney damage with mild ↓ GFR
Observe; control blood pressure and risk factors
3A 45–59 Moderate ↓ GFR
3B 30–44
4 15–29 Severe ↓ GFR Prepare for end-stage kidney disease
5 < 15 End-stage kidney disease Dialysis, transplantation or conservative care
p: the addition of p to a stage (e.g. 2p, 3Bp) means that there is significant proteinuria. Proteinuria is quantified on the basis of an
albumin : creatinine (ACR) or protein : creatinine (PCR; see Box 12.4).
T: the addition of T to a stage (e.g. 4T) indicates that the patient has a renal transplant.
D: the addition of D to stage 5 CKD (i.e. 5D) indicates that the patient is on dialysis.
< 2
Dialysis access
Drug history
Family history
Face
12
Social history
General appearance
General appearance
dehydrated patient the eyes may appear sunken and the mucous
Palpation
Peripheral oedema
Weight
12
Abdominal examination
Examination sequence
Inspection
Percussion
Investigations
Auscultation Urinalysis
concentrate urine
Joints
Nervous system
Prostate
Fig. 12.13 Urine dipstick test. From Pitkin J, Peattie AB, Magowan BA.
Obstetrics and Gynaecology: An Illustrated Colour Text. Edinburgh:
Churchill Livingstone; 2003.
Investigation of renal function
ADH, antidiuretic hormone (vasopressin); AKI, acute kidney injury; ANCA, antineutrophil cytoplasmic antibody; CKD, chronic kidney disease; (e)GFR, (estimated) glomerular
filtration rate.
Mrs Measham, 60 years old, is attending to discuss the results of her recent blood tests. She has presented with a 3-month history of tiredness and
you know that her renal function was normal 1 year ago.
Investigations
Haemoglobin: 101 g/L (10.1 g g/dL) (normal range female 115–165 g/L (11.5–16.5 g/dL); male 130–180 g/L (13.0–18.0 g/dL))
White cell count: 8.9 × 109/L (normal range 4.0–11.0 × 109/L)
Platelet count: 510 × 109/L (normal range 150–400 × 109/L)
Potassium: 5.2 mmol/L (normal range 3.5–5.0 mmol/L)
Urea: 14.5 mmol/L (40.6 mg/dL; normal range 3.0–7.0 mmol/L (8.4–19.6 mg/dL))
Creatinine: 163 μmol/L (1.84 mg/dL; normal range 60–120 μmol/L (0.68–1.36 mg/dL))
Dipstick urinalysis: blood: 3+, protein 3+
Take a history from the patient
Introduce yourself to the patient and clean your hands.
Obtain consent to take a history.
Establish that the patient was well until 3 months ago and that the main symptoms are tiredness and breathlessness on exertion.
Ask about:
weight loss, appetite and bowel motions
peripheral oedema
haemoptysis
urinary symptoms: dysuria, nocturia, urgency, hesitancy, incontinence, loin pain
back pain, fevers and rigors. 12
Confirm details of the past medical history.
Document current medication and any relevant recent changes.
Determine how symptoms are affecting the patient’s lifestyle: both work and leisure.
Establish the family history.
Thank the patient and clean your hands.
Summarise your findings
The patient has presented with 3 months of lethargy and investigations reveal that he has anaemia in the context of renal impairment.
Suggest a differential diagnosis
The most likely diagnosis is an intrinsic renal disease, probably a glomerulonephritis, which may be part of a multisystem disorder. Infection is also
possible.
Suggest additional investigations
Relevant further investigations might include erythrocyte sedimentation rate, C-reactive protein, vasculitis and myeloma screens, and iron stores.
Renal ultrasound, chest X-ray and mid-stream urine for microscopy and culture could be considered. The patient would benefit from a referral to a
nephrologist.
THE RENAL SYSTEM
Mr Logan, 45 years old, is known to have adult polycystic kidney disease, and has a history of intermittent loin pain and hypertension.
Please examine the abdomen
Introduce yourself and clean your hands.
Obtain permission to examine the patient.
Perform a peripheral examination, including hands, arms and face. Look for leuconychia, pallor, and an arteriovenous fistula for haemodialysis (if
functioning, it will have a palpable thrill).
Measure the blood pressure.
Inspect the abdomen. Examine for scars from a previous nephrectomy (increasingly, these will be laparoscopic, rather than scars from an open
nephrectomy), or from a current or previous renal transplant in the right or left iliac fossa, and a distended abdomen if polycystic kidneys are large.
Ask if the abdomen is painful. Start with light palpation and then proceed more deeply across all abdominal regions. Assess for specific
organomegaly, including liver, spleen, kidneys and bladder. Findings may include an irregular enlarged liver (polycystic liver), or palpable masses in
one or both flanks (polycystic kidneys; it is key to distinguish these from the liver or spleen). Remember to ballott both kidneys.
Percuss over any mass.
Assess for shifting dullness due to ascites.
Auscultate over the abdomen and over masses.
Summarise your findings
This man has bilateral flank masses, which are ballottable. I can get above the masses and the percussion note over them is resonant. These are most
likely to represent bilaterally enlarged kidneys. The patient also has a functioning left arteriovenous fistula, most likely for haemodialysis.
Suggest a diagnosis
The most likely cause is autosomal dominant polycystic kidney disease.
Suggest initial investigations
An ultrasound scan would be the simplest test to show the presence of cysts. Magnetic resonance imaging would provide more detail about renal size.
Advanced level comments
In addition to hypertension and renal failure, complications of APCKD include cyst haemorrhage and infection, and subarachnoid haemorrhage due to a
ruptured berry aneurysm.
arthritis can develop over 24 hours, or more insidiously. Crystal fever and gonococcal arthritis. If intermittent, with resolution
arthritis (gout and pseudogout) causes acute, severe pain that between episodes, it may be palindromic rheumatism.
develops quickly, often overnight. Joint sepsis causes pain that
develops over 1–2 days. Exacerbating/relieving factors
Pain from joints damaged by intra-articular derangement or
Character osteoarthritic degeneration worsens with exercise. Pain from
Bone pain is penetrating, deep or boring, and is characteristically inflammatory arthritis worsens with rest. Pain from a septic joint
worse at night. Localised pain suggests tumour, osteomyelitis is present both at rest and with movement.
(infection), osteonecrosis or osteoid osteoma (a benign bone
tumour). Generalised bony conditions, such as osteomalacia, Severity
usually cause diffuse pain. Apart from trauma, the most severe joint pain occurs in septic
Fracture pain is sharp and stabbing, aggravated by attempted and crystal arthritis. Disproportionately severe pain is seen
movement, and relieved by rest and splintage. acutely in compartment syndrome (increased pressure in a
Muscle pain is often described as ‘stiffness’ or aching, and fascial compartment, compromising perfusion and viability of
is aggravated by use of the affected muscle(s). compartmental structures) and chronically in complex regional
‘Shooting’ pain is often caused by impingement of a peripheral pain syndrome. Neurological involvement in diabetes mellitus,
nerve or nerve root: for example, buttock pain, which ‘shoots leprosy (Hansen’s disease), syringomyelia and syphilis (tabes
down the back of the leg’, caused by lumbar disc protrusion. dorsalis) may impair joint sensation, reducing pain despite obvious
Progressive joint pain in patients over 40 years of age is pathology on examination. Grossly abnormal joints may even
commonly caused by osteoarthritis. be pain-free (Charcot joints). Partial muscle tears are painful;
Fibromyalgia, a chronic pain syndrome, causes widespread, complete rupture may be less so.
constant pain with little diurnal variation, which is poorly controlled
by conventional analgesic/anti-inflammatory drugs.
Patterns of joint involvement
Radiation
Different patterns of joint involvement aid the differential diagnosis
(Fig. 13.3). Are the small or large joints of the arms or legs
13
Pain from nerve compression radiates to the distribution of affected? How many joints are involved? Involvement of one
that nerve or nerve root (see Fig. 7.23), such as lower leg pain joint is called a monoarthritis; 2–4 joints, oligoarthritis; and more
in intervertebral disc prolapse, or hand pain in carpal tunnel than 4, polyarthritis.
syndrome. Neck pain radiates to the shoulder or scalp. Hip pain
is usually felt in the groin but may radiate to the thigh or knee. and feet suggests an inflammatory arthritis, such as
Common patterns of radiation are summarised in Box 13.3. rheumatoid arthritis or systemic lupus erythematosus (SLE).
Associated symptoms
For example, swelling and redness of a joint indicate inflammatory
arthritis. 13.4 Clinical vignette: arthralgia and fatigue
Timing (frequency, duration and A 34-year-old mother-of-two presents to her GP with a 1-year history
periodicity of symptoms) of gradually worsening pain and persistent fatigue. The pain moves
around and involves the back, neck, shoulders, elbows, hands and
A history of several years of pain with a normal examination
knees. All joints are described as swollen, particularly her hands,
suggests fibromyalgia (Box 13.4). A history of several weeks of which swell ‘all over’. Further history reveals poor sleep with the
pain, early-morning stiffness and loss of function is likely to be patient wakening every 2 hours and feeling unrefreshed in the
an inflammatory arthritis. ‘Flitting’ pain starting in one joint and morning. She has a difficult social background and a past history of
moving to others over a period of days is a feature of rheumatic depression and irritable bowel syndrome. Examination shows no skin
or joint abnormality but there is widespread tenderness, particularly
across her shoulders, in her neck and down her back (see figure).
13.3 Common patterns of referred and radicular Blood tests are all normal.
musculoskeletal pain She is diagnosed with fibromyalgia.
Site where pain is perceived Site of pathology
Occiput C1, 2
Interscapular region C3, 4
Tip of shoulder, upper outer aspect of arm C5
Interscapular region or radial fingers and thumb C6, 7
Ulnar side of forearm, ring and little fingers C8
Medial aspect of upper arm T1
Chest Thoracic spine
Buttocks, knees, legs Lumbar spine
Lateral aspect of upper arm Shoulder
Forearm Elbow A B
Anterior thigh, knee Hip Typical tender points in fibromyalgia. A Anterior view. B Posterior
Thigh, hip Knee view.
254 THE MUSCULOSKELETAL SYSTEM
Stiffness
Ask what the patient means by stiffness. Is it:
Swelling
Ask about the site, extent and time course of the swelling.
The speed of onset of swelling is a clue to the diagnosis:
<30 minutes), severe swelling suggests a
haemarthrosis (Fig. 13.4). This occurs when vascular
structures such as bone or ligament are injured, and is
worse in the presence of anticoagulants or bleeding
disorders.
such as with a meniscal tear or articular cartilage abrasion. Fig. 13.4 Joint swelling. A Olecranon bursitis. B Right-knee
haemarthrosis.
marked swelling, tenderness, redness and extreme
reluctance to move the joint actively or passively.
255
septic arthritis. It commonly starts overnight or early in the A 32-year-old lady is seen in the outpatient clinic with fatigue and
intermittent pain and swelling in her hands, which she has had for the
morning due to the rise in serum urate following the
last year. She noticed a rash across her cheeks and on her arms while
evening meal.
she was on holiday in Spain recently and this seems to have sparked
off painful mouth ulcers and worsening joint pain. She has no other
Erythema and warmth relevant history. Examination shows a ‘butterfly’ rash across the cheeks
Erythema (redness) occurs in infective, traumatic and and nose, several mouth ulcers and two swollen metacarpophalangeal
crystal-induced conditions, and mild erythema may be present joints. Blood tests reveal anaemia, lymphopenia, positive antinuclear
antibody and raised anti-double-stranded DNA antibodies.
in inflammatory arthritis. All affected joints will be warm. Erythema
A diagnosis of systemic lupus erythematosus is made.
associated with DIP joint swelling helps to distinguish DIP joint
psoriatic arthritis from the Heberden’s nodes of osteoarthritis.
Triggering is a block to extension of a finger, which then ‘gives’
Weakness suddenly when extending from a flexed position. In adults it usually
affects the ring or middle fingers and results from nodular tendon
thickening or fibrous thickening of the flexor sheath due to chronic
problem may be focal or generalised.
low-grade trauma, which may be occupational or associated
Joint disorders cause weakness, either through inhibition of
with inflammatory arthritis. Triggering can be congenital, in which
function by pain, or by disruption of the joint or its supporting
case it usually affects the thumb.
structures.
Nerve entrapment may be the cause: for example, carpal Extra-articular symptoms
tunnel syndrome at the wrist.
Muscle disorders can produce widespread weakness Patients may present with extra-articular features of disease (Box
associated with pain and fatigue, such as in myositis, and with 13.5) that they may not connect with musculoskeletal problems.
a rash, as in dermatomyositis. Ask about:
Proximal muscle weakness can occur in endocrine disorders:
for example, hypothyroidism or excess of glucocorticoids. nodosum. Ask whether they are photosensitive (SLE,
Box 13.6).
Locking and triggering
rheumatoid arthritis and SLE. High-spiking fevers in the
‘Locking’ is an incomplete range of movement at a joint because
evening, accompanied by a rash, occur in adult-onset
of an anatomical block. It may be associated with pain. Patients
Still’s disease.
use ‘locking’ to describe various problems, so clarify exactly
what they mean.
tenderness: features of temporal arteritis.
True locking is a block to the normal range of movement
caused by mechanical obstruction, such as a loose body or Connective tissue disease may present with multiple
torn meniscus, within the joint. The patient is characteristically extra-articular features:
able to ‘unlock’ the joint by trick manœuvres.
Pseudolocking is a loss of the range of movement due to pain.
256 THE MUSCULOSKELETAL SYSTEM
Drug Possible adverse musculoskeletal effects To describe altered limb position due to joint/bone deformity,
Glucocorticoids Osteoporosis, myopathy, osteonecrosis, use:
infection
Statins Myalgia, myositis, myopathy midline
Angiotensin-converting Myalgia, arthralgia, positive antinuclear
enzyme inhibitors antibody In the wrist and hand, use:
Antiepileptics Osteomalacia, arthralgia
Immunosuppressants Infections side
Quinolones Tendinopathy, tendon rupture
side.
257
Fig. 13.5 Nail-fold infarcts caused by small-vessel vasculitis. Fig. 13.7 Rheumatoid nodules at the olecranon and ulnar border.
258 THE MUSCULOSKELETAL SYSTEM
A B
Fig. 13.10 Assessing the wrist. A Extension. B Flexion. There is a
reduced range of movement at the right wrist.
Gait
Ask the patient to walk ahead in a straight line, then turn
and walk back towards you. Look for smoothness and
symmetry of the gait.
Fig. 13.8 Osteoarthritis of the hand. Heberden’s (single arrow) and
Bouchard’s (double arrow) nodes.
Arms
Stand in front of the patient.
Inspect the dorsum of the hands and check for full
extension at the metacarpophalangeal (MCP), PIP and DIP
joints.
Gently squeeze across the MCP joints. Tenderness
suggests inflammation, as in rheumatoid arthritis.
Ask the patient to:
Clench their fists and then open their hands flat.
Squeeze your index and middle fingers.
Touch each of their fingertips with the thumb.
Make a ‘prayer sign’, with their elbows as high as
possible. Then reverse this with the backs of their
hands together and elbows low (Fig. 13.10).
Put their arms straight out in front of their body.
Bend their arms up to touch their shoulders.
Place their elbows by the side of their body, bent at 90
degrees. Turn their palms up and down.
Fig. 13.9 Gouty tophi.
Put their hands behind their head, with their elbows
back.
Joints: the GALS screen Put their hands behind their back.
Hypermobility
replacement
Some patients have a greater than normal range of joint movement.
If this is severe, patients may present with recurrent dislocations
or sensations of instability. Milder cases may develop arthralgia A high-stepping gait occurs in foot drop due to common
or be symptom-free. Mild hypermobility is normal but Marfan’s, peroneal nerve palsy. The knee is raised high to allow clearance
Ehlers–Danlos and benign joint hypermobility syndromes (Box of the weak foot.
13.8) cause significant hypermobility. Increased tone
This occurs with upper motor neurone lesions, such as
Detailed examination of the cerebrovascular accident (stroke) or cerebral palsy. The gait
depends on the specific lesion, contractures and compensatory
musculoskeletal system mechanisms (see Fig. 7.17).
C1
C2 C1 1
2 2 Cervical
C3 3
3 4 lordosis
C4
C5, C6 – Arm abduction 4 5 Scoliosis
C5 6 Kyphosis
Elbow flexion 5
C6 7
C6, C7 – Wrist extension 6 8
C7, C8 – Elbow extension C7 7 1
C8, T1 – Finger abduction C8 T1 2
Hand grasp T1 2 3
T2 3 4
T3
4 5 Thoracic
T4 6 kyphosis
T2–T7 – Chest muscles 5 A B
T5 7
6
T6 8
7 9
T7
8 10
T8 11
9
T9 12
10 1
Gibbus
T10 2
T9–T12 – Abdominal muscles 11 3
4
T11 5
12 1
2
T12 3 Increased
L1, L2, L3 – Hip flexion L1 4 lumbar
L1 5
lordosis
2
L2
L1, L3, L4 – Knee extension Lumbar C D
3 lordosis
Cauda
L3 Fig. 13.12 Spinal deformities.
equina 4
L4, L5, S1, S2 – Knee flexion L4
L4, L5 – Ankle dorsiflexion 5 posteriorly and the intervertebral discs and neurocentral joints
anteriorly. The nerve roots, particularly in the lower cervical spine,
L5, S1 – Great toe extension L5
may be compressed or irritated by lateral disc protrusion or by
S1, S2 – Ankle plantar flexion S1
S2 osteophytes arising from the facet or neurocentral joints. Central
S2, S3, S4 – Voluntary S3 disc protrusions may press directly on the cord (see Fig. 7.30).
rectal tone
S4
S5 The history
Co The most common symptoms are pain and difficulty turning
the head and neck. Neck pain is usually felt posteriorly but
Fig. 13.11 The normal spinal curves and root innervations. may be referred to the head, shoulder, arm or interscapular
region. Cervical disc lesions cause radicular pain in one arm
or the other, roughly following the dermatomes of the affected
13.9 Common spinal problems nerve roots (see Box 13.3). If the spinal cord is compromised
(cervical myelopathy), upper motor neurone leg weakness, altered
Mechanical back pain sensation and sphincter disturbance may occur.
Prolapsed intervertebral disc
Spinal stenosis The physical examination
Ankylosing spondylitis Be particularly careful when examining patients with rheumatoid
Compensatory scoliosis from leg-length discrepancy arthritis, as atlantoaxial instability can lead to spinal cord damage
Cervical myelopathy
when the neck is flexed.
Pathological pain/deformity, e.g. osteomyelitis, tumour, myeloma
In patients with neck injury, never move the neck. Splint it
Osteoporotic vertebral fracture resulting in kyphosis (or rarely
lordosis), especially in the thoracic spine with loss of height and check for abnormal posture. Check neurological function
Cervical rib in the limbs and X-ray to assess bony injury.
Scoliosis
Spinal instability, e.g. spondylolisthesis Examination sequence
Ask the patient to remove enough clothing for you to see
their neck and upper thorax, then to sit on a chair.
Cervical spine
Look
Anatomy and physiology Face the patient. Observe the posture of their head and
neck. Note any abnormality (Box 13.10), such as loss of
Head nodding occurs at the atlanto-occipital joint, and rotational
lordosis (usually due to muscle spasm).
neck movements mainly at the atlantoaxial joint. Flexion, extension
and lateral flexion occur mainly at the mid-cervical level. The neural Feel
canal contains the spinal cord and the emerging nerve roots, Feel the midline spinous processes from the occiput to T1
which pass through exit foramina bounded by the facet joints (usually the most prominent).
261
13.10 Causes of abnormal neck posture 13.11 Causes of thoracic spine pain
Loss of lordosis or flexion deformity Adolescents and young adults
Acute lesions, rheumatoid arthritis, trauma Scheuermann’s disease Disc protrusion (rare)
Axial spondyloarthritis
Increased lordosis
Middle-aged and elderly
Ankylosing spondylitis Degenerative change Osteoporotic fracture
Torticollis (wry neck) Any age
Sternocleidomastoid contracture, trauma Tumour Infection
Pharyngeal/parapharyngeal infection
Lateral flexion
Thoracic spine
Erosion of lateral mass of atlas in rheumatoid arthritis
Anatomy and physiology
This segment of the spine is the least mobile and maintains
a physiological kyphosis throughout life. Movement is mainly
rotational with a very limited amount of flexion, extension and
lateral flexion.
The history
Presenting symptoms in the thoracic spine are localised spinal
pain (Box 13.11), pain radiating round the chest wall or, less
Neutral Rotation
frequently, signs of cord compression: upper motor neurone
leg weakness (paraparesis), sensory loss, and loss of bladder
13
or bowel control. Disc lesions are rare but may cause pain
radiating around the chest that mimics cardiac or pleural disease.
Osteoporotic vertebral fractures may present with acute pain,
or painless loss of height with increased kyphosis.
Vertebral collapse due to malignancy may cause cord
compression. Infection causes acute pain, often with systemic
The principal movements are flexion, extension, lateral flexion Insidious onset of back or buttock ache and stiffness in an
and rotation. In flexion, the upper segments move first, followed adolescent or young adult suggests inflammatory disease of the
by the lower segments, to produce a smooth lumbar curve. sacroiliac joints and lumbar spine (axial spondyloarthritis, Box
However, even with a rigid lumbar spine, patients may be able 13.13). Symptoms are worse in the morning or after inactivity,
to touch their toes if their hips are mobile. and ease with movement. Morning stiffness is more marked
In the adult, the spinal cord ends at L2. Below this, only the than in osteoarthritis, lasting at least 30 minutes. Other clues
spinal nerve roots may be injured by disc protrusion. to the diagnosis are peripheral joint involvement, extra-articular
features or a positive family history.
The history Acute onset of low back pain in a young adult, often associated
Low back pain is extremely common. Most is ‘mechanical’, with bending or lifting, is typical of acute disc protrusion (slipped
and caused by degenerative changes in discs and facet joints disc). Coughing or straining to open the bowels exacerbates the
(spondylosis). pain. There may be symptoms of lumbar or sacral nerve root
Analyse the symptoms using ‘SOCRATES’. For back pain, compression. Cauda equina syndrome occurs when a central disc
ask specifically about: prolapse, or other space-occupying lesion, compresses the cauda
equina. There are features of sensory and motor disturbance,
back including diminished perianal sensation and bladder function
disturbance. The motor disturbance may be profound, as in
(Box 13.12) paraplegia. Cauda equina syndrome and spinal cord compression
are neurosurgical emergencies.
Radicular pain caused by sciatic nerve root compression
radiates down the posterior aspect of the leg to the lower leg
or ankle (sciatica). Groin and thigh pain in the absence of hip
abnormality suggests referred pain from L1–2. 13.13 Clinical vignette: back pain
Consider abdominal and retroperitoneal pathology, such as
abdominal aortic aneurysm. A 34-year-old man attends his general practitioner’s surgery with back
Mechanical low back pain is common after standing for too pain. He first developed pain in his late teens but it improved for a few
years. He has had persistent pain in his lower back and sometimes his
long or sitting in a poor position. Symptoms worsen as the day
buttocks for 5 years now. It wakes him from sleep and he can be very
progresses and improve after resting or on rising in the morning.
stiff in the mornings, although this eases as the morning progresses.
There is no radiation to the leg. He is stiff after sitting or driving. He
has always put it down to his occupation. He has used ibuprofen to
good effect but has had diarrhoea and abdominal pain recently, which
13.12 ‘Red flag’ and ‘yellow flag’ features for he attributes to this drug. Examination in the outpatient clinic shows a
acute low back pain thin man with reduced lumbar mobility (modified Schober’s index,
‘Red flag’ features reduced at 2 cm; see Fig. 13.15), pain on sacroiliac joint compression,
Features that may indicate serious pathology and require urgent and tenderness at his Achilles insertion. Investigations show him to
referral have a raised C-reactive protein, an anaemia of chronic disease, a
History positive human leucocyte antigen B27 and a raised faecal calprotectin,
Age < 20 years or > 55 years Faecal incontinence suggesting inflammatory bowel disease. Magnetic resonance imaging
Recent significant trauma Motor weakness confirms bilateral sacroiliitis and inflammatory changes in the lumbar
(fracture) Sensory changes in the spine.
Pain: perineum (saddle anaesthesia) A diagnosis of axial spondyloarthritis is made.
Thoracic (dissecting Sexual dysfunction, e.g.
aneurysm) erectile/ejaculatory failure
Non-mechanical (infection/ Gait change (cauda equina
tumour/pathological syndrome)
fracture) Bilateral ‘sciatica’
Fever (infection)
Difficulty in micturition
Past medical history
Cancer (metastases)
Previous glucocorticoid use (osteoporotic collapse)
System review
Weight loss/malaise without obvious cause, e.g. cancer
‘Yellow flag’ features
Psychosocial factors associated with greater likelihood of long-term
chronicity and disability
A history of anxiety, depression, chronic pain, irritable bowel
syndrome, chronic fatigue, social withdrawal
A belief that the diagnosis is severe, e.g. cancer. Faulty beliefs can
lead to ‘catastrophisation’ and avoidance of activity
Lack of belief that the patient can improve leads to an expectation
that only passive, rather than active, treatment will be effective
Ongoing litigation or compensation claims, e.g. work, road traffic
accident Ankylosing spondylitis. The patient trying to touch his toes.
263
Examination sequence
Ask the patient to stand with their back fully exposed.
Look
Look for obvious deformity (decreased/increased lordosis,
scoliosis) and soft-tissue abnormalities such as a hairy
patch or lipoma that might overlie a congenital
abnormality: for example, spina bifida.
Feel
Palpate the spinous processes and paraspinal tissues.
Note overall alignment and focal tenderness.
After warning the patient, lightly percuss the spine with
your closed fist and note any tenderness.
Move (Fig. 13.14) Fig. 13.15 Schober’s test. When the patient bends forward maximally
Flexion: ask the patient to try to touch their toes with their with the knees straight, distance BC should increase by at least 5 cm.
legs straight. Record how far down the legs they can
reach. Some of this movement depends on hip flexion.
Usually, the upper segments flex before the lower ones,
and this progression should be smooth.
Place the end of the tape measure on the upper mark (B).
Extension: ask the patient to straighten up and lean back
Ask the patient to touch their toes. The distance from B to
as far as possible (normal 10−20 degrees from a neutral
C should increase from 15 to more than 20 cm.
erect posture).
Lateral flexion: ask them to reach down to each side, Root compression tests
touching the outside of their leg as far down as possible
Intervertebral disc prolapse causing nerve root pressure occurs
while keeping their legs straight.
most often in the lower lumbar region, leading to compression
Special tests of the corresponding nerve roots.
The femoral nerve (L2–4) lies anterior to the pubic ramus, so
Schober’s test for forward flexion
straight-leg raising or other forms of hip flexion do not increase
its root tension. Problems with the femoral nerve roots may
Examination sequence cause quadriceps weakness and/or diminished knee jerk on
Mark the skin in the midline at the level of the posterior that side.
iliac spines (L5) (Fig. 13.15; mark A). The sciatic nerve (L4–5; S1–3) runs behind the pelvis.
Use a tape measure to draw two more marks: one 10 cm Straight-leg raise tests L4, L5 and S1 nerve-root tension (L3/4,
above (mark B) and one 5 cm below this (mark C). L4/5 and L5/S1 disc prolapse, respectively).
264 THE MUSCULOSKELETAL SYSTEM
Sciatic nerve stretch test (L4–S1) Flip test for functional overlay
Upper limb
The prime function of the upper limb is to position the hand
appropriately in space. This requires shoulder, elbow and wrist
Negative
Fig. 13.16 Stretch test: sciatic nerve. A Straight-leg raising limited by
the tension of the root over a prolapsed disc. B Tension is increased by
A B
dorsiflexion of the foot (Bragard’s test). C Root tension is relieved by
flexion at the knee. D Pressure over the centre of the popliteal fossa Fig. 13.18 Sciatic nerve: ‘flip’ test. A Divert the patient’s attention to
bears on the posterior tibial nerve, which is ‘bowstringing’ across the the tendon reflexes. B The patient with physical nerve root compression
fossa, causing pain locally and radiation into the back. cannot permit full extension of the leg.
265
movements. The hand may function in both precision and power 13.14 American College of Rheumatology/European League
modes. The intrinsic muscles of the hand allow grip and fine Against Rheumatism classification criteria for rheumatoid
manipulative movements, and the forearm muscles provide arthritis, 2010
power and stability.
Criteria Score
Distinguish between systemic and local conditions. Systemic
conditions, such as rheumatoid arthritis, usually cause pathology Duration of symptoms (as reported by patient)
at several sites. Differentiate local conditions from referred or < 6 weeks 0
> 6 weeks 1
radicular pain. Establish whether the condition is inflammatory
or not from the pattern of diurnal stiffness and pain. Joint distribution (0–5)
1 large jointa 0
2–10 large joints 1
Hand and wrist 1–3 small jointsb (large joints not counted) 2
Motor and sensory innervation of the hand is shown in Fig. 4–10 small joints (large joints not counted) 3
7.27. The wrist joint has metacarpocarpal, intercarpal, ulnocarpal >10 joints (at least 1 small joint) 5
and radiocarpal components. There is a wide range of possible Serology (0–3)
movements, including flexion, extension, adduction (deviation Negative RF and negative ACPA 0
towards the ulnar side), abduction (deviation towards the radial Low positive RF or low positive ACPA 2
High positive RF or high positive ACPA 3
side) and the composite movement of circumduction (the hand
moves in a conical fashion on the wrist). Always name the affected Acute-phase reactants
finger (index, middle, ring and little) in documentation to avoid Normal CRP and normal ESR 0
Abnormal CRP or abnormal ESR 1
confusion. The PIP and DIP joints are hinge joints and allow
only flexion and extension. The MCP joints allow flexion and Patients must have at least 1 swollen joint not better explained by
extension, and some abduction/adduction, which is greatest another disease.
A score of ≥ 6 classifies the patient as having definite rheumatoid
when the MCP joints are extended.
arthritis. A score of 4–5 is probable rheumatoid arthritis, i.e. a patient 13
The history may have clinical rheumatoid arthritis but not fulfil all criteria.
The patient will often localise symptoms of pain, stiffness, loss of a
Large joints: shoulders, elbows, hips, knees and ankles
function, contractures, disfigurement and trauma. If symptoms b
Small joints: all metacarpophalangeal and proximal interphalangeal joints, thumb
are vague or diffuse, consider referred pain or a compressive interphalangeal joint, wrists and 2nd–5th metatarsophalangeal joints.
neuropathy, such as carpal tunnel syndrome (see Box 7.11). If ACPA, anti-cyclic citrullinated peptide antibody; CRP, C-reactive protein;
ESR, erythrocyte sedimentation rate; RF, rheumatoid factor.
PIP or MCP joint swelling is prominent, consider inflammatory Reproduced from Aletaha D, Neogi T, Silman AJ, et al. Rheumatoid arthritis
arthritis. classification criteria: an American College of Rheumatology/European League
Painful, swollen and stiff hand joints are common and important Against Rheumatism collaborative initiative. Arthritis & Rheumatism 2010; 62(9):
presenting symptoms, and scoring systems (Box 13.14) are used 2569–2581, with permission from John Wiley and Sons.
to define the presence of rheumatoid arthritis.
Supination Pronation
B
Dorsal Radial Ulnar
Palmar
Neutral
Fig. 13.23 T1 root lesion (cervical rib) affecting the right hand.
Wasting of the thenar eminence and interossei, and flexed posture of the
fingers due to lumbrical denervation.
A B
13
C D
Radial nerve (wrist and finger extensors): ask the patient to Feel
extend the wrist and fingers fully (‘paper sign’). Palpate the bony contours of the lateral and medial
Ulnar nerve (hypothenar muscles, interossei, two medial epicondyles and olecranon tip.
lumbricals, adductor pollicis, flexor carpi ulnaris and the Feel for sponginess, suggesting synovitis, on either side of
ulnar half of flexor digitorum profundus): ask the patient to the olecranon when the elbow is fully extended.
make the ‘scissors sign’. Feel for focal tenderness over the lateral or medial
Median nerve (thenar muscles that abduct and oppose the epicondyle (see ‘Special tests’).
thumb, the lateral two lumbricals, the medial half of flexor Feel for olecranon bursa swelling, and nodules or tophi.
digitorum profundus, flexor digitorum superficialis, flexor Feel for rheumatoid nodules on the proximal extensor
carpi radialis, palmaris longus and pronator teres): ask the surface of the forearm.
patient to clench the fist fully (‘stone sign’). The best test
of median nerve motor function is the ability to abduct the Move
thumb away from the palm because of inconstant Assess the extension–flexion arc: ask the patient to touch
crossover in the nerve supply to the thenar eminence their shoulder on the same side and then straighten the
muscles other than abductor pollicis brevis. However, elbow as far as possible. The normal range of movement
clenching the fist fully also depends on median function is 0–145 degrees; a range of less than 30–110 degrees
because of its flexor supply. will cause functional problems.
Anterior interosseous nerve (flexor pollicis longus, the index Assess supination and pronation: ask the patient to put
finger flexor digitorum profundus and pronator quadratus): their elbows by the sides of their body and flex them to 90
ask the patient to make the ‘OK’ sign. This depends on degrees. Now ask them to turn the palms upwards
the function of both flexor pollicis longus and index finger (supination: normal range 0–90 degrees) and then
flexor digitorum profundus. downwards (pronation: normal range 0–85 degrees).
13
13.16 Common conditions affecting the shoulder
Non-trauma
Rotator cuff syndromes, e.g. Adhesive capsulitis (‘frozen
supraspinatus, infraspinatus shoulder’)
tendonitis Calcific tendonitis
Impingement syndromes Bicipital tendonitis
(involving the rotator cuff and Inflammatory arthritis
subacromial bursa) Polymyalgia rheumatica
Trauma
Rotator cuff tear Fracture of the clavicle
Glenohumeral dislocation Fracture of the head or neck Fig. 13.28 Right anterior glenohumeral dislocation. Loss of the normal
Acromioclavicular dislocation of the humerus shoulder contour.
Examination sequence
Ask the patient to sit or stand and expose their shoulder
completely.
Look Fig. 13.29 ‘Winging’ of the left scapula. This caused by paralysis of the
Examine from the front and back, and in the axilla, for: nerve to serratus anterior.
Deformity: the deformities of anterior glenohumeral and
complete acromioclavicular joint dislocation are obvious
(Fig. 13.28), but the shoulder contour in posterior Muscle wasting, especially of the deltoid, supraspinatus
glenohumeral dislocation may appear abnormal only when
you stand above the seated patient and look down on the infraspinatus indicates a chronic tear of their tendons.
shoulder. Size and position of the scapula: that is, whether it is
Swelling. elevated, depressed or ‘winged’ (Fig. 13.29).
270 THE MUSCULOSKELETAL SYSTEM
Feel hand behind their back and feel as high up the spine as
Feel from the sternoclavicular joint along the clavicle to the possible. Document the highest spinous process that they
acromioclavicular joint. can reach with the thumb.
Palpate the acromion and coracoid (2 cm inferior and External rotation: in the same position, with the elbow
medial to the clavicle tip) processes, the scapula spine tucked against their side, ask them to rotate their hand
and the biceps tendon in the bicipital groove. outwards.
Extend the shoulder to bring supraspinatus anterior to the Deltoid: ask the patient to abduct their arm out from their
acromion process. Palpate the supraspinatus tendon. side, parallel to the floor, and resist while you push down
on the humerus. Compare each side.
Move Rotator cuff muscles
Active movements (Fig. 13.30) To test the component muscles of the rotator cuff, the effect
Ask the patient to flex and extend their shoulder as far as
of other muscles crossing the shoulder needs to be
possible.
neutralised.
Abduction: ask the patient to lift their arm away from their
Internal rotation of the shoulder – subscapularis and
side.
pectoralis major:
Palpate the inferior pole of the scapula between your
To isolate subscapularis, place the patient’s hand
thumb and index finger to detect scapular rotation and
behind their back. If they cannot lift it off their back, it
determine how much movement occurs at the
suggests a tear (Gerber test).
glenohumeral joint. The first 0–15 degrees of abduction
Pain on forced internal rotation suggests tendonitis.
are produced by supraspinatus. The middle fibres of
Abduction of the arm – supraspinatus:
the deltoid are responsible for the next 15–90 degrees.
Past 90 degrees the scapula needs to be rotated to
Loss of power suggests a tear.
achieve abduction, which is carried out by the trapezius
Pain on forced abduction at 60 degrees suggests
and serratus anterior muscles (Fig. 13.31). If the
tendonitis.
glenohumeral joint is excessively stiff, movement of the
External rotation – infraspinatus and teres minor:
scapula over the chest wall will predominate. If there is
Test external rotation with the arm in the neutral
any limitation or pain (painful arc) associated with
position and at 30 degrees to reduce the contribution
abduction, test the rotator cuff.
of deltoid. Loss of power suggests a tear.
Internal rotation: with the patient’s arm by their side and
Pain on forced external rotation suggests tendonitis.
the elbow flexed at 90 degrees, ask them to put their
No movement or fixed internal rotation suggests a
frozen shoulder.
Bicipital tendonitis
Internal External Palpate the long head of biceps in its groove on the head
of the humerus, noting any tenderness. Ask the patient to
supinate their forearm and then flex the arm against
resistance. Pain occurs in bicipital tendonitis. A rupture of
the long head of biceps causes the muscle to bunch
distally (the Popeye sign).
External 90 degrees
Flexion and extension Abduction
Internal
180
degrees Rotation in
abduction
90
degrees Elevation
0 degrees 0 degrees
Neutral Glenohumeral alone Neutral Total
(scapula immobilised) Glenohumeral
and scapular
Abduction Fig. 13.31 Contribution of the glenohumeral joint and scapula to
Fig. 13.30 Movements of the shoulder. shoulder abduction.
271
Lower limb Ask how the pain restricts activities. Record walking ability in
terms of the time and distance the patient manages outside and
Hip on stairs, and note whether walking aids are used.
Anatomy The physical examination
The hip is a ball-and-socket joint and allows flexion, extension,
abduction, adduction, internal/external rotation and the combined Examination sequence
movement of circumduction.
Patients should undress to their underwear and remove socks
The history and shoes. You should be able to see the iliac crests.
Pain is usually felt in the groin but can be referred to the anterior Look
thigh, the knee or the buttock. Hip pain is usually aggravated by Assess gait.
activity, but osteonecrosis and tumours may be painful at rest Carry out a general inspection: ask the patient to stand.
and at night. Lateral hip or thigh pain, aggravated when lying From the front, check if:
on that side, suggests trochanteric pain syndrome. Fracture stance is straight
of the neck of the femur is common following relatively minor shoulders lie parallel to the ground and symmetrically
trauma in postmenopausal women and those aged over 70 years. over the pelvis (this may mask a hip deformity or true
The classical appearance is a shortened, externally rotated leg shortening of one leg)
272 THE MUSCULOSKELETAL SYSTEM
Move
brim is perpendicular to the spine.
Check the range of flexion of each hip in turn.
Abduction and adduction: stabilise the pelvis by placing
B
hand, abduct the patient’s leg until you feel the pelvis start
to tilt (normal 45 degrees). Test adduction by crossing one
of the patient’s legs over the other and continuing to move
it medially (normal 25 degrees) (Fig. 13.34A).
Internal and external rotation: with the patient’s leg in full
extension, roll it on the couch and watch the foot to
indicate the range of rotation. Test with the knee (and hip)
flexed at 90 degrees. Move the foot medially to test
external rotation and laterally to test internal rotation
(normal 45 degrees for each movement) (Fig. 13.34B).
Extension: ask the patient to lie prone on the couch. Place
your left hand on the pelvis to detect any movement. Lift
each of the patient’s legs in turn to assess the range of C
extension (normal range 0–20 degrees) (Fig. 13.34C).
Fig. 13.34 Testing hip movement. A Abduction. B Flexion.
Thomas test C Extension.
This reveals fixed flexion deformity (incomplete extension) that
may be masked by compensatory movement at the lumbar
spine or pelvis and increased lumbar lordosis.
Place your left hand under the patient’s back (to detect
any masking of hip limitation by movement of the pelvis
and lumbar spine).
Passively flex both legs (hips and knees) as far as possible
(Fig. 13.35A).
Keep the non-test hip maximally flexed and by feeling with
your left hand confirm that the lordotic curve of the spine
remains eliminated.
Ask the patient to extend the test hip. Incomplete
extension in this position indicates a fixed flexion deformity
at the hip (Fig. 13.35B).
If the contralateral hip is not flexed sufficiently, the lumbar
lordosis will not be eliminated and fixed flexion deformity of
the ipsilateral knee confuses the issue. In this case,
perform the test with the patient lying on their side.
Do not perform the test if the patient has a hip
replacement on the non-test side, as forced flexion may Fig. 13.35 Thomas test. A Passively flex both legs as far as possible.
cause dislocation. B Extend the test leg. Limitation indicates fixed flexion deformity.
273
Medial malleolus 13
Special tests
Shortening
Shortening occurs in hip and other lower limb conditions (Box Fig. 13.36 True and apparent lengths of the lower limbs.
13.17). Apparent shortening is present if the affected limb appears
shortened, usually because of an adduction or flexion deformity
at the hip.
Examination sequence
Ask the patient to lie supine and stretch both legs out as
far as possible equally, to eliminate any soft-tissue
contracture/abnormal posture.
Measure with a tape:
from umbilicus to medial malleolus: the apparent length
from anterior superior iliac spine to medial malleolus:
the ‘true length’ (Fig. 13.36).
Confirm any limb length discrepancy by ‘block testing’:
Ask the patient to stand with both feet flat on the
ground.
Raise the shorter leg, using a series of blocks of
graduated thickness until both iliac crests feel level.
Trendelenburg’s sign
Fig. 13.37 Trendelenburg’s sign. Powerful gluteal muscles maintain the
Examination sequence position when standing on the left leg. Weakness of the right gluteal
muscles results in pelvic tilt when standing on the right leg.
Stand in front of the patient.
Palpate both iliac crests and ask the patient to stand on
one leg for 30 seconds. Knee
Repeat with the other leg.
Anatomy
or down. The knee is a complex hinge joint with tibiofemoral and
Normally, the iliac crest on the side with the foot off the patellofemoral components. It has a synovial capsule that
ground should rise. The test is abnormal if the extends under the quadriceps muscle (the suprapatellar pouch),
unsupported hemipelvis falls below the horizontal (Fig. reaching 5 cm above the superior edge of the patella. The joint
13.37). This may be caused by gluteal weakness or is largely subcutaneous, allowing easy palpation of the patella,
inhibition from hip pain, such as in osteoarthritis, or tibial tuberosity, patellar tendon, tibial plateau margin and femoral
structural abnormality of the hip joint, such as in coxa vara condyles. The knee depends on its muscular and ligamentous
or developmental hip dysplasia. structures for stability (Fig. 13.38).
274 THE MUSCULOSKELETAL SYSTEM
A 2 B C D
8 6 8 SP
1 1 7
G
PP
l 10 m M
3 6 L
5 10
5 SM
4
IP
6
8
3
8
9 5
Key
G Bursa under the medial head 1 Extensions of synovial sheath 7 Posterior ligament
of gastrocnemius on either side of patella 8 Horns of lateral (l) and medial
IP Infrapatellar bursa 2 Extension of synovial sheath (m) menisci
L Lateral tibiofemoral articulation at upper pole of patella 9 Connection of anterior horns
M Medial tibiofemoral articulation 3 Lateral ligament 10 Unattached margin of meniscus
PP Prepatellar bursa 4 Medial ligament
SM Semimembranosus bursa 5 Anterior cruciate ligament
SP Suprapatellar pouch (or bursa) 6 Posterior cruciate ligament
Fig. 13.38 Structure of the right knee. A Anterior view, showing the common synovial sheath. B Anterior and lateral views, showing the ligaments.
C Plan view of the menisci. D Bursae.
Swelling
13.18 Bone conditions associated with pathological fracture
The normal volume of synovial fluid is 1–2 mL and is clinically
Osteoporosis Renal osteodystrophy undetectable. An effusion indicates intra-articular pathology.
Osteomalacia Parathyroid bone disease Haemarthrosis (bleeding into the knee) is caused by injury to a
Primary or secondary tumour Paget’s disease vascular structure within the joint, such as a torn cruciate ligament
Osteogenesis imperfecta or an intra-articular fracture. The menisci are predominantly
avascular and do not cause a haemarthrosis, unless torn at their
periphery, or in conjunction with some other internal derangement.
The hamstring muscles flex the knee. Extension involves the Locking
quadriceps muscles, quadriceps tendon, patella, patellar tendon Two common causes in the knee are a loose body, such
and tibial tuberosity. Any disruption of this ‘extensor apparatus’ as from osteochondritis dissecans, osteoarthritis or synovial
prevents straight-leg raising or produces an extensor lag (a chondromatosis, and a meniscal tear. Bucket-handle and anterior
difference between active and passive ranges of extension). beak meniscal tears are especially associated with locking.
The medial and lateral collateral ligaments resist valgus and Posterior horn tears commonly cause pain and limit movement
varus stress, respectively. The anterior cruciate ligament (ACL) in the last few degrees of flexion. Meniscal tears also cause local
prevents anterior subluxation of the tibia on the femur, and the joint-line tenderness. Congenital discoid meniscus may present
posterior cruciate ligament resists posterior translation. The medial with locking and clunking.
and lateral menisci are crescentic fibrocartilaginous structures
that lie between the tibial plateaux and the femoral condyles. Instability (‘giving way’)
There are several important bursae around the knee: Any of the four main ligaments may rupture from trauma or
become incompetent with degenerative disease. The patella
patella and the overlying skin) and infrapatellar bursae is prone to dislocate laterally because the normal knee has a
(between the skin and the tibial tuberosity/patellar valgus angle.
ligament)
The physical examination
(Fig. 13.38D).
Examination sequence
The history Observe the patient walking and standing, as for gait. Note
Pain posture and deformities such as genu valgum (knock knee) or
genu varum (bow legs).
Generalised knee pain is likely to be due to pathology in the
tibiofemoral joint (Box 13.18). Anterior knee pain, particularly after Look
prolonged sitting or going downstairs, suggests patellofemoral joint Ask the patient to lie supine on the couch. Expose both legs
pathology. Medial or lateral pain could come from the collateral fully and look for:
ligaments or meniscal tears. Scars, sinuses, erythema or rashes.
Pain in the knee may be referred from the hip. Muscle wasting: quadriceps wasting is almost invariable
Take a detailed history of the mechanism of any injury. The with inflammation, internal derangement or chronic pain,
direction of impact, load and deformation predict what structures and develops within days. Measure the thigh girth in both
are injured. legs 20 cm above the tibial tuberosity.
275
Look for
fluid bulge
on medial
Medial Lateral side
Fig. 13.39 Testing for effusion by the patellar tap. Fig. 13.40 Bulge or ripple test to detect small knee effusions.
276 THE MUSCULOSKELETAL SYSTEM
A B
Fig. 13.41 Testing the ligaments of the knee. A Collateral ligaments. B Cruciate ligaments.
1 Lateral malleolus
2 Medial malleolus
3 Lateral (external) ligament
4 Medial ligament
5 Deep fibres of medial ligament
4
6 Navicular
3 6 7 Spring ligament
3 9 5
8 Calcaneus
9 Talus
1 2
3
3 9 5 7 8
4
Fig. 13.42 Ankle ligaments.
Neutral Dorsiflexion
(extension)
Plantar
(flexion) 13
Forefoot Forefoot
adduction abduction Flexion Extension
Eversion Inversion
Fig. 13.43 Terminology used for movements of the ankle and foot.
The history Forefoot pain, often localised to the second metatarsal, after
A ‘twisted’ ankle is very common, and is usually related to a excessive activity such as trekking, marching or dancing, suggests
sporting injury or stepping off a kerb or stair awkwardly. Establish a stress fracture (Fig. 13.44). Symptoms are relieved by rest and
the exact mechanism of injury and the precise site of pain. aggravated by weight bearing.
Frequently there has been a forced inversion injury stressing
the lateral ligament. A sprain occurs when some fibres are torn Non-traumatic conditions
but the ligament remains structurally intact. A complete ligament Anterior metatarsalgia with forefoot pain is common, especially
tear allows excessive talar movement in the ankle mortise with in middle-aged women. Acute joint pain with swelling suggests
instability. an inflammatory arthropathy such as rheumatoid arthritis or gout.
Achilles tendon rupture is associated with sudden plantar In severe cases the metatarsal heads become prominent and
flexion at the ankle. It is common in middle-aged patients doing walking feels like walking on pebbles or broken glass.
unaccustomed activity such as squash, and is associated with Plantar surface heel pain that is worse in the foot-strike phase
some medications such as oral glucocorticoids and fluoroquinolone of walking may be caused by plantar fasciitis and tends to affect
antibiotics. Sudden pain occurs above the heel and there is often middle-aged patients and those with seronegative arthritides.
a sensation or noise of a crack. Patients may feel as if they have Posterior heel pain may be caused by Achilles tendonitis or
been kicked or even shot. enthesitis.
278 THE MUSCULOSKELETAL SYSTEM
Examination sequence
Ask patients to remove their socks and shoes.
Look
Examine the soles of the shoes for abnormal patterns of
wear.
Assess gait. Look for: Fig. 13.45 Hallux valgus overriding the second toe.
increased height of step, indicating ‘foot drop’
ankle movement (dorsiflexion/plantar flexion)
Passive foot inversion/eversion
position of the foot as it strikes the ground (supinated/
Examine the subtalar joint in isolation by placing the foot
pronated)
into dorsiflexion to stabilise the talus in the ankle mortise.
hallux rigidus – loss of movement at the
Move the heel into inversion (normal 20 degrees) and
metatarsophalangeal (MTP) joints.
eversion (normal 10 degrees).
From behind and with the patient standing:
Examine the combined mid-tarsal joints by fixing the heel
Observe how the heel is aligned (valgus/varus).
with your left hand and moving the forefoot with your right
From the side:
hand into dorsiflexion, plantar flexion, adduction,
Observe the position of the midfoot, looking particularly
abduction, supination and pronation.
at the medial longitudinal arch. This may be flattened
(pes planus – flat foot) or exaggerated (pes cavus).
Passive hallux and lesser toe movements
Assess flexion and extension at MTP and interphalangeal
If the arch is flattened, ask the patient to stand on
joints. Pain and stiffness at the first MTP joint suggest
tiptoe. This restores the arch in a mobile deformity but
hallux rigidus.
not in a structural one.
If there is toe deformity, assess impingement on the other
A ‘splay foot’ has widening at the level of the metatarsal
toes. Claw toes result from dorsiflexion at MTP joints and
heads, often associated with MTP joint synovitis.
plantar flexion at PIP and DIP joints. Hammer toes are due
Examine the ankle and foot for scars, sinuses, swelling,
to dorsiflexion at MTP and DIP joints, and plantar flexion at
bruising, callosities (an area of thickened skin at a site of
PIP joints. Mallet toes describe plantar flexion at DIP joints.
repeated pressure), nail changes, oedema, deformity and
position. Special tests
Look for deformities of the toes such as hallux valgus
Achilles tendon
(Fig. 13.45) or overriding toes.
Observe any bunion (a soft-tissue bursal swelling) over the
first metatarsal head that may be inflamed or infected.
Examination sequence
Ask the patient to kneel with both knees on a chair.
Feel Palpate the gastrocnemius muscle and the Achilles tendon
Feel for focal tenderness and heat.
for focal tenderness and soft-tissue swelling. Achilles
In an acute ankle injury, palpate the proximal fibula, both
tendon rupture is often palpable as a discrete gap in
malleoli, the lateral ligament and the base of the fifth
the tendon about 5 cm above the calcaneal insertion
metatarsal.
(Fig. 13.46A).
Gently compress the forefoot. Assess the lesser toe MTP
joints for swelling and tenderness suggestive of Thomson’s (Simmond’s) test
inflammatory arthritis.
Move (see Fig. 13.43) Examination sequence
Active movements Squeeze the calf just distal to the level of maximum
Assess plantar flexion/dorsiflexion at the ankle, inversion/ circumference. If the Achilles tendon is intact, plantar
eversion of the foot and flexion/extension of the toes. flexion of the foot will occur (Fig. 13.46B).
Passive movements
Mulder’s sign for Morton’s neuroma
Grip the patient’s heel from below with the cup of your left
hand, with your thumb and index finger on the malleoli.
Put the foot through its arc of movement (normal range 15
Examination sequence
degrees dorsiflexion to 45 degrees plantar flexion). Squeeze the metatarsal heads together with one hand, at
If dorsiflexion is restricted, assess the contribution of the same time putting pressure on the interdigital space
gastrocnemius (which functions across both knee and with your other hand. The pain of the neuroma will be
ankle joints) by measuring ankle dorsiflexion with the localised to the plantar surface of the interdigital space
knee extended and flexed. If more dorsiflexion is possible and may be accompanied by a ‘clunk’ as the neuroma
with the knee flexed, this suggests a gastrocnemius slides between the metatarsal heads. Paraesthesia will
contracture. radiate into the affected toes.
279
13
Move
Establish whether the patient can move joints distal and
13.19 Describing a fracture
proximal to the fracture.
What bone(s) is/are involved?
Do not move a fracture site to see if crepitus is present; Is the fracture open (compound) or closed?
this causes additional pain and bleeding. Is the fracture complete or incomplete?
Describe the fracture according to Box 13.19. For each Where is the bone fractured (intra-articular/epiphysis/physis/
suspected fracture, X-ray two views (at least) at perpendicular metaphysis/diaphysis)?
planes of the affected bone, and include the joints above and What is the fracture’s configuration (transverse/oblique/spiral/
below. comminuted (multifragmentary)/butterfly fragment)?
What components of deformity are present?
Translation is the shift of the distal fragment in relation to the
proximal bone. The direction is defined by the movement of the
distal fragment, e.g. dorsal or volar, and is measured as a
percentage.
Angulation is defined by the movement of the distal fragment,
measured in degrees.
Rotation is measured in degrees along the longitudinal axis of
the bone, e.g. for spiral fracture of the tibia or phalanges.
Shortening: proximal migration of the distal fragment can cause
shortening in an oblique fracture. Shortening may also occur if
there has been impaction at the fracture site, e.g. a Colles’
fracture of the distal radius.
Is there distal nerve or vascular deficit?
What is the state of the tissues associated with the fracture (soft
tissues and joints, e.g. fracture blisters, dislocation)?
Investigations
Fig. 13.48 Ankle deformity. A Clinical appearance. B Lateral X-ray Common investigations in patients with musculoskeletal disease
view showing tibiotalar fracture dislocation. are summarised in Box 13.20.
Mr Hunt, 38 years old, has a 2-month history of right shoulder pain with no history of trauma.
Please examine the shoulder
Introduce yourself and clean your hands.
Expose both of the patient’s shoulders and arms.
Comment on acromioclavicular deformity and muscle wasting; look for winging of the scapula.
Compare the right shoulder to the normal left shoulder.
Perform active and passive movements. In particular, look for frozen shoulder, which is diagnosed by limitation of external rotation and flexion.
Finally, examine the arm, looking for conditions such as biceps rupture.
If all movements of the shoulder are normal, conduct a full examination of the neck.
Thank the patient and clean your hands.
Summarise your findings
The patient reports pain between 120 and 60 degrees of abduction when lowering the abducted shoulder. Pain is reproduced on abduction against
resistance.
Suggest a differential diagnosis
The most common cause of these symptoms is impingement syndrome, which can be confirmed by carrying out special tests (Neer and Hawkins–
Kennedy). Differentials include frozen shoulder, calcific tendonitis, acromioclavicular joint pain, arthritis (osteoarthritis, rheumatoid arthritis or
post-traumatic), long head of biceps rupture and referred pain from the neck.
Suggested investigations
X-ray will reveal degenerative changes in osteoarthritis or tendon calcification. Ultrasound may demonstrate effusions, calcific deposits and tendon
damage/rupture.
282 THE MUSCULOSKELETAL SYSTEM
Mrs Hill, 46 years old, presents with an 8-week history of insidious onset of pain, stiffness and swelling of her hands. She smokes 15 cigarettes per day.
Please examine her hands
Introduce yourself and clean your hands.
Look:
In this case there is swelling of two MCP joints on the right, and one PIP joint on the left.
Normal nails and skin (therefore psoriatic arthropathy is unlikely).
Feel:
Ask first what is sore and seek permission to examine gently.
Tender, soft swelling of the MCP and PIP joints in the hands and left elbow.
In feet: tender across her MTP joints on squeeze test but no palpable swelling.
Move:
Painful MCP joints in right hand on active and passive flexion, reducing handgrip and fine movements.
Summarise your findings
The patient has tender, soft swelling of two MCP joints and one PIP joint. There is pain on active and passive movement of the affected joints, resulting
in limitation of hand function.
Suggest a differential diagnosis
The pattern of joint involvement, patient’s gender, duration of symptoms and history of smoking support a clinical diagnosis of rheumatoid arthritis. The
differential diagnosis of psoriatic arthropathy is less likely because of her normal nails and lack of the typical skin changes of psoriasis.
Suggest initial investigations
Full blood count, renal function tests, calcium, phosphate and liver function tests to assess for anaemia of chronic disease and to determine suitability
for disease-modifying antirheumatic drugs; C-reactive protein to assess the degree of systemic inflammation; anti-CCP antibody to confirm whether
seropositive rheumatoid arthritis is present; application of the 2010 American College of Rheumatology/European League Against Rheumatism criteria
(see Box 13.14) for classification of rheumatoid arthritis; hand and foot X-rays to detect any bony erosions; chest X-ray to look for rheumatoid lung
disease.
Dermatological conditions are very common (10–15% of general (Box 14.1). It has three layers, the most superficial of which
practice consultations) and present to doctors in all specialties. is the epidermis, a stratified squamous epithelium, containing
In the UK, 50% are lesions (‘lumps and bumps’), including skin melanocytes (pigment-producing cells) within its basal layer, and
cancers, and most of the remainder are acute and chronic Langerhans cells (antigen-presenting immune cells) throughout.
inflammatory disorders (‘rashes’), including infections, with genetic The dermis is the middle and most anatomically complex layer,
conditions accounting for a small minority. containing vascular channels, sensory nerve endings, numerous
Dermatological diagnosis can be challenging: not only is there a cell types (including fibroblasts, macrophages, adipocytes and
vast number of distinct skin diseases, but also each may present smooth muscle), hair follicles and glandular structures (eccrine,
with a great variety of morphologies and patterns determined by sebaceous and apocrine), all enmeshed in collagen and elastic
intrinsic genetic factors, with the diagnostic waters muddied still tissue within a matrix comprising glycosaminoglycan, proteoglycan
further by external influences such as rubbing and scratching, and glycoprotein.
infection, and well-meaning attempts at topical and systemic The deep subcutis contains adipose and connective tissue.
treatment. Even in one individual, lesions with the same pathology Dermatoses (diseases of the skin) may affect all three
can have a very variable appearance (for example, melanocytic layers and, to a greater or lesser extent, the various functions
naevi, seborrhoeic keratoses and basal cell carcinomas). of the skin.
Many skin findings will have no medical significance, but it is
important to be able to examine the skin properly in order to
identify tumours and rashes, and also to recognise cutaneous
signs of underlying systemic conditions. The adage that the skin
is a window into the inner workings of the body is entirely true,
and an examination of the integument will often provide the 14.1 Functions of the skin
discerning clinician with important clues about internal disease
processes, as well as with information about the physical and Protection against physical injury and injurious substances, including
psychological wellbeing of an individual. ultraviolet radiation
Anatomical barrier against pathogens
Immunological defence
Anatomy and physiology Retention of moisture
Thermoregulation
Calorie reserve
Skin Appreciation of sensation (touch, temperature, pain)
Vitamin D production
Absorption – particularly fetal and neonatal skin
The skin is the largest of the human organs, with a complex
Psychosexual and social interaction
anatomy (Fig. 14.1) and a number of essential functions
Shaft of hair
Sweat duct
Subpapillary vascular plexus
Sebaceous gland
Dermis
Arrector pili muscle
Sweat gland
Hair follicle
Subcutaneous adipose tissue
Muscle layer
Hair
Hair plays a role in the protective, thermoregulatory and sensory
functions of skin, and also in psychosexual and social interactions. Ask:
There are two main types of hair in adults:
body surface
Nails
example, exercise or exposure to heat may precipitate
The nail is a plate of densely packed, hardened, keratinised cells cholinergic urticaria.
produced by the nail matrix. It serves to protect the fingertip
and aid grasp and fingertip sensitivity. The white lunula at the
base of the nail is the visible distal aspect of the nail matrix (Fig. ameliorate urticaria, and topical glucocorticoids may help
14
14.2). Fingernail regrowth takes approximately 6 months, and inflammatory reactions.
toenail regrowth 12–18 months.
such as joint pain (psoriasis), muscle pain and
weakness (dermatomyositis), fever, fatigue or
The history
The possible diagnoses in dermatological conditions are broad
and some diseases have pathognomonic features. Thus, in order
to ensure that your history taking is focused and relevant, it
may be appropriate to ask to glimpse the lesion or rash before Past medical and drug history
embarking on detailed enquiry.
Ask about general health and previous medical or skin conditions;
Common presenting symptoms a history of asthma, hay fever or childhood eczema suggests
atopy. Coeliac disease is associated with dermatitis herpetiformis.
These include: Take a full drug history, including any recent oral or topical
prescribed or over-the-counter medication. Enquire about allergies
not just to medicines but also to animals or foods.
Lateral nail fold Distal edge of nail plate Hyponychium Nail plate Proximal nail fold (paronychium)
(paronychium)
Nail bed Cuticle Matrix
Lunula
Nail plate
Cuticle
Eponychium
Distal phalanx
A B
Fig. 14.2 Structure of the nail. A Dorsal view. B Cross-section.
286 THE SKIN, HAIR AND NAILS
C
Fig. 14.6 Rash morphology. A Koebner response. B Pemphigoid.
C Granuloma annulare.
C
Fig. 14.5 Lichen planus. A Discrete flat-topped papules on the wrist.
B Wickham striae, visible on close inspection. C A white lacy network of extravasation and entrapment in the collagen and elastic fibres
striae on the buccal mucosa.
of the dermis.
The tint of the erythema may be helpful: a violaceous hue
distinguishes lichen planus; a beefy-red or salmon-pink colour
The vascular contribution to the colour of a rash can be pivotal often typifies psoriasis; and a heliotrope (pink–purple) colour is
in diagnosis since erythematous and purpuric eruptions usually a feature of dermatomyositis, especially on the eyelids.
have very different underlying causes. It is not sufficient to describe Macular purpura may be the result of thrombocytopenia or
a rash as ‘red’ or ‘pink’; it is essential to demonstrate whether capillary fragility, but palpable purpura (often painful) usually
or not a rash blanches on direct pressure or when the skin indicates vasculitis (Fig. 14.7A) and necessitates exclusion of
is stretched. Blanchable redness (erythema) indicates that the vasculitic inflammation in other organs. Purpura elicitable by
red blood cells causing the colour remain within blood vessels; pinching the skin (‘pinch purpura’) may be indicative of AL
non-blanchable redness (purpura) is the result of erythrocyte (light-chain) amyloidosis (Fig. 14.7B).
289
A B
Fig. 14.7 Purpura. A Cutaneous vasculitis. B AL (light-chain) amyloidosis.
14
A B
A B
Fig. 14.11 Basal cell carcinoma. A Viewed with the naked eye. B Dermatoscopy highlights distinctive telangiectasia.
Dermatoscopy
A dermatoscope consists of a powerful light source (polarised or
non-polarised) and a magnifying lens, and enables considerably
more cutaneous anatomical detail to be seen (Fig. 14.14).
14
Fig. 14.12 Alopecia areata. Fig. 14.14 Dermatoscope.
C
Fig. 14.13 Nail appearances in systemic diseases. A The typical linear pattern of dermatomyositis with Gottren’s papules on the dorsum of the hand.
B Nail-fold telangiectasia in dermatomyositis, viewed through the dermatoscope. C Yellow nail syndrome in a patient with lymphoedema and pleural
effusions.
292 THE SKIN, HAIR AND NAILS
Diascopy
The pressure of a glass slide on the skin will compress the
cutaneous blood vessels and blanch the area of contact. If blood
is still visible through the glass, it is because red blood cells have
Wood’s lamp
OSCE example 2: Pigmented lesion Integrated examination sequence for the skin
Ms Forsythe, 55 years old, presents with a 6-week history of a Prepare the patient:
changing pigmented lesion on her right calf. Arrange for privacy.
Please examine her skin Arrange for a chaperone, if necessary.
Remove sufficient clothing.
Introduce yourself to the patient and clean your hands. Remove makeup and wigs, if face and scalp are being examined.
Ask her to undress to underwear. Carry out a general examination of the skin:
Carry out a general inspection of the skin, estimating her Fitzpatrick Look for excoriations, xerosis (dry skin), actinic damage and
skin type, and observing for signs of actinic damage and for other suspicious lesions, for example.
lesions that might require close assessment. Carry out a specific examination of a rash:
Observe the lesion on her calf for size, symmetry, regularity of Extent.
margins, variation of pigmentation and ulceration. Distribution: symmetry, pattern.
Palpate the lesion. Morphology.
Examine for enlargement of regional lymph nodes. Colour.
Examine the abdomen for an enlarged liver. Erythema/purpura.
Undertake a similar examination of any other suspicious lesions. Specific features, e.g. scale, signs of infection/infestation.
Thank the patient and clean your hands. Mouth, hair and nails.
Suggest a differential diagnosis Regional lymph nodes.
Carry out a specific examination of a lesion:
Any changing lesion should raise suspicion of malignant melanoma,
Site, size, colour.
although melanocytic naevi, seborrhoeic keratoses, dermatofibromas,
Symmetry.
haemangiomas and pigmented basal cell carcinomas can cause
Surface texture.
diagnostic confusion.
Consistency.
Suggested investigations Mobility.
If, after examination, there is still suspicion regarding the malignant Pattern of vasculature.
potential of the lesion, it should be excised for histological examination. Regional lymph nodes.
14
Section 3
Applying history
and examination skills
in specific situations
15 Babies and children 297
16 The patient with mental disorder 319
17 The frail elderly patient 329
18 The deteriorating patient 339
19 The dying patient 347
Ben Stenson
Steve Cunningham
15
Babies and children
Babies 298 The physical examination 310
The history 298 Normal growth and development 310
Maternal history 298 Physical examination techniques in children 312
Pregnancy history 298 The acutely unwell child 313
Birth history 298 General examination 313
Infant’s progress 298 Ears, nose and throat 314
Presenting problems and definitions 298 Cardiovascular examination 315
Respiratory examination 315
The physical examination of newborns 299
Abdominal examination 315
Timing and efficacy of the routine neonatal examination 299
Neurological examination 315
General examination 299
Spotting the sick child 315
Cardiovascular examination 301
Respiratory examination 302 Child protection 315
Abdominal examination 303 OSCE example case 1: Cyanotic episodes 317
Neurological examination 304 OSCE example 2: Asthma 317
Limbs 305
Integrated examination sequence for the newborn child 318
Weighing and measuring 306
Final inspection 307
The physical examination of infants beyond the newborn period 307
Older children 307
The history 307
Obtaining a history from children compared with adults 307
Common presenting symptoms 308
Past medical history 310
Birth history 310
Vaccination history 310
Developmental history 310
Drug history 310
Family and social history 310
Systematic enquiry 310
298 BABIES AND CHILDREN
BABIES
A baby is a neonate for its first 4 weeks and an infant for its first
year. Neonates are classified by gestational age or birthweight
Presenting problems and definitions
(Box 15.1).
The history
Pallor
Ask the mother and look in the maternal notes for relevant
history:
Maternal history
of < 120 g/L (<
hereditary illnesses)?
Respiratory distress
> 60 breaths
Pregnancy history
Cyanosis
delivery?
Acrocyanosis
Jaundice
Infant’s progress
birth?
Jitteriness
Examination sequence
Observe whether the baby looks well and is well grown.
Look for:
cyanosis
Dysmorphism
Skin
Hypotonia
Normal findings
and nails.
15
Apgar score
This first clinical assessment of a neonate is made immediately
Abnormal findings
General examination
Occiput
Lambdoid suture
Posterior fontanelle
Parietal bone
and eminence
Sagittal suture
Anterior fontanelle
Frontal bone
Frontal suture
Fig. 15.2 Mongolian blue spot.
Sinciput
Fig. 15.3 The fetal skull from above.
Head
Examination sequence
Normal findings
Abnormal findings
Ophthalmoscopy
Examination sequence
Fig. 15.4 Coloboma.
Ears
Examination sequence
Nose Neck
Examination sequence Examination sequence
Mouth
swellings do not.
Examination sequence
Normal findings
Abnormal findings
Normal findings
Cardiovascular examination
Abnormal findings
Examination sequence
Candida albicans
BABIES AND CHILDREN
Fig. 15.5 Palpating the femoral pulses. The pulse can be difficult to
feel at first. Use a point halfway between the pubic tubercle and the
anterior superior iliac spine as a guide.
Normal findings
(Box 15.4).
8 9 10
Abnormal findings
4
5 3
1
6 2
7
aorta. Radiofemoral delay is not identifiable in the newborn.
later in childhood.
Examination sequence
by 4).
Listen for additional noises with breathing.
the nostrils.
1 and S2
Normal findings
Abnormal findings
Examination sequence
fossa.
15
the right costal margin.
finger.
Examination sequence
Abnormal findings Female
BABIES AND CHILDREN
Penoscrotal
A B
Male
Fig. 15.11 Hypospadias and chordee. A Penile shaft hypospadias.
be adherent in babies. B Lateral view showing the ventral curvature of the penis (chordee). From
Lissauer T, Clayden G. Illustrated Textbook of Paediatrics. 2nd edn.
Edinburgh: Mosby; 2001.
Examination sequence
Normal findings
< 5 mm in diameter
and <
Abnormal findings
Normal findings
× 1 cm across. investigation.
Neurological examination
Abnormal findings
Examination sequence
the baby cries. Most cases are transient.
Normal findings
Examination sequence
Grasp responses
Place-and-step reflexes
15
Moro reflex
Root-and-suck responses
Limbs
Examination sequence
Fig. 15.12 Erb’s palsy. The right arm is medially rotated and the wrist is
flexed. From Lissauer T, Clayden G. Illustrated Textbook of Paediatrics. 2nd
edn. Edinburgh: Mosby; 2001.
BABIES AND CHILDREN
Normal findings
Abnormal findings
is dislocatable.
15.5 Developmental attainment of preschool children at different ages*
Skills 4 months 6 months 10 months 1–2 years 2–3 years 3–5 years
Gross motor Has good head control on Supports weight Sits unsupported Walks without Runs Pedals a
pull to sit on hands when Pulls to stand support Bounces on tricycle
Keeps back straight when laid prone trampoline
held in sitting position Rolls front to back
Fine motor Opens hands Transfers objects Uses pincer grip Holds a crayon Can draw a circle Can draw a
Holds objects placed in from hand to hand bilaterally without and scribbles cross, square,
hand and to mouth hand preference face/person
Personal Shows interest in toys Has a variety of Starts to understand Has 10–20 Can communicate Has 500–1500
social Laughs, vocalises speech noises some words recognisable verbally words
Plays peep-bo Claps hands words Is dry by day
*Development is extremely variable and failure to attain only one milestone is of little significance whereas failure to attain several milestones is cause for concern.
15
The physical examination of infants
beyond the newborn period
Fig. 15.15 Measurement of head circumference.
OLDER CHILDREN
The history
}
Acute
Headache ** Low Acute (simple) headache, migraine, meningitis/
encephalitis
Unsteady gait * High Varicella encephalomeningitis, vestibular neuronitis
Vomiting, fever, neck stiffness,
Seizurea * High Febrile seizure, meningitis/encephalitis
photophobia
Epilepsy, metabolic disorder
Disturbed level of * High Encephalitis, intoxication/drug ingestion
consciousness (accidental/ deliberate)
Chronic
Headacheb ** Low Vomiting Brain tumour, migraine, chronic non-specific
Abdominal pain headache
Failure to pass * Moderate Widening gap between age and Cerebral palsy, neglect
developmental age when ‘normal’ milestone
milestones should have been passed
Developmental * High Muscular dystrophy, inborn error of metabolism,
regression neurodegenerative conditions
Seizure * High Epilepsy; rarely, long QT syndrome or inborn error
of metabolism
a
An acute seizure can be confused with a rigor in a febrile child. A seizure involves slow (1 beat per second), coarse, jerking that cannot be stopped, loss of consciousness
and postictal drowsiness. A rigor is characterised by rapid (5 beats per second), fine jerking that can be stopped by a cuddle with no loss of consciousness. bChronic
headache can also arise from the mouth (e.g. dental abscess) or face.
Staphylococcus aureus).
BABIES AND CHILDREN
Systematic enquiry
Birth history
gestation)?
Vaccination history
Drug history
Growth
Family and social history
Ask:
A child on the 0.4th centile for height may be thriving if this has
height centile ±
height lies on the 50th centile will have children whose height will
several caregivers.
Neurological development
Weight-for-age BOYS
Birth to 2 years (z-scores)
17 3 17
16 16
2
15 15
14 14
13 13
12 0 12
11 11
Weight (kg)
10 -2 10
9 -3
9
8 8
7 7
6 6
5 5
4 4
3 3
2 2
Months 1 2 3 4 5 6 7 8 9 10 11 1 2 3 4 5 6 7 8 9 10 11
Birth 1 year 2 years
Age (completed months and years)
WHO Child Growth Standards
Weight-for-age GIRLS
Birth to 2 years (z-scores)
15
17 3 17
16 16
15 2 15
14 14
13 13
12 12
0
11 11
Weight (kg)
10 10
9 -2 9
8 -3 8
7 7
6 6
5 5
4 4
3 3
2 2
Months 1 2 3 4 5 6 7 8 9 10 11 1 2 3 4 5 6 7 8 9 10 11
Birth 1 year 2 years
Age (completed months and years)
WHO Child Growth Standards
Fig. 15.17 Growth charts. World Health Organization standard centile charts for girls and boys. From WHO Child Growth Standards. http://www.who.int/
childgrowth/standards/weight_for_age/en/ © World Health Organization 2017. All rights reserved.
Puberty
Female
Height of growth spurt
in the illness.
12 years
Similarities in examination between
children and adults
Age of menarche
121/4 –121/2 years that takes time to learn. The key skills involve being:
Breast stage IV
III
II
III
II
Penis stage IV
III
II
Testicular volume
12 mL
4 mL
III
II
3–5 years
8 9 10 11 12 13 14 15 16 17 18 19 20
Years
Fig. 15.18 Timing of puberty in males and females.
BI BII BIII BIV BV
Prepubertal Breast bud Juvenile smooth Areola and papilla Adult
Breast development
FEMALE contour project above breast
Pubic hair
Fig. 15.19 Stages of puberty in males and females. Pubertal changes according to the Tanner stages of puberty.
15
Calibration checked
15.10 Serious signs requiring urgent attention
Head straight, eyes and ears level
Poor perfusion with reduced capillary refill and cool peripheries
(indicating shock) Gentle upward traction on mastoid process
Listless, poorly responsive, whimpering child (suggesting sepsis)
Petechial rash over the trunk (suggesting meningococcal sepsis)
Headache with photophobia or neck stiffness (suggesting meningitis)
Respiratory distress at rest (rapid rate and increased respiratory
effort, indicating loss of respiratory reserve due to pneumonia or
asthma)
Knees straight
5+ years
Barefoot with feet flat on floor
Heels touching back of board
General examination
investigation and management (Box 15.10).
Height
BABIES AND CHILDREN
Fig. 15.21 How to hold a child to examine the mouth and throat.
Examination sequence
Vital signs
Normal ranges for vital signs vary according to age (Box 15.11).
Examination sequence
Lymphadenopathy
Normal findings
15.13 Clinical signs associated with severe
15.12 Causes of lymph node enlargement illness in children
Cervical lymphadenopathy Fever > 38°C
Tonsillitis, pharyngitis, sinusitis Drowsiness
‘Glandular fever’ (infectious mononucleosis/cytomegalovirus) Cold hands and feet
Tuberculosis (uncommon in developed countries) Petechial rash
Neck stiffness
Generalised lymphadenopathy
Shortness of breath at rest
Febrile illness with a generalised rash Tachycardia
‘Glandular fever’ Hypotension (a late sign in shocked children where blood pressure
Systemic juvenile chronic arthritis (Still’s disease) is initially maintained by tachycardia and increased peripheral
Acute lymphatic leukaemia vascular resistance)
Drug reaction
Mucocutaneous lymph node syndrome (Kawasaki disease)
Abdominal examination
Child protection
Neurological examination
strength against gravity. Ask them to lift their arms above their
BABIES AND CHILDREN
Patient details
PRESCHOOL (1–4 years) Name
DOB CHILDREN’S
UNIT
Hosp No
COAST: CHILDREN’S UNIT
CHILDREN’S OBSERVATION AND SEVERITY TOOL
SOUTH COAST CHILDREN’S EARLY WARNING SCORE: CHILDREN’S UNIT
Date
Time
Doctor/Nurse/Family Concern?
40
39
38
Temperature
(°C) 37
36
35
34
220
210
200
190
180
170
Heart Rate 160
(bpm) 150
140
and 130
120
110
Blood Pressure 100
(mmHg)* 90
80
*nb BP does not score 70
in COAST Scoring 60
50
40
Heart Rate (number)
70
60
Resp Rate 50
(bpm) 40
30
(over 1 minute) 20
10
Resp Rate (number)
Receiving O2 (L/min)
O2 saturations (%)
Resp. Mod/Severe
Distress None/Mild
Distress None/Mild
Level Decreased
GCS*
Pain Score*
TOTAL COAST SCORE
Number of shaded boxes
Observer’s initials
ACTIONS 0–1 Continue normal observations.
2 Nurse in Charge review. Hourly observations.
NB: Scores 3 should
be recorded overleaf
3 Nurse in Charge & Doctor to review patient. Half-hourly observations.
4 Nurse in Charge & SpR to review patient. Consider informing Consultant.
5–6 Nurse in Charge & Senior Doctor to see immediately.
If airway compromise, call ITU Registrar immediately.
*nb: BP, GCS and Pain Score values do not contribute to the overall COAST score.
Fig. 15.23 Rapid cardiopulmonary evaluation. BP, blood pressure; bpm, beats/breaths per minute; GCS, Glasgow coma scale score; ITU, intensive
treatment unit; SpR, specialist registrar. Courtesy Dr Sandell.
OSCE example case 1: Cyanotic episodes
Charlie, 4 months old, is brought in to see you by his mother Helen. She is anxious, as he has ‘turned blue’ on three occasions since discharge from
hospital. Two of the episodes have been during breastfeeding, when he has become agitated and breathless.
Please perform a newborn examination, focusing on the cardiovascular system
Introduce yourself to the parent and clean your hands
Carry out a general inspection: are there any signs of congenital heart disease?
Look for signs of respiratory distress (tachypnoea, indrawing, accessory muscle use).
Check for scars on the chest.
Look at the colour and perfusion of the patient (cyanosis, pallor, sweatiness).
Look for signs of dysmorphic features that might indicate an associated chromosomal abnormality.
Look for signs of poor weight gain.
Palpate: is the infant warm and well perfused? Are there any palpable cardiac abnormalities?
Check central capillary refill. Feel the temperature.
Palpate peripheral pulses (brachial, femoral).
Palpate the precordium for palpable murmurs (thrills), ventricular heave or abnormal position of the apex.
Assess whether there is palpable hepatomegaly or finger clubbing.
Auscultate: is there a murmur?
Auscultate the heart in a systematic fashion.
Describe any murmur by documenting timing, grade (1–6), character, location, radiation, and variation with position and respiration.
Auscultate the back to check whether the murmur radiates.
Clean your hands and thank the parent.
Suggest a diagnosis
Congenital heart disease is possible with this presentation. There are many possible types and further investigation is needed for diagnosis. Tetralogy
of Fallot consists of four features: ventricular septal defect, right ventricular outflow obstruction, right ventricular hypertrophy and an overriding aorta. It
requires surgical correction. Children with tetralogy of Fallot are more likely to have chromosome disorders (Down’s syndrome or Di George syndrome).
Finger clubbing is not usually present in young infants.
Suggest investigations 15
Pulse oximetry, echocardiogram, electrocardiogram, chest X-ray.
John, 8 years old, who has been diagnosed with asthma, is brought to see you by his parent. He has had more frequent episodes of wheeze and
night-time cough over the last 3 months, each lasting longer and responding less well to regular doses of bronchodilator.
Please perform a chest examination, focusing on the respiratory system
Introduce yourself to the parent and patient, and clean your hands.
Carry out a general inspection: are there any signs of acute or chronic respiratory distress?
Look for chest wall deformity (pectus excavatum, Harrison’s sulcus).
Look for signs of respiratory distress (tachypnoea, indrawing, accessory muscle use).
Count the respiratory rate over 1 minute.
Look at the colour and perfusion of the patient (cyanosis, pallor, sweatiness).
Look for finger clubbing and poor weight gain.
Palpate: consider palpation if there are chest-wall abnormalities or differential chest expansion on inspection, to look for differential chest-wall
movement.
Auscultate: warm the stethoscope.
Auscultate the respiratory system in all lung regions, anteriorly and posteriorly, with the chest fully exposed.
Wheeze is auscultated in all lung regions. No crepitations are heard. Air entry is reduced to all lung regions. The respiratory rate is raised at 40
breaths per minute.
Heart sounds are normal with no murmur.
Clean your hands and thank the parent and patient.
Summarise your findings
This child has tachypnoea and a widespread, loud, polyphonic wheeze on expiration.
Suggest a diagnosis
Acute asthma attack on the background of unstable asthma is the likely diagnosis with these symptoms and signs. This requires treatment of the acute
episode with bronchodilator and oral glucocorticoids, and consideration of how to improve background control. Stabilising background control includes
an assessment of adherence and technique for current therapies, consideration of new triggers and how exposure may be reduced (by history and/or
skin-prick testing) and, if required, a trial of a stepwise increase in baseline asthma therapy.
Suggest initial investigations
Peak expiratory flow or spirometry, and oxygen saturation.
BABIES AND CHILDREN
Mental disorders are very common, frequently coexist with physical death) or incriminating (illicit drug misuse, other crime, homicidal
disorders and cause much mortality and morbidity. Psychiatric ideas). For interviews undertaken in non-clinical settings such as
assessment is therefore a required skill for all clinicians. It consists police stations or prisons, or for the provision of court reports,
of four elements: the history, mental state examination, selective the latter is obviously especially pertinent, and it is important to
physical examination and collateral information. Each element can be clear with the patients about any limits to confidentiality in
be expanded considerably, so the assessment must be adapted your interview.
to its purpose. Is it a quick screening of a patient presenting Try to develop rapport early in the interview, if possible, and to
with other problems, a confirmation of a suspected diagnosis consolidate it before raising a sensitive topic, although sometimes
or a comprehensive review for a second opinion? you must cover such material without delay. It is particularly
important to ask about suicidal thoughts.
Appearance
16.1 Content of a psychiatric history Think of this as a written account of a still photograph, prepared
for someone who cannot see it. Observe:
Referral source
Reason for referral
History of presenting symptom(s)
Systematic enquiry into other relevant problems and symptoms previous self-harm)
Past medical/psychiatric history
Prescribed and non-prescribed medication
Substance use: illegal drugs, alcohol, tobacco, caffeine
Family history (including psychiatric disorders) alcoholic liver disease)
Personal history
from thyrotoxicosis).
Behaviour
16.2 Personal history
Think of this as a written account of a video, observing such
Childhood development Partner(s) and children features as:
Losses and experiences Housing
Education Leisure activities
Occupation(s) Hobbies and interests withdrawal)
Financial circumstances Forensic history
Relationships
unobserved stimuli
321
This is not a description of what the patient says (that is, content),
pleasure?’ Abnormalities of mood include a problematic pervasive
but of how they say it (form). Assess:
mood, an abnormal range of affect, abnormal reactivity and
inappropriateness or incongruity. Some terms relating to mood
are defined in Box 16.5.
Some patients prompt affective responses in the interviewer,
via the process of countertransference. The elated gaiety of some
hypomanic patients can be infectious, as can the hopeless gloom
of some people with depression. Recognising these responses in
yourself can be helpful in understanding how the patient relates
Box 16.4). to others and vice versa.
may be understandable but unusually rapid, as in the flight of The main difference between them is that delusions either
ideas that characterises hypomania, or unduly ‘single track’ and lack a cultural basis for the belief or have been derived from
perseverative, as in some cases of dementia. Sometimes thinking abnormal psychological processes.
appears to be very circumstantial, and the patient hard to pin
down, even when asked simple questions. Overvalued ideas
More severe disruption of the train of thought is termed
These are usually beliefs of great personal significance. They
loosening of associations or formal thought disorder, in which
fall short of being full delusions but are abnormal because of
their effects on a person’s behaviour or wellbeing. For example,
direction that the interviewer cannot follow. This is a core feature
in anorexia nervosa, people may still believe they are fat when
of schizophrenia. Concrete thinking, in the sense of difficulty
they are seriously underweight – and then respond to their belief
handling abstract concepts, is a common feature of dementia,
rather than their weight, by further starving themselves.
and can be assessed by asking the patients to explain the
meaning of common proverbs. Delusional beliefs
It may help to illustrate your assessment with verbatim examples
from the interview, chosen to illustrate the patient’s manner of These beliefs also matter greatly to the person, resulting in
thinking and speaking. powerful emotions and important behavioural consequences;
they are always of clinical significance. They are classified by
their content, such as:
Thought content
the patient’s mind. It will become apparent when taking the history
but may need to be explored further via specific enquiries. It
may broadly be divided into preoccupations, ruminations and
abnormal beliefs. These are defined in Boxes 16.7 and 16.8.
Preoccupations
Preoccupations occur in both normal and abnormal mood states. withdrawal)
Sadly dwelling on the loss of a loved one is entirely normal in
bereavement; persisting disproportionate guilty gloom about the
state of the world may be a symptom of depression. Bizarre delusions are easy to recognise, but not all delusions
are weird ideas: a man convinced that his partner is unfaithful
Ruminations may or may not be deluded. Even if a partner were unfaithful,
These are preoccupations that are in themselves abnormal – held without evidence or for some unaccountable reason, such
and therefore symptoms of mental disorder – by reason of as finding a dead bird in the garden.
repetition (as in obsessional disorders) or groundlessness (as
in hypochondriasis).
Abnormal beliefs
These beliefs fall into two categories: those that are not diagnostic 16.8 Abnormal beliefs: definitions
of mental illness (such as overvalued ideas, superstitions and
Term Definition
magical thinking) and those that invariably signify mental illness
(that is, delusions). Delusion An abnormal belief, held with total conviction, which
is maintained in spite of proof or logical argument to
the contrary and is not shared by others from the
same culture
16.7 Thought content: definitions Delusional A delusion that arises fully formed from the false
perception interpretation of a real perception, e.g. a traffic light
Term Definition turning green confirms that aliens have landed on
Hypochondriasis Unjustified belief in suffering from a particular the rooftop
disease in spite of appropriate examination and Magical An irrational belief that certain actions and outcomes
reassurance thinking are linked, often culturally determined by folklore or
Morbid thinking Depressive ideas, e.g. themes of guilt, burden, custom, e.g. fingers crossed for good luck
unworthiness, failure, blame, death, suicide Overvalued Beliefs that are held, valued, expressed and acted
Phobia A senseless avoidance of a situation, object or ideas on beyond the norm for the culture to which the
activity stemming from a belief that has caused person belongs
an irrational fear Thought The belief that the patient’s thoughts are heard by
Preoccupation Beliefs that are not inherently abnormal but which broadcasting others
have come to dominate the patient’s thinking Thought The belief that thoughts are being placed in the
Ruminations Repetitive, intrusive, senseless thoughts or insertion patient’s head from outside
preoccupations Thought The belief that thoughts are being removed from the
Obsessions Ruminations that persist despite resistance withdrawal patient’s head
323
Delusions can sometimes be understood as the patient’s way when going to sleep (hypnagogic) or waking up (hypnopompic).
of trying to make sense of their experience, while the content of Hallucinations are categorised according to their sensory modality
the delusions often gives a clue that may help type the underlying as auditory, visual, olfactory, gustatory or tactile.
illness: for example, delusions of guilt suggest severe depression, Any form of hallucination can occur in any severe mental
whereas grandiose delusions typify mania. disorder. The most common are auditory and visual hallucinations,
Some delusions are characteristic of schizophrenia. They the former associated with schizophrenia and the latter with
include a delusional perception (or primary delusion) and ‘passivity delirium. Some auditory hallucinations are characteristic of
phenomena’: namely, the belief that thoughts, feelings or acts schizophrenia, such as voices discussing the patient in the
are no longer controlled by a person’s own free will. third person or giving a running commentary on the person’s
activities (‘Now he’s opening the kitchen cupboard’). Ask, for
Perceptions example, ‘Do you ever hear voices when nobody is talking?’
and ‘What do they say?’
People normally distinguish between their inner and outer worlds Pseudohallucinations are common. The key distinction from
with ease: we know what is real, what reality feels like, and what a true hallucination is that they occur within the patient, rather
resides in our ‘mind’s eye’ or ‘mind’s ear’. In mental illness this than arising externally. They have an ‘as if’ quality and lack the
distinction can become disrupted, so that normal perceptions vividness and reality of true hallucinations. Consequently, the
become unfamiliar, while abnormal perceptions seem real. affected person is not usually distressed by them, and does
Abnormal perceptions are assessed via the history and specific not normally feel the need to respond, as often happens with
enquiries, backed up by observation. They fall into several true hallucinations.
categories, defined in Box 16.9.
Perceptions may be altered (as in sensory distortions or illusions) Cognition
or false (as in hallucinations and pseudohallucinations). In a third
category, what is altered is not a perception in a specific sensory If the history and observation suggest a cognitive deficit, it must
modality but a general sense of disconnection and unreality be evaluated by standard tests. History, observation, MSE and
in oneself (depersonalisation), the world (derealisation) or both. rating scales (see later) are then used together to diagnose and
People find depersonalisation and derealisation intensely distinguish between the ‘3Ds’ (dementia, delirium and depression),
unpleasant but hard to describe. They may occur in association which are common in the elderly and in hospital inpatients.
with severe tiredness or intense anxiety but can also arise in most Core cognitive functions include:
types of mental illness. Ask, for example, ‘Have you ever felt that
you were not real or that the world around you wasn’t real?’
16
new information; once this has registered, check retention be neither overstated nor ignored. Any others at risk are most
after 5 minutes, with a distracting task in between. Do the likely to be family or, less commonly, specific individuals (such
as celebrities in cases of stalking) or members of specific groups
significant. Alternatively, use a six-item name and address (defined by age, ethnicity, occupation and so on). Sometimes the
(in the format: Mr David Green, 25 Sharp Street, Durham). risk applies non-specifically to strangers, or to anyone preventing
More than one error indicates impairment. the patient from achieving their goals.
There may be direct risk to life and limb (as in suicide, self-harm
history. Gaps and mistakes are often obvious but some or violence to others), or it may be an indirect risk, either to health
patients may confabulate (that is, fill in the gaps with (through refusal of treatment for physical or mental illness) or
plausible but unconsciously fabricated facts), so check the welfare (through inability to provide basic care – food, warmth,
account with a family member or other informant if shelter, hygiene – for oneself or one’s dependents). The risk may
possible. Confabulation is a core feature of Korsakoff’s be imminent, as in a patient actively attempting self-harm, or
syndrome, a complication of chronic alcoholism. Failing remote, as in a patient refusing prophylactic medical treatment.
long-term memory is characteristic of dementia, although Direct risks tend to be imminent and indirect risks remote, although
this store of knowledge can be remarkably intact in the this is not always so. A patient declining renal dialysis because
presence of severe impairment of other cognitive functions. their depression makes them feel unworthy is at imminent but
indirect risk of death. Finally, the likelihood of the risk may range
Impaired attention and concentration from near certainty to hypothetical possibility.
A risk assessment should readily distinguish between cases
These occur in many mental disorders and are not diagnostic.
where there is an imminent, direct and near-certain risk to the
Impaired attention is observed as increased distractibility, with
patient’s life (such as a man actively trying to throw himself from
the patient responding inappropriately to intrusive internal events
the window to escape delusional persecutors), and those where
(memories, obsessions, anxious ruminations) or to extraneous
any risks apply to the welfare of other people, at some point
stimuli, which may be either real (a noise outside the room) or
in the future, and amount to possibilities (such as a depressed
unreal (auditory hallucinations).
woman who may be neglecting her frail elderly father). The former
Concentration is the patient’s ability to persist with a mental
case calls for urgent intervention, probably via mental health
task. It is tested by using simple, repetitive sequences, such as
legislation; the latter requires engagement over time, preferably
asking the patient to repeat the months of the year or days of
in a voluntary way.
the week in reverse, or to do the ‘serial 7s’ test, in which 7 is
While all psychiatric evaluations require some assessment of
subtracted from 100, then from 93, then 86 and so on. Note
risk, it should be considered in depth whenever the presentation
the finishing point, the number of errors and the time taken.
includes acts or threats of self-harm or reports of command
Intelligence hallucinations, the past history includes self-harm or violent
behaviour, the social circumstances show a recent, significant
This is estimated clinically from a combination of the history loss, or the mental disorder is strongly associated with risk (as
of educational attainment and occupations, and the evidence in severe depression).
provided at interview of vocabulary, general knowledge, abstract Assessing suicidality is the element of risk assessment that is
thought, foresight and understanding. If in doubt as to whether most often needed. If a patient presents after an act of self-harm
the patient has a learning disability, or if there is a discrepancy or overdose, the questions arise naturally (‘What did you want
between the history and presentation, a psychologist should to happen when you took the tablets? Did you expect to die?
formally test IQ. Is that what you wanted? How do you feel about that now? Do
you still feel you’d be better off dead? Have you had thoughts
Insight about doing anything else to harm yourself?’).
Insight is the degree to which a patient agrees that they are but do not fear that you may be putting ideas in the patient’s
ill. It can be broken down into the recognition that abnormal mind (‘You’ve told me how bad you have been feeling. Have
mental experiences are in fact abnormal, agreement that these you ever felt life is not worth living? Have you had any thoughts
abnormalities amount to a mental illness, and acceptance of the about ending your life? How close have you come? What has
need for treatment. Insight matters, since a lack of it often leads stopped you acting on those thoughts so far?’).
to non-adherence, and sometimes to the need for compulsory
detention. You might ask ‘Do you think anything is wrong with
you’ or ‘If you are ill, what do you think needs to happen to Capacity
make you better?’
Assessing capacity is a skill required of all doctors and should not
be delegated to psychiatrists. The legal elements vary between
Risk assessment
The first is the presumption of capacity: clinicians should treat
Risk assessment is a crucial part of every psychiatric assessment.
patients as retaining capacity until it is proven that they have lost
Consider:
it. Secondly, capacity is decision-specific: patients may not be
able to understand the risks and benefits of complex medical
treatment options, while retaining the ability to decide whether
or not to enter a nursing home. Thirdly, residual capacity should
The person usually at risk, if anyone, is the patient themselves. be maximised: if a patient’s ability to understand is impaired by
The risk posed to others by people with mental disorder must sensory deficits or language barriers, these should be corrected
325
16.14 Clinical vignette: overdose 16.15 Clinical vignette: confusion, agitation and hostility
A 19-year-old woman attends the accident and emergency An 85-year-old man in a medical ward, where he is undergoing
department, having taken a medically minor overdose. She has intravenous antibiotic treatment for a chest infection, now appears
presented in this way three times in the last 2 years. She needs no confused, agitated and hostile, in a way not previously evident to his
specific medical treatment. family.
Your assessment should concentrate first on the circumstances of You need to approach him carefully to establish rapport and to
the overdose and her intentions at the time. Collateral information interview him as much as he will allow, while anticipating that you may
should include assessments after previous presentations and any have to rely heavily on collateral information, and a mental state
continuing psychiatric follow-up. Mental state examination should examination limited to observation of appearance and behaviour. It will
screen for any new signs of mental disorder emerging since her last be crucial to talk to his family to establish his normal level of cognition
assessment, and in particular any mood problems or new psychotic and independence, and to the nursing staff to establish the diurnal
symptoms. She will clearly have undergone a detailed physical pattern of his problems. If there is any history of previous episodes,
assessment, but even if the overdose appears medically trivial, you acquire the results of previous assessments. He will need a
need to undertake a risk assessment to judge the chances of further neurological examination and assessment of his cognition via a
self-harm or completed suicide in the near future. She probably does standard scale. Risk assessment should focus on the indirect risks to
not need a detailed cognitive assessment or psychiatric rating scales. his health if he tries to leave hospital against advice, generating a view
about his detainability under mental health legislation. A capacity
assessment of his ability to consent to continuing antibiotic treatment
is required, and may result in the issue of an incapacity certificate.
327
A 35-year-old woman attends her general practitioner, presenting with A 42-year-old man attends a psychiatric outpatient clinic for the first
fatigue. time, having been referred by his general practitioner for longstanding
Assessment of possible physical causes is required, via history, paranoid thoughts.
examination and appropriate blood tests, but as these proceed, the It will be particularly important to establish rapport with a patient
interview should also cover possible symptoms of depression, previous who is likely to be very wary. The interview needs to cover the
episodes, family history and recent stressors. Mental state examination psychiatric history in some detail, considering substance misuse, family
should concentrate on objective evidence of lowered mood. Formal history of mental illness and a full personal history in particular. Mental
assessment of cognition is probably not necessary, but a standard state examination should explore the paranoid thoughts in detail, to
rating scale for mood disorder may help establish a diagnosis and a establish whether they are preoccupations or overvalued ideas
baseline against which to measure change. Risk assessment is not a (suggesting a personality disorder), or delusions (suggesting a
prominent requirement, unless a depressive illness is suspected and psychotic illness). Risk assessment should concentrate on the risk to
she reports thoughts of self-harm, or is responsible for young children, others about whom the patient has paranoid fears. Neither detailed
in which case the chance of direct or indirect harm to them needs to cognitive assessment nor a specific rating scale is likely to add much
be considered. to the initial assessment.
Miss Gardiner, 27 years old, presented to the accident and emergency department the previous day after taking an overdose of paracetamol while
intoxicated with alcohol. She has undergone treatment with acetylcysteine overnight and is now medically fit for discharge.
Please assess her risk of self-harm and suicide
Introduce yourself and clean your hands.
Explain the purpose of your assessment; try to gain rapport.
Enquire how she is feeling physically (specifically asking about nausea, vomiting and abdominal pain).
Tactfully introduce the subject of the overdose.
Establish the number and type of tablets taken.
16
Establish how much alcohol she drank, whether this was with the tablets (to ‘wash them down’) or whether she was already intoxicated at the time
of the overdose.
Clarify the circumstances. Who else was present or expected? Did she write a note or otherwise communicate what she had done or was planning
to do?
Clarify how she was found and either came or was brought to hospital.
Explore recent or chronic stressors.
Establish her intent at the time of the overdose. Did she expect to die? Is that what she wanted?
Confirm her view now. Does she still wish to die? Does she have any thoughts about another overdose or other form of self-harm?
Establish relevant past history. Are there any previous overdoses? Any previous or continuing psychiatric follow-up?
Confirm whether she has parental or caring responsibilities for young children. Tactfully enquire about any thoughts of harming them.
Establish who will be with her when she leaves hospital.
Thank the patient and clean your hands.
Summarise your findings
The risk assessment should concentrate most on the short-term risk of suicide.
Advanced level comments
More advanced students would be expected to tabulate short- and long-term risk of both suicide and further self-harm, and to quote the risk of
completed suicide in the first year after an act of self-harm (1–2%).
328 THE PATIENT WITH MENTAL DISORDER
Mr Duncan, 82 years old, is admitted to an orthopaedic ward after falling and breaking his hip. Forty-eight hours after surgery he became restless and
agitated overnight, pulling out his intravenous line. He is now settled and cooperative.
Please assess the likely cause of this episode
Introduce yourself and clean your hands.
Explain the purpose of your assessment; try to establish rapport.
Enquire how he is feeling physically (specifically asking about pain, fever, constipation, and urinary and respiratory symptoms).
Establish his awareness of where he is, why he is there and how long he has been in hospital.
Ask how much he remembers of the night’s events and enquire specifically about any recollection of hallucinations or persecutory fears.
Enquire about any continuing hallucinations or fears.
Ask about any previous similar episodes.
Clarify how active he was before his fall, and whether there is any awareness of memory impairment leading up to it.
Ask about alcohol intake.
Administer simple tests of cognitive function, especially of attention and memory (advanced performers should know the Abbreviated Mental Test
questions).
Undertake a basic physical examination, assessing for tremor, ophthalmoplegia and nystagmus.
Gain the patient’s permission to speak to his next of kin, general practitioner and others.
Thank the patient and clean your hands.
Summarise your findings
The diagnosis is delirium, with further enquiries needed to establish the likely cause (which may be alcohol withdrawal, given the timing), as well as
the possibility of pre-existing cognitive impairment as a vulnerability factor.
Review the relevant information to clarify the reason for referral or mode of self-presentation.
Establish rapport to reduce distress and assist assessment.
Cover the key headings for the history (presenting symptoms, systematic review, past medical and psychiatric history, current medication, substance
misuse, family history, personal history).
Cover the headings for the personal history (childhood development, losses and experiences, education, occupation, financial circumstances,
relationships, partner(s) and children, housing, leisure activities, hobbies and interests, forensic history).
Make the extent, order and content of the assessment appropriate to the presentation and setting.
Observe closely to gain objective evidence of mental state, especially non-verbal information.
Cover the headings for the mental state examination systematically (appearance and behaviour, speech, mood, thought form and content,
perceptions, cognition and insight).
Use brief formal tests to assess cognitive function (Abbreviated Mental Test, Mini-Mental State Examination, Montreal Cognitive Assessment).
Consider your own emotional response to your patient.
Consider standardised rating scales as a screening tool (and sometimes to monitor progress).
Undertake physical examination as appropriate to the setting and the presentation.
Gather further background information from other sources to the degree necessary (with permission).
As well as a diagnosis and management plan, be sure to consider:
assessment of risk to self or others
capacity to take decisions
need to use mental health or incapacity legislation.
Andrew Elder
Elizabeth MacDonald
17
The frail elderly patient
Assessment of the frail elderly patient 330 The physical examination 333
Factors influencing presentation and history 330 General examination 333
The history 331 Systems examination 334
The presenting symptoms 331 Functional assessment 335
Common presenting symptoms 331 Interpretation of the findings 337
Past medical history 331 OSCE example 1: History in a frail elderly patient with falls 337
Drug history 331
OSCE example 2: Examination of an acutely confused frail
Family history 332 elderly patient 337
Social and functional history 332
Integrated clinical examination for the frail elderly patient 338
Systematic enquiry 332
330 THE FRAIL ELDERLY PATIENT
The presenting symptoms the problem is true vertigo or worse on standing (p. 123) 17
Frail elderly patients often have multiple symptoms. Take time or any joint pain, especially in the back, neck or lower
to detail each symptom, and separate those arising from new limbs
acute illness from those due to background disabilities.
Ask:
Try to establish what the patient’s symptoms, functional abilities Past medical history
and mental status were before the new presenting problem. This
helps set realistic goals for treatment and rehabilitation. Detail the past history and known comorbidities from all available
The patient’s perspective may vary from yours, particularly sources, including any previous records. Comorbidities may not
in acute settings. For example, a patient referred following be directly relevant to the current problem but may influence
sudden loss of consciousness may be unconcerned by this prognosis and the feasibility and appropriateness of potential
but anxious about longstanding back pain. These symptoms investigations and treatments (Box 17.3).
are not coincidental; if it is important to your patient, it should
be important to you.
Drug history
Common presenting symptoms Polypharmacy is associated with drug interactions, adverse events
and difficulties with adherence. Take a detailed drug history,
Decreased mobility
supplemented by the following:
Ask about:
preparations.
change was abrupt
recently, or doses of regular medications altered.
inhalers correctly.
332 THE FRAIL ELDERLY PATIENT
}
Anticholinergics Dry mouth
Diuretics Urinary frequency A symptom is caused by drug treatment rather than disease
Some calcium antagonists Ankle swelling
}
Vasodilators, diuretics Postural hypotension
Beta-blockers Bradycardia A sign is caused by drug treatment rather than disease
L-dopa (usually long-term) Dyskinetic limb movements
Beta-blockers No tachycardia in gastrointestinal bleeding An expected sign does not occur because of drug treatment
the house.
Family history
A first presentation of disease with a strong genetic basis is relevant to their condition and gives insight into their past
unlikely, but family history is still important to patients who have life. Retirement can lead to social isolation, which
lost siblings or children to specific conditions and who may contributes to mood disorders.
believe that their own symptoms are related.
Do they do their own shopping and prepare their own problems or has anyone else commented on their
mobility and sleep. Postural Less specific than in younger patients; may be
hypotension caused by drugs, disease or age-related
abnormal autonomic responses to postural
leakage from their bladder or bowels. Are they aware
change
Decreased skin Decreased collagen elasticity and reduced
turgor subcutaneous fat can mimic reduced turgor.
prostatic symptoms (p. 235) in particular. Do these
Best assessed at the sternum
Impaired capillary Less reliable in the frail elderly because less
refill time specific
and whether they wear glasses. Can they can see the
Dry mouth A non-specific finding caused by other problems
aid, find out if it is working and whether they are such as anticholinergic drugs or mouth breathing 17
wearing it. Tachycardia in Less sensitive due to drug- or age-related
hypovolaemia abnormal autonomic responses
Ask specifically about any falls in the past year and obtain
a careful description of these (p. 331). Find out how they
would call for help if they fell and could not get up.
pressure occurs because there is decreased arterial compliance. drug therapy. Kyphosis often occurs from painless osteoporotic
Isolated systolic hypertension and postural hypotension occur vertebral collapse and may affect postural stability and respiratory
more frequently. The latter may result from age-related function.
baroreceptor reflex change, disease or drugs. It may not be Always examine the feet. Bunions, onychomycosis with or
symptomatic but increases the risk of a fall. without nail overgrowth, and foot ulcers are common. All can
Medial sclerosis and arterial calcification can make it difficult compromise mobility and stability, be a source of sepsis or pain,
to feel peripheral pulses but do not cause impaired perfusion and affect gait. Observe your patient walking. A wide variety of
and circulation in isolation. The carotid artery may become more pathologies can produce distinctive abnormalities of gait, including
tortuous and its pulsations more easily visible. This can create Parkinson’s disease (see Fig. 7.17). Gait abnormalities are a risk
a false impression of arterial dilatation. factor for falls and can exacerbate joint problems.
Atrial contribution to left ventricular filling increases with age,
partly due to diastolic dysfunction of the heart, and a fourth
heart sound (S4) is more commonly heard. Functional assessment
Respiratory examination Functional assessment is divided into an analysis of:
posture and gait and any inappropriate footwear. Are they Look for signs of acute illness (see Box 17.4) and pain
(see Box 17.6).
Examine the skin, large joints, lungs, heart valves,
Cardiovascular system: check for postural hypotension. prostheses and abdomen for signs of sepsis.
Examine for any new neurological features.
in the lower limbs, and look for evidence of Parkinson’s Perform pulse oximetry (SpO2).
disease (Ch. 7). Feel for a distended bladder.
Musculoskeletal system: look for muscle wasting or Consider a rectal examination (p. 111) to check for faecal
fasciculation, joint abnormality and foot deformity. impaction.
Consider specific investigations (Box 17.8). Consider specific investigations (see Box 17.8).
The acutely confused frail elderly person The frail elderly person with falls
If patients have problems with vision or hearing, ensure Look for signs of bony or soft-tissue injury and acute
they wear their glasses or a working hearing aid. illness such as sepsis (see Box 17.4).
Cardiovascular system: check for postural hypotension,
arrhythmias and aortic stenosis.
17.9 A problem-based approach in a frail elderly patient with immobility and confusion
Problem Potential contributory factors Management plan
Urinary incontinence Urinary tract infection Perform urinalysis
Faecal impaction Send a midstream specimen of urine to confirm
Carry out a rectal examination
Hyponatraemia Bendroflumethiazide Withhold bendroflumethiazide
Monitor serum sodium
Confusion with features of delirium Urinary infection As above plus:
Hyponatraemia Check Mini Mental State Examination
Underlying dementia Obtain a collateral history from a carer
Check thyroid function
Arrange an occupational therapy review
Foot ulcer Absent pedal pulses Check ankle : brachial pressure index
Discuss a dressing with the nurse
Poor mobility Urinary infection As above plus:
Hyponatraemia Prescribe simple analgesia
Pain from foot ulcer Carry out a full neurological/gait examination
Underlying cerebrovascular disease Assess vascular risk factors
Arrange a physiotherapy review
337
Follow a standard systematic approach, including aspects that are important in frail patients. Remember that examination is tiring for frail patients
and may have to be done in stages, and that they benefit from assessment by the full multiprofessional team (see Box 17.1).
Introduce yourself and clean your hands.
Ensure that the patient is comfortable and wearing any glasses and hearing aids. Ask if they want someone to be with them.
Throughout the examination, observe for signs of pain (see Box 17.6) or distress.
Assess the general appearance: ill kempt, restless or anxious, withdrawn.
Test vision and hearing: check with the patient wearing any glasses or hearing aids.
Assess cognition: screen for cognitive deficit (p. 323), low mood or anxiety.
Establish nutritional status: body mass index, weight loss or dehydration (see Box 17.5).
Check skin health: inflammation, ulcers, breaks in pressures areas.
Look at mobility: decreased balance or gait abnormality.
Perform a systems examination, noting particularly:
Chest: symmetrical air entry, added sounds.
Cardiovascular system: cardiac rhythm, heart murmurs, postural blood pressure.
Abdomen: distended bladder. Consider rectal examination.
Locomotor system: joints – swelling, deformity, pain or inflammation. Feet – overgrown nails, deformities or ulcers.
Neurology: abnormal speech, asymmetry of neurology, signs of Parkinson’s disease.
After the examination help your patient to dress.
Thank the patient and clean your hands.
Ross Paterson
Anna R Dover
18
The deteriorating patient
Vital signs 340 Sepsis 345
Early warning scores 340 Ongoing management 346
Initial assessment 341 OSCE example: The unwell patient 346
The ABCDE approach 341 Integrated examination sequence for the deteriorating patient 346
A: Airway 341
B: Breathing 342
C: Circulation 343
D: Disability 344
E: Exposure 345
340 THE DETERIORATING PATIENT
A deteriorating patient is one who becomes acutely unwell in NEWS Key Date:
the hospital setting. This can occur at any stage of a patient’s 0 1 2 3 Time:
illness but is more common if the patient has been admitted ≥25 3
as an emergency, undergone surgery or spent time in a 21–24 2
Respiratory 12–20
high-dependency or intensive care setting. Common causes Rate
9–11 1
for deterioration include sepsis, bleeding, myocardial infarction, ≤8 3
hypoglycaemia and pulmonary embolism. Chronic
Default
Sp02 Hypoxia
Early assessment and intervention is required, as these patients ≥96
are at high risk of cardiac arrest; once this occurs, fewer than Medical signature
≥88 94–95 1
20% of patients survive to hospital discharge. required to use scale
for patients with
86–87 92–93 2
Chronic Hypoxia ≤85 ≤91 3
Sign
Unrecordable 3
Vital signs Inspired 02 % 2
2
≥39°
1
Temperature 38°
Physiological observations are monitored routinely in patients who
37°
are admitted to hospital. The vital signs that are measured include 36°
heart rate, blood pressure, respiratory rate, oxygen saturations, Mark 1
≤35°
temperature and level of consciousness. Additional monitoring 3
3
may include urine output, pain assessment and blood glucose NEWS 230
3
testing. SCORE 220
uses 210
Systolic BP
200
Early warning scores 190
180
170
Vital signs are recorded using track-and-trigger systems in the 160
form of early warning scores designed to assess illness severity. 150
Measurements are made of the patient’s respiratory rate, the 140
Mark 130
use of oxygen therapy, oxygen saturation, temperature, heart
120
rate, blood pressure and level of consciousness, and points
110
are assigned for physiological derangement in each organ Manual 100
1
system. Increased frequency of observations is recommended BP 2
90
3
for patients with abnormal signs, and a rising score triggers a 80
3
graded response. 70
3
In the UK there is a validated track-and-trigger system, the 60
3
National Early Warning Score (NEWS; Fig. 18.1). This system 50
3
will trigger a graded response, due to either an aggregated high Unrecordable 3
score or a single severe physiological derangement, with the >140
3
urgency and seniority of the team being summoned escalating 3
130
2
as the score rises (Box 18.1). For example, a NEWS score of 120
2
between 1 and 4 is escalated to the nurse in charge of the 110
1
ward, a score of 5 or 6 (or a single observation scoring 3) is 100
1
escalated to the doctor covering the ward, and a score of 7 90
Heart Rate
80
should be escalated to a senior doctor and discussed with the
70
supervising consultant, with consideration of referral to a critical 60
care team. 50
The early warning score is designed to complement clinical 1
40
3
judgement. If you or another member of your team is concerned 30
3
about a patient, do not dismiss this instinct purely because Regular Y/N
the early warning score is low. A patient may just look unwell Alert
or feel cold to the touch and, although these features are not Conscious V/P/U 3
Level
captured by the early warning scoring systems, they may signify New confusion 3
early deterioration, particularly in young patients with greater Total NEWS score
physiological reserve. Urine output recorded Y/N
Blood Glucose
Frequency of observations
Structured Response Tool Y/N
Escalation Y/N
Pain score (0–10)
Nausea score (0–3)
Motor Block score (0–3)
Circulation
Sensation
Movement
Fig. 18.1 An example of a National Early Warning Score (NEWS)
Initials
chart. The scoring of physiological variables is shown. BP, blood pressure;
V/P/U, responding to voice/pain/unresponsive.
341
Initial assessment
When you are reviewing a deteriorating patient, a rapid assessment
should replace the usual systematic history taking and physical
examination in order to identify abnormal physiology quickly and
to administer immediate life-saving interventions to prevent further
deterioration and death.
The approach to the acutely deteriorating patient is time-critical
and attending to this patient should be prioritised; do not wait to finish
other tasks or ward rounds. Make every effort to go and see the
patient for yourself, as your immediate first impressions can provide
much more information than can be obtained by several minutes Fig. 18.3 Chin lift for opening the airway.
of discussion by telephone; if patients look sick, they probably are. 18
Examination sequence
A: Airway
Always ensure your own safety and use the appropriate
personal protective equipment. If a patient is able to speak normally, you can be confident that
Approach the patient and assess their response by asking the airway is patent. If there is no response or if the patient
‘Are you alright?’ Gently shake the patient by the appears to have difficulty in breathing, perform a more detailed
shoulders and shout loudly into both ears if unresponsive. assessment. Airway obstruction is a medical emergency; call
A normal response confirms that the airway is clear and for expert help immediately.
there is perfusion of the brain.
If the patient is unresponsive, check for a pulse and Examination sequence
assess whether the patient is breathing. If in cardiac or
respiratory arrest, ask a colleague to summon the cardiac Look for signs of airway obstruction. There may be use of
arrest team and begin cardiopulmonary resuscitation in the accessory muscles of respiration, supraclavicular or
accordance with guidelines. subcostal indrawing, or paradoxical movements where the
Monitor the vital signs; attach an electrocardiogram (ECG) abdomen moves out as the chest moves in (‘seesaw’
monitor, a non-invasive blood pressure monitor and a breathing). Cyanosis is a late sign.
pulse oximeter as soon as possible. Ensure the patient Look in the mouth for foreign objects, blood, vomit or
has an intravenous cannula inserted. secretions. These can be removed by gentle suction with
If the patient does not respond or looks unwell, seek a Yankauer suction catheter (Fig. 18.2).
senior help immediately. Listen for abnormal airway noises (Box 18.2).
Open the airway with a chin-lift or jaw-thrust manœuvre
(Figs 18.3 and 18.4).
The ABCDE approach In patients with altered consciousness it may be necessary
to maintain the airway by insertion of an oropharyngeal
The ABCDE approach provides a standardised framework for (Guedel) or nasopharyngeal airway adjunct (Fig. 18.5), or
simultaneously assessing and treating life-threatening problems by tracheal intubation, which must be performed by an
in critically ill patients. This systematic approach will help you to experienced clinician.
break down complex and stressful clinical situations into more Administer high-concentration oxygen via a non-rebreather
manageable components. mask at a flow rate of 15 L/minute (Fig. 18.6).
342 THE DETERIORATING PATIENT
Fig. 18.4 Jaw thrust for opening the airway. Place your fingers behind
the angle of the patient’s jaw, and then lift it to open the airway.
18.3 Situations in which pulse oximetry may give cage to move independently. Feel for subcutaneous
misleading values emphysema due to pneumothorax or trauma.
Percuss and auscultate the chest to identify
Inadequate waveform
pneumothorax, effusions, consolidation or oedema. A
Hypoperfusion – ear-lobe sensor may be better than finger probe if silent chest can occur when airflow is poor, such as in
poor hand perfusion life-threatening asthma.
Hypothermia
Consider further evaluation of gas exchange with an arterial
Movement artefact
Rapid irregular pulse – e.g. atrial fibrillation blood gas (ABG) measurement; it will give valuable information
on arterial oxygen, carbon dioxide and acid–base status but
Falsely normal or high reading requires skill and competence to obtain. Prolonged attempts at
Abnormal haemoglobins: taking an ABG sample should not detract from other aspects of
Carboxyhaemoglobin (e.g. carbon monoxide poisoning) the resuscitation. It is usually appropriate to obtain a portable
Methaemoglobina chest X-ray in a breathless or hypoxic patient.
Sulphaemoglobina
High levels of HbA1c
Falsely low reading
C: Circulation
Abnormal haemoglobins: Consider hypovolaemia as the most probable cause of shock
Methaemoglobina
in any acutely unwell patient.
Sulphaemoglobina
Severe anaemia
Nail varnish, false fingernails Examination sequence
Skin pigmentation
Look at and feel the skin; a shocked patient will be cold
Excessively dirty fingers
with pale, white or mottled skin.
a
Depending on the levels of methaemoglobin or sulphaemoglobin, pulse Check capillary refill by pressing on a fingertip (held at the
oximetry may underestimate or overestimate the true arterial oxygen saturation level of the heart) for 5 seconds. This will cause it to
(usually low). blanch. When the pressure is released the colour should
HbA1c, haemoglobin A1c, glycated haemoglobin.
return to the fingertip in less than 2 seconds. This is
roughly the same time as it takes you to say ‘capillary refill
time’. If the capillary refill time is delayed, this indicates
poor peripheral perfusion or shock.
18.4 Respiratory patterns: common causes Assess the pulse rate and rhythm (p. 47). A heart rate of
less than 50 beats per minute (bpm) or more than 90 bpm
Tachypnoea requires further investigation. A heart rate of more than
130 bpm requires immediate attention.
18
Anxiety Chest injury
Pain Pneumothorax Palpate peripheral and central pulses, assessing the
Asthma Pulmonary embolus volume and character (p. 48); poorly felt peripheral pulses
Metabolic acidosis Brainstem stroke may indicate hypovolaemia or poor cardiac output,
Bradypnoea/apnoea whereas a bounding pulse may indicate sepsis. As
blood pressure falls, peripheral pulses diminish, with
Cardiac arrest Central neurological causes
Opioids/other sedative (stroke, head injury) loss of the radial, then femoral and finally carotid pulsation.
overdose As a rule of thumb, if the radial pulse is present, the
systolic blood pressure is likely to be greater than
Cheyne–Stokes respiration
90 mmHg but once the femoral pulse becomes
Left ventricular failure Overdose (barbiturates, impalpable, the systolic blood pressure is likely to be
Central neurological causes gamma-hydroxybutyrate, less than 60 mmHg.
(stroke, head injury) opioids)
Attach an ECG monitor to the patient to assess heart rate
Kussmaul respiration and rhythm. A 12-lead ECG should also be recorded in
Metabolic acidosis, e.g. Shock (lactic acidosis) patients with suspected acute coronary syndrome or
diabetic ketoacidosis Overdose (methanol, ethylene arrhythmia.
Uraemia glycol, salicylate) Check the blood pressure (p. 49). Use a manual
Hepatic failure sphygmomanometer, as automated blood pressure
Paradoxical respiration devices may be inaccurate in the acutely unwell patient.
Airway obstruction High spinal cord lesions Hypotension is a late and serious sign, particularly in
Respiratory failure Guillain–Barré syndrome young patients who may be able to maintain blood
Flail segment pressure by peripheral vasoconstriction.
Examine the jugular venous pressure (p. 52).
Auscultate the heart to identify added sounds or
murmurs (p. 55).
Palpate the trachea in the suprasternal notch. It should be Insert one or more wide-bore (14- or 16-gauge)
central; if it is not, it suggests mediastinal displacement by intravenous cannulae, and take blood for routine
pneumothorax or collapse. Gently palpate any areas of haematological, biochemical and coagulation tests and for
injury to assess for a flail segment, where multiple rib cross-matching. If the patient is hypotensive, give a bolus
fractures in more than one place allow a part of the rib of 250–500 mL warmed crystalloid solution.
344 THE DETERIORATING PATIENT
Look for other signs of inadequate organ perfusion such component (‘E4 eyes open spontaneously; V2 sounds only;
as reduced consciousness (see later) and oliguria M6 obeying commands’) when communicating by telephone
(< 0.5 mL/kg/hour). A fluid balance chart should be to remove ambiguity.
commenced. Consider urinary catheterisation. Urinary Testing for response to a painful stimulus should be done
catheters have their own associated morbidity, in particular only if the patient is not responding to speech. The stimulus
catheter-associated urinary tract infection. However, if the should be administered centrally by applying firm supraorbital
patient is obtunded or unable to pass urine, a catheter pressure or a trapezius pinch; sternal rub should be avoided, as
should be inserted. it can cause distressing bruising to the patient’s chest. Peripheral
painful stimuli should be avoided, as they can elicit misleading
D: Disability spinal reflexes.
Any change in a patient’s conscious level should raise concern. Examination sequence
Causes of unconsciousness can include hypoxia, hypercapnia,
Assess the patient’s conscious level using either the AVPU
cerebral hypoperfusion, hypoglycaemia or the use of sedative
scale or GCS.
medications such as opiates.
Examine the pupils for size, symmetry and light reflex.
Conscious level is often recorded using the AVPU scale, which
Pupil size will vary with ambient lighting but should be
categorises the patient as:
symmetrical and constrict to light. Symmetrical change in
alert
pupil size suggests a drug or metabolic cause. Constricted
voice
pupils (miosis) can be a sign of opiate overdose or
pain
organophosphate poisoning, whereas pupillary dilatation
unresponsive.
(mydriasis) may indicate toxicity from anticholinergics (such
This measure is incorporated into many early warning scores as atropine or tricyclic antidepressants) or
and has the advantage of being a fast and easily understood sympathomimetics (such as cocaine). Asymmetrical pupils
verbal description of the patient’s conscious level. It is not suggest a structural lesion. A unilateral dilated pupil in a
designed as a measure to track small changes in a patient’s patient with altered conscious level is a medical
neurological condition. emergency and should prompt further investigation with
The Glasgow Coma Scale (GCS) is more sensitive to changes emergency computed tomography of the head.
in a patient’s conscious level but is more complex. It measures Check the drug chart for reversible causes of reduced
eye opening, vocal and motor responses (Box 18.5). The GCS consciousness.
was initially validated as a measure of conscious level in patients Check the capillary blood glucose using a bedside glucose
with traumatic brain injury. Its use has been extrapolated to meter (Fig. 18.7 and Box 18.6). The acronym after ABC of
many situations of altered consciousness and it may not always ‘DEFG’ (‘Don’t ever forget glucose’) is a good reminder. If
perform as intended. the blood glucose is less than 4 mmol/L (72 mg/dL) and
The GCS should always be reported in its component parts – the patient is unconsciousness, administer 75–100 mL of
for example, E4 V5 M6 – and it can be useful to describe each 20% glucose intravenously over 15 minutes; thereafter,
follow national guidelines for the management of
hypoglycaemia.
Delirium is a common complication affecting 10–20% of hospital
patients; the incidence is greatest in the elderly. It should not be
overlooked or dismissed, as it may be a sign of an underlying
18.5 Glasgow Coma Scale (GCS) deterioration and should prompt a search for an underlying cause
such as infection, metabolic derangement, hypoxia or cerebral
Eye opening (E)
hypoperfusion.
4 Spontaneously
3 To speech
2 To pain
1 No response
Best verbal response (V)
5 Orientated
4 Confused
3 Inappropriate words
2 Incomprehensible sounds
1 No verbal response
Best motor response (M)
6 Obeys commands
5 Localises painful stimulus
4 Normal flexion
3 Abnormal flexion
2 Extends to painful stimulus
1 No response
Prepare equipment for the procedure: If there is clinical suspicion of infection and 2 or more of the criteria
Gloves below, think ‘Could this be sepsis?’
Glucose meter Systemic inflammatory response syndrome (SIRS) criteria
Test strips
Single-use lancet Temperature: < 36°C or > 38°C
Cotton swab Pulse: > 90 beats per minute
Introduce yourself, explain the procedure and obtain consent White cell count: < 4 × 109/L or > 12 × 109/L
Clean your hands and put on gloves Respiratory rate: > 20 breaths per minute
Clean the patient’s fingertip and allow it to dry. Note that any Mental state: new confusion
glucose on the patient’s finger will give a falsely high reading Blood glucose: > 7.7 mmol/L (138 mg/dL) in a patient without
Inset the test strip into the glucose meter after checking it is in date diabetes
Prick the side of the patient’s finger with the lancet (no lower than qSOFA score
the nail bed) and gently massage (or milk) the finger to promote
Respiratory rate ≥ 22 breaths per minute
bleeding. Apply this drop of blood to the test strip until the meter
Systolic blood pressure ≤100 mmHg
confirms an adequate sample has been received
Glasgow coma scale < 15
Give the patient the swab to stop the bleeding and safely dispose of
gloves, lancet and test strip
Clean your hands and thank the patient for their cooperation
Sleeping Taking less interest why the focus of treatment, monitoring and care will change to
more in surroundings making sure the person is comfortable. Explain what to expect
Mouth and eyes open when the person dies and what to do if the person is at home.
when unconscious Eating and drinking
less Most people stop breathing gradually but may take a final breath
Upper airway secretions after a long pause. A brief muscle spasm may be observed at
due to pooling of saliva Difficulty in that time, so warn relatives about this.
swallowing
Increased
respiratory rate Irregular breathing/
Moist secretions
Cheyne–Stokes Confirming and certifying death
pattern of
in chest respiration
The confirmation and certification of death are important to allow
the legal requirements and cultural and religious traditions that
Low-volume happen after a person has died to be fulfilled. Some people will
pulse Cool peripheries have decided to be organ donors. Notification of the relevant
team in advance and the prompt diagnosis of death can make
Moist skin this possible for many of them.
Muscle weakness In the UK death is defined as ‘the irreversible loss of the essential
or stiffness characteristics necessary to the existence of a living person – to
be able to sense and interact with the environment and to maintain
Skin that blisters the fundamental bodily functions of respiration and circulation’.
or marks easily Consciousness and respiratory and circulatory function are
Peripheral oedema controlled within the brainstem. Irreversible damage to the
associated with low brainstem, either after cardiorespiratory arrest or due to direct
albumin and altered damage to the brainstem itself, always results in death.
fluid metabolism
Fig. 19.2 Signs that suggest a patient will die soon.
The history
19.2 Common potentially reversible causes of deterioration A decision will usually have been made and documented in
in advanced illness advance, stating that CPR will not be given because it would
not work or would have a very poor outcome for this person.
Dehydration Occasionally, a person with one or more advanced illnesses
Infection
deteriorates more rapidly than expected or a decision that CPR will
Opioid toxicity or other drug toxicity or poisoning
not be given has not been made in advance. In those situations
Glucocorticoid withdrawal or a new diagnosis of adrenal insufficiency
Acute kidney injury the professionals who are present decide if CPR should not start
Delirium or should be stopped. 19
Hypercalcaemia If you are not familiar with the patient and their recent medical
Hypoglycaemia or hyperglycaemia history, read their records before going to see them or speaking
Hyponatraemia to their family. Being aware of whether the death was sudden or
expected and how the person has been during their final illness
helps you to prepare for speaking with the family.
Care in the last days of life
The physical examination
If the patient is likely to die soon, their care needs to be planned
to anticipate problems. It is important to review a patient who is After the person has died, it is important for the clinical team to
dying at least daily, and more often if they are unsettled or have continue to care for them as they would any other patient. This
complex clinical problems. If a patient deteriorates rapidly or their includes speaking about the person by name to family members
symptoms change, urgent assessment is required. Find out if who are present at the time of death or while you are carrying
the other people who are caring for the dying patient have any out the examination to confirm death. Some relatives choose
concerns and work with them to maintain the person’s comfort to remain in the room and you need to explain each part of the
and dignity. Involve and support family members and close friends. examination in simple terms and conduct it in a respectful and
Cultural, religious and spiritual care is very important when professional manner.
a person is dying, at the time of death and afterwards. Always The person who has died should be observed for a minimum
ask the person and those close to them about their wishes and of 5 minutes to establish that irreversible cardiorespiratory arrest
what you and other staff members can do to help support them. has occurred. This provides an opportunity for you to spend
This may include wishes about how the person is touched or time supporting and listening to any family members who are
cared for after death. present. After death the body cools gradually and stiffens; bowel
sounds may persist for a time until the sphincters relax and the
bowels and bladder empty.
Communication with patients and families
Brainstem death
Find out what the patient and their family know and what they
expect. Explain what happens when a person is dying. Talk The diagnosis of brainstem death must be made by at least two
about the changes that will be seen and what they mean. Explain doctors who have been fully registered for at least 5 years. They
350 THE DYING PATIENT
should have experience in the assessment of brainstem function. always be discussed and confirmed with a senior colleague. Some
One of the doctors must be a consultant or equivalent senior medical certificates of death require additional information such
physician. The tests are performed on two occasions. The first as the duration of the final illness, so make sure you are familiar
set of tests is to diagnose brainstem death. The second set is to with these requirements. You should also know or seek advice
confirm the diagnosis. There is no minimum time required between about when a medical certificate of death should not be issued
tests; they can occur concurrently. If the tests demonstrate that because the death has to be reported (Box 19.3).
brain death has occurred, then the time of death is recorded
as the time of diagnosis: that is, the time at which the first set
of tests was completed. Looking after yourself and others
Communication with families Caring for a patient who is dying and their family is very
rewarding but can also be stressful and emotionally demanding.
Communicating with family members to tell them that someone It is important to recognise this and look for help and support
has died should be done as soon as possible. Speak to relatives when you need it. You may need advice on how to manage
in a quiet, private room and try to avoid interruptions. If the death a patient’s symptoms, decide on a care plan or communicate
is sudden and unexpected, this will be breaking bad news so it sensitively and effectively with people who are experiencing loss
needs to be done clearly and sensitively. If contacting a family and bereavement. Talk to colleagues and support them too.
member by telephone to inform them of a patient’s death, it is
important to decide if it is safe to do so or whether it would
be better instead to contact someone such as the police and
ask them to go and inform the family member in person about 19.3 Deaths that may require further investigation
a sudden death. Explain what has happened and what will
happen next. Offer the family time with the person who has The cause of death is unknown
died if they wish. Death was violent or unnatural
Death was sudden and unexplained
The person who died was not visited by a medical practitioner
Documentation during their final illness
A medical certificate is not available
Document the place, time and date of death in the patient’s Death occurred during an operation or before the person came
medical record. In some countries the time of death is when round from the anaesthetic
the person was observed to have died by those present or the The medical certificate suggests that the death may have been
person was found to have died. In other countries the time of caused by an industrial disease or industrial poisoning
death is when death is confirmed by a doctor, so make sure Death occurred in legal custody
you know which time to record. Include details of who was A complaint has been received over the medical treatment or
standards of care received by the deceased
present when the person died and what the primary and main
Death was due to a notifiable disease
secondary causes of death were. The cause of death should
Mr Jenkins, 80 years old, has severe chronic obstructive pulmonary disease. He is on domiciliary oxygen therapy. He was admitted to the ward 3 days
ago with severe pneumonia. After initially responding to treatment, his condition has deteriorated. He is becoming breathless, confused and distressed.
He has been seen by the intensive care consultant, who has stated, ‘The patient would not benefit from ICU care.’ She has suggested that Mr Jenkins
should be treated with a focus on good symptom control and care appropriate for the last days of life. The nurses ask you to speak to Mr Jenkins’s
son about what has happened and what the next steps should be in terms of treatment. You should talk about cardiopulmonary resuscitation and
explain why this would not be the right treatment when his father dies.
To prepare:
Ask for a private room.
Ask if you can leave your bleep and /or telephone with the nursing staff.
Ask for a nurse to accompany you.
Introduce yourself to the son and clarify his relationship to the dying person:
– ‘Hello. My name’s Dr Smith. Are you Mr Jenkins’s son, John? Thank you for seeing me, Mr Jenkins. I’m sorry to tell you that your father has
become much more unwell today. Is there anyone else you’d like to be with you at this time?’
Establish the son’s perceptions:
– ‘What do you understand about your father’s illness and what’s happened so far?’
Explain the medical facts in lay terms:
– ‘He’s been unwell for a while, not really getting out of the house for a long time. He’s been in and out of hospital a lot lately and never really
seemed to get better.’
Inform the son of the severity of his father’s illness and what the frequent hospital admissions reflect about its progression.
Explain that, because his father has advanced lung disease and is not responding to antibiotics, he is likely to deteriorate further.
Pause.
Explain that this means Mr Jenkins is likely to die.
Allow time for silence.
Express your condolences.
Gently rebuff any false hopes.
351
The nurse-in-charge calls you to tell you that Mr Williams, an 83-year-old inpatient, has died.
Please describe the process for establishing and certifying death, and how you would communicate with staff and family
Introduce yourself to the nursing team on the ward:
– ‘Hello, my name’s Dr Smith. I’m here to see Mr Williams.’
Ask if the death was expected.
Confirm that the patient was not for resuscitation.
Ask if the team know why Mr Williams was in hospital and what the likely cause of death might be.
Ask for the patient’s notes and check you have the correct name, hospital number and date of birth.
On entering the patient’s bed space:
Clean your hands and introduce yourself to any relatives or staff present.
Express your condolences and explain why you need to examine the patient:
– ‘I’m sorry to intrude at a sad time. I’m here to examine Mr Williams to confirm that he’s died. If you have any questions about what I’m doing
or what happens next, please ask me and I’ll do my best to answer.’
Check the patient’s identity on their wristband.
From the end of the bed, respectfully inspect the patient. If necessary, make sure the patient looks dignified before continuing with examination:
for example, position their head, clean any obvious secretions, and lift their limbs into appropriate and peaceful positions.
Gently stimulate the patient and say their name: 19
– ‘Mr Williams, Mr Williams, can you hear me?’
Inspect for any respiratory effort, carotid pulsation or limb movement.
Note the colour and temperature of the skin.
Say:
– ‘I’m just going to look into your eyes.’
Respectfully retract the eyelids and inspect the eyes. The pupils should be dilated and unresponsive.
Shine a torch into each eye, looking for both a direct response and a consensual response.
Test for corneal reflexes by stimulating the cornea with cotton wool and look for a motor response. To ensure that the cornea is stimulated, the
cotton wool must touch the area over the iris. Close the eyelids after examination.
Apply supraorbital pressure and check for a response.
Respectfully expose the upper anterior chest wall and palpate for a pacemaker on both sides. This is felt as a firm, subcutaneous object with a
clear geometrical shape and an associated linear operation scar.
Palpate for carotid pulsation for 1 minute.
Listen for heart sounds for 1 minute.
Listen for breath sounds for 1 minute.
Cover the patient in a dignified manner.
Clean your hands.
Document the examination and confirmation of death in the notes:
Date and time of death:
– Mr Williams died at 01:00h on 1 January 2016.
– No response to stimulation.
– Pupils unreactive to light and dilated.
– No corneal reflex.
– No central pulse palpated for 1 minute.
– No heart sounds auscultated for 1 minute.
– No breath sounds auscultated for 1 minute.
Write your full name, qualifications, contact number and formal signature.
If appropriate, write the cause of death in the notes, indicating that this will need to be discussed with a senior member of the team before a
death certificate can be issued.
If appropriate, make arrangements for the patient’s relatives to be informed.
Thank the nursing staff on the ward.
352 THE DYING PATIENT
Section 4
Putting history and
examination skills to use
20 Preparing for assessment 355
21 Preparing for practice 361
Anna R Dover
Janet Skinner
20
Preparing for assessment
General principles 356 Approach to assessment 359
Methods of assessment 356 Professionalism 359
Clinical simulation 357 Managing time 359
OSCEs 357 Communication during assessment 359
Managing unexpected difficulties 360
Marking structures 357
Putting it all together 360
Approach to preparation 358
356 PREPARING FOR ASSESSMENT
The most widely used clinical assessment methods include Knows how
OSCEs, short cases, long cases and clinical simulation scenarios
(Box 20.1), during which you may be observed performing an Knows
integrated sequence of clinical, practical and/or communication
skills. Fig. 20.1 Miller’s pyramid of clinical competence and assessment
Different assessment formats test different aspects of your methods. Adapted from Miller G. The assessment of clinical skills/
professional competence or expertise. Short cases, for example, competence/performance. Academic Medicine 1990; 65(suppl):S63–S67.
Marking structures
Examiners award marks for your performance in assessments
using a standardised marking structure. While this varies from
358 PREPARING FOR ASSESSMENT
run revision courses or mock examinations, and these can be down and to have long hair tied back. Ensure that you have the
excellent ways to experience what the examination itself will be appropriate clinical equipment with you (such as stethoscope, pen
like. Daily clinical encounters are always opportunities for practice, torch and so on) and are familiar with their use. If you are going
as are more formal encounters with senior colleagues such as to have physical contact with a patient during the assessment,
workplace-based assessments and bedside or simulation-based always clean your hands with alcohol-based gel or soap and water
teaching events. Make sure you also ask colleagues for honest (see Fig. 3.1) and observe basic safety principles, including the
and critical feedback after clinical encounters so that you can use of personal protective equipment and safe sharps disposal.
reflect on which areas you can improve.
You may be offered technical and non-technical (such as
team working and leadership) skills training in your local clinical
Managing time
skills centre, and these occasions will also allow you to practise
Managing your time, both in advance of and during the
repeatedly those techniques that you will be asked to demonstrate
assessment, can have a major impact on your performance.
during assessments. Deliberate practice, repeating the skills and
Make sure that you know where the examination is to be held,
sequences of examination that you will be expected to execute
rehearse your journey and give yourself plenty of time to get
on the day, helps to make these behaviours automatic and
there.
reduces the chances of you forgetting an aspect of history taking
Pay particular attention to the timings within the examination
or physical examination under pressure.
and ensure that you have practised completing your assessment
within the allocated time. Some assessments will be broken into
Approach to assessment different stages, and it is worth finding out as much as you can
about the format; you may think you have 10 minutes to complete
the OSCE station but in reality you may be allowed to spend only
Professionalism part of the time with the patient with the remaining time reserved
for questioning from the examiners. Marks will be awarded for
Make sure you are smartly dressed, look professional and adhere your answers to these questions. If you take too long assessing
to any local infection control and uniform policies (Box 20.5). the patient, you may not be able to take advantage of these
Most institutions would expect you to be bare from the elbows marks; similarly, if you finish your assessment too quickly, you
risk the examiners moving on to more challenging questions to
fill the remaining time. Assessments will often have short breaks
between stations to allow candidates to read the instructions for
20.5 Professionalism during assessment the next station; once again, it is helpful to familiarise yourself
with these aspects of the examination in advance.
or brief that often includes information that they will volunteer to your final mark will be a composite of all of the components of
you from the outset, and further information that they will divulge the assessment, and it is often possible to fail a station or two
only if asked. It is therefore important to ensure that you take a and still pass overall.
structured approach to your questioning, making sure you start
with open questioning and then focus on pertinent aspects, not
forgetting to enquire about the patient’s own concerns. Putting it all together
Managing unexpected difficulties Preparing for assessment starts long before the examination itself.
Deliberate repeated practice of clinical and communication skills
Even with thorough preparation, things may not go to plan, is key to performing well on the day. This should include timed
because of examination pressure or nerves, or through you practice within the format itself, as well as practice in presenting
misunderstanding the format of a station or the question you are your findings to a surrogate examiner. A detailed understanding
asked. Remember that examiners generally want you to succeed of the examination format and timing, as well as the marking
and will have experienced similar assessments themselves. They structure, will help to ensure you are well prepared.
will understand that you may be very nervous and will try to Take time to review the information provided in the relevant
support you if you are finding the experience difficult. If you feel system-based chapters, as well as the more general guidance
you have performed poorly in a station, try to put it behind you in Section 1, and watch the clinical videos for examples of
and focus your attention on the next one, where you may be able comprehensive systematic examination techniques.
to recover your position. Remember that in most assessments Good luck!
Karen Fairhurst
Gareth Clegg
21
Preparing for practice
Adapting history and examination skills appropriately 362 Assessment of a patient with minor injury or illness 364
Integrated examination 362 Assessment of a critically ill patient 364
Diagnostic strategies 362 Documenting your findings 364
Pre-test probability 362 Communicating with colleagues 365
Rare diseases 362 Verbal communication 365
Approach to the patient with medically unexplained symptoms 363 Written communication 374
362 PREPARING FOR PRACTICE
History and examination skills are adapted by doctors to suit the Pre-test probability
situation. For example, elective surgical or unscheduled emergency
admissions may require a systematic and comprehensive history Where doctors are unable to recognise patterns in presentations
and examination. Patients attending a specialist outpatient clinic, quickly, various refinement strategies are used to arrange the
will already have been screened by a referring clinician, however, possible diagnoses in order of probability. The pre-test probability
and a history and examination focused on the presenting condition of a disease in an individual depends on the context in which
is appropriate. If the patient is attending a review clinic, history and the symptom has appeared because the prevalence of disease
examination may be restricted to monitoring an existing condition. varies between populations. In general practice populations the
The information-gathering process may appear to be sequential: incidence of serious disease is much lower than in hospital
the history suggests a differential diagnosis; examination and populations; serious conditions still usually need to be excluded,
then investigation help confirm or refute diagnostic possibilities. however. This may involve identification of ‘red flag’ symptoms
In reality, these elements often occur in parallel. For example, and signs for serious disease, or the use of clinical prediction
sequential history then examination may be abandoned in rules such as the Wells score for deep vein thrombosis. Positive
favour of a more opportunistic approach to avoid distressing ‘red flag’ features or above-threshold prediction scores increase
a reluctant child. In critically ill patients a highly focused history the probability of a disease in individuals and generally trigger
and examination aimed at rapidly identifying the main problems further investigations.
while initiating resuscitation is imperative. Additional factors affecting the pre-test probability of disease in
patients with the same presenting symptoms include age, gender,
past medical history, family history and lifestyle. Few doctors use
Integrated examination formal probabilistic reasoning in making diagnoses, but most
know the relationship between these factors and the likelihood
Although in an individual it is rarely necessary to carry out a of a specific disease and use this understanding intuitively to
comprehensive history and examination of all systems, a rapid select likely diagnoses (hypotheticodeductive reasoning, Fig.
screening examination may be useful to direct more detailed 21.1). History, examination and investigation results are used
examination if the diagnosis is unclear or when patients are to support or refute putative diagnoses. These components are
being admitted to hospital. There is no single correct procedure rarely independent, however, and returning to clarify the history
for performing a physical examination and you will develop your or re-examine when signs are ambiguous allows an iterative
own approach, but a reasonable routine is outlined in Box 21.1. approach to accurate diagnosis.
Gather clues 10
Pathological cause
Formulate hypothesis 8
a
ni a
in
ss
ai n
s
e
in
Diagnosis
es
gu
em
oe
ch
pa
pa
i ne
om
lp
n
da
pn
ti
Management
mb
st
ck
Fa
na
Oe
Ins
a
s
Diz
e
Ba
Dy
He
mi
Ch
Nu
do
Ab
Fig. 21.2 Percentage of symptoms presenting in primary care with
Follow up an underlying pathological cause.
Approach to the patient with medically patient’s symptoms at face value. Remember that patients with
unexplained symptoms MUS may also have or develop disease. Even if a functional
diagnosis is suspected, a comprehensive history and examination
Much of this book deals with the association between a patient’s remain imperative. This helps patients to feel that they are being
history and examination findings and the presence of underlying taken seriously; in addition, organic disease, however unlikely,
disease. Symptoms are not synonymous with disease, however, is less likely to be missed. 21
but are subjective experiences with many possible sources: Patients’ illness beliefs matter hugely and should be explicitly
pathological, physiological, psychological, cultural, behavioural acknowledged. What do they think is wrong? Why have they
and external. Many patients experience symptoms that impair come to you now and what do they hope you can do for them?
function but do not fit characteristic patterns of disease, and Inconsistencies in the history should be explored with the patient;
persist despite normal examination and investigations. These are for example, a patient with severe chest pain and normal coronary
called ‘functional’ or ‘medically unexplained symptoms’ (MUS, Fig. angiography may still firmly believe they have angina. Normal
21.2). Over 30% of patients attending their general practitioner investigations need to be explained clearly to help demonstrate
have MUS and they are also common in secondary care, although that the evidence does not support their belief.
disease prevalence is much higher there. Some symptoms are Patients may complain about previous doctors or treatments.
more likely to be medically unexplained than others: for example, Allowing a patient to express dissatisfaction shows interest, and
persistent fatigue, abdominal pain and back pain. The causes helps to avoid suggesting treatments they are likely to reject.
of MUS are poorly understood but various predisposing and Always remain professional and avoid being drawn into criticism
precipitating factors (Box 21.2) may contribute. Most functional of other healthcare providers.
symptoms are transient but some become persistent, causing Patients can be acutely sensitive to questions that suggest a
similar disability to those resulting from disease and also significant doctor thinks there is a psychological basis for their symptoms
emotional distress. If MUS are not recognised and managed (‘all in the mind’). Frame questions carefully in terms of their
appropriately, attempts to alleviate them can result in harm from symptoms: for example, ‘Do your symptoms ever make you feel
fruitless investigations, inappropriate interventions or drugs, and down or frustrated?’ rather than ‘Do you ever feel depressed?’
increased fear of disease. Abuse is one possible precipitant of MUS but seek this history
Patients with MUS commonly feel that doctors do not think judiciously. Follow local guidelines for any abuse you discover.
their symptoms are real, leading to a breakdown in trust between The physical assessment includes observing the patient
patient and doctor, and frustration for both. Crucially, doctors throughout the consultation. Watch for inconsistent signs,
must use an empathic and non-judgemental approach so the though this does not indicate whether they are consciously or
patient feels believed. Keep an open mind and accept all the subconsciously produced. Usually there are no physical signs
364 PREPARING FOR PRACTICE
but some non-pathological signs are associated with MUS; for that they are being taken seriously and assessed thoroughly.
instance, in irritable bowel syndrome you may find evidence of Conversely, not examining a patient risks them feeling you are
bloating and some tenderness, but otherwise gastrointestinal being dismissive of their problems.
examination will be normal. The history often suggests MUS, so
focus on excluding any unexpected physical findings, as well as
demonstrating to patients that you are taking them seriously. Any Assessment of a critically ill patient
signs you do find may vary between examinations but overall
the examination is commonly normal with MUS. A critically unwell patient requires a very different approach to
Investigations are used in MUS mainly to reassure both those with minor ailments. Examination and interventions often
physician and patient. Exhaustive investigations to exclude all occur simultaneously as the clinician attempts to identify the
physical illness are costly and unhelpful, risk side effects and main problems. Initially, your aim is to gain control of the situation
do not reassure patients in the longer term. Before requesting and stabilise the patient’s condition. A fuller history and clinical
investigations, discuss with the patient the likelihood and examination can follow after initial resuscitation.
significance of a normal result. Patients are more likely to be The approach to recognising and assessing the acutely ill and
satisfied when your explanation makes sense to them, removes deteriorating patient is covered in detail in Chapter 18.
blame and helps generate ideas about how they can manage
their symptoms.
Documenting your findings
Assessment of a patient with minor Documenting clinical findings in a clear and concise medical
record is a crucial aspect of medical practice. It should include
injury or illness a structured account of the history and examination – both
positive and important negative findings. Some circumstances
In patients with minor injury or illness, usually presenting in the demand additional detail: for example, forensic documentation
accident and emergency department or general practice, a history of the length and position of wounds.
and examination focused on the presenting symptoms are usually The appropriate level of detail varies with the context but adopt
sufficient. It is, however, crucial to establish the reason for the and use a consistent format. This format quickly becomes a habit,
patient’s presentation, as well as clearly defining their clinical reduces your need to think about what to record next, and lessens
problem, as their concerns about their symptoms and their the likelihood of forgetting something important. A consistent
expectations of investigation and treatment influence the outcome. format also allows others to locate specific information quickly
Carefully eliciting the mechanism of injury, progression of in your documentation. An example of clear and comprehensive
symptoms and their impact on the patient (for example, whether clinical documentation of a case is shown in Fig. 21.3.
they can walk and go to work/school) will help detect problems One widely used overall structure for organising your written
that are not as ‘minor’ as they might seem. Be wary of the documentation is SOAP, an acronym for subjective, objective,
apparently minor injury or illness that is actually the tip of a assessment and plan.
diagnostic iceberg, for example:
Subjective
fact a pathological fracture secondary to an underlying
This records information you obtain directly from the patient (or
lung malignancy
someone speaking on their behalf). It constitutes the body of
the history, as covered in Chapter 2. What is the patient’s chief
caused by cardiac arrhythmia
symptom? What is the patient’s current condition? It is best
to avoid describing the problem in medical terms at this point
fact the first presentation of angina
and more useful to record the patient’s own words. What is the
history of the problem? If an injury, what was the mechanism?
at odds with the history, suggesting possible
Past medical history, family medical history, social history
non-accidental injury.
(including smoking and alcohol or recreational drug use), current
Focus your examination on the system or body part implicated medications and any allergies should also be noted here.
in the history, as outlined in previous chapters. If the findings
are not consistent, carry out a more comprehensive history and Objective
examination. If the system affected is unclear (such as arm pain,
This is information you gather about the patient. Here you record
which may be musculoskeletal, vascular, neurological or referred
vital signs, findings from your physical examination and the results
cardiac pain), examine all of these systems.
of any initial investigations. Again, it is useful to use a standard
As you formulate a differential diagnosis, check for other
format to record physical findings, so others can find specific
systemic features of disease in addition to examining the
information quickly.
obvious source of symptoms. A swollen ankle may trigger a
systematic enquiry and examination if the history suggests a
Assessment
reactive arthropathy rather than a simple sprain.
Focusing the clinical examination comes with practice, but This starts with a brief summary of the information obtained. It
if in doubt, be comprehensive. Start with the body part that then lists the patient’s main symptoms, together with a differential
is causing the most trouble and follow leads. Elements of the diagnosis. If the patient has several pressing issues, compile a
examination likely to cause discomfort should be left until last. ‘problem list’. Not all of these problems may be medical but they
A careful and courteous examination can also increase trust will all influence the best plan for what to do next. For example,
between the patient and clinician. Even when you feel it is unlikely ‘worsening soft-tissue infection of the left lower leg’ is a problem
to yield important information, examination reassures the patient with a diagnosis, but ‘not taken any of the prescribed antibiotics
365
Verbal communication
but would have serious consequences if missed?
Verbal communication about a patient needs to be structured
worth taking a moment to reflect on whether there is and concise to be effective. Be clear about your expectations
another condition that may present in a similar way, of the person you are communicating with, especially if you are
particularly if an obvious diagnosis suggests itself quickly. requesting that they do something, such as coming to review
the patient.
underlying the presentation be a social, psychological or SBAR (situation, background, assessment, recommendation)
emotional one? is a simple tool to help standardise communication. It is
recommended by the World Health Organization for use as a
Plan tool to increase patient safety. It allows staff to share similar
This should include all relevant actions: procedures performed, expectations about what is to be communicated and how the
medications given, explanations and advice offered, referrals and communication is structured. SBAR can be used face to face,
recommendations made. Additionally, record here any further over the telephone or even in some written communication.
investigations and information still required to refine the diagnosis
and inform further management.
Using SBAR
Sign and date your notes, including your position and contact
details (pager number, for example). think through what you want to achieve by the
communication: for example, informing a colleague, asking
for immediate help or requesting advice. Consider some
Communicating with colleagues brief notes under the SBAR headings.
An essential part of a doctor’s work is the accurate and with. Introduce yourself. If face to face, make eye contact.
timely sharing of information about patients with colleagues. If possible, use the person’s name.
Communication failures are strong predictors of healthcare- – ‘Hello, Dr Jones. My name is Dr Smith. I’m one of
related harm. the junior doctors in the emergency department.’
Typical situations include: Situation: give a one- or two-sentence description
covering why you are calling, what is happening and what
(Box 21.3) the acute change is.
– ‘I’m concerned about a 53-year-old man who came
into the emergency department this morning
hospital (Box 21.4) complaining of severe headache. His headache’s
getting worse and he’s begun to vomit.’
referring consultant 21
21.4 Contents of a patient discharge letter following a
hospital admission
21.3 Contents of a referral letter Demographic information about the patient, the consultant and the
preferred GP (the GP who has been most involved, if known)
Demographic details about the patient and the referring doctor Ward
practice Date of discharge/transfer or date of death
Consultant/receiving practitioner and/or clinic, ward or specialty Reason for admission/transfer
The urgency of the referral Mode of admission: elective, emergency or transfer
Clinical information: Source of admission
History of presenting symptoms/examination findings/results of Diagnosis/problem list
any investigation Significant operations/procedures (dates)
Reason for referral and expected outcome Relevant investigations
Past medical history Complications/adverse reactions
Current and recent medication (including any complementary Medication (including start and stop dates, recommendations for
therapies and self-medication known to the referring doctor) altering dose or stopping medication after discharge, use of aids
Clinical warnings, e.g. allergies, blood-borne viruses such as a dosette box)
Smoking status/alcohol history Discharge plans:
Additional relevant information, e.g.: Further information about destination
– Relevant social or personal circumstances Care package
– Patient/family’s understanding of the condition and their Primary care support needed
expectations Information given to patient/carers
– Information about any advanced directives or resuscitation Results awaited
orders Hospital review plan/referral to other hospital services
Similar information will be required when a patient is referred Other relevant clinical or personal information
internally to another hospital consultant. Contact name and telephone number of author
366 PREPARING FOR PRACTICE
HPC
Severe pain ‘like a band around chest’ while watching TV, which has now lasted 2 hours despite using GTN,
aspirin and diltiazem.
Radiates to jaw and inner aspect of L arm.
Has gradually become breathless over the last hour and dizzy in last 30 minutes.
First began 6 months ago: episode of lower retrosternal chest pain after walking about 1/2 mile uphill:
2 months ago: visited GP who diagnosed angina. Prescribed GTN, which gave effective relief.
1 week ago: three episodes of chest pain at rest, all immediately relieved by GTN.
°Blackouts, °pain in calves on exertion.
Breast cancer 79
aged 50
1 aunt died aged 57 of acute MI
Fig. 21.3 Case notes example. CCU, coronary care unit; CHI, community health index.
367
Demographic details
Always record:
tient’s name and address, date of birth (DOB) and age
Any national health identification number, such as Community Health
Index number in Scotland or National Health Service number in England
and Wales
referral, e.g. from emergency department or general practitioner
SH
Retired cleaner.
Widow for 3 years. Lives alone in sheltered housing.
Smoked 20/day from age 19.
Teetotal.
HH once a week for cleaning and shopping. Daughter nearby visits regularly.
SE
CVS: See above.
RS: Longstanding cough most days with white sputum on rising in morning only. °Haemoptysis.
Wheezy in cold weather.
GI: Weight steady.
Nil else of note.
GUS: PARA 1 + 0. °PMB, °urinary symptoms.
CNS: Nil of note.
MSS: Occasional pain and stiffness in right knee on exertion for 5 years.
ES: Nil of note.
O/E
Anxious, frail, cachectic lady.
Weight 45 kg. Height 1.25 m.
2 cm craggy mass in upper, outer quadrant L breast. Fixed to underlying tissues.
Patient unaware of this
1 cm node in apex of left axilla.
°Pallor, °cyanosis, °jaundice, °clubbing.
CVS
P90 reg, small volume, normal character.
BP 140/80 JVP + 3 cm normal character, °oedema, AB 5ICS MCL, °thrills.
HS I + II + 2/6 ESM at LLSE °radiation.
°Bruits.
PP:
Radial Brachial Carotid Femoral Popliteal Post. Tibial Dorsalis pedis
R + + + + +/- +/- +/-
L + + + + + + +
+
(Normal +, Reduced /-, Absent -)
RS
Trachea central. Reduced cricosternal distance and intercostal indrawing on inspiration.
Expansion reduced but symmetrical.
PN resonant.
Breath sounds normal, no wheeze or crackles heard.
VR normal and symmetrical.
l
ug use (if appropriate)
rt in the frail or disabled
HH – Home help
ugular v
ankle oedema
ex bea , presence of thrills
y added sounds, murmurs and grade
eripheral pulses (PP) and bruits 21
– 5th intercostal space
– vicular line
– mur
– er left sternal edge
Respiratory system (RS)
y chest-wall deformity
Trachea central or deviated
hyperinflation
y
ercussion note (PN) and site of any abnormality
y added sounds and site of abnormality
abnormality
AS Scar
Normal oral mucosa
Upper midline scar
Hernial orifices intact
°Tenderness or guarding
°Masses
°LKKS or ascites
BS normal
PR not done
PV not performed
CNS
AMT 9/10
Cranial nerves II–XII: PERLA, NAD
Speech normal
RIGHT LEFT
UL LL UL LL
Power 5 5 5 5
Tone normal (n) n n n
Light touch n n n n
Position n n n n
Coordination n n n n
+ +
++ ++
Reflexes K A B T S Pl + +
R ++ + ++ + + flexor
L ++ + ++ + + flexor
++ ++
(increased +++, normal ++, diminished +, absent -)
+ +
MSS
Heberden’s nodes on index and middle fingers bilaterally.
Full ROM in all joints.
Crepitus in right knee. No other bony abnormality.
IMPRESSION
Active problems
1 Chest pain suggestive of acute coronary syndrome
2 Left breast lump and axillary node suspicious for cancer
3 Smoker
Inactive problems
1 Stable COPD
2 Perforated duodenal ulcer 1977
3 Possible osteoarthritis of right knee
nial orifices
enderness and guarding; site of these
these
liver, kidneys or spleen (LKKS)
present
mal speech
ves: record abnormalities only
y
Tabulate the remaining examination
If it is relevant, record the presence or absence of tremor, gait
abnormality, fasciculation, dyspraxia, two-point discrimination,
stereognosis or sensory neglect.
Plan
ECG performed on admission shows sinus rhythm and deep ST depression in leads II, III and aVF
Troponin at 12 hours
Repeat ECG in 1 hour
Chest X-ray
Full blood count
Urea and electrolytes, glucose
Oxygen and cardiac monitor
IV morphine and metoclopramide
Aspirin and clopidogrel
Low-molecular-weight heparin
Continue aspirin and diltiazem
Discuss beta-blocker with consultant in view of COPD
Advice to stop smoking
When stable
1 Review anti-anginal management
2 Referral for mammography and fine-needle aspiration of breast lump
3 Spirometry and assessment of inhaler technique
Information given
Diagnosis and treatment explained to patient and daughter
N.B. Breast lump not mentioned at this stage until discussed with senior staff
A. Doctor (signed)
A. DOCTOR (Date and Time) capitals
Progress notes
3.8.13
1800 Ward Round – Dr Consultant
No further chest pain
O/E
P70 BP 100/70
JVP not elevated, °oedema
HS I + II and ESM as above
Chest clear
Breast lump noted
ECG at 4 hours – resolution of inferior ST changes
Impression
Acute coronary syndrome – no ST segment elevation
Plan
Await troponin
Continue LMW heparin
Check lipid profile
For echocardiography in view of murmur then consider ACE inhibitor
Spirometry and assessment of inhaler technique
Consultant to discuss finding of breast lump A. Doctor (signed)
with patient and daughter A. DOCTOR (Date and Time) capitals
Plan
List the investigations required. When a result is already
available, e.g. an ECG, record it.
Record any immediate management instigated.
If uncertain about an investigation or treatment, precede with
a ‘?’ and discuss with a more senior member of staff.
Information given
Document what you have told the patient and any other family
member. It is also important to document any diagnosis that you
have not discussed.
If the patient voices any concerns or fears, document these too.
Progress notes
Follow the same structure with these additions:
tient’s symptoms
tion findings
esults of new investigations
the patient’s progress
ther management, particularly drug changes.
21
Make progress notes regularly depending on the speed of
change in the patient’s condition; in an intensive therapy setting,
this may be several times a day but, in a stable situation, daily or
alternate days.
Date, note time and sign all entries.
Record any un pected change in the patient’s condition as well
as routine progress notes.
Background: the information needed to make an SBAR can be applied as a standard framework to transfer
assessment: important information in many situations. By using this method
Relevant history: what were the key events leading up you are proactively giving the listener the information that they
to the present situation? would be requesting anyway to assess the problem. You save time
Vital signs. by assimilating and presenting information in a structured way.
– ‘Mr Jackson had a sudden onset of severe
headache after waking at about 07:00 this
morning. The pain hasn’t improved despite Written communication
painkillers and he appears to be getting
worse. He’s hypertensive at 210/110 and Conventionally, information was transferred between doctors
vomiting.’ by post, but increasingly communication is done electronically.
Assessment: what is your assessment of the Whatever the medium, the quality of written communication is
problem? crucial. Handwritten forms must be clear and legible. Doctors
– ‘I’m concerned that Mr Jackson may be having an should write clear, well-structured referral, discharge or transfer
intracranial bleed.’ letters (see Boxes 21.3 and 21.4). More and more, these letters
Recommendation/request: what do you think should be are copied to, or read by, patients as well as other clinicians, so
done? What assistance are you asking for? Be clear about they must always contain appropriate language.
what you need and when you need it. Clinical information is confidential and sensitive. It should never
– ‘I’d like you to come and review the patient urgently be transmitted by insecure electronic means. Nor should it be
please.’ stored on, or copied to, equipment that could be stolen or lost,
If you are feeling out of your depth and need support from a breaching confidentiality. Encryption should be used wherever
senior colleague, be clear about that. It is better to endure the possible to protect electronic records, and all clinical information
brief discomfort of having to admit that you need help than to should always be managed in accordance with local information
put a patient’s wellbeing in jeopardy. governance regulations.
Index
Page numbers followed by “f ” indicate figures, and “b” indicate boxes.
Babies (Continued) pain (mastalgia), 213 Chest wall deformity, in deteriorating Colour, of hands, 23, 23f
head shapes in, 300b skin changes, 213, 213f patient, 342 Coma
history in, 298–299 Breast examination, 212–216, Chest wall pain, 81 Glasgow Coma Scale (GCS), 344,
birth, 298 214b–215b, 214f–216f, 236b Chest X-ray, 63, 63f 344b
infant’s progress and, 298 anatomy and physiology in, Cheyne-Stokes respiration, 84, 343b see also Consciousness
maternal, 298 212–216, 212f Chilaiditi’s sign, 108 Comedo, 287b
physical examination of, 299–307 common presenting symptoms in, Children, 297–315 Common peroneal nerve, 147, 147b
general, 299–301 212–214 abdominal examination in, 315 Communication
timing and efficacy of, 299 Breath sounds, in auscultation, 88–89 cardiovascular examination in, 315 during assessment, 359–360
presenting problems and definitions Breathing, 342–343, 342b–343b developmental attainment of, 307b with colleagues, 365–374, 365b
in, 298–299 Breathlessness. see Dyspnoea growth and development in, in frail elderly, 330–331, 330b
weighing and measuring of, (breathlessness) 310–312, 311f terminally ill patient and, 349–350,
306–307, 306b–307b, 307f Bristol stool form scale, 100, 100f neurological, 310–312 350b–351b
see also Children; specific disorders Broca’s area, 125 history in, 307–310 Comorbidities, 331, 332b
Babinski sign, 140 Brown-Séquard syndrome, 145 birth, 310 Compartment syndrome, 66
Bad breath, 94 Brudzinski’s sign, 124b common presenting symptoms Compassion, 7
Balance, in frail elderly, 333 Bruising, in frail elderly, 334 in, 308–309, 308b–309b Compulsion, 321b
Ballism, 137 Buerger’s test, 69, 69b compared with adults, 307–308 Computed tomography (CT), 64
Barlow manoeuvre, 306, 306f Bulbar palsy, 125b, 129b developmental, 310 Concentration, impaired, 324
Bartholin’s abscess, 221f Bulge test, 275, 275f drug, 310 Concordance, 13
Basal cell carcinoma, 290f Bulimia, 99 family and social, 310 Concrete thinking, 321b
Basal ganglia, 135f Bulla, 287b past medical, 310 Confabulation, 324
lesions of, 134 Burning retrosternal pain, 81 systematic enquiry in, 310 Confidentiality, clinical encounters
Beau’s lines, 25f Burrow, 287b vaccination, 310 and, 7
Beckwith-Wiedemann syndrome, 301 neglect or abuse of, 315b Confusion, 331, 336, 336b–337b
Behaviour C neurological examination in, 315 clinical vignette for, 326b
of doctor, 7 CAGE questionnaire, 325b pain in, 308, 308b Conjunctiva, 152
of patients, 321b Callus (callosity), 287b physical examination of, 310–315 Conjunctival pallor, 27f
Beighton scoring system, 259b Cannon waves, 53, 53b acutely unwell child, 313, 313b Conjunctivitis, 158b
Bell’s palsy, 131 Capillary blood glucose measurement, ears, nose, and throat in, 314, allergic, 158b–159b
Bell’s phenomenon, 131 345b 314f bacterial, 158b–159b
Benign prostatic hyperplasia, Cardiac catheterisation, 63–64 general, 313–314, 313f viral, 158b–159b
112–113 Cardiac output, mechanical obstruction, height in, 313, 313f Consciousness
Bicipital tendonitis, 270 44 lymphadenopathy in, 314, 315b assessment of, 124
Bilateral testicular atrophy, 235 Cardiac tamponade, 50f similarities with adults, 312 clouding of, 323
Bilirubin, 101 Cardiomegaly, 302 techniques in, 312–313 level of, 323
see also Jaundice Cardiovascular disease preschool, 311 transient loss of, 122
Bimanual examination, of female common symptoms of, 40–44, 40b protection of, 315 Consent, clinical encounters and, 7
reproductive system, history for, 40–45 puberty. see Puberty Constipation, 100, 100f
222–223, 222b–223b, 223f drug, 44 respiratory examination in, 315 Constructional apraxia, 142
Biopsy family, 45 school-age, 311 Continuous murmurs, 61
endometrial, 223, 224f past medical, 44, 45b sick, identification of, 315, 315b, Conventional smear, cervical, 222
skin, 292 social, 45 316f Coordination, motor system and,
Bivalve speculum, 221f other symptoms of, 44, 45f vital signs in, 314, 314b 141–142, 141b
Bleeding, gastrointestinal, 100–101 physical examination for, 45–61 see also specific disorders Cord compression, in abdominal pain,
haematemesis, 100 see also specific disorders Cholestatic jaundice, 102 97b
melaena, 101 Cardiovascular examination Cholesteatoma, 176f Cornea
rectal, 101 in babies, 301–302, 301b–302b Chordee, 304, 304f infection of, 158b
Rockall and Blatchford score, 101, in children, 315 Chorea, 137 reflex of, 129, 129f
101b in frail elderly, 334–335 Chromosomal abnormalities, 34–36 ulcer/abrasion in, 158b–159b
Blind spot, 162–163 Cardiovascular system, 39–73, 74b see also specific abnormalities Corneal arcus, 46f, 47, 334–335
Blister, 287b Carotene, 26 Chronic kidney disease (CKD), 241–242 Corneal disease, 156b
Blood pressure, 49–52 Carotid artery, pressure, 52b definition of, 241, 242b Cortical function, 126–127, 126f
ambulatory monitoring of, 61 Carotid pulse, 47, 47f Chronic obstructive pulmonary disease Costochondritis, 80
British hypertension Society Carpal tunnel syndrome, features of, (COPD), 77, 79b Cough, 77–78
classification of, 50b 146b Chronic pain syndrome. see causes of, 78, 79b
in frail elderly, 333b Cataract, 156b–157b, 157f Fibromyalgia Courvoisier’s sign, 108
Korotkoff sounds, 51, 51f Catastrophic reaction, 321b Chronic skin excoriation, in children, Crackles, 89, 335
measuring, 49, 50f Cauda equina syndrome, 262 309 Cranial nerves, 127–133, 127b, 128f
in renal disease, 244 Cellulitis, orbital, 158b–159b Chronic venous ulceration, 72 see also individual nerves
see also Hypertension; Hypotension Central abdominal pain, 96 Circinate, 287b Cremasteric reflex, 140
Bloody diarrhoea, 100 Central ataxia, 135b Circle of Willis, 123f Critically ill patient, assessment of, 364
Blue toes, 66 Central cyanosis, of tongue, 86, 86f Circulation, 343–344, 343b–344b Crust (scab), 287b
Blunting, 321b Central retinal arterial occlusion, 156b, Circumstantiality, 321b CSF. see Cerebrospinal fluid
Bone pain, 253 157f Clang associations, 321b CT. see Computed tomography
Borborygmi, 99 Central retinal vein occlusion, 156b, 157f Cleft palate, 301 Cultural factors, in managing clinical
Bouchard’s nodes, 257, 258f Cephalhaematoma, 300 Clinical simulation, 356b–357b, 357, encounters with patient, 4
Bovine cough, 78 Cerebellum, 120 357f Cushing’s syndrome, 26, 202, 203f
Bowel habit, altered, 99–100 Cerebral infarct, vision and, 156b Clinical vignettes, 325–326 physical examination for, 202, 202b
see also Constipation; Diarrhoea Cerebrospinal fluid (CSF), 120 for confusion, agitation, and hostility, Cyanosis, 28
Brachial plexus injuries, 305 Cervical nodes, 33, 34f 326b in babies, 298
Brachial pressure index, 69, 69b Cervical smear, 222, 222b, 222f for fatigue, 327b central, 28, 28f
Brachial pulse, 47, 47f Cervical spine disorders, 260–261 for overdose, 326b peripheral, 28
Brachycephaly, 300b anatomy and physiology in, 260 for paranoid thoughts, 327b Cyanotic episodes, 317b
Bradycardia, 47–48 history of, 260 Clitoris, 216 Cyst, 287b
Bradypnoea, 343b physical examination for, 260–261, Clonus, 138 Cystocoele, 219
Brain, 120 260b–261b Coarctation of the aorta, 48–49, 49f
see also individual regions feel, 260–261 Coarse crackles, 89 D
Brainstem, 120 look, 260, 261b Co-codamol, drug history, 13b Deafness, 330b
death, 349–350 move, 261, 261f Cog wheeling, 138 see also Hearing loss
lesions of, 145–146 see also Neck Cognition, 323–324 Death, 349–350, 351b
Breast disorders Cervix, 216 in frail elderly, 330–331 brainstem, 349–350
abscesses, 215 Chest deformity, in respiratory disease, Cognitive difficulties, 16 care for others after, 350
cancer, 213f, 215 84, 84f Cognitive impairment, 335 communication with families, 350,
cysts, 215, 216f Chest pain, 40–42, 80–81 Colicky pain, 96 350b–351b
gynaecomastia, 214, 214b, 214f acute, 41–42 Collapsing pulse, 47 definition of, 349
investigations in, 216, 216f angina pectoris causing, 40–41 Collateral history, 325 documentation of, 350, 350b
lump, 212–213, 216b cardiovascular causes of, 41b Colles’ fracture, 279, 279f history of, 349
nipple changes, 213–214, 213f intermittent, 40–41 Coloboma, 300, 301f physical examination and, 349–350
INDEX 377
Decision-making, hypotheticodeductive Down’s syndrome, 36, 36f, 226b Electromyography (EMG), 149 examination for
method of, 363f glossoptosis, 301 Emmetropia, 153 in babies, 300–301, 300b
Deep vein thrombosis, 72b Dressing apraxia, 142 Empathy, 10–11 in children, 314
Dehydration, in frail elderly, 333b Driving, 332 Encryption, 374 musculoskeletal conditions and, 257
Delirium, 330b Drug-induced gastrointestinal End-stage renal disease, 242 Eyelid, 152
assessment of, 328b conditions, 102b Endocrine disease ptosis, 161b
Delusional beliefs, 322–323, 322b Drugs adrenals, 201–204
Delusional perception, 322b adverse musculoskeletal effects anatomy and physiology in, 201 F
Demeanour, of patients, 5, 23 caused by, 256, 256b common presenting symptoms Face, examination of
Dementia, 16, 330b allergies, 13 in, 201–202 for heart diseases, 47, 47b
Dental caries, 189f history, 13–14, 13b past history in, 202 for respiratory disease, 86, 86b, 86f
Dentition, 185f in respiratory disease, 81, 82b physical examination for, Facial expression, 23, 23b
Depersonalisation, 323b Dry eyes, 158b–159b 202–204 Facial flushing, 27b, 28f
Depression, 330b, 331 Dupuytren’s contracture, 23f clinical features of, 194b Facial (VII) nerve, 130–131, 130b,
Derealisation, 323b of palmar fascia, 104 diabetes, 205–208 131f–132f
Dermatitis herpetiformis, 286–287 Dysaesthesia, 143 anatomy and physiology in, 205, Facial nerve palsy, 305
Dermatoscopy, 291–292, 291f Dysarthria, 125, 330b 206b Facial pain, 181–182
Dermatoses, 284 Dysdiadochokinesis, 142 common presenting symptoms Facial weakness, types of, 132f
Dermis, 284 Dysmorphism, in babies, 299 in, 205 Faecal incontinence, 336b
Deteriorating patient, 339–346, 346b Dysmotility-like dyspepsia, 95 investigations in, 207b Faecal masses, 112
ABCDE approach to, 341–345 Dyspareunia, 218 past medical, drug, family and Fallopian tubes, 216–217
airway, 341–342, 341b, Dyspepsia, 95–96 social history, 205–206, Falls, 331, 333, 336, 336b–337b
341f–342f Dysphagia, 98–99, 186 206b Family history, 14, 14f
breathing, 342–343, 342b–343b Dysphasias, 125, 125b, 330b physical examination for, Fasciculation, 136
circulation, 343–344, 343b–344b expressive (motor), 125 206–208 Fast alcohol screening test (FAST)
disability, 344, 344b, 344f global, 125 gonads, 204 questionnaire, 326b
exposure, 345, 345b receptive (sensory), 125 parathyroids, 198–199 Fat intolerance, in dyspepsia, 95–96
early warning scores of, 340, 340f, Dysphonia, 125, 186, 187b, 330b anatomy and physiology in, Fatigue, 253f
341b Dyspnoea (breathlessness), 42–43, 77, 198 clinical vignette for, 327b
initial assessment of, 341, 341b 77b common presenting symptoms Female reproductive system disorders,
ongoing management of, 346 causes of, 77, 78f in, 198–199 216–223
sepsis in, 345, 345b in later pregnancy, 228 past medical, drug, family and anatomy and physiology in,
vital signs of, 340 medication and, 44b social history in, 199 216–217, 217f–218f
Deterioration, 348, 349b, 349f paroxysmal nocturnal, 42, 42f physical examination for, 199, common presenting symptoms in,
Developmental attainment, 307b Dystonia, 137 199b 217–219
Diabetes, 205–208 Dysuria, 239 pituitary, 200–201 abdominal distension and
anatomy and physiology in, 205, thyroid, 194–198 bloating, 218
206b E anatomy and physiology in, 194, abnormal vaginal bleeding,
common presenting symptoms in, Ear, 172–179 195f, 196b 217–218
205 anatomy and physiology of, 172–173 common presenting symptoms lower abdominal pain, 218
investigations in, 207b external ear, 172, 172f in, 194–196 prolapse, 219, 219f
past medical, drug, family and social inner ear, 173 past medical, drug, family and urinary incontinence, 219
history, 205–206, 206b middle ear, 172–173, 172f social history of, 196 vaginal discharge, 219
physical examination for, 206–208 Ear discharge, 173 physical examination for, drug history in, 219
assessment of newly diagnosed Ear disorders 197–198 family and social history in, 220
diabetic patient, 206, 206b, common presenting symptoms in, Endocrine system, 193–208 investigations in, 223, 224b, 224f
207f 173–174 Endometrial biopsy, 223, 224f physical examination for, 220–223,
diabetic foot, 207–208, ear discharge, 173 Enlarged organs, in gastrointestinal 220b
207b–208b, 208f hearing loss, 173, 173b disorders, 105–106 sexual history in, 220, 220b
routine review of diabetic patient, nystagmus, 174, 174b Enterocoele, 219 Females
207, 207b pain and itching, 173, 173b Epidermis, 284 puberty in, 312f
Diabetes mellitus, retinal abnormalities tinnitus, 173–174 Epididymal cyst, 235, 235f stages of, 313f
in, 165, 166f vertigo, 174, 174b Epididymitis, 235 urinary tract, 239f
Diabetic foot, 207–208, 207b–209b, drug history and, 175 Epilepsy. see Seizure Femoral fracture, 271, 271f
208f family history and, 175 Episcleritis, 158b–159b Femoral hernia, 110
Diabetic ketoacidosis, in abdominal investigations in, 179, 179f–180f Epistaxis, 180–181 Femoral nerve stretch test, 264, 264b,
pain, 97b past medical history in, 175 Epitrochlear nodes, 33, 34f 264f
Diabetic maculopathy, gradual loss of physical examination for, 175–179, Epstein’s pearls, 301 Femoral pulses
vision and, 156b–157b 175b, 191b Epworth Sleepiness Scale, 81 in babies, 302, 302f
Diagnostic strategies, 362–363 in babies, 301, 301b Erb’s palsy, 305, 305f examination of, for peripheral arterial
Dialogue, 5, 7 in children, 314, 314b, 314f Erectile dysfunction, 232–233 disease, 68, 69f
Diarrhoea, 116b inspection in, 175 Erosion, 287b Femoral triangle, 68f
Diascopy, 292 otoscopy in, 175, 175f–176f Erythema, 287b Fetal movements, reduced, in later
Diastolic murmurs, 60–61 palpation in, 175 tint of, 288 pregnancy, 226
Digital ischaemia, 66 testing hearing, 177–178 Erythema ab igne, 26f Fetor hepaticus, 104
Digital mammogram, 216f testing vestibular function, Erythema multiforme, in children, 309 Fetus, skull of, 300f
Diplopia, 155 178–179 Erythema toxicum, 299 Fever, 81
see also Double vision Earache, 173b Erythroderma, 287b Fibrocystic changes, in breast, 215
Direct inguinal hernia, 110 Easy bruising, 26 Essential tremor, 137 Fibromyalgia, 253, 253f
Disability, 344, 344b, 344f Ecchymosis (bruise), 287b Estimated date of delivery (EDD), 225b Fine crackles, 89
Discharge, from eye, 155, 160b ECG. see Electrocardiography Exanthem, 287b Finger clubbing, 24, 24b, 25f, 46, 85,
Discharge letter, 365b Echocardiography, 63 Excoriation, 287b, 289 104
Discoid, 287b Echolalia, 321b Exertional dyspnoea, 42 Finger jerk, 140
Discoloration, 26–28, 27f Ectopic beats (extrasystoles), 43 Exomphalos, 303, 303f Finger-to-nose test, 141, 142f
Disinhibition, 321b Eczema, 286 Exposure, of deteriorating patient, 345, Fingers
Dissecting aortic aneurysm, in of nipple and areola, 213 345b deformities of, 265, 266f
abdominal pain, 97b EEG. see Electroencephalography External abdominal hernia, 110 rotational, 265, 266f
Disturbance of smell, 181 Elbow, 268 External auditory meatus, exostosis of, flexors and extensors of, testing,
Dix-Hallpike positional test, 178, 178b, anatomy and physiology of, 268 176f 267, 267f
178f physical examination of, 268, 268b Extraocular muscles, 152–153, Fissure, 287b
Dizziness, 43, 123 feel, 268 152f–153f Fistula test, 179, 179b
Doctors, duties of, 6, 6b look, 268 Extrasystoles, 43, 43b Fitzpatrick scale of skin types, 286b
Dolichocephaly, 300b move, 268 Eye, 152, 152f FLACC scale, 308b
Doll’s-eye reflex, 164, 164b, 165f special tests for, 268 movements of, 152–153, 152f, 164, Flashes, 155
Domestic activities of daily living, 335 Elderly, frail. see Frail elderly 164b Flattening, 321b
Dorsal root, peripheral nerves and, Electrocardiography (ECG), 61, 62f refractive elements of, 153, 153f Flatulence, 99
144–145, 144f, 146f ambulatory, 61 Eye disorders Flights of ideas, 321b
Dorsalis pedis pulse, 69, 69f exercise, 61 coloboma as, 300, 301f Floaters, 155
Double vision, 155, 159b, 159f, 169b Electroencephalography (EEG), 149 discharge, 155, 160b Fluid thrill, in ascites, 109, 109f
378 INDEX
Focal seizure, 122 Gastrointestinal disorders Haemosiderin, 26 physical examination of, 271–272,
Fontaine classification, of lower limb history of Hair, 283–292 271b–272b
ischaemia, 64b drug, 102, 102b anatomy of, 285 feel, 272
Food intolerances, in gastrointestinal family, 102 asynchronous cycles of, 285 look, 271–272
disorders, 102 past medical, 102 signs, 290–291, 291f move, 272, 272f
Foot (feet), 276–278 social, 102–103 Hair loss, in children, 309 shortening, 273, 273b, 273f
anatomy of, 276–277 investigations in, 113, 113b–114b, Half-and-half (Lindsay’s) nails, 243, 243f special test for, 273
Foot drop, 135b 113f, 115f–116f Halitosis, 94 Trendelenburg’s sign, 273, 273b,
Foot trauma symptoms of, 94–102 Hallucination, 323b 273f
history of, 277–278, 277f mouth, 94 Hallux valgus, 278, 278f Hirsutism, 204, 205f, 290
physical examination for, 278, 278b see also specific disorders Haloes, 155 History taking, 9–17
active movements, 278 Gastrointestinal examination, 103–113 Hammer toes, 278 in babies, 298–299
feel, 278 abdominal, 104–110 Hand, 265–268 beginning the history, 10–11
inversion/eversion, 278 auscultation in, 109–110 extra-articular signs of, 265 in children, 307–310
look, 278 in frail elderly, 335 finger clubbing, 46 concordance and adherence in, 13
move, 277f, 278 general, 103–104 history of, 265, 265b consultation and, 10–11
passive movements, 278 inspection in, 104–105 physical examination of, 265–268, in difficult situation, 16–17
special tests for, 278 palpation in, 105–107 265b–268b drug history for, 13–14, 13b–14b
Foot ulcer, 336b percussion in, 107–109 active movement, 266–267 empathy during, 10–11
Foreign body, corneal, 158b proctoscopy in, 113 feel, 266 and examination skills, 362
Fornices, 216 rectal, 111–113, 111b for heart diseases, 46–47, 46b family history in, 14, 14f
Fracture, 279–280 sequence of, 103b–107b, 103f, look, 265 gathering information during, 10–16
Colles’, 279, 279f 109b–113b move, 266–268 history of the presenting symptoms,
femoral, 271, 271f Gastrointestinal system, 93–113 passive movement, 267 11–12, 11b–13b
history of, 279 anatomy and physiology of, 94, 94b, for respiratory disease, 85, 85b, importance of a clear history in, 10
metatarsal, 277, 277f 94f–95f 85f past medical history for, 13
pain, 253 integrated examination sequence for, rheumatoid arthritis, 265, 266f of patient with mental disorder, 320
physical examination for, 279–280, 117b swelling, 265, 266f general approach to, 320
279b–280b Gastro-oesophageal reflux disease, 95 T1 root lesion and, 265, 267f sensitive topics in, 320
describing, 280b Gastroschisis, 303 with wound, examining, 268 uncooperative patient in, 320
feel, 279 General examination. see Physical Hand hygiene, 21f preparation for, 10
look, 279 examination Handshake, 20b, 23 social history and lifestyle in, 14–16
move, 280 General medical Council, 7 Hawkins-Kennedy test, 271, 271f systematic enquiry in, 16, 17b
Frail elderly, 329–337, 338b Genital examination. see Reproductive Head see also Physical examination
assessment of, 330–331 system examination of, in babies, 300, 300b Hoarseness, 190b, 342b
cognition and mood of, 330–332 Gestation, 225b shapes of, neonatal, 300b see also Dysphonia
communication difficulties in, see also Pregnancy Head impulse test, 178–179, Hoffmann’s reflex, 139
330–331, 330b Giant cell arteritis, 156b 178b–179b Holmes-Adie syndrome, 162
with decreased mobility, 331, Gibbus, 259, 260f Head thrust test, 178–179, 178b–179b Home environment, 332
335–336, 336b Gilbert’s syndrome, 102 Head tremor, isolated, 137 Hoover’s sign, 139, 139f
functional decompensation in, 330f Glabellar tap, 141b Headache, 120b, 122 Horn, 287b
history of, 331–333 Glandular fever. see Infectious history of, example of, 149b Horner’s syndrome, 162
drug, 331–332, 332b mononucleosis Hearing, testing of, 177–178, 180f Hostility, clinical vignette for, 326b
factors influencing, 330–331 Glasgow Coma Scale (GCS), 344, 344b Hearing loss, 173, 173b, 334 Hydration, 30–31
family, 332 Glaucoma, 156b–157b Heart, 40–64 in frail elderly, 333–334, 333b
past medical, 331 angle-closure, 158b–159b anatomy and physiology of, 40, 40f Hydrocephaly, 300b
presenting symptoms in, 331 haloes and, 155 auscultation of, 54b–55b, 54f, Hydrocoele, 234, 304
social and functional, 332 Glenohumeral dislocation, 269, 269f 55–61, 56f Hyperaesthesia, 143
systematic enquiry in, 332–333 Glossopharyngeal (IX) nerve, 131–132, normal resting pressure (mmHg), 40f Hyperalgesia, 143
interpretation of findings in, 337 132b, 132f palpation of, 54–55, 54b, 55f Hyperandrogenism, 204
multiprofessional team in, 330b Glossoptosis, 301 surface anatomy of, 54f Hypercarotenaemia, 26, 27f
physical examination of, 333–336, Glucocorticoids, side effects of, 256b Heart block, 53b Hyperkeratosis, 287b
333b Goitre, 194–195 Heart failure Hyperlipidaemia, 46f
cardiovascular, 334–335 Golfer’s elbow, 268, 268b causes of, 42b Hypermetropia, 153, 153f
functional assessment in, Gonads, 204 JVP and, 53b Hypermobility, 259
335–336 GORD. see Gastro-oesophageal reflux New York Heart Association Beighton scoring system, 259b
gastrointestinal, 335 disease classification of, 42b Hyper-reflexia, 140–141
general, 333–334 Gout, 252, 252f, 255b Heart murmurs, 58–61, 58b–59b Hypertension, 50–51
musculoskeletal, 335 Gouty tophi, 257, 258f continuous, 61 secondary, 50–51
neurological, 335 in frail elderly, 335 diastolic, 60–61 white coat, 50
respiratory, 335 ‘Graham Steell murmur’, 60 systolic, 59–60, 59b Hypertensive retinopathy, 51, 165,
sequence of, 335b–336b Graphaesthesia, 144 Heart rate, in babies, 302, 302b 167f
systemic, 334–335 Grasp reflex, 141b Heart sounds, 55–58, 56b–57b, 56f–57f Hypertonia, 137–138
presentation of Grasp response, 305 Heart valves, 40f Hypertrichosis, 290
factors influencing, 330–331 Graves’ disease, 194 mechanical, 58 Hypoaesthesia, 143
Frailty, definition of, 330 Graves’ hyperthyroidism, 195f, 196b Heartburn, 95 Hypochondriasis, 322b
Freckle, 287b Groin swellings, 102 Heberden’s nodes, 255, 257, 258f Hypoglossal (XII) nerve, 133, 133b,
Frontal lobe, 127 Grommet in situ, 176f Heel-to-shin test, 141, 142f 133f
Functional assessment, in frail elderly, Growth, in children, 310–312, 311f Hemiparesis, 30 Hypogonadism, 204
335–336 Grunting, 342b Hemiplegic gait, 135 Hyponatraemia, 336b
Functional gait, 135b Gurgling, 342b Hepatic encephalopathy, grading of, Hypopituitarism, 26, 200
Fundus, 165f Gynaecological malignancy, 112 108b physical examination for, 201, 201b,
Furuncle, 287b Gynaecomastia, 104, 214, 214b, 214f Hepatic jaundice, 102 202f
Gyrate, 287b Hepatomegaly, 106–107, 107f Hyposmia, 128
G causes of, 107b Hypospadias, 304, 304f
Gait, 22–23, 258–259, 259b H palpation for, 303 Hypotension
increased tone of, 259 Haemarthrosis, 254f Hernias, 102, 110–111, 110b, 110f abdominal pain and, 97
pain, 259 Haematemesis, 100 anatomical structure of, 111f postural, 44
structural change of, 259 Haematoma, 175f, 287b Herpes simplex virus keratitis, 157f Hypotheticodeductive method, of
weakness, 259 cephalhaematoma, 300 Herpes zoster infection decision-making, 363f
Gait abnormalities, 135, 135b, 136f Haematuria, 240 in abdominal pain, 97b Hypothyroidism, 194
antalgic gait, 259 non-visible, 240 in chest pain, 80–81 Hypotonia, 137
in frail elderly, 335 principal sources of, 240, 240f trigeminal nerve and, 130, 130f in babies, 299, 305
Gait apraxia, 135b visible, 240 High-volume diarrhoea, 100 Hysterosalpingogram, 224f
Galactorrhoea, 213–214 Haemochromatosis, 26, 26f Hip, 271–273
Gallbladder, 94b Haemodialysis, 242 anatomy of, 271 I
GALS screen, 258–259 fistula, 243, 244f developmental dysplasia of, Ichthyosis, 287b
initial questions in, 258–259, Haemoptysis, 79 305–306, 306f Idiopathic cough, 79b
258b–259b Haemorrhoids, 112 history of, 271 Iliac fossa pain, 218
INDEX 379
Illness trajectories, 348, 348f ligament testing of, 275–276, 276f Lumbar spine disorders, history of, integrated examination sequence for,
Illusion, 323b anterior cruciate, 276, 276b 262–263, 262b, 262f 328b
Immunosuppressants, side effects of, collateral, 275, 275b Lumps physical examination for, 325
256b locking, 274 breast, 212–213, 216b Mental state examination (MSE),
Incongruity, 321b pain, 274, 274b groin, 31–32, 32b, 32f, 102 320–325
Incontinence, in frail elderly, 336, 336b patella, 276, 276b neck, 186–187, 187f, 188b, 191b appearance in, 320
Indirect inguinal hernia, 110 physical examination of, 274–275, see also Swelling behaviour in, 321b
Infants. see Babies 274b–275b Lung cancer, 79b capacity in, 324–325
Infectious mononucleosis, 186, 186f feel, 275 in pleuritic pain, 80 cognition in, 323–324
Infective diarrhoea, 100 look, 274–275 Lungs. see Respiratory disease insight in, 324
Infective endocarditis, 44 move, 275 Lymph nodes, 31–34, 33b, 33f mood in, 321, 321b
Ingestion, 95 swelling, 274 Lymphadenopathy, in children, 314, perceptions in, 323, 323b
Inguinal hernia, 110, 111f, 303f, 304 Koebner (isomorphic) phenomenon, 315b personal, 320b
Inguinal nodes, 33, 34f 286–287, 288f Lymphoedema, 31, 31f psychiatric, 320b
Insight, 324 Koilonychia, 25f of breast, 213 risk assessment in, 324
Integrated examination, 362, 362b Korotkoff sounds, 51, 51b, 51f speech in, 321
Intelligence, 324 Kussmaul respiration, 343b M thought content in, 322–323,
Intention tremor, 137 Kussmaul’s sign, 53 Macroglossia, 301 322b
Intermittent claudication, 64–65, 65b Kyphosis, 259, 260f Macular degeneration thought form in, 321–322, 321b
Interstitial lung diseases, 79b dry age-related, 156b–157b, 157f Mesenteric ischaemia, 66
Intestinal obstruction, 98b L wet age-related, 156b, 157f Metatarsal fracture, 277, 277f
Intracranial lesions, 145–146 Labia majora, 216 Macular purpura, 288 Microcephaly, 300b
Itching Labia minora, 216 Macule, 287b Microglial cells, 120
in ear, 173 Lability, 321b Magical thinking, 322b Micrognathia, 301
see also Pruritus Lachmann test, 276 Magnetic resonance imaging (MRI), 64 Microtia, 175f
Lactational abscesses, 215 Male reproductive system disorders, Migraine, vision and, 156b
J Laryngomalacia, 303 230–235 Milia, 287b, 299
Janeway lesions, 46, 46f Last menstrual period (LMP), 225b anatomy and physiology in, 230, Miller’s pyramid of clinical competence
Jaundice, 27, 101–102, 101b, 101f, Lateral cutaneous nerve, of thigh, 147, 231f and assessment methods,
117b 147b common presenting symptoms in, 356f
in babies, 298 Lateral meniscus, 276 231–233 Mini-Mental State Examination (MMSE),
hepatic, 102 Left ventricular hypertrophy, 55 erectile dysfunction, 232–233 325
posthepatic/cholestatic, 102 Leg pain, 64–66 penile discharge or dysuria, 231 Minor injury or illness, assessment of,
prehepatic, 102 Legs, 258 penile skin lesions, 232, 233f 364
urine and stool analysis of, 102b see also Lower limb scrotal swelling or pain, 231–232, Miscarriage, 225b
Jaw jerk, 129, 129f Lentigo, 287b 232b, 232f Mitral regurgitation, 58f
Jendrassik’s manoeuvre, 139 Leuconychia, 25f, 104 urinary symptoms, 231 Mitral stenosis, 57–58, 60f
Jitteriness, in babies, 299 Leucoplakia, 189f drug history in, 233 Mobility, 331, 335–336, 336b
Joint pain, 252, 252b Lichen planus, 286–287, 288f investigations in, 235 Mongolian blue spot, 299, 300f
exacerbating factors of, 253 Lichenification, 287b past medical history in, 233 Mood
progressive, 253 Lifestyle, 14–16 physical examination for, 233–235 in frail elderly, 330–331
radicular, 253b Light reflex, direct and consensual, 161, penis, 233–234, 233b–234b of patient, 321, 321b
referred, 253b 161b prostate, 235, 235b Morbid thinking, 322b
severity of, 253 Light touch, 143 scrotum, 234–235, 234b, 234f Moro reflex, 305, 306f
Joints Limb swelling, 72 skin, 233, 233b Morton’s neuroma, Mulder’s sign for,
erythema, 255 Limbs social history in, 233 278, 278b
extra-articular symptoms of, examination of, in babies, 305–306, Males Motor retardation, 321b
255–256, 255b 305b–306b puberty in, 312f Motor system, 133–142, 134f
GALS screen, 258–259 lower. see Lower limb stages of, 313f see also Muscles; Tendon reflexes
involvement, patterns of, 253–254, upper. see Upper limb urinary tract, 238f Mouth disorders, 184–190
254f Linea nigra, 225b Mallet toes, 278 anatomy and physiology in, 184,
locking and triggering, 255 Liquid-based cytology, cervical smear Mallory-Weiss syndrome, 100 184f–185f
physical examination of, 246, and, 222, 222f Malnutrition Universal Screening Tool common presenting symptoms in,
256–259 Liquor, 225b (MUST) score, 334f 184–187
position sense, 144 Live birth, 225b Mammary duct fistula, 216f sore mouth, 184–185, 185b
stiffness, 254 Liver, 94b Marfan’s syndrome, 30, 30f drug history in, 187
structure of, 252, 252f Liver disease, 103f, 104 ‘Mechanical’ dysphagia, 99 investigations in, 190, 190b
swelling, 254–255, 254f risk factors for, 103 Mechanical heart valves, 58 past medical history in, 187
warmth, 255 Localised oedema, 30–31 Meconium, 303 physical examination for, 187–189,
weakness, 255 Locking, 255 Medial meniscus, 276 187b–188b, 188f–189f
see also Musculoskeletal disorders; knee, 274 Median nerve, 146, 146b, 267–268, in babies, 301, 301b
individual joints Locomotor system, integrated 267f social history in, 187
Jugular venous pressure (JVP), 52–53, examination sequence for, Medical Research Council (MRC) see also specific disorders
52b, 52f–53f, 86, 244 282b breathlessness scale, 77, 77b MRI. see Magnetic resonance imaging
abnormalities of, 53b Loin pain, renal disease causing, 239 Medically unexplained symptoms, Muehrcke’s lines, 243, 243f
carotid artery pressure versus, 52b Long case assessment, 356b 363–364, 363b, 363f Mulder’s sign for Morton’s neuroma,
JVP. see Jugular venous pressure Longstanding dysphagia, 99 Medication 278, 278b
Loosening of associations, 321b angina pectoris and, 44b Multimorbidity, 330
K Lordosis, 259, 260f dyspnoea and, 44b Murmurs, of heart, 302
Keratosis, 287b Low back pain, 262, 262b oedema and, 44b Murphy’s sign, 108
Kernig’s sign, 124b, 125f Low-volume diarrhoea, 100 palpitation and, 44b Muscle bulk, 136
Kidney, 94b Lower abdominal pain, 96 Megalencephaly, 300b Muscle pain, 252–253, 252b
anatomy of, 238, 238f female reproductive system and, 218 Melaena, 101 Muscles
auscultation of, 246 Lower limb, 271–278 Melanin, 26 fasciculation and, 136
inspection of, 245, 245f peripheral arterial disease and, 68 Melanocytic naevi, 290, 299 inspection and palpation of,
nephron, 238f shortening, 273, 273f Memory, 323–324 136–137, 136b
palpation of, 245–246, 245f see also individual parts Men. see Males myoclonic jerks and, 136
percussion of, 246 Lower motor neurone, lesions of, 134, Meningeal irritation, 124, 124b, 125f power, 138–139, 138b–139b, 139f
see also entries under renal 134b Meninges, 120 tendon reflexes
Klinefelter’s syndrome (47XXY), 36, 204, Lower urinary tract, functional Meningism, 124 deep, 139–141, 139b–140b,
205f assessment of, 247, 247b Meniscal provocation test, 276, 276b 140f
Klumpke’s palsy, 305 Lumbar puncture, 149 Mental disorder, 319–326 primitive, 141, 141b
Knee, 273–276 Lumbar spine, 261–264 clinical vignettes for, 325–326, tone, 137–138, 137b
anatomy of, 273–274, 274f anatomy and physiology of, 261–262 326b–327b tremor. see Tremor
flexion/extension physical examination of, 263, 263b collateral history in, 325 Musculoskeletal chest pain, 80
active, 275 feel, 263 history of, 320 Musculoskeletal disorders
passive, 275 look, 263 general approach to, 320 extra-articular symptoms of,
history of, 274 move, 263, 263f sensitive topics in, 320 255–256, 255b
instability, 274 special tests for, 263–264 uncooperative patient in, 320 general examination of, 257–259
380 INDEX
Musculoskeletal disorders (Continued ) Nervous system disorders, 119–149 family history in, 225, 226b onset of, 252–253
history of, 252–256 anatomy and physiology in, 120, 121f information of previous pregnancies, radiation in, 253, 253b
drug, 256, 256b cranial nerves, 127–133, 127b, 128f 225b severity of, 253
family, 256 examination of, 124–127, 246 investigations in, 226, 227b site of, 252
past medical, 256 history of, 120–124 occupational history in, 226, 226b timing of, 253, 253b, 253f
social, environmental and common presenting symptoms, past medical history in, 225 ocular, 155, 158b
occupational, 256 122–123 social history in, 225–226 Pallor, 27–28
investigations in, 280, 280b–281b drug history, 124 Obstructive jaundice, 102 in babies, 298
look-feel-move in, 256 family history, 124 Obstructive sleep apnoea (OSA), 81 conjunctival, 27f
OSCE example on, 281b–282b occupational history, 124 Obstructive sleep apnoea/sleep Palmar erythema, 104
physical examination for, 256–259 past medical history, 123 hypopnoea (OSASH), 81 Palmomental reflex, 141b
presenting symptoms of, 252–256 social history, 124 Occipital lobe, 127 Palpable mass, in gastrointestinal
see also specific disorders integrated examination sequence for, Occupational disorder, 15, 15b disorders, 105, 106f
Musculoskeletal system, 251–280 150b Occupational exposure, in respiratory Palpable purpura, 288
detailed examination of, 259–278 interpretation of findings in, 147 disease, 82 Palpation, 54–55, 54b, 55f
of frail elderly, 335 investigations in, 147–149 Occupational history, 15–16 in gastrointestinal disorders,
Mutism, 321b initial, 147, 148f Ocular alignment, 163–164 105–107
Myalgia. see Muscle pain lumbar puncture, 149 Ocular pain, 155, 158b enlarged organs, 105–106
Mycology, 292 neurophysiological tests, 149 Oculocephalic reflex, 164, 164b, 165f hepatomegaly, 106–107
Myocardial infarction, 41b motor system, 133–142, 134f Oculomotor (III) nerve, 128 palpable mass, 105
in abdominal pain, 97b peripheral nerves, 146–147 Odours, 29 spleen, 108–109, 108f
Myoclonic jerks, 136 sensory system, 142–146, 143f Odynophagia, 96 tenderness, 105
Myopathic gait, 135b see also specific disorders Oedema of kidney, 245–246, 245f
Myopia, 153, 153f Neurocardiogenic syncope, 43 cardiac, 44 in respiratory disease, 87, 87b, 87f
Myotonia, 137–138 Neurofibromatosis, 29f medication and, 44b Palpitation, 43
Neurological dysphagia, 98 peripheral, 245 medication and, 44b
N Neurological examination Oesophageal Pancreas, 94b, 205
Naevus, 287b in babies, 304–305, 304b–305b dysmotility, 98 Pansystolic murmurs, 59–60
Nail disorders in children, 315 pain, 40–41, 41b Papilloma, 287b
history in, 285–286 in frail elderly, 335 reflux, 79b Papule, 287b
common presenting symptoms Neurological symptoms, functional, 123 Olecranon bursitis, 254f Paradoxical respiration, 343b
in, 285 Neuromuscular dysphagia, 98 Olfaction, 179 Paraesthesia, 143
family and social history in, 286 Neurone, 120 Olfactory (I) nerve, 127–128, 127b–128b Paranasal sinuses, 183f
past medical and drug history, Neurophysiological tests, 149 Oligodactyly, 306 Paranoid thoughts, clinical vignettes for,
285 Night pain, 65 Oligodendrocytes, 120 327b
see also specific disorders Night sweats, 81 Oligohydramnios, 225b Paraphimosis, 233f
Nail-fold infarcts, 257, 257f Nipple, 212 Oliguria, 239 Parathyroid disease, 198–199, 199f
Nails, 24, 24b, 25f, 283–292 changes in, 213–214, 213f Omphalocoele, 303 anatomy and physiology in, 198
anatomy of, 285 discharge, 213 Onycholysis, 25f, 287b common presenting symptoms in,
investigations in, 292 eczema of, 213 Ophthalmology, integrated examination 198–199
physical examination of, 257, inversion, 213, 213f sequence for, 169b past medical, drug, family and social
286–292 Paget’s disease of, 213f Ophthalmoscopy, 164, 164b, 165f, history in, 199
signs in, 290–291, 291f Nocturia, 239 166b physical examination for, 199, 199b
splinter haemorrhages, 46, 46f Nodules, 257, 257f–258f, 287b in babies, 300–301, 300b–301b Parietal lobe, 127
structure of, 285f Non-lactational abscesses, 215 Optic disc pallor, differential diagnosis Parity, 225b
Nasal abnormalities, 181f Non-pleuritic chest pain, 81 of, 166b Parkinsonian gait, 135b, 136f
Nasal deformity, 182, 182f Non-traumatic conditions, of ankle and Optic disc swelling, causes of, 164, 166b Parkinson’s disease, tremor and, 137
Nasal discharge, 180 foot, 277–278 Optic (II) nerve, 128 Parosmia, 128
Nasal obstruction, 180 Non-verbal communication, 5 Optic neuritis, 156b, 157f, 158b Parotid duct, 184
Nasal pain, 181–182 Nose and sinuses, disorders of, Optic neuropathy pus in, 187f
Nasal polyps, 181f 179–183 anterior ischaemic, 156b Parotid gland, 184
Nasal septum perforation post-surgery, anatomy and physiology in, compressive, 156b–157b, 157f Paroxysmal nocturnal dyspnoea, 42, 42f
181f 179–180, 181f Oral thrush, 189f Past medical history, 13
National Early Warning Score (NEWS), common presenting symptoms in, Orbit, 152 Patch, 287b
340, 340f 180–182 examination of, 161, 161b, 161f Patch testing, 292, 292f
Nausea and vomiting, 99 disturbance of smell, 181 Orientation, 323 Patella, 276, 276b
Neck, 184–190 epistaxis, 180–181 Orthopnoea, 42 meniscal provocation test for, 276,
abnormal posture of, 261b nasal and facial pain, 181–182 Osler’s nodes, 46, 46f 276b
anatomy and physiology of, 184, nasal deformity, 182, 182f Osteoarthritic changes, in frail elderly, meniscal tears, test for, 276
185f nasal discharge, 180 335 Patellar apprehension test, 276
common presenting symptoms in, nasal obstruction, 180 Osteoarthritis, 257, 258f Patellar tap, 275, 275f
184–187 sneezing, 181 Osteogenesis imperfecta, 34 Patent ductus arteriosus, 302
neck lump, 186–187, 187f, 188b, drug history in, 182 Otitis externa, 176f Patients
191b family history in, 182 Otitis media, 176f appearance of, 320
drug history in, 187 investigations in, 183, 183b, 183f with effusion, 176f behaviour of, 321b
investigations in, 190, 190b past medical history in, 182 fluid level, 176f clinical encounters with, 3–7
past medical history in, 187 physical examination for, 182–183, Ovaries, 216–217 addressing the problem during, 6
physical examination of, 189–190, 182b, 183f, 191b pain in, 218 clinical environment and, 4, 4f
189b–190b, 190f in babies, 301, 301b torsion of, 97b concerns during, 5
in babies, 301, 301b in children, 314, 314f Overdose, clinical vignette for, 326b concluding, 6
for peripheral arterial disease, 68 social history in, 182 Overvalued ideas, 322, 322b cultural sensitivity and, 6
for respiratory disease, 86, 86b, see also specific disorders dialogue with, 7
86f Nummular, 287b P empathy in, 5–6
social history in, 187 Nutrition, in frail elderly, 333–334, 334f Paget’s disease, of nipple, 213f gathering information during, 5
stiffness of, 124b Nystagmus, 164, 174, 174b Pain opening, 5
in children, 315 testing for, 178, 178b abdominal. see Abdominal pain personal responsibilities in, 7
swelling of, 301 in breast, 213 professional responsibilities in,
Neck lump, 186–187, 187f, 188b, O chest. see Chest pain 6–7, 6b
191b Obesity, 29 in children, 308 reasons for, 4, 4b
Necrobiosis lipoidica diabeticorum, Objective findings, 364 in ear, 173, 173b sensitive information and third
288f Objective structured clinical in frail elderly, 333–334, 334b parties in, 5
Neer test, 271 examinations (OSCEs), in gastrointestinal disorders, 95–98 with cognitive difficulties, 16
Neglect, of children, 315, 315b 356b–358b, 357, 358f knee, 274, 274b with communication difficulties, 16
Nelson’s syndrome, 26 Obsessions, 322b loin, renal disease causing, 239 emotional or angry, 16–17
Neologism, 321b Obstetric history and examination, of mouth, 95, 95f with mental disorder, 319–326
Neonates. see Babies reproductive system, 225–226 musculoskeletal, 252–254 uncooperative, 320
Nephron, 238f checklist for, 225b associated symptoms of, 253 Peau d’orange, of breast, 213f
Nephrotic syndrome, 240 drug, alcohol and smoking history in, character of, 253 Pedigree chart, 14f
Nerve conduction studies, 149 225 exacerbating factors of, 253 Pedunculated, 287b
INDEX 381
Pelvic inflammatory disease, 98b Plantar response, 140, 140f Pull test, 135 presenting symptoms of, 242
Pelvic masses, 218 Plaque, 287b Pulmonary embolism, JVP and, 53b storage symptoms of, 239
Pelvic response to back stimulation, Pleural rub, 89 Pulmonary embolus, in chest pain, 80 voiding symptoms of, 239–240
305 Pleurisy, in abdominal pain, 97b Pulmonary infarcts, in pleuritic pain, 80 see also specific disorders
Pelvis, 216, 217f Pleuritic pain, 80 Pulmonary regurgitation, 60 Renal system, 237–247
pain in, 219b–220b Pleuropericardial rub, 58 Pulse. see Arterial pulses Renal transplant, 242
ultrasound of, 224f Pneumaturia, 240 Pulse pressure, in renal disease, 244 Reproductive system disorders,
Penile discharge or dysuria, 231 Pneumonia, in pleuritic pain, 80 Pulse rate, in frail elderly, 333b 211–235
Penile skin, 230 Pneumothorax, in pleuritic pain, 80 Pulse volume, 48–49, 49b breast, 212–216
lesions, 232, 233f Poikiloderma, 287b Pulsus alternans, 49 anatomy and physiology in,
Penis, 230, 231f Polyarthritis, 253–254, 254f Pulsus bisferiens, 49 212–216, 212f
physical examination of, 233–234, Polycythaemia, 27–28 Pulsus paradoxus, 49 common presenting symptoms
233b–234b Polydactyly, 306 Pupillary pathways, 153, 154f in, 212–214
Perceptions, 323, 323b Polyhydramnios, 225b Pupils, 161–162 investigations in, 216, 216f
Percussion Polypharmacy, 331–332 defects of physical examination for,
in gastrointestinal disorders, Polyuria, 239 Adie’s pupil, 162 214–215, 214b–215b,
107–109, 107b, 107f Pons, lesions of, 131f Argyll Robertson pupil, 162 214f–216f, 236b
ascites, 109 Popliteal pulse, examination of, for examination of, 161–162 female, 216–223
splenomegaly, 108–109 peripheral arterial disease, 68, Purpura, 287b, 289f anatomy and physiology in,
of kidney, 246 69f Pustule, 287b 216–217, 217f–218f
in respiratory disease, 87–88, 87b, Posterior drawer test, 276 Pyrexia. see Fever common presenting symptoms
88f Posterior tibial pulse, examination of, for in, 217–219
Perforated peptic ulcer, with acute peripheral arterial disease, 68, Q drug history in, 219
peritonitis, 98b 69f Quinolones, side effects of, 256b family and social history in, 220
Pericardial constriction, 53b Posthepatic jaundice, 102 Quinsy, 186 investigations in, 223, 224b, 224f
Pericardial effusion, 53b Postural hypotension, 44 physical examination for,
Pericardial pain, 41–42, 41b in frail elderly, 333b R 220–223, 220b
Pericardial rub, 58 Posture, 22–23 Radial nerve, 146, 146b, 267–268, 267f sexual history in, 220, 220b
Perineum, 216 Posturing, 321b Radial pulse, 47, 47f male, 230–235
in babies, 303–304, 303b–304b Practice Radionuclide studies, 63 anatomy and physiology in, 230,
Peripheral arterial system, 64–69 of diagnostic strategies, 362–363 Ramsay Hunt syndrome, 131 231f
anatomy and physiology, 64, 64f of history and examination skills, 362 Ranula, 301 common presenting symptoms
history for, 64–67 of integrated examination, 362, 362b Rare diseases, diagnostic strategies for, in, 231–233
drug, 67 preparing for, 361–374 362–363 drug history in, 233
family, 67 Precordium, 53–61, 54f Rash investigations in, 235
past medical, 67 Pre-eclampsia, in later pregnancy, 227 distribution of, 286, 286f, 288f past medical history in, 233
social, 67 Pregnancy, routine antenatal check in, morphology of, 286–289, 288f–289f physical examination for,
investigations for, 69, 70b 226–230 pattern of, 286 233–235
physical examination of, 67–69, common presenting symptoms in, Raynaud’s phenomenon, 66, 67f, 257 social history in, 233
68b–69b 226–228 Reactive arthritis, 255b obstetric history and examination,
Peripheral nerve map, 145f abdominal pain, 227 ‘Rebound tenderness’, 105 225–226
Peripheral nerves, 120, 146–147 breathlessness, 228 Rectal bleeding, 101 routine antenatal check in later
Peripheral oedema, 245 fetal movements, reduced, 226 Rectal examination, 111–113, pregnancy, 226–230
Peripheral venous system, 70–73, physiological symptoms, 226 111b–112b, 112f common presenting symptoms
70f–71f, 71b pre-eclampsia, 227 abnormal stool appearance in, 112b in, 226–228
investigations for, 73 pruritus, 227 indications for, 111b history in, 226–228
past history for, 73b–74b vaginal bleeding, 226–227 position in, 112f investigations in, 227b, 230
physical examination of, 72–73, history in, 226–228 Rectocoele, 219 physical examination in, 228–230
72b–73b investigations in, 227b, 230 Red eye, 155, 158b–159b Respiration, haemodynamic effects of,
Peritoneal dialysis, 242 physical examination in, 228–230, Reducible hernia, 110–111 48b
Peritonsillar abscess, 186, 186f 228b–229b Referral letter, 365b Respiratory disease
Perseveration, 321b Prehepatic jaundice, 102 Reflexes. see Tendon reflexes findings of, interpretation of, 89, 89b
Persistent patent ductus arteriosus, 61f Preoccupations, 322b Reflux-like dyspepsia, 95 history, 76–82, 76b, 90b–91b
Personal responsibilities, of doctor, 7 Preschool child, 311 Refractive error, gradual loss of vision drug and allergy, 81, 82b
Personality disorder, 325b examination of throat in, 314, 314b, and, 156b–157b family, 81
Petechiae, 33–34, 34f, 46, 46f, 287b 314f Relative afferent pupillary defect (RAPD), occupational, 82, 83f
Phaeochromocytoma, 51b Pressure of speech, 321b 162, 162b past medical, 81, 82b
Phenothiazine-induced pigmentation, Pressure of thought, 321b Renal disease social, 81–82
27f Presyncope, 43–44 abdominal examination in, 245–246, home circumstances in, 82
Phobia, 322b Pre-test probability, 362, 363f 245b–246b investigations in, 89, 90b
Physical examination, 19–36, 362b Primary dysmenorrhoea, 218 auscultation, 246 physical examination for, 82–89, 91b
of babies, 299–307 Primitive reflexes, 141, 141b, 305, inspection, 245, 245f auscultation in, 88–89
of children, 310–315 305b, 306f palpation, 245–246, 245f inspection in, 82–87, 83f–84f
equipment for, 20b Probability, pre-test, 362, 363f percussion, 246 sequence of, 84b–88b, 85f–87f,
of frail elderly, 333–336, 333b Proctoscopy, 113, 113b anatomy and physiology in, 238 92b
initial observations in, 22–23, 22f Professionalism, during assessment, end-stage, 242 symptoms of, 77–81
medically unexplained symptoms, 359, 359b, 359f fluid balance assessment, 244–245 systematic enquiry in, 82
363–364, 363b, 363f Prolactinoma, 200 charts, 245 see also specific disorders
of patients with mental disorders, Prolapse chest examination, 245 Respiratory distress, in babies, 298
325 assessment of, 222, 222f general appearance, 244 Respiratory examination
preparing for, 20, 20b female reproductive system, 219, weight, 245 in babies, 302–303, 302b
sequence for, 21–22 219f history of, 239–243 in children, 315
spot diagnoses, 34–36, 35b, 35f Prostate, 230 drug, 243 in frail elderly, 335
see also specific body systems physical examination of, 235, 235b, family, 243 Respiratory rate
Physiological symptoms, in later 246 past medical, 243 in babies, 302b
pregnancy, 226 Prostatitis, 239 social, 243 of deteriorating patient, 342
Physiological tremor, 137 Proteinuria, 240 integrated examination sequence for, Respiratory system, 75–89, 76f
Pierre Robin syndrome, 301 quantification of, 241, 242b 250b Rest pain, 65
Pigmentation, 287b Pruritus, 292b interpretation of findings in, 246 Reticulate, 287b
Pigmented lesion, 293b in later pregnancy, 227 investigations in, 246–247 Retinal detachment, 156b, 157f
Pinna, 175, 175f Pseudobulbar palsy, 129b blood and urine, 248b Retinitis pigmentosa, 156b–157b, 157f
Pipelle, for endometrial biopsy, 224f Pseudohallucination, 323b imaging for, 248b Retinopathies, 165
Pituitary gland, 200–201 Psoriatic arthritis, 255b OSCE example on, 249b–250b hypertensive, 165, 167f
Pituitary macroadenoma, 200f Psychiatric interview, 320 physical examination for, 243–246 Retraction pocket, of pars tensa, 176f
Pituitary tumours, 200 Psychiatric rating scales, 325 dialysis access, 243, 244f Retrobulbar neuritis, 156b
Pityriasis rosea, 286 Puberty, 312 face, 243–244 Rheumatoid arthritis, 255b
Place-and-step reflexes, 305, 306f stages of, 313f general appearance, 243–244 causing finger deformities, 265, 266f
Plagiocephaly, 300b timing of, 312f hands, 243, 243f Rheumatoid nodules, 257, 257f
Plan, 365 Puerperium, 225b skin, 244, 244f Rhinitis, with postnasal drip, 79b
382 INDEX
Thyrotoxicosis, 194, 197 Upper limb, 264–271 Ventral suspension, 305 Vitiligo, 26, 26f
Tics, 137 movements of, 267, 267f Ventricular tachycardia, 43, 43b Vitreous haemorrhage, 156b
Tietze’s syndrome, 80 peripheral arterial disease and, 68 Verbal communication, 365–374 Vocal resonance, 89
Timed Get Up and Go test, 335f respiratory disease and, 85, 85b, 85f Verrucous, 287b Vomiting. see Nausea and vomiting
Tinnitus, 173–174 see also specific parts Vertigo, 123, 174, 174b Vulva, 216
Tissue loss, 65 Upper motor neurone, lesions of, 134, Vesicle, 287b inspection of, 221f
Tone, motor system and, 137–138, 134b Vestibular function, testing of, 178–179
137b Uraemia, 242 Vestibulocochlear (VIII) nerve, 131 W
Tongue, 29 Uraemic fetor, 29 Vibration, sensory system and, 143–144 Weakness
ankyloglossia, 301 Urinalysis, 246–247, 247b Visceral abdominal pain, 96 facial, 132f
glossoptosis, 301 Urinary incontinence, 219, 220b, 336b Vision, examination of, in frail elderly, gait, 258
macroglossia, 301 Urinary symptoms, of male reproductive 334 joint, 255
Tonic-clonic seizure, 122 system, 231 Visual acuity, 160, 160b Weber’s test, 177, 177b, 177f
Torsion, of testis/ovary, in abdominal Urinary tract in frail elderly, 334 Weight, 29, 29b
pain, 97b female, 239f Visual fields, 162–163, 162b–163b, 163f Weight gain. see Obesity
Torus palatinus, 188f lower, functional assessment of, defects, 154f Weight loss, 29
Transient ischaemic attack, 123 247, 247b Visual loss, example of, 168b in gastrointestinal disorders,
Transient murmurs, 302 male, 238f Visual pathway, 153, 154f 94–95
Trauma, red eye and, 158b–159b see also individual parts Visual system, 151–165 in respiratory diseases, 81
Travel history, 16 Urine anatomy and physiology of, Wernicke’s area, 125
Tremor, 137 blood. see Haematuria 152–153, 152f Wheal, 287b
example of, 149b–150b investigations, 248b extraocular muscles, 152–153, Wheeze, 76–77, 89, 342b
Trendelenburg’s sign, 273, 273b, 273f jaundice and, 102b 152f–153f polyphonic, in children, 315
Tricuspid regurgitation, JVP and, 53b protein. see Proteinuria eye, 152, 152f Whispered voice test, 177, 177b
Tricuspid stenosis, JVP and, 53b test. see Urinalysis pupillary pathways, 153, 154f ‘Whispering pectoriloquy’, 89
Trigeminal (V) nerve, 128–130, Urine dipstick test, 246–247, 246f, refractive elements of eye, 153, ‘Whistling’ sounds, in wheeze, 77
128f–130f, 129b 247b 153f ‘White coat hypertension’, 50
Triggering, 255 Urological disease, investigations of visual pathway, 153, 154f Wind, 99
Trimester, 225b blood and urine, 248b history, 155–159 Winging, of left scapula, 269, 269f
Trisomy 21. see Down’s syndrome imaging for, 248b common presenting symptoms, Women. see Females
Trochlear (IV) nerve, 128 Urticaria, 286 155 Wood’s lamp, 292
Trousseau’s sign, 199f Urticaria pigmentosa, 289 drug and allergy history, 159 Word salad, 321b
Tubal pregnancy, in abdominal pain, Uterine examination, in later pregnancy, family history, 159 Wrist, 265–268
97b 228–229, 228f–230f past medical history, 159 assessing, 258f
Tuning fork tests, 177–178, 178b Uterus, 216–217 past ocular history, 159 examining, 268
Turbinate hypertrophy, 181f external prolapse of, 219f social history, 159 extra-articular signs of, 265
Turner’s syndrome (45XO), 36 Uveitis, 158b investigations for, 165, 168b history of, 265, 265b
Tympanic membrane abnormalities, acute anterior, 158b–159b physical examination of, 160–165 physical examination of, 265–268,
176f general examination, 160 265b–268b
Tympanosclerosis, 176 V ocular alignment and eye active movement, 266–267
Vagina, 216 movements, 163–164 feel, 266
U bleeding ophthalmoscopy, 160–165 look, 265
Ulcer, 287b abnormal, 217–218, 220b orbit and periorbital examination, move, 266–268
Ulcer-like dyspepsia, 95 in later pregnancy, 226–227 161, 161b, 161f passive movement, 267
Ulnar nerve, 146–147, 147b, 267–268, discharge in, 219, 220b pupils, 161–162 swelling, 265, 266f
267f Vaginal wall prolapse, 219f retinopathies, 165, 166f–167f Written communication, 374
Umbilical hernia, 303 Vagus (X) nerve, 131–132, 132b, 132f visual acuity, 160
Umbilication, 287b Varicocoele, 234 visual fields, 162–163, 163f X
Uncooperative patient, 320 Vasculitic rash, 244, 244f see also Eye disorders; specific Xanthelasma, 46f, 47
Undernutrition, 333–334 Vasculitis, 288, 289f parts Xerosis, 287b
Unexplained symptoms, medically, Veins, examination, in gastrointestinal Vital signs
363–364, 363b, 363f disorders, 104 in children, 314, 314b Y
Unterberger’s test, 179, 179b Vellus hair, 285 of deteriorating patient, 340 Yellow nail syndrome, 85, 85f