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Housestaff Manual: July 2020 - June 2021
Housestaff Manual: July 2020 - June 2021
Housestaff Manual
July 2020 - June 2021
Department of Medicine
Massachusetts General Hospital
Harvard Medical School
Boston, MA
Editors
Jacqueline Henson, MD
Alexandra Wick, MD
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The White Book is comprised of a collective of clinical experiences on the medical services as well as an annual review of the
literature. This book is a product of diligent work of many resident contributors (listed on the bottom of each page) as well as past
generations of authors and editors.
We extend our sincere gratitude to those junior and senior residents who contributed significant time and energy in editing entire
sections of this manual:
Cardiology: Shawn Li, Avanthi Raghavan Endocrinology: Max Petersen, Seth Tobolsky
Pulmonology & Critical Care: Robert Arao, Anna O’Kelly Allergy & Immunology: Jessica Plager
Gastroenterology: Ryan Flanagan, Sally Knooihuizen Neurology: Jeffrey Gluckstein
Nephrology: Daniel Gromer, Elizabeth Kurtz Psychiatry: Alexandra Wick
Infectious Disease: Rebecca Abelman, Hawra Al-Lawati Primary Care: Nate Alhalel
Hematology: Nora Abo-Sido Consultants: Jacqueline Henson, Alexandra Wick
Oncology: Leon Pappas, Vinayak Venkataraman Radiology: Sam Cartmell
Geriatrics & Palliative Care: Paige McLean Procedures: Sean Mendez, Chitra Mosarla
Rheumatology: Leslie Chang
We would like to thank the many faculty and fellows who assisted with this book, particularly Jonathan Dau for his work on the
Rheumatology section. In addition, we are grateful for the contributions from residents in the neurology and radiology programs.
Multiple sections have had significant updates and there are some new articles including: Infectious Disease – COVID-19;
Hematology – Anticoagulation Management; Allergy & Immunology – Mast Cell Disorders; Primary Care – Eye & Ear Complaints;
Consultants – OB/GYN; Logistics – Peri-Procedural Anticoagulation.
Our work would not be possible without the countless hours of work by the previous editors of the MGH Department of Medicine
Housestaff Manual. We hope we have lived up to their example:
1994 Albert Shaw & Ravi Thadhani 2009 David Dudzinski & Elizabeth Guancial
1995 Barry Kitch 2010 Roby Bhattacharya & Paul Cremer
1996 Sam Hahn 2011 Kerry Massman & Vilas Patwardhan
1998 Marc Sabatine 2012 Michelle Long & Mihir Parikh
2000 Sherri-Ann Burnett & Bill Lester 2013 Molly Paras & David Sallman
2001 Jose Florez 2014 Zaven Sargsyan & George Anesi
2003 Andrew Yee 2015 Ang Li & Jehan Alladina
2004 Ishir Bhan 2016 Nino Mihatov & Tessa Steel
2005 Aaron Baggish & Yi-Bin Chen 2017 Michael Abers & C. Charles Jain
2006 Bobby Yeh & Eugene Rhee 2018 Kelsey Lau-Min & Jonathan Salik
2007 Rajeev Malhotra 2019 Melissa Lumish & Shilpa Sharma
2008 Maha Farhat & W. Steve Sigler
And of course, none of this would be possible without the guidance and support of so many amazing people that make up the
Department of Medicine. In particular, we extend special thanks to Gabby Mills, Libby Cunningham, and Paula Prout for supporting
this project. In addition, we would like to thank our Chief Residents – Pierre Ankomah, Alyssa Castillo, Kelsey Hills-Evans, and
Aisha James – as well as Jay Vyas and Katrina Armstrong for their undying support and endless devotion to the housestaff and our
education. We will always be grateful for their unwavering leadership during the COVID-19 pandemic.
It has been an incredible honor to edit The White Book. We look forward to the contributions of future generations of authors and
editors in the years to come.
As with any other medical reference, this manual is NOT intended to provide specific clinical care decisions in an individual case,
and should NOT substitute for clinical judgment. Every clinical care decision must be made by the exercise of professional
judgment by the individual responsible for the care of a patient based on the facts of that individual case, which may differ from the
facts upon which entries in this manual are based. You should consult other references and your fellow residents, fellows, and
attendings whenever possible. We have carefully inspected every page, but errors may exist. If you find any errors, we would
appreciate it if you would inform next year’s editors (via this link: bit.ly/mghwhitebook) to make sure these errors are corrected.
MGH Housestaff Manual Table of Contents
CARDIOLOGY Sodium Disorders 94 Calcium Disorders 175
ACLS: Cardiac Arrest & Cooling 1 Potassium Disorders 95 Osteoporosis 176
ACLS: Bradycardia 3 Magnesium & Phosphorus Disorders 96 Thyroid Disorders 177
ACLS: Tachycardia 4 IV Fluids & Electrolyte Repletion 97 ALLERGY & IMMUNOLOGY
ACLS: Defibrillation, Cardioversion, Pacing 5 Urinalysis 98 Drug & Contrast Allergy 179
EKG Interpretation 6 The Nephron 99 Angioedema & Anaphylaxis 181
Narrow & Wide Complex Tachycardia 8 INFECTIOUS DISEASE Mast Cell Disorders 182
Atrial Fibrillation & Flutter 10 Empiric Antibiotics 100 Primary Immunodeficiency 183
QTc Prolongation 12 Gram Stain Interpretation 101 NEUROLOGY
Chest Pain 13 Multidrug Resistant Organisms 102 Altered Mental Status 184
Acute Coronary Syndrome 14 Community Acquired Pneumonia 103 Delirium 185
MI Complications 17 HAP/VAP & Aspiration Pneumonia 104 Dementia 186
Cardiac Catheterization 19 Viral Respiratory / Head & Neck Infections 105 Headache & Vertigo 187
Non-Invasive Cardiac Testing 20 COVID-19 106 Stroke & TIA 188
Echocardiography 22 Urinary Tract Infections 108 CNS Emergencies 190
Inpatient Heart Failure 23 Skin & Soft Tissue Infections 109 Seizures 191
Right Ventricular Failure 26 Osteomyelitis 110 Weakness & Neuromuscular Disorders 192
Pulmonary Artery Catheterization 27 Bacteremia & Endocarditis 111 Neuroprognostication 193
Mechanical Support & Transplant 28 Meningitis & Encephalitis 112 PSYCHIATRY
Cardiac Devices: PPM & ICD 29 C. Difficile Infection 113 Psychosis & Agitation 194
Valvular Heart Disease 30 Invasive Fungal Infections 114 Consent & Capacity 195
Pericardial Disease 32 Tuberculosis 115 Catatonia, NMS & Serotonin Syndrome 196
Aortic Disease 33 HIV/AIDS & Opportunistic Infections 116 Depression & Anxiety 197
Syncope 35 Transplant ID 117 Alcohol Use Disorder & Withdrawal 198
Hypertensive Urgency & Emergency 36 STIs & Travel Medicine 118 Opioid Use Disorder & Withdrawal 200
Peripheral Artery Disease / Cardio-Onc 37 Tick-Borne Diseases 119 Other Substance Use 201
Outpatient CV Health 38 Fever of Unknown Origin 120 PRIMARY CARE
Anti-Arrhythmic Medications 40 Rare Diseases 121 Health Screening & Maintenance 202
PULMONOLOGY & CRITICAL CARE Infectious Precautions 122 Women’s Health 204
Respiratory Distress 41 Vancomycin & Renal Antibiotic Dosing 123 LGBTQ Health 206
Hypoxemia & Hypercarbia 42 MGH Antibiogram 124 Immigrant & Refugee Health 207
Noninvasive Oxygenation/Ventilation 43 HEMATOLOGY Musculoskeletal Pain 208
Asthma 44 Anemia & Pancytopenia 125 Respiratory Complaints 210
COPD 45 Thrombocytopenia 127 Eye & Ear Complaints 211
Bronchiectasis & Hemoptysis 46 Eosinophilia 128 Nodules 212
Interstitial Lung Disease 47 Coagulation Disorders 129 CONSULTANTS
VTE 48 Anticoagulation Agents 130 Calling Consults 213
Pulmonary Hypertension 50 Anticoagulation Management 131 Perioperative Medicine 214
Mechanical Ventilation 51 Transfusion Medicine 132 Dermatology 216
ARDS 53 Transfusion Reactions 134 Surgery 219
ECMO 55 ONCOLOGY Urology 220
Sedation 56 Acute Leukemia 135 ENT 221
Shock 57 Lymphoma 137 Ophthalmology 222
Sepsis 58 Plasma Cell Disorders 138 OB/GYN 223
Vasopressors 60 MDS & MPN 139 RADIOLOGY
Toxicology 61 Stem Cell Transplantation 140 Contact Information 224
GASTROENTEROLOGY CAR T-Cell Therapy 143 Radiology Basics 225
Upper GI Bleeding 63 Solid Organ Malignancies 144 Contrast 226
Lower GI Bleeding 64 Chemotherapy & Toxicities 146 Protocols 227
GERD & Peptic Ulcer Disease 65 Immune Checkpoint Inhibitors 148 Interpretation of Common Studies 229
Nausea & Vomiting 66 Oncologic Emergencies 150 PROCEDURES
Diarrhea 67 Febrile Neutropenia 151 Ultrasound Basics 231
Constipation & Colonic Disorders 69 GERIATRICS & PALLIATIVE CARE Ultrasound-Guided Peripheral IV 233
Motility Disorders 70 Frailty & Polypharmacy 152 Central Line 234
Inflammatory Bowel Disease 71 Pain Management 153 Arterial Line 236
Intestinal Ischemia 72 Non-Pain Symptom Management 155 Intraosseous Line 237
Nutrition & Feeding 73 Adv Care Planning & Code Status 156 Paracentesis 238
Pancreatitis 74 End of Life & Pronouncement 158 Arthrocentesis 239
Liver Chemistry Tests 75 Organ Donation 159 Lumbar Puncture 240
Biliary Disease 76 RHEUMATOLOGY Thoracentesis 241
Acute Liver Injury & Failure 77 Approach to Rheumatologic Disease 160 Pericardial Drain 242
Viral Hepatitis 78 Arthritis 161 Fluid Analysis 243
Alcohol-Related Liver Disease 79 Connective Tissue Diseases 163 Tube Management 244
End Stage Liver Disease 80 Vasculitis 164 Exposures & Needle Sticks 247
Hepatorenal Syndrome 84 Miscellaneous Rheumatologic Diseases 166 LOGISTICS
Liver Transplant 85 Autoantibodies 167 Monitoring & Prophylaxis 248
NEPHROLOGY Rheumatologic Medications 168 Peri-Procedural Anticoagulation 249
Acute Kidney Injury 86 ENDOCRINOLOGY Senior On Encounters 250
Glomerular Disease 88 Outpatient Type 2 Diabetes 169 Post-Acute Care 251
Chronic Kidney Disease 89 Inpatient Diabetes Management 171 Formulas 252
Dialysis & Transplant 90 DKA/HHS 172 MGH Directory 254
Advanced Diuresis 91 Adrenal Insufficiency 173 NWH Directory 256
Acid-Base Disorders 92 Pituitary Disorders 174
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1
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Cooling Criteria
• Comatose (GCS<8, not following commands, no purposeful movements to noxious stimuli) within 6 hours of cardiac arrest
• Able to maintain a blood pressure +/- vasopressors +/- IABP following ROSC
Brad Petek
2
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Alexandra Wick
3
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NO YES
Drug Dosing
• Amiodarone: 150 mg IV over 10 min (may repeat x1); then infusion at 1 mg/min x6hrs followed by 0.5 mg/min x18h
(max 2.2 g/24 hours). May complete 10g load with up to 400mg PO TID.
• Lidocaine: 1-1.5 mg/kg IV bolus—usually 100 mg (may repeat 0.5-0.75 mg/kg q5-10min, max 3mg/kg); then
maintenance infusion at 1-4 mg/min; agent of choice when prolonged QT
• Procainamide: 20 mg/min until either VT ceases or hypotension or QRS duration prolongs by 50% from baseline or
total 17 mg/kg given (~1.2 g for 70kg person); then maintenance infusion at 1-4 mg/min (adjusted for CrCl); avoid in
prolonged QT
• Sotalol: 1-1.5 mg/kg IV over 5 min; then maintenance infusion at 10 mg/min; avoid in prolonged QT
• Adenosine: 6mg rapid IV push (followed by NS flush) 12 mg for second dose if required
Alexandra Wick
4
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Pearls:
- CPR ok to perform while pacing, take R-sided pulses (L not reliable)
- Failure to capture? Increase output, ensure pads are in correct location,
Manual consider ddx (barrel chest, COPD, tamponade/pericardial effusion, acidosis,
hyperK, obesity, MI, cardiac drug tox [dig, anti-arrhythmic])
- Failure to sense? Only happens with synchronous pacing – can switch to
asynchronous pacing, reposition pads
Andrew Abboud
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LAFB: left axis deviation, QRS <120, qR in I, aVL and rS in II, RBBB: QRS >120, rSR’ in V1, wide LBBB: QRS >120, wide negative QS
III, aVF. Common, nonspecific. qRS in V6, shallow broad S in I in V1, wide tall R in V6
LPFB: right axis deviation, QRS <120, rS in I, aVL and qR in
II, III, aVF. No alternate reason (RVH, emphysema, lateral MI,
PE). Rare to see in isolation, usually occurs with RBBB.
Bifascicular block: RBBB with either LAFB or LPFB
Paula Rambarat
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Other
• J-Point Elevation Syndromes: J point is when QRS transitions to ST segment
o Early repolarization pattern: benign STE in absence of chest pain, terminal QRS slur, or terminal QRS notch
Suspicious features: FH of sudden cardiac arrest or early unexplained death, eval and workup suggestive of
channelopathy, h/o unheralded sycnope suggestive of arrhythmogenic pathogenesis (Circ 2016;133:1520) Wellens Type B
o Brugada Syndrome: autosomal dominant SCN5A loss of function mutation in 10-30%, M>F, more common to have
nocturnal cardiac arrest, p/w VT/VF or sudden cardiac death (Circ Arrhythm Electrophys 2012;5:606).
o Osborn wave: hypothermia T<93ºF, elevation of J point height ~ proportional to degree of hypothermia
o Epsilon wave: found in ARVC, most specific in V1 (30% with ARVC), low frequency, positive terminal deflection in
V1-V3
• Electrolyte Abnormalities
Electrolyte Derangement Characteristic ECG Findings
Hypokalemia Prolonged QT, ST depression, flattened T wave, prominent U wave
Hyperkalemia Peaked, symmetric T wave, prolonged PR, flattened P and widened QRS (severe)
Hypocalcemia Prolonged QT, unchanged T wave
Hypercalcemia Shortened QT
Paula Rambarat
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Long RP Tachycardias
Short RP Tachycardias
Sinus Tachycardia
Junctional Tachycardia
• Gradual in onset
• Arises from increased automaticity in the AV junction
• Most important to determine underlying cause: hypovolemia,
• Usually short RP, can be no RP
hemorrhage, withdrawal (EtOH, BZD, opiate, BB), intoxication,
• If P waves present, must be negative in aVF
fever/infection, pain, hypoxemia, PE, anemia, tamponade,
dissection, hormonal (hyperthyroidism, adrenal insufficiency, Atrioventricular Re-entrant Tachycardia (AVRT)
pheo) • Arises from true re-entry via bypass tract
Atrial Tachycardia (AT) • Usually short RP, uncommonly long RP
• Single P morphology, non-sinus P wave axis • Ventricular activation via AV node (orthodromic, narrow
QRS) more common than accessory tract (antidromic,
• Arises from increased automaticity at single atrial focus
wide QRS)
• Classic digoxin toxicity is AT w/ variable AVB
• Rates usually 150-250
Multifocal Atrial Tachycardia (MAT)
Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)
• ≥3 P wave morphologies
• Arises from functional re-entry within AV node
• Irregular d/t varying PP, PR, and RR intervals
• Short RP (when conducting fast-slow), however more
• Seen in COPD, pHTN, CAD, electrolyte disarray, theophylline
commonly no RP (when conducting slow-fast)
Atrial Flutter (AFL) • Trigger PAC (slow-fast) > PVC (fast-slow)
• Arises from true (isthmus-dependent, typical) or functional • Young adults, F>M
(isthmus-independent, atypical) re-entry in R atrium
• PP interval constant but RR may vary (variable AV block) No RP Interval
• Counterclockwise: negative flutter waves in II, III, aVF
Atrial Fibrillation (AF)
• Clockwise: positive flutter waves in II, III, aVF
• No coordinated atrial activity (P wave absent), irregular
• Signature: no isoelectric baseline, atrial rate ~300, always
• Arises from numerous re-entrant tracts in atria or
>250, usually with 1:2 conduction
pulmonary veins
AVNRT vs AVRT
• Both are regular, paroxysmal, re-entrant NCTs w/ variable RPs that
terminate w/ adenosine/vagal/AV block
• Use baseline ECG, trigger, terminal activity to help distinguish
AVNRT: look for terminal pseudo-r’ in V1-2 (below) during
tachycardia that is absent on baseline ECG
AVRT: look for pre-excitation on baseline ECG (short PR or delta
wave/WPW), followed by a PAC which triggers NCT (QRS often
more narrow than baseline)
Andrew Abboud 8
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Polymorphic VT that
1. Non-sustained VT (>3 complexes, <30 secs) 1. Evaluate for ischemia & need for
occurs with underlying
nodal blockade (e.g. BB/CCB) revascularization
prolonged QTc (congenital
2. Stable and sustained (>30 seconds) 2. Stable magnesium 2-4g, HR
or acquired). Can be
antiarrhythmic agent (e.g. amiodarone) (dopa, epi, iso, overdrive pacing), QTc
prompted by PVC falling
3. Unstable synchronized cardioversion (100J) (lido), avoid bradycardia (amio, CCB/BB)
on T wave of previous beat
if pulse; defibrillation if pulseless 3. Unstable defibrillation
(R on T phenomenon)
Andrew Abboud 9
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Cardioversion (ALWAYS consider high risk of embolic stroke if any breaks in AC for one month prior)
• Indications: Urgent: ischemia, end-organ hypoperfusion, symptomatic hypotension, severe pulmonary edema; Elective: new-onset AF or
unacceptable symptoms from persistent AF
• Synchronized Electrical Cardioversion (DCCV): start with 150J (biphasic), increase energy in stepwise fashion if sinus rhythm not
achieved
o Use procedural sedation if possible (consult cardiac anesthesia). If elective, should be performed in ICU or EP lab.
o Consider anti-arrhythmic drugs as adjunct (e.g. amiodarone)
• Chemical Cardioversion: success rate significantly higher for acute (<7d) compared with longer duration AF
o Pill-in-pocket (flecainide, propafenone), dofetilide, ibulitide
o Amiodarone (IV infusion weakly effective for cardioversion, PO load over 3-4wk 27% rate of cardioversion)
• Anticoagulation (applies to BOTH chemical and electrical)
o Pre-procedure: if definitive new onset <48 hrs: may proceed without anticoagulation. If onset >48 hrs: must anticoagulate for 3 wks
prior to DCCV or obtain TEE immediately prior to DCCV (NEJM 2001;344:1411)
o Post-procedure: anticoagulate for at least 4 weeks after DCCV (due to myocardial stunning)
Long-Term Rate vs. Rhythm Control
• Overall, rate control is noninferior to rhythm control for AF symptoms, CV mortality, and stroke risk. (AFFIRM, RACE, PIAF, STAF, HOT
CAFÉ, AF-CHF).
o Consider rhythm control if persistent AF sx impairing quality of life, age <65, or comorbid HF (esp if systolic dysfxn). Restoration of
NSR may lead to increased quality of life and exercise performance (NEJM 2005;352:1861, JACC 2004;43:241).
Krishan Sharma
10
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Krishan Sharma
11
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Mubeen Shakir
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PTX PNA
Pericarditis NSTEMI STEMI Signs of PE
Diffuse upsloping 0.5mm STD or New ≥1mm STE in RAD, new RBBB,
STE and PR TWI (consider any 2 consecutive TWI V1-4, Widened
depression, PR leads compared to S1Q3T3 Normal
posterior infarct) mediastinum
elevation in AVR prior ECG or new suggestive of RV
LBBB strain (Sp, not Sn)
+/- hs-troponins
Consider PE, Consider non- Consider
valvulopathy, or cardiopulmonary Aortic
ACS Pathway myopathy etiology Dissection
Daniel Amponsah
13
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14
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15
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*Consider concomitant PPI therapy if patient on triple therapy or high-risk for GI bleeding
5Initiate at a dose of 0.75 mcg/kg/min (NO
Peri-operative P2Y12 Bridging
bolus) for a minimum of 48 hours and a
maximum of 7 days
6 600 mg loading dose of clopidogrel as soon
16
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Cardiology MI Complications
Mechanical Complications (JACC 2013;61:e78)
Cardiology MI Complications
Electrical Complications
• Overview
o Bradyarrhythmia/conduction block: may be due to coronary artery occlusion (see below) or Bezold-Jarisch reflex (Anes 2003;98:1250)
o Tachyarrhythmia: related to creation of re-entrant circuit from scar formation and/or automaticity from adrenergic surge
Second degree
Usually inferoposterior MI ( vagal Usually transient; observe
AV block: Usually within first 24h of MI
tone narrow QRS) Atropine if symptoms or HR < 45
Mobitz Type I
Second degree Usually anterior MI with infranodal Consider temporary pacing
AV block: conduction injury, wide QRS, HR Usually within first 24h of MI In infranodal block, atropine may
Mobitz Type II often < 30, 33% progress to CHB paradoxically worsen AV block
3-7% acute MI
If inferior MI: intra-nodal lesion; Recovery 3-7 days; temp pacing required
Inferior: gradual, stable, more
Third degree AV narrower QRS escape Inferior: more benign, resolves on own
common
block If anterior MI: infra-nodal lesion; Anterior: carries high mortality rate (80%)
Anterior: sudden, 12-24h
wide, unstable escape rhythm b/c indicates extensive necrosis
after MI
50% already present on 1st ECG, Pts w/ BBB are more likely to have
Intraventricular may represent antecedent disease comorbid conditions, less likely to have
2-5% of MI
Conduction Blocks of conduction syndrome received therapies, have larger area
Suggests more extensive infarct infarcts, and have high mortality
Undesirable b/c decreases coronary
Persistent sinus tach. may be
Sinus perfusion time, increases O2 demand,
Supraventricular
common in anterior MI
Treat underlying cause
Atrial premature
May reflect LA pressure
beats
Early: due to atrial ischemia 6-8%, may be >30% of acute Associated with mortality, particularly if
Atrial fibrillation
Late: due to atrial stretch/HF MI late (>30d) AF (Circ 2011;123:2094)
Premature Correct electrolyte deficits. Do NOT treat
Due to electrical instability and
Ventricular Variable with class I anti-arrhythmic a/w
increased sympathetic tone
Contractions mortality (NEJM 1991;324:781)
Accelerated 50-110bpm, higher V- vs. A-rate; in Up to 20% of STEMI Do not treat unless symptomatic or
Ventricular Tachyarrhythmias
Idioventricular 40%, considered a reperfusion Usually within 12-48 h, hemodynamically unstable, usually short
Rhythm (AIVR) rhythm occurs after reperfusion duration and does not affect prognosis
NSVT 1-7%, sustained VT
Monomorphic VT<170bpm is Antiarrhythmic agents
(2-3% of STEMI, <1%
unusual early after STEMI; Cardioversion/defibrillation as ppx
Ventricular NSTEMI)
suggests pre-existing against VF and restore hemodynamic
Tachycardia Usually 48h post STEMI, late
arrhythmogenic scar (mono VT) vs instability
VT (>48h) has very poor
recurrent ischemia (poly VT) Correct underlying abnormalities (pH, K)
prognosis
Risk factors: age, prior MI (scar),
ACLS/defibrillation
anterior MI, cardiogenic shock,
Ventricular 5% of STEMI Anti-arrhythmic infusion (24-48h
LVEF, CKD
Fibrillation 1% of NSTEMI amiodarone post-defibrillation)
VF >48h post-MI may indicate LV
Maintain K>4, Mg>2
dysfunction
18
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Anatomy
• LCA and RCA w/ their branches create two rings around the heart: RCA + LCX in AV plane; LAD + PDA in IV plane (see above)
• 80% of PDA arises from RCA (right dominant), thus inferior MI more likely due to RCA lesion
Preparation for Catheterization
• NPOpMN; INR<2; monitor Cr closely, no ppx abx. Continue ASA, statin, BB, heparin gtt (hold when on call) or lovenox (hold 24h prior
to cath; see Logistics: Peri-Procedural AC). Hold metformin (usually 1d pre-, 2d post-proc.). May need to hold/delay starting ACEi.
• Document bilateral radial, femoral, popliteal, DP pulses, and Allen’s test prior to cath. Check for bruit. Note hx of HIT, PVD, Ao
aneurysm/dissection.
• Contrast allergy: pre-treatment with steroids and benadryl if patient has documented allergy. See Radiology section for MGH 13h
protocol. Consult allergy service for expedited protocol if the cath is required emergently.
• Respiratory distress: patient will need to lie flat; consider intubation if prohibitive hypoxemia/pulmonary edema
• Pre-hydration w/ crystalloids and NAC/bicarb have not been shown to prevent CIN in most patients with moderate CKD (Lancet
2017;389:1312; NEJM 2018;378:603); CIN risk calculator; diagnostic cath = 25cc contrast (CT-PE = 80-100cc)
Percutaneous Coronary Intervention Considerations
• Access: fewer bleeding/vascular complications if radial (vs. femoral), possible death in ACS (JACC 2018;71:1167)
• BMS vs DES: in-stent thrombosis with DES subsequent revascularization; however, risk of late stent re-stenosis
requires longer duration of DAPT
• Contraindications to stents: predicted DAPT non-adherence, anticipated major surgery within treatment time, elevated bleeding risk
• Antiplatelet Tx: 81 mg ASA indefinitely (Circ 2016;134:e123). P2Y12 inhibitor added after cath.
o No high bleeding risk: for ACS, 12 mos of DAPT (DES or BMS); for stable ischemic heart disease, at least 6 mos of DAPT (DES)
or 1 mo (BMS)
o High bleeding risk: for ACS, 6 mos of DAPT (DES or BMS); for stable ischemic heart disease, at least 3 mos of DAPT (DES) or 1
mo (BMS)
o Triple therapy: See ACS section
Post-Procedure Care
• Groin access: 4-6 hrs bedrest after procedure. Closure devices decrease time needed for bedrest.
o Groin checks immediately post- and 6h, 8h post-procedure: check bilateral pulses, palpate for pulsatile masses, auscultate
for bruits
o Sheaths: during pass-off, ask interventional fellow about timing of arterial removal; only cardiology fellows remove sheaths
Radial access: TR band x 4-6h
Post-Catherization Complications
• Access site complications: always inform the interventional fellow who performed the procedure, diagnose by exam and U/S
o Hematoma: mass w/out bruit. Apply compression. If unable to control, may require Fem-Stop device to apply external pressure.
o Pseudoaneurysm: presents as pulsatile mass with bruit at access site. Treat with compression; if <2 cm, may require thrombin
injection or surgery if >2 cm. Urgent U/S and vascular surgery consult.
o AV fistula: presents as continuous bruit with no mass. Evaluate w/ U/S. Surgical repair is usually necessary.
o Limb ischemia: from thrombus, dissection, or malpositioned closure device. Evaluate pulses, limb warmth, and PVRs.
o Retroperitoneal bleed: presents within hours post-cath, often with hemodynamic instability +/- flank pain +/- ecchymoses.
STAT CT A/P if stable. Transfuse, IV fluids, discussion with attending re: stopping/reversing anticoagulation.
• Other complications:
o Infection: more common in setting of vascular closure devices
o Atheroembolism: eosinophilia; livedo reticularis; blue toes; mesenteric ischemia; acute, subacute, or chronic renal dysfunction
o CIN: peak Cr 2-5d post contrast load, risk correlated with contrast load and initial GFR
o Tamponade: post-cath hypotension from coronary or cardiac perforation. Check pulsus paradoxus (Δ >10mmHg), STAT TTE,
alert cath fellow. Give IVF.
o MI/CVA: due to in-stent thrombosis (MI) or distal embolization post-cath (CVA). Discuss all CP/neuro changes with cath fellow
o Radiation injury: more common in CTO cases. Occurs days to weeks after PCI. Ranges from erythema to skin ulceration.
Shauna Newton
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VIABILITY TESTING
• Indication: determine viability of ischemic myocardial tissue (“hibernating myocardium”)
• Imaging modalities: SPECT (thallium or sestamibi), PET, TTE, MRI
o SPECT is performed using exercise or pharmacologic stress. PET/TTE/MI performed using pharmacologic stress only.
REST IMAGING
Coronary CTA: used to evaluate for presence and extent of CAD (JACC 2010;55:2663)
• Requires cardiac gating (goal HR 60-70, may need to give BB) and respiratory gating (breath hold for 5+ sec)
• Indications:
o Should NOT be used to screen asymptomatic pts
o Low risk pts: has high NPV (99%) for CAD rule-out (JACC 2008;52:1724)
o Moderate risk pts: reasonable for further risk stratification in pts at intermediate risk of CAD or pts with equivocal stress test
results
• Findings: 2 yr ACS risk significantly elevated if high-risk plaque (16%) and/or stenotic disease (6%) (JACC 2015;28:337)
o Higher sensitivity and specificity for coronary stenosis compared to cMRI (Annals 2010;152:167)
• Less useful in pts with extensive calcifications or stented vessels due to “blooming” artifact (can’t evaluate patency)
Cardiac MRI:
• Modality of choice for assessment of funtional and tissue properties of the heart than cannot be adequately assessed with
echocardiography or CCTA (inflammation, infiltration, cardiac tumors, pericardial disease)
• Preferred for post-CABG vessel imaging, evaluation of suspected or known congenital or acquired coronary abnormalities
Shauna Newton
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Cardiology Echocardiography
View/Description Position View
Patient: lying on left side, with left arm under head.
PARASTERNAL LONG AXIS Probe: 2-3 inches left of sternum at 3rd-4th intercostal
• LV size, function, wall thickness space, probe indicator at 10 o’clock (facing R shoulder).
(septum/posterior wall)
• MV/AoV function/flow (w/
Doppler)
• LVOT diameter, aortic root size
Reviewing the MGH Report: for questions or clarification of findings, call Echo Lab (x6-8871) or page on-call Echo Fellow
• Valvulopathy: look for stenosis/regurgitation (valve area, gradients, severity), leaflet numbers/motion, vegetations
• Structure/chamber dimensions:
AoSinus = aortic sinus ASC AO = ascending aorta
LVIDd = LV internal diameter in diastole (range 37-52 mm) LVIDs = LV internal diameter at end-systole (range 22-35 mm)
PWT = posterior wall thickness ( thickness seen in LVH, IVS = intraventricular septum (if along with PWT, consider diastolic
diastolic dysfxn) dysfunction; if isolated consider HOCM)
• EF: “preserved” EF ≥50%, “borderline” EF 40-50%, “reduced” EF <40%
• WMA: territory correlates w/ coronary vessels (anterior + septal = LAD, inferior = RCA, lateral = LCx). If global WMA, r/o diffuse ischemia vs non-
ischemic insult (sepsis, stress)
• RVSP: RVSP=4v2 + RAP. RAP assumed to be 10 mmHg (often not clinically accurate) and v = TR jet velocity.
o Clinically, often used as surrogate marker for pHTN (present if >35; not gold standard for dx and requires euvolemia)
Clinical Questions and Associated TTE Findings:
• Right heart strain in acute PE: RV WMA or hypokinesis, RV dilation (RV:LV ratio >1), interventricular septal bowing, IVC collapse
o McConnell’s sign: RV free wall akinesia w/ normal RV apex motion (77% Sn / 94% Sp for acute PE)
o D sign: septal flattening due to overloaded RV bowing into LV (ventricular interdependence)
• Tamponade: large effusion, swinging heart, R-sided chamber collapse, interventricular septal bowing, dilated IVC (no w/ inspiration)
• ACS/mechanical complications of ACS: regional WMA, septal/free wall rupture, acute MR, LV thrombus
• Stress (Takotsubo) cardiomyopathy: LV apical ballooning and akinesis/hypokinesis
• Heart failure: depressed EF, RV/LV hypertrophy and/or dilation, regional WMA
• Constrictive pericarditis: thickened or hyperechoic pericardium, abnormal septal motion, respiratory variation in ventricular size, dilated IVC
Indications for STAT Echocardiography:
• Evaluation of hemodynamic instability of suspected cardiac etiology (assess for biventricular dysfunction, acute valvular dysfunction, tamponade)
• Evaluation of early MI complication (myocardial free wall, septal, or papillary muscle rupture)
• Evaluation of acute chest pain with suspected MI in patients with non-diagnostic lab markers and ECG
• Identify the cause of cardiac arrest (i.e. PE with RV dysfunction, ACS with WMAs or EF decrement, tamponade)
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Tailored Therapy: uses invasive hemodynamic monitoring (i.e. PAC) to guide medical therapy
• Goals: tissue perfusion ( CO, MAP), decongestion ( CVP, PCWP), ventricular unloading (minimize myocardial O2 demand)
1. Preload: LVEDV ∝ LVEDP ≈ PCWP; goal PCWP 14-18, PAD 16-20, CVP 8-12
o Diuresis, UF with RRT, or TNG
2. Afterload: wall stress ∝ MAP (Laplace’s law); SVR = (MAP - CVP)/CO; goal MAP >60, SVR <800-1200
o Vasodilators: captopril, hydralazine, nitroprusside, TNG, IABP
o Vasopressors: afterload but sometimes necessary to stabilize MAP in mixed shock or to counteract vasodilatory effect
of inodilators
3. Contractility: ∝ CO for given preload/afterload; goal CO>4, CI >2.0-2.2, MvO2 >65
o Dobutamine (inodilator): β1>β2 agonist ( production of cAMP)
• Watch for tachycardia, increased ventricular response to AF, arrhythmias, ischemia, HoTN, tachyphylaxis in
infusions >24-48 hrs
o Milrinone (inodilator): PDE-3 inhibitor ( breakdown of cAMP)
• Watch for tachycardia, arrhythmias, ischemia, HoTN. Compared to dobutamine, milrinone has longer half-life,
greater pulmonary vasodilatation, slightly less chronotropy, fewer arrhythmic events.
• Preferred in patients on βB and w/ RV failure. Is renally cleared. Often choice for home inotrope for palliative therapy
o Epinephrine, norepinephrine, dopamine (inopressors): use if severe HoTN, unable to tolerate inodilators
• Watch for tachycardia, arrhythmias, end-organ hypoperfusion
4. Advanced: consideration of need for mechanical circulatory support or transplant
o Goal of mechanical circulatory support: improve systemic perfusion while reducing myocardial oxygen demand (in
contrast to inotropes which CO at the expense of increased oxygen demand)
o Types of MCS at MGH: IABP, Impella, VAD, VA-ECMO (see MCS & Transplant) – if considering, obtain SHOCK c/s
(p11511)
• Limitations:
o CO measured via thermodilution or calculated using Fick equation: CO = VO2/(13.4 x Hgb x [SpO2-MvO2]); CI = CO/BSA; VO2
estimate = 125 x BSA
Thermodilution: uses temp gradient between two points on PAC. Less reliable if shunt/valvular insufficiency (e.g. TR)
Fick equation: assumes a VO2 (oxygen consumption) that in reality varies depending on physiologic state (e.g. infxn)
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Heart Transplant
2018 UNOS Adult Heart Allocation Criteria:
Status 1: VA-ECMO, MCS with life-threatening vent. arrhythmia; Status 2: non-dischargeable LVAD, MCS + device malfunction, IABP;
Status 3: ≥2 inotropes or single high-dose + continuous hemodynamic monitoring, dischargeable LVAD for discretionary 30 days, VA-
ECMO after 7d, IABP after 14d; Status 4: re-transplant, inotropes without hemodynamic monitoring, dischargeable LVAD without
discretionary 30 days; Status 5: awaiting dual organ Tx; Status 6: all others; Status 7: inactive listing
Transplant evaluation at MGH: (orders are typically placed by transplant coordinators)
• Labs: blood typing (2 samples on separate days), second sample for PRA (check with tissue typing x63722), BMP, LFTs, amylase,
CBC+diff, INR/PTT, TFTs, lipids, PTH, 25-OH-D, 1,25-Vit-D, HIV, CMV, Toxo Igs, EBV, VZV serology, MMR, RPR, hepatitis
serologies, IGRA, UA, 24h urine CrCl (and 24h urine protein if diabetic)
• Vaccines: HBV, PPSV23, Tdap
• Consults: Psychiatry (Dr. John Purcell), SW (Kathryn Tsagronis), Tx coordinators (Sally Keck, Coral Haggan, Kerry Gaj, Karen
Turvey – they can all consent patient for Tx), Dental (Panorex, inpatient consult), Nutrition, Endocrine, Palliative Care
• Diagnostics: RHC (eval for presence & reversibility of pHTN with vasodilator challenge; if unsuccessful vasodilator challenge, note
that PVR often declines after 24-48h of treatment [e.g. diuretics, inotropes, vasoactive agents]), +/- LHC, level 1 CPET (x4-7825),
abdominal U/S, carotid U/S, TTE, ECG, CXR, DXA, ABIs +/- angiography, cancer screening up-to-date
Post-transplant immunosuppression: steroids (typically tapered off over 6 months, 1st line for acute rejection), calcineurin inhibitors
(cyclosporine/tacrolimus), anti-proliferatives (azathioprine/mycophenolate), mTOR inhibitors (sirolimus/everolimus – most effective for
coronary allograft vasculopathy; avoid in immediate post-tx phase as inhibit wound healing)
Monitoring: protocolized schedule of RV biopsies to r/o cellular/humoral rejection, RHC/LHC and TTE to assess graft function and for
coronary artery vasculopathy
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Hardware Overview: system consists of pulse generator + leads. Usually Position I Position II Position III Position IV
implanted SQ in upper chest (L>R) >> abdominal. Chamber(s) Chamber(s) Response to Rate
• Types: traditional (SQ pulse generator + IV leads in ventricle), leadless Paced Sensed Sensing Modulation
(pulse generator directly implanted into RV; no pocket complications; when O = None O = None O = None O = None
battery dies, device retrieval is rare), SQ ICD (no IV hardware; low risk for A = Atrium A = Atrium T =Triggered
R = Rate
infection but NO pacing capabilities) Modulation
• Placement: RA lead RA appendage; RV lead RV apex; LV lead V = Ventricle V = Ventricle I = Inhibited
coronary sinus branches of great cardiac vein D = Dual D = Dual D = Dual
(A+V) (A+V) (A+V)
• Interrogation: page EP Technician (PPM, p16939) during normal business
hours; EP fellow on call if after-hours/weekend.
• MRI compatibility: not all devices are MRI Code Action Use
compatible, however even non-MRI compatible Single Chamber Modes
devices may be safe to scan after re-programming Atrial Demand; atrium paced, atrium Isolated SN dysfxn,
AAI
(NEJM 2017;376:755). Determined on case-by-case sensed, atrial activity inhibits PM intact AV node
basis by radiology. Need to know device model. High-grade AV blocks,
Ventricular Demand; ventricle paced,
bradycardia; does not
VVI ventricle sensed, ventricular activity
track atrial activity (i.e.
PPM Indications (Class I): (JACC 2013;61:e6) inhibits PM
chronic AF)
Sinus Node Dysfunction: Asynchronous; atrium or ventricle Obsolete (AOO), Temp
• Symptomatic sinus bradycardia (± sinus pauses) AOO / VOO
paced, no sensing wire pacing (VOO)
or chronotropic incompetence Dual Chamber Modes
• Symptomatic medication-induced bradycardia if Tracking Modes
medication (e.g. βB) is required for underlying Allows coordination of
Synchronous; paces and senses in
medical condition A and V pacing; most
DDD atrium and ventricle; atrial activity is
AV Block (AVB)/Conduction Disease: closely mimics intrinsic
tracked/triggers ventricular activity
conduction system
• Symptomatic 2° AVB or 3°AVB
Atrial Synchrony Possible; ventricle
• Asymptomatic 2° AVB Mobitz II or 3° AVB with: Rarely used; high-
VDD paced, atrium and ventricular activity is
asystole ≥3 sec (≥5 seconds if in AF), escape grade AV block
sensed
rate ≤ 40 BPM (or >40 BPM if cardiomegaly also Non-Tracking Modes
present), or wide-complex escape rhythm AV Sequential; paces and senses in
SSS or sinus brady
• Permanent 2° AVB Mobitz II or intermittent 3° AVB DDI
atrium and ventricle; atrial activity not
with intermittent atrial
(regardless of symptoms) tracked; atrial tachyarrhythmia does not
tachycardias
• Alternating bundle branch block trigger RVR
Neurocardiogenic: Avoid sensing
Asynchronous Fixed Rate; paces electrocautery or
• Recurrent syncope AND inducible asystole ≥ 3 sec DOO
atrium and ventricle, no sensing electromagnetic
with carotid massage interference
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• ACC/AHA: one-time abdominal U/S in all men • General population: not recommended
>60 w/ FHx of AAA (IIC) and all men >65 that • Indications: at time of dx of Marfan (IC), Turner (IC),
have ever smoked (IA) Loeys-Dietz, Takayasu or GCA. 1° relatives of pt w/
• USPSTF: one-time abdominal U/S for men TAA, dissection, bicuspid valve (IB/IC)
age 65-75 who have ever smoked (Grade B) • Surveillance: if aneurysm only, then same as AAA. If
Screening/ and selective screening for male never also with dissection, image at 1, 3, 6, & 12 months then
Surveillance smokers 65-75 (Grade C). Screening women annually. Image entire aorta (CT/MRI) if multiple
not recommended. aneurysms (~25% TAA will have AAA; ~25% AAA will
• Surveillance: have TAA).
o 3-3.4 cm: U/S q3y
o 3.5-4.4 cm: U/S or CT q12mo
o 4.5-5.4 cm: U/S or CT q6mo
• Abdominal U/S: screening and surveillance of infrarenal AAAs. High Sn/Sp (>90%), operator-dependent
• CT w/ contrast: high Sn/Sp, better than U/S for suprarenal AAAs
Imaging
• MRI/MRA: good Sn/Sp, preferred for aortic root imaging and for imaging tortuous aortas
Modalities
• CXR: “enlarged aorta” nonspecific (tortuous aorta vs. aneurysm)
• TTE: useful for root and proximal thoracic aorta; TEE: will visualize entire thoracic aorta but rarely used.
Medical Medical
• Smoking cessation (slows AAA growth by up • Reduce BP (<140/90 or <130/80 if DM or CKD; little
to 25%) actual evidence, IB)
• Reduce BP in accordance with ACC/AHA • Meds: BBs (decrease TAA growth in Marfan pts), ARBs
standards (slow aortic root aneurysm in expansion in Marfan pts,
• Meds: statins (reduce all-cause mortality in likely via TGF-β inhibition), statins (goal LDL<70)
pts s/p surgery); BBs (may slow expansion; IA • Smoking cessation
for perioperative use); ACEi (controversial; • Avoid straining
Treatment may prevent rupture but may speed growth); • Stress test used to guide BP management (follow SBP
low dose ASA (may slow growth) response to stress)
Surgical Surgical
• Men: >5.5cm OR growing >0.5cm/yr OR sx • Root/ascending TAAs: usually concomitant aortic valve
Women: >4.5-5cm (controversial) replacement
• Open repair (~4-6% 30 day mortality) vs. • Arch/descending TAAs: mostly open graft (EVAR).
EVAR (only ~50% suitable, c/b endoleaks) Ischemic brain/spine injury most worrisome
complication.
• Rupture: devastating mortality. AAA annual rupture rates are 4%, 7%, 20% at 5, 6, and 7cm, respectively.
Risk factors: size, rate of expansion, female gender.
Complications Sx: triad of abd/back pain + pulsatile abd mass + HoTN immediate OR (don’t image)
• Dissection: pain (chest/abdomen/back), occlusion of aortic vessels, thromboembolism
• Post-repair: EVAR: endoleak, graft failure, thrombosis. Open: MI, embolization, AKI, ischemic colitis
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Cardiology Syncope
Overview:
• Definition: transient (self-limited) loss of consciousness due to cerebral hypoperfusion that is associated with loss of postural tone,
followed by complete spontaneous recovery; excludes metabolic causes (e.g. hypoglycemia, hypoxia, intoxication)
• Risk assessment and need for hospitalization:
o High-risk symptoms: preceding palpitations, exertional syncope, bleeding, syncope while supine, lack of prodrome, trauma
o High-risk features: angina, CHF, mod-severe valvular or structural heart disease, ECG features of ischemia/arrhythmia, FHx of
SCD, preexcitation syndromes, high-risk occupation (e.g. airline pilot)
o Risk calculators (e.g. SFSR, SRS) have high NPV (>95%) but do NOT replace clinical judgment
San Francisco Syncope Rule (SFSR): admit pt if >1 of: EKG changes or non-sinus rhythm, dyspnea, Hct<30, SBP<90, HF
• Ddx: seizure, metabolic causes (hypoglycemia, hypoxia), intoxication, vertebrobasilar TIA, fall, psychiatric
Etiology and Diagnosis: 2017 AHA/ACC/HRS Syncope Guidelines
Etiology Historical Features Diagnosis Treatment
Reflex (60%) Vasovagal: prodrome of dizziness, • Vasovagal: can dx w/ tilt table test • Avoid provocative stimuli
• Vasovagal nausea, warmth, diaphoresis, (Class IIa) (Sn 32-85%, Sp 90%) • Isometric counterpressure
• Situational pallor; a/w intense emotion, pain, (JACC 1996;28:263) maneuvers of the limbs
• Carotid sinus or stress. • Carotid sinus syncope: diagnose via carotid (e.g. leg crossing, hand
syncope Situational: cough, sneeze, laugh, sinus massage (if no underlying bruits or grip, Valsalva, squatting)
micturition, defecation CVA history) • Meds used in select cases
CSS: neck only (i.e. midodrine,
turning/surgery/irradiation fludrocortisone, βB).
(NEJM 2005;352:1004)
Orthostasis (15%) Prodrome of dizziness, nausea, • Orthostatic vital signs (systolic 20mmHg • Primary: fludrocortisone
• Autonomic failure warmth, diaphoresis, pallor. or diastolic 10mmHg within 3 min of (0.1-0.2mg QD),
(1° or 2°) Risk factors for autonomic failure: standing) midodrine (5-20mg TID),
• Drug-induced - 1°: PD, Lewy body, Shy-Drager - HR is NOT part of definition pyridostigmine, droxidopa
• Volume - 2°: DM, amyloid, spinal cord • Consider: Hct, A1C, SPEP if c/f amyloid, (for PD-associated
depletion injury, chronic EtOH, Lyme, RPR, B12 orthostasis)
syphilis, B12 deficiency, meds • Secondary: treat
(vasodilators, diuretics, BB, TCAs, underlying etiology, replete
PD meds, opiates, α-blockers) volume, d/c culprit meds
Cardiac (15%) No prodrome, syncope while in • Causes of cardiac syncope in young people • Based on etiology, follow
• Arrhythmia sitting or supine position, (+ ECG signs): guideline-directed
• Structural (AS, palpitations, FHx or personal 1. WPW (delta wave) management and therapy
LVOT obs.) history of heart disease 2. HOCM (LVH, apical TWI)
• Obstruction 3. Brugada (pseudo-RBBB with
(e.g.,PE, coved/saddleback pattern in V1-V2)
tamponade) 4. Long QTc syndrome (QTc >500ms)
• Dissection 5. ARVC (Epsilon wave)
• Consider cardiac monitoring on basis of
frequency and nature of syncope events
(inpatient telemetry, Holter, Zio patch,
implantable cardiac monitor).
• ONLY consider TTE if hx suggestive of
cardiac cause (<1% yield if no underlying
heart disease and normal ECG)
• Consider PE if no other apparent cause
identified in 17.3% of pts hospitalized with
1st syncope episode (and 25.4% of pts with
no other apparent cause for syncope)
(NEJM 2016;375:1524)
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TREATMENT:
• Supplemental oxygen therapy (see Oxygen Delivery Therapies section for more detail):
o NC: for every liter increase in O2, FiO2 0.03/L (max: 6L = 0.40 FiO2)
o Venturi masks: pre-set FiO2 (0.24, 0.28, 0.31, 0.35, 0.40) (flow rate decreases with increasing FiO2)
o NRB: can give FiO2 ~0.90, but in tachypneic patient, FiO2 ~0.60 (due to entrainment of room air)
o HFNC: FiO2 0.6 to 1.0 at 10-60 L/min (humidified air); 90-day mortality vs. NIPPV for pts with hypoxemic respiratory
failure not due to pulmonary edema or obstructive lung disease (NEJM 2015;372:2185)
• NIPPV (BIPAP for COPD; CPAP for CHF): RR >25-30, accessory muscle use, pH <7.35, PaCO2 >45mmHg
• Intubation: See red flags above
Rapid Response x6-3333 (Senior On, nursing supervisor, RT, pharmacy) | STAT page RICU x6-3333
• RICU communication guide: have information ready for RICU prior to intubation; greet RICU in patients’ room
Code status Urgency/acuity of decline
Hemodynamics – LV, RV, valves, volume status, access Difficult airway (look for prior intubation notes)
Aspiration risk – NPO status, last meal, risk factors Allergies
• Have ready: sedation (propofol/fentanyl/versed), pressor (Neo >> Levo), IV fluids w/ push line; RICU brings paralytic
• MICU/CCU: Resource RN will call for RICU; make sure attending/OI, fellow, RT and RN are aware of plan
• INTUBATION IS NOT AN ACT OF WEAKNESS: do not delay intubation in patients with impending respiratory failure
O2 sat (%)
PaO2 (mmHg)
P:F Ratio
Quick surrogate for A-a gradient
Can’t use if significant pCO2
P=PaO2 / F=FiO2
P:F<300 = mild ARDS
P:F<200 = moderate ARDS
P:F<100 = severe ARDS
BiPAP/HFNC on the floor: huddle with nursing and RT (also notify Senior On). Trial BiPAP or HFNC no more than 2-3
hours and assess response; consider ABG/VBG to assess change in oxygenation or ventilation. If no improvement,
discuss escalation of care to ICU.
REMEMBER: BiPAP/HFNC should NOT be used to delay intubation!
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PERT (x47378): call if large PE w/ abnormal VS (tachycardia, hypotension), evidence of RH strain (TTE, EKG, biomarkers),
central/saddle PE. Order (if not already obtained): CBC w/ diff, BMP, LFTs, lactate, D-dimer, ABG, PT/INR, PTT, T&S, NT-
proBNP, hs-troponin, EKG, CT-PE protocol, LENIs, TTE.
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WHO Functional Classes: similar to NYHA for CHF & guides intensity of therapy. Class I = asx w/ ordinary activity, class II = sx w/
ordinary activity, class III = sx w/ minimal activity, class IV = sx at rest.
Management: Treat underlying etiology: CTD, CHF, hypoxemia (O2), VTE, etc. Advanced therapies (see below): guided by WHO
functional class (reserved for II-IV). Most evidence in Group 1. Surgery: pulmonary thromboendarterectomy (CTEPH), atrial septostomy
(R L shunt), lung txp in select pts. General: exercise/pulm rehab, O2, diuresis (for RHF), contraception in ♀
Mechanism Medication Route Indication Side effects
Endothelin Bosentan, Group 1: sx, 6MWT (NEJM 2002;346:896, Circ Anemia, PNA, edema, hepatotox.
receptor ambrisentan, PO 2008;117:3010) Macitentan: also flu, HA, UTI,
antagonists macitentan Macitentan: morbid/mortality (NEJM 2013;369:809) bronchitis
Group 1: sx, 6MWT (NEJM 2005;353:2148, Erythema, flushing, indigestion,
PDE5 inhibitors:
PO NEJM 2009;361:1864) HA, insomnia, epistaxis, rhinitis,
sildenafil, tadalafil
(NO)-cGMP retinal hemorrhage
enhancers Group 1 & Group 4: sx, 6MWT (NEJM BP, n/v/d/constipation, GERD,
sGC stimulator:
PO 2013;369:330) anemia, dizziness, HA,
riociguat
hemorrhage
Analogues: IV or inh.; Group 1: 6MWT, QOL; reserved for sickest CP, BP, HR, flushing, abd pain,
Prostacylin epoprostenol, treprostinil patients (NEJM 1996;334:296) anorexia, n/v/d, jaw pain, MSK
pathway treprostinil, iloprost also SC Group 5: some etiologies pain, dizziness, HA, hemorrhage
agonists Receptor agonist: Group 1: hospitalization; no Δ mortality (NEJM Diarrhea, nausea, jaw pain, HA,
PO
selexipag 2015;373:2522) anemia
Positive vasoreactivity test (mPAP by ≥10 BP, LE edema
CCB Nifedipine, diltiazem PO
mmHg & to ≤ 40 mmHg w/o CO). RV failure.
• Per CHEST guidelines: If WHO FC II or FC III w/o rapid progression, start w/ ambrisentan/tadalafil combo (pref. over monotx w/ ERA,
PDE5i, or riociguat; NEJM 2015;373:834). If FC III w/ rapid progression or FC IV, start w/ IV prostanoid. If unacceptable clinical status,
add 2nd/3rd class (Chest 2019;156:187).
Ventilator Complications:
• Dynamic hyperinflation (auto-PEEP): due to incomplete alveolar emptying during expiration; measured during expiratory hold
o Diagnosis: end-expiratory flow >0 (residual pressure); see graphic Auto-PEEP (Adapted from Medscape)
o Risk factors: vent strategy causing hyperinflation (high RR, I:E ratio)
or obstructive disease (asthma, COPD, CF)
o Consequences: adverse hemodynamic effects (hypotension due to
venous return), alveolar over-distention (volu-/barotrauma); effort
for pt to trigger ventilator-assisted breath
o Treatment: allow longer exhalation ( I:E ratio, RR), set exogenous
PEEP to 2/3 auto-PEEP, bronchodilators for obstruction
o If severe hemodynamic or resp. compromise, transiently disconnect pt
from ventilator and manually bag ventilate to allow deflation
• Ventilator-induced lung injury (VILI): alveolar injury alveolar permeability, interstitial & alveolar edema, alveolar hemorrhage,
hyaline membranes, & alveolar collapse (similar to ARDS) (NEJM 2013;369:2126). Avoid w/ lung protective ventilation (see ARDS).
o Volutrauma: over-distension of alveoli due to high VT; or, if there is heterogenous consolidation or atelectasis, a disproportionate
volume from each breath is delivered to open alveoli
o Atelectrauma: shear forces from cyclic alveolar recruitment and de-recruitment injure adjacent alveoli/airways
o Biotrauma: cytokine release from lung epithelium multi-organ dysfunction
o Oxytrauma: elevated FiO2 free radical production and lung injury
o Barotrauma: injury from high Pplat (highest risk >35) PTX, subcutaneous emphysema, pneumomediastinum
• Other complications: ventilator-associated pneumonia, laryngeal edema, tracheal stenosis
Air leak PE
increased (eg, >40)
↓airway resistance extrathoracic process
Pplat
normal increased (eg, >30)
↑airway resistance = PIP – Pplat (nl <10) ↓ lung compliance =
VT
(nl >60)
Pplat −PEEP
- Bronchospasm
- Asynchronous breathing
- Secretions
- Auto-PEEP - Pulmonary edema
- Aspiration
- Pneumothorax - PE
- Ventilator tubing problem
- Pneumonia - ILD
Monitoring Mechanics
• Target values: VT ≤6cc/kg IBW, Pplat ≤30; driving pressure (ΔP = Pplat-PEEP) ≤15; compliance >50; resistance <10
o Non-ARDS: VT 10cc/kg vs 4cc/kg no difference in mortality or vent-free days (PReVENT JAMA 2018;320:1872)
• Ventilator maneuvers for monitoring mechanics:
o Expiratory hold: end expiratory pause; measures auto-PEEP
o Inspiratory hold: end inspiratory pause; measures Pplat and compliance
At end-inspiration, resistive pressure is 0 and PIP = Pplat
Liberation & Extubation (ATS/CHEST: AJRCCM 2017;195:115 & Chest 2001;120:375S; NEJM 2012;367:2233; ERJ 2007;29:1033)
• Requirements for extubation: (1) adequately treated underlying disease process, (2) adequate oxygenation and ventilation:
PaO2/FiO2 ≥150-200, PEEP ≤5-8, FiO2 ≤0.4-0.5, pH >7.25, (2) ability to cough, (3) able to manage secretions, (4) hemodynamic
stability. Ideally sufficient mental status (alert, following commands), but as long as protecting airway, AMS does not preclude
extubation.
o Rapid Shallow Breathing Index (RSBI) = RR/VT; RSBI >105 predicts extubation failure (Sn>Sp) (NEJM 1991;324:1445)
• Liberation protocol:
o Daily Spontaneous Awakening Trial (SAT) + Spontaneous Breathing Trial (SBT)
SAT: ventilator time, ICU LOS, and mortality if paired with SBT (NEJM 2000;342:1471, Lancet 2008;371:126)
SBT: ~30min (up to 2hrs) daily trials with little/no support (PEEP ≤5 on PSV; generally 0) = vent time (NEJM 1996;335:1864;
NEJM 1995;332:345)
- Ways to fail SBT: hypoxemia (SaO2 <90%, PaO2<60), hypercarbia (PaCO2 by >10), inadequate VT, respiratory
distress (HR, RR, HTN, accessory muscle use, diaphoresis), arrhythmia, hemodynamic instability, anxiety/agitation,
somnolence
- Causes of SBT failure: underlying etiology not corrected, volume overload, cardiac dysfunction, neuromuscular
weakness, delirium, anxiety, metabolic abnormalities
• Extubation strategies:
o Extubation to NIPPV or HFNC in patients with hypercarbia / risk factors for reintubation post-extubation respiratory failure
(Lancet 2009;374:1082, JAMA 2016;316:1565). HFNC w/ intermittent NIV post-extubation reintubation compared to HFNC
alone (JAMA 2019;322:1465).
o Check for absence of cuff leak before extubation (concerning for laryngeal edema) consider methylpred 20mg IV q4h
12hrs prior to extubation or IV methylpred 40mg x1 4hrs prior or IV dexamethasone 5mg q6h (Eur J Anaesthesiol 2010;27:534)
o If agitation is limiting ability to extubate, consider dexmedetomidine may improve odds of extubation (JAMA 2009;301:489)
• Post-extubation respiratory failure: usually due to poor secretion clearance, CHF, aspiration, bronchospasm, laryngeal edema.
o NB: no benefit to NIPPV as rescue therapy during post-extubation respiratory failure and may be associated w/ worse
outcomes (NEJM 2004;350:2454). Not recommended per ERS/ATS guidelines (ERJ 2017;50).
• Tracheostomy: usually performed if still intubated for 14 days
o Early tracheostomy (7 days) if expect intubation >14 days comfort, allows sedation, risk of tracheal stenosis, vent-
free and ICU days, though no change in VAP rate (JAMA 2010;303:1483, Crit Care 2015;19:424, Br J Anaesth 2015;114:396)
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Mechanical Ventilation
Is the patient stable, tolerating NO
noninvasive ventilation, P:F > - VT 4-6cc/kg predicted body weight (PBW), Pplat ≤30, ΔP ≤15
200mmHg? - Optimal PEEP titration
- Keep PaO2 55-80 mmHg or SpO2 88-95% with pH ≥7.25
YES
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Krishan Sharma
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Krishan Sharma
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Passive leg raise: raise legs to 45° w/ torso horizontal x1 min. in mech.
ventilated patient to provide “autotransfusion” of ~250-350cc; assess Δ in Pulse pressure ≥10%
hemodynamics (surrogate for SV if invasive
measures of CO not available)
Δ in IVC diam: measure 1cm prox. to hepatic vein junction in M-mode; if mech. vent, calc. distensibility: dIVC ≥15%
dIVC = (Dmax-Dmin)/Dmin; if spont. breathing, calc. collapsibility: cIVC= Dmax-Dmin/Dmax cIVC ≥40%
Fluid challenge: bolus 250-500cc fluids; measure CVP before and immediately after and if by ≥2 Improvement in
then was appropriate volume challenge. If chosen parameter(s) improve, then fluid responsive. If do BP/vasopressors, UOP, lactate;
not, then not fluid responsive. in pulse pressure ≥10%
• Resp. variation w/ vent: pos. pressure during expiration venous return & RV preload LV preload. If on ascending portion of
Starling curve, sensitive to Δs in preload. Volume responsive pts will show larger variations in PP or SV during respiratory cycle.
• Lack of volume responsiveness suggests patient is on the flat part of the Frank-Starling curve; use/increase vasopressors instead.
• Targets of resusc.: lactate clearance (normalization or >20%/2hrs) (JAMA 2010;303:739); cap. refill (<30s) (JAMA 2019;321:654)
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Sirus Jesudasen
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Hepatorenal syndrome
Low: β1 >β2 >α1: ACLS (1st) HR, arrhythmias
Low: 1-4 mcg/min
Epinephrine CO, neutral SVR Anaphylaxis (1st) Myocardial ischemia
Adrenalin Symptomatic bradycardia (2nd) lactate
“Epi” High: α1 > β1>β2: Septic shock splanchnic SVR High: 5-35 mcg/min
CO, SVR Bronchospasm FSBG
Low: D1 >β1: Symptomatic bradycardia
CO, UOP Tachyarrythmia Low: 1-2 mcg/kg/min
Septic shock w/ bradycardia
Dopamine Myocardial ischemia
Med: β1>D1: mortality vs. levophed in
Intropin BP (low dose) Med: 5-10 mcg/kg/min
CO, SVR septic (CCM 2017;45:486) &
“Dopa” PCWP, pulm shunt
High: α1>β1>D1: cardiogenic shock (SOAP-II NEJM FSBG High: 10-50 mcg/kg/min
SVR 2010;362:779)
Refractory vasoplegia due to Falsely SpO2
sepsis/anaphylaxis Arrhythmias Initial: 1-2 mg/kg
NO and cGMP
Methylene Post-cardiopulm bypass PVR
Sm musc tone:
blue Amlodipine overdose Rash, hemolysis,
SVR Max: 5 mg/kg
Metformin overdose serotonin syndrome
Methemoglobinemia Contraindicated in G6PD
Refractory septic shock
Angiotensin II ANG-II agon.: SVR Peripheral ischemia 10-20ng/kg/min; max 40
(NB: not avail at MGH)
BP, HR Initial: 0.5-1 mcg/kg/min
Dobutamine
β1, β2>α1 agonist: Cardiogenic shock Arrhythmias (2.5 if more severe)
Dobutrex
CO, SVR Sepsis + LV EF (added to NE) Myocardial ischemia
“Dobuta” Max: 20-40 mcg/kg/min
Tachyphylaxis
PDE inhibitor
Initial: 0.125 mcg/kg/min
INOTROPES
(cAMP) Hypotension
Milrinone Cardiogenic shock
inotropy, Arrhythmias
Primacor RV failure (PVR, LVEDV)
vasodilation: Myocardial ischemia Max: 0.75 mcg/kg/min
CO, PVR/SVR
BP, HR 2-10 mcg
Isoproterenol β1 = β2 agonist: Symptomatic bradycardia Arrhythmias (can bolus 2-6mcg first)
Isuprel HR, SVR Mg-refractory Torsades Myocardial ischemia
30 mcg/min
Flushing, anxiety
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Nathan Kunzler
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Dialyzable Toxins
EtOH, methanol, isopropyl
alcohol Acid Diuresis Alkaline Diuresis
Glycols (give Vitamin C) (give NaHCO3)
Acetone Quinine Phenobarbital
Lithium PCP Salicylates
Salicylates Methotrexate
Barbiturates TCAs
INH
Atenolol, sotalol
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Urgent Assessment & Management of GI Bleeding Etiologies of Upper GIB (Dig Dis Sci 2018;63:1286)
• Assess & reassess V/S for hemodynamic stability Ulcers (~50%): PUD: H. pylori, NSAID, ZE, EtOH
• Attempt to quantify amount & rate of blood loss Varices (~5%): EVB (esophageal) > gastric
• ≥ 2 PIV (18G or larger) – rarely done by IV nurse; look at their arms Esophagitis or gastritis (~30%): GERD, pill, ASA,
(green = 18; pink = 20; blue = 22) NSAIDs, clopidogrel, EtOH, infectious
• Type & screen (type & cross if plan to transfuse), IVF (and blood if Vascular lesions (~5-10%): Dieulafoy’s, AVM, GAVE,
indicated): liberal transfusion if active bleed or unstable VS. Hct drop HHT, XRT, aortoenteric fistulae
lags 24-72h from onset of bleeding. Traumatic (~5%): Mallory-Weiss, foreign body,
• Correct coagulopathy: IV vit K, FFP, Plt, PCC. If severe/life- Boerhaave’s
threatening, consider reversal agent. If uremic, consider ddAVP (0.3 Neoplastic (~5%): primary > metastatic
mcg/kg); if ESLD, consider amicar, avoid FFP (volume). Post-procedural (varies): polypectomy, sphincterotomy
• Transfusion goals: Hb >7 (avoid overtransfusion if EVs), Plt >50k, INR <2 (unless ESLD), PTT <50, Fibrinogen >100
o See Transfusion Medicine for Massive Transfusion; generally, give FFP/plts after 4U
• GI consult for EGD and/or colonoscopy High Risk Features in UGIB
• Surgery or IR consult if hemodynamic instability or difficult endoscopic correction Hypotension
• Intubation: if high volume hematemesis, AMS, variceal bleeding requiring balloon tamponade Tachycardia
Coagulopathy (INR > 1.5)
Acute Upper GI Bleeding (International Guidelines: Annals 2019;171:805; NEJM 2016;374:2367) AMS
• Definition: bleeding proximal to ligament of Treitz Syncope
• S/Sx: hematemesis, melena (+LR 25); brisk UGIB can p/w hematochezia, orthostasis; BUN/Cr Age > 65
>30 (⊕ LR 7.5; JAMA 2012;307:1072), especially >35 (100% Sp; J Clin Gastro 1990;12:500). Liver Dx
CHF
• Risk stratification (30d mortality): Glasgow-Blatchford Score recommended over AIMS65
(Annals 2019;171:805, BMJ 2017;356:6432); Machine Learning Scoring System with > specificity (100%) than both (Gastro 2020;158:160)
• Management: EGD generally within 24hrs (debated), but no Δ in outcomes if between 0-6hrs vs. 6-24hrs (NEJM 2020;382:1299)
Pre-EGD Post-EGD
- Transfusion: Hb >7 (NEJM 2013;368:11). Consider higher - If high risk PUD, intensive PPI x72 hr re-bleeds & need
threshold if CVD (Annals 2019;171:805). Avoid overtransfusion in for repeat EGD: pantoprazole 40mg IV BID (intermittent dosing
variceal bleed – can portal pressures and worsen bleeding. non-inferior to bolus+gtt; JAMA Intern Med. 2014;174:1755). Oral
- IV PPI: high-risk lesions requiring endoscopic therapy, but PPI may replace IV PPI if good PO intake.
unclear clinical impact pre-EGD (Cochrane Rev. 2010) - Treat H. pylori if positive
- IV erythromycin or azithromycin: 250mg 30m prior to EGD - If variceal bleed: continue octreotide x 3-5d, consider TIPS or
gut motility & visualization (AJG 2006;101:1211) BRTO if refractory to EGD
- If cirrhosis: IV octreotide: 50 mcg x1 50 mcg/hr + IV CTX 1g - If angiodysplasia: consider long-term octreotide (AJG
q24hr x7 days for ppx against bacterial infections (Gastro 2007;102:254), bevacizumab or thalidone w/ GI help
2006;131:1049; APT 2011;34:509); stop β-blockers - If re-bleed: repeat EGD, consider angiography, surgical/IR
- If continues to bleed, consider amicar (5 g bolus followed by 1 consult. If variceal, consider balloon tamponade, TIPS, BRTO
g/hr, max ~24g in 24h), ddAVP (if uremia)
Management of anticoagulation/antiplatelet agents (ASGE Guidelines: Gastrointest Endosc 2016;83:3)
Warfarin: hold during bleed; resume after hemostasis (w/ UFH bridge at ~48hrs if indicated; see Hematology section); risk of
thrombosis, death in AF if resumed w/in 7d (Am J Cardiol 2014;113:662)
DOAC: hold during bleed; no data to guide, but generally resume 48-72hr after hemostasis
ASA: hold during bleed (unless recent PCI/ACS – see below); resume in pts w/ CAD (2° prev.) after hemostasis, best if w/in 1-7d;
risk of 30d mortality if not resumed (Annals 2010;152:1); if PUD, add PPI to risk of bleeding
DAPT for PCI/ACS: d/w cardiologist though generally if very recent (<30d PCI, <90d ACS) continue both unless life-threatening; if more
distant, continue ASA but less risk in holding P2Y2i. Resume w/in 1-7d if able, esp if low rebleed risk.
In general, restarting AC/AP sooner risk of vasc. events, though risk of bleeding (APT 2019;50:8)
• Prognosis:
o PUD rebleeding w/o med management: 90% if active bleed, 50% if visible vessel, 30% if clot, 20% if oozing, else < 10%
o Esoph variceal bleed: 50% resolve spontaneously; 30% mortality 70% if continued bleeding; 60% risk re-bleeding overall
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P E P T I C U L C E R D I S E A S E ( P U D ) (BMJ 2019;367:I5495)
Signs & Sx: intermittent gnawing, dull, aching, or “hunger-like” epigastric pain relieved w/ antacids though 70% are asx; duodenal
ulcers p/w pain 2-5hrs after meal & at night night (persistent acid w/o buffer). Associated sx: early satiety, bloating, n/v.
Etiology: 90% caused by H. pylori or NSAIDs. Others: meds (bisphosphonates, steroids, clopidogrel, sirolimus), ZES, mastocytosis,
HSV, CMV, EBV, fungal infxn, post-surgical, XRT, ischemia (crack cocaine), Crohn’s, sarcoid, critical illness
Ddx: other causes of dyspepsia: biliary disease, gastric CA, celiac, chronic pancreatitis, drug-induced, functional dyspepsia
Evaluation: H. pylori testing in all w/ dyspepsia; if >60 EGD to exclude CA. (ACG Guidelines for Dyspepsia: AJG 2017;112:988)
• H. pylori testing: Stool Ag or urea breath test (not avail. at MGH) preferred to assess for active infection though affected by
PPI & abx ( false ⊝). Serology (IgG) not affected by PPI/abx/bismuth but cannot accurately distinguish active vs. past
infection; a ⊝ serology is helpful in excluding infection if low pre-test probability. Bx w/ urease, histolology, Cx.
• EGD: biopsy malignant-appearing & select benign-appearing ulcers; obtain samples for H. pylori testing.
Management: PPI (duration depends on etiology), add sulcralfate if duodenal ulcer 2/2 acid, H. pylori tx, d/c offending agents; if
need to continue ASA, continue w/ PPI (NEJM 2005;352:238, Gastro 2010;138:82). F/u EGD after 8-12w if refractory sx (see below) or
gastric ulcer w/o clear etiology (ASGE Guidelines: Gastrointest Endosc 2010;71:663)
H. pylori treatment: (ACG Guidelines: Gastro 2017:112:2)
• First line = quadruple therapy (assuming resistance of clarithromycin >15%): PPI BID, bismuth 300mg QID, tetracyline 500mg
QID (alternative: doxy 100mg BID), metronidazole 500 QID x 14d. Combo pill (Pylera) available; add PPI BID for quad tx.
• Triple therapy: clarithromycin 500mg BID + amoxicillin 1g BID (or flagyl 500mg TID if PCN-allergic) + PPI BID x14d. Addition of
bismuth may eradication (CGH 2020;18:89).
• Confirmation of eradication: stool Ag, urea breath test (not avail. at MGH) or EGD >4 wks after completion of abx and PPI.
Refractory PUD: ulcer that does not heal after 8-12wks adequate tx; 5-10% of ulcers are refractory to PPI tx.
• Ensure H. pylori eradicated, NSAIDs & other contributing meds discontinued. Test for ZES w/ fasting serum gastrin ( if on PPI,
recheck 1 week s/p cessation); secretin stimulation test if non-diagnostic.
• Continue PPI x additional 12w and then reassess w/ EGD. If still refractory, surgical tx: resection, vagotomy, partial gastrectomy
Complications and Management: ulcer consider complicated if any of the following are present:
Bleeding: IVF/pRBC, IV PPI, EGD. Perforation: IVF, IV PPI, abx ± surgery. Penetration. Gastric outlet obstruction: pyloric channel/
duodenal ulceration spasm, edema, inflammation, dysmotility fibrosis/scarring; Tx: IVF, correct electrolytes, NGT; may need
endoscopic dilatation or surgical tx if persists w/ medical mgmt.
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Gastroenterology Diarrhea
Acute Diarrhea: ≥3 loose stools/d for <14 days (ACG: AJG 2016;111:602; IDSA: CID 2017;65:e45; NEJM 2014;370:1532)
• Evaluation: character of sx (small bowel=watery, large vol., +cramping/bloating; large bowel=freq., small vol., painful, +/- fever, blood,
mucus), exposure hx (travel, abx/hospitalization, food, sick contacts, daycare), immunocompromised, s/sx volume depletion
• Workup: BMP if vol. depletion; BCx if fever/ill, immunocompromised; stool Cx if severe (>6BMs/d, severe pain), inflammatory, high-
risk host (age >70, immunocompromised, IBD), or persistent >2w; O&P if persistent, immunocompromised, MSM; C. diff if RFs
• Common pathogens: Viral (most cases): norovirus (outbreaks during winter; n/v prominent), rotavirus (often daycare-assoc.),
adenovirus. Bacterial (most severe cases): E. coli (toxigenic = traveler’s diarrhea; hemorrhagic, O157:H7 = undercooked meats, a/w
Shiga toxin, HUS), Campylobacter (undercooked/unpasteurized foods, can be a/w reactive arthritis or GBS), Salmonella (eggs,
poultry, milk, often bacteremic), Shigella (low inoculum, often hematochezia), Vibrio spp. (shellfish/salt water; *cirrhosis), Yersinia
(undercooked pork, “pseudoappendicitis”), C. diff (see Clostridium difficle). Parasitic: Giardia (outdoor streams; watery stool
progressing to malabsorptive/greasy), Cryptosporidia (water-related outbreaks), Cyclospora (contaminated produce); E. histolytica
(contam food/water outside US, a/w liver abscesses). Immunocompromised: CMV, C. diff, Cryptosporidia, Isospora, Microsporidium,
MAC, TB, Histoplasma, Cryptococcus.
• Treatment: Volume & lyte repletion critical (PO if able). Empiric abx: controversial; if febrile, septic, inflammatory diarrhea: FQ or
azithro. Consider in age ≥70, hospitalized, serious comorbidities. Avoid abx if suspect EHEC as can risk of HUS. Caution w/
loperamide (OK if no fever or bloody stool). Probiotics controversial: not recommended by ACG except for post-abx diarrhea.
Chronic Diarrhea: ≥3 loose stools/d for >4wk. 5 types: secretory, osmotic, Disease Process Physical Exam Findings
functional, malabsorptive, and inflammatory. See table below. Dehydration, neuropathy Orthostasis, hoTN
Evaluation: (Gastro 2017;152:515, CGH 2017;15:182, Gut 2018;67:1380) Hyperthyroidism Tremor, lid lag
• Hx: freq., stool vol., tenesmus, abd pain, fever, bloating, wt loss, Addison’s disease Hyperpigmentation
nocturnal sx, postprandial sx, steatorrhea, surg hx (CCY, resection,
Carcinoid Flushing, murmur, wheezing
bariatric, vagotomy), travel, immunocompromised, meds, radiation
Amyloidosis Hepatomegaly, macroglossia
• Labs: CBC, BMP, ESR/CRP, LFTs; TSH; stool lytes (Na, K, pH), fecal
HIV, lymphoma, CA Lympadenopathy
WBC/calprotectin, fecal fat (24-48h coll.), FOBT
Glucagonoma Migratory nec. erythema
• Stool osmotic gap for watery diarrhea: 290 – 2*(stool [Na] + [K]);
Celiac disease Dermatitis herpetiformis
Normal 50-100 mOsm/kg
Watery Fatty
Inflammatory
Secretory Osmotic Functional Malabsorptive/Maldigestive
Addison’s, neuroendocrine
Malabsorption: mesenteric IBD, invasive
tumors, hyperthyroidism, Lactose
IBS, ischemia, mucosal disease bacterial/parasitic
medullary CA of thyroid, intolerance,
functional (CD, Whipple’s), short gut infxn (C. diff, E.
mastocytosis, microscopic mannitol,
diarrhea syndrome, SIBO histolytica, Yersinia,
Etiologies colitis (lymphocytic or sorbitol,
Maldigestion: bile acid TB), ulcerating viral
collagenous), DM autonomic magnesium,
(see Motility malabsorption (ileal disease) infxn (CMV, HSV),
neuropathy, laxative
Disorders) or ↓ synthesis, pancreatic colon CA, lymphoma,
amyloidosis, bile salt (4-5%), use/abuse
exocrine insufficiency radiation colitis
lymphoma, villous adenoma
Structural problem, mucosal Inflammation
Secretagogue, rapid transit, Osmotic Multi-
Mechanism disease, panc. or bile acid interferes w/ nml
surface area substance factorial
insufficiency function/absorption
Osmotic gap <50 >125 50-100
Response to
No change Improves Variable Improves No change
fasting
Exclude infxn. +/- colo with bx Sudan stain, 24hr fecal fat
Stool pH (<6), Exclude infxn.
(esp. if immunosupp). As (>20g likely panc dysfxn, 14-
Further H2 breath ESR/CRP,
appropriate: chromogranin, None 20g likely small bowel
Testing test, laxative calprotectin, colo w/
gastrin, somatostatin, calcitonin, cause), stool elastase or
screen biopsies
5-HIAA, TSH, ACTH stim, SPEP chymotrypsin, see celiac
Bile salt: cholestyr. 4g QD-QID Fiber
Microscopic colitis: budesonide (Citrucel >
Pancreatic enzyme
VIP: somatostatin (octreotide 50- D/c offending Metamucil),
replacement therapy Abx vs.
Treatment 250 ug TID SQ) agent; dietary Viberzi
(pancrealipase 500-2500 immunosuppression
Other: opiates via mu receptor review (+pain),
units/kg/meal),
(eg loperamide 2-4mg QID, Rifaxamin
diphenoxylate 2.5-5mg QID) (+bloating)
Celiac Disease (NEJM 2012;367:2419): abnormal immune response to gluten diarrhea, wt loss, abd pain, Fe def anemia, vit D def
Diagnosis: tTG-IgA (Sn >95%, Sp >95%) + total IgA. If IgA def, DGP- & TTG-IgG. If any ⊕, EGD w/ biopsies. If gluten-free &
⊝ serologies, HLA-DQ2/DQ8. If ⊝, dx excluded. If ⊕, should challenge w/ gluten x2-8w and then serologies and EGD w/ bx.
Bx: intraepithelial lymphs, elongation of crypts, villous atrophy. If Bx & serologies discordant, HLA. (ACG: AJG 2013;108:656)
• Treatment: strict adherence to gluten-free diet; IgA anti-tTG titer should decrease and return to normal over time. Ensure no
deficiency in vitamins (A, D, E, B12), Cu, Zn, carotene, folic acid, Fe +/- thiamine, vit B6, Mg, and selenium.
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24μg BID for STC/NTC; Binds Cl- channel & increases secretion, small bowel &
Lubiprostone (Amitiza)
8μg BID for IBS-C colon transit. Most common side-effect is nausea.
Secretory drugs Linaclotide: 145μg QD for
Linaclotide (Linzess),
STC/NTC; 290μg QD for Agonists of guanylate cyclase-C; Cl, HCO3 secretion &
plecanitide
IBS-C colonic transit.
(Trulance)
Plecanatide: 3g daily
Methylnaltrexone: At MGH, methylnaltrexone approved only if on stable
1 dose SQ QOD PRN dose of opioids ≥ 2 weeks x3d w/o BM AND failed
Peripheral Methylnaltrexone,
- 38-62kg: 8mg multiple other laxatives. Contraindicated in obstruction,
opioid receptor naloxegol (pegylated
- 62-114kg: 12 mg small risk of perforation. See AGA Guidelines for opioid-
antagonists naloxone), alvimopan
- <38, >114kg: 0.15mg/kg induced constipation: Gastro 2019;156:218 & Gastro
- CrCl <30: 1/2 dose 2019;156:229.
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(solids + liq.)
(Chicago classification: Neurogastro Motil 2015;27:160)
Intrinsic: tumor, XRT, trauma/surgical resection, Zenker’s Intrinsic: tumor, stricture, infxn, EoE, rings, webs (e.g.
Structural Extrinsic: anterior mediastinal mass, goiter, cervical Plummer-Vinson), pills (NSAIDs, doxy, tetracyc., bisphosph)
(solids >
liquids) spondylosis Extrinsic: vascular rings (e.g. dysphagia lusoria), Ao. enlarge.,
LA compression, mediastinal, substernal thyroid, LAD
History: sx onset & duration, solid/liq & localization of dysphagia, +/- odynophagia, underlying conditions (e.g. CNS,
malignancy, thyroid, DM, scleroderma), use of offending meds (pill esophagitis), immunocompromise (Cand., CMV,
Work-up HSV infectious esophagitis or lymphoma in HIV), radiation, etc. Dysphagia in older adults, is not normal aging. PE: gen
appearance (?systemic disease or CNS issue), HEENT exam (?evidence of LAD, tumor, asymmetry), FOBT Labs
(consider): CBC, TFTs, ANA, α-Scl-70, α -centromere, α -RNP, α -Jo, HgbA1C, iron studies, HIV, AChR-Ab
1) Modified barium swallow, ENT and neuro evals, +/- 1) EGD is the most useful test +/- barium swallow (mucosal
EGD to identify obstructive structural problem pathology or structural abnormality)
Diagnostics
2) Consider chest/neck CT to dx extrinsic compression 2) if normal esoph. manometry to diagnose motility d/o
3) Consider chest/neck CT to dx extrinsic compression
Zenker’s diverticulum: p/w halitosis, regurgitation of food/aspiration, cough. Tx w/ endoscopic surgery (rigid vs. flexible).
Strictures & rings: if lumen <13mm, dysphagia common. Tx PPI, dilation, intralesion steroid inj, stent
Distal esophageal spasm: uncoordinated peristalsis a/w intermittent chest pain & regurgitation; barium swallow:
corkscrew (vs. nml). Hypercontractile esophagus: similar sx; nml barium swall. Tx (both): PPI, nitrates/CCB/PDEi,TCA.
Selected Infectious esophagitis: odynophagia; often immunosuppressed – Candida, HSV, CMV
Conditions Eosinophilic esophagitis (EoE): dysphagia, refractory GERD sx. EGD w/ stacked rings, strict. Bx >15 eos/hpf. Tx PPI,
diet Δs (dairy, wheat > soy, eggs, nuts, fish), topical steroids (MDI/neb/liq.); consider dilation. (AGA: Gastro 2020;158:1776)
Achalasia: progressive dysphagia solids/liquids, + regurgitation; barium swallow with bird’s beak appearance of distal
esophagus; manometry: absent distal peristalsis, incomplete LES relaxation; EGD to r/o pseudo-achalasia (2/2 CA); tx w/
pneumatic dilation, Heller myotomy, POEM, botox, CCBs. (AGA Guidelines: AJG 2013;108:1238; JAMA 2015;313:18)
Gastroparesis Ileus
Definition: decreased gastric motility w/o obstruction Definition: slow motility of the gut w/o obstruction, often post-op
Sx: n/v, early satiety, postprandial fullness, bloating +/- abd pain Sx: nausea/vomiting, BMs and flatus, abd distention
Etiologies: diabetes (vagus nerve damage 2/2 hyperglycemia), Studies: KUB/CT w/ colonic dilatation w/o mechan. obstruction
post-surgical (e.g. vagus nerve injury post-bariatric surgery), Paralytic ileus: s/p intra-abdominal surgery or a/w peritonitis,
post-viral, systemic disease (thyroid, critical illness, Parkinson’s, ischemia, meds (opioids, anti-cholinergics); worsened by hypoK
connective tissue d/o), meds (opiates, CCB, anti-cholinergics) Tx: bowel rest, decompression via NGT if mod/severe/ongoing
Exam: +/- TTP in epig, succussion splash (sloshing on abd ausc) sx, avoid opiates, replete lytes. Methylnaltrexone PRN if opioids.
Dx: exclude mech obstruction w/ EGD, CTE/MRE/SBFT Acute colonic pseudo-obstruction (Ogilvie’s): typically in elderly,
gastric emptying nuc. study (hold motility meds 48 hrs prior) hospitalized, ill pts. A/w severe illness (e.g. sepsis, pancreatitis,
Labs: TSH, ANA, A1c, tot protein, alb, CBC w/ diff. peritonitis), systemic disease (thyroid dis., DM, renal or liver
Treatment: small meals w/ low fat & non-digestible fiber, failure), neuro (spinal cord compression or trauma, Parkinson’s,
prokinetic agents before meals (metoclopramide or erythromycin; MS), meds (opiates, CCB, anticholinergics).
give drug holidays due to tachyphylaxis / to assess benefit), Tx: conservative (NPO, IVF, NGT/rectal tube), neostigmine if
antiemetics; venting G-tube if refractory sx, J-tube for nutrition if cecal diam. >12 or if fail conserv tx. Colonic decomp. if fails.
wt loss. (ACG Guidelines: AJG 2013;108:18) (ASGE Guidelines: Gastro Endosc 2020;91:228)
FUNCTIONAL GI DISORDERS: GI disorders caused by aberrant neuronal signaling (dysfunction of the gut-brain axis) rather than
structural or known molecular abnormality. Classification of >20 disorders per the Rome IV Criteria. (Gastro 2016;150:1393)
Functional dysphagia Sense of dysphagia w/o structural d/o, abnl motility, GERD or EoE. Sx ≥ 1x/wk. Tx: CCB, TCA
Functional dyspepsia Early satiety, epigastric pain. Must r/o structural/organic cause. Tx: PPI/H2RA, TCA, metoclopramide
Globus sensation Sensation of obstruction in the throat when there is none, Tx: PPI, antidepressants, CBT
Episodic, stereotyped. Kids>adults. Often trigger and prodrome. May be better w/ hot shower. Tx:
Cyclical vomiting syndrome
anti-emetics (Zofran), benzos to sedate, triptans may abort, TCAs may ppx; overall limited evidence
Cannabis hyperemesis syndrome Frequent cannabis, n/v (temp. relieved by MJ), relieved by hot shower. Tx: topical capsaicin; MJ
Sphincter of Oddi dysfunction Biliary pain, +/- pancreatitis 2/2 inability to relax, often post-CCY. Tx: trial CCB/nitrate; ERCP
Irritable Bowel Syndrome (IBS):
Definition (per Rome IV Criteria): recurrent abd discomfort ≥ 1x/wk on average for 3 months a/w 2+ of the following: (1) related to
defecation, (2) change in stool frequency, (3) change in stool form. No nocturnal pain, weight loss, bleeding, or calprotect/lactoferrin.
Types: IBS-C (constipation-predominant), IBS-D (diarrhea-predominant), IBS-M (mixed), IBS-U (unclassified), by Bristol Stool Score
Epidemiology: risk w/ younger age, ♀ > ♂, psychosocial stressors, low QoL, hypochondriasis; gastroenteritis may be trigger.
Treatment: all: exercise, diet Δ (low FODMAP), fiber (psyllium), rifaximin (esp. non IBS-C), anti-spasmodics (dicyclomine), peppermint oil,
TCAs, CBT. IBS-C: laxatives (linaclotide, plecanatide, lubiprostone); IBS-D: eluxadoline, loperamide, alosetron (♀) (ACG: AJG 2018;113:1)
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peritonitis, pouchitis,
Aminosalicylates (UC>>CD) IV steroids† +/- rectal steroids, IV Fluids/lytes perforation, high fever,
Budesonide oral/topical (UC/CD) High-risk DVT ppx‡, +/- Cipro/FlagylΔ leukocytosis, bandemia
PO prednisone (UC/CD) Tspot, Hep serologies, TPMT enzyme ϒ
risk of tox meg in UC
Antibiotics (CD) No NSAIDs/opiods/antidiarrhealsϒ * Bridge to maintenance tx
Thiopurines (UC/CD) NPO for endoscopy (c/s IBD team, inform outpt GI), ADAT σAnti-TNF, anti-integrin, etc.
Refractory disease/toxic Resolution* Refractory after 3-5 days: Advance therapyσ, surgical consult
Indications for surgery: CD: undilatable stricture, fistulae, abscess failing medical tx. UC: refractory disease, perforation, toxic megacolon
Management guidelines: CD: ACG: AJG 2018;113:481, AGA: Gastro 2017;152:271; UC: ACG: AJG 2019;114:384, AGA: Gastro 2019;156:748 & 2020;158:1450
Class Drug* Use Notes & Adverse Effects (AE)
PO budesonide 1st-line in mild CD, 2nd-line to ASA for mild UC, but can
Budesonide (PO/PR), Pred
Steroids Induction be 1st-line for mod
(PO), Methylpred (IV)
AE: osteoporosis, infection, AVN, AI, weight gain, mood lability, delirium
Sulfasalazine Induction + Sulfasalazine: pro-drug with more AEs, also systemic effects
Amino-
Mesalamine (PO: Pentasa, Maintenance for Mesalamine forms differ in gut penetration: Pentasa (ileum, R>L colon),
salicylates
Ascol, Lialda, Apriso. mild-moderate Ascol (R>L colon), Lialda & Apriso (pancolon), Canasa & Rowasa (distal).
(UC>>CD)
PR: Canasa, Rowasa) disease AE: HA, fever, rash, diarrhea, pancreatitis, sperm count, kidney injury
Typically as combination therapy for induction; can be monotherapy for
Azathioprine (pro-drug) Induction +
Thiopurines maintenance
6-MP Maintenance
AE: n/v, hepatitis, BM suppression, pancreatitis, NHL, skin cancer
Contraindicated if toxic megacolon, pyogenic infections.
Infliximab (Remicade) Induction +
If flare during maintenance: measure trough (24hrs prior to dose) and
Adalimumab (Humira) Maintenance for
Anti-TNF antidrug Ab levels, determine if dose escalation or new drug is required.
Certolizumab (Cimzia)-CD mod-severe
If pt non-responsive despite adequate levels, switch to another class
Golimumab (Simponi)- UC
AE: site rxn, infxn, TB/HBV reactiv., demyelinating dz, HF, malignancy
Induction + VARSITY3- In mod-severe UC, achieved clinical remission at 52wks vs.
Anti-integrin Vedolizumab1,2 (Entyvio) Maintenance for adalimumab, but w/ greater steroid use
mod-severe AE: infusion reactions, nasopharyngitis
IL-12, -23 Induction + AE: infection, HA, nasopharyngitis, nausea, abdominal pain, arthralgias
Uztekinumab4,5 (Stelara)
inhibitor Maintenance
JAK Induction + Consider if previously failed anti-TNFs
Tofacitinib6 (Xeljanz)
inhibitor Maintenance AE: infection, herpes zoster, HA, nasopharyngitis, arthralgias
Calcineurin Induction only C/i in s/o toxic megacolon. Labs: troughs (q2-3d) Cr, Mg, lipids, LFTs
Cyclosporine
inhib (IV) for severe UC AE: renal injury,K, infxn, neurotox/seizures (esp. if Mg or cholesterol)
*For UC and CD unless otherwise noted
1. NEJM 2013;369:699, 2. NEJM 2013;369:711, 3. NEJM 2019 381:13, 4. NEJM 2016;375:1946, 5. NEJM 2019;381:13, 6. NEJM 2017;376:1723
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Gastroenterology Pancreatitis
E T I O L O G Y (CGH 2007;5:648)
- Gallstones/sludge (40-75%): #1 in women - Drugs (<5%): Class Ia: ACEi, dapsone, lasix, flagyl, pentamidine,
- Alcohol (30%): #1 in men statins, sulfa, tetracycline, valproate, mesalamine; Class Ib:
- Hypertriglyceridemia (10%): #3; suspect if TG>1000 amiodarone, azathioprine/6-MP, dexamethasone; Class II:
- Anatomic: ampullary diverticula/stenosis, duodenal didanosine, estrogen, propofol, tamoxifen, hydrochlorothiazide
stricture, tumor, divisum, parasites, foreign body - Toxins: organophosphates, scorpion venom, methanol, smoking
- Post-ERCP (3-5%): in high-risk pts, rectal NSAIDs rate - Infections: viral (Coxsackie, EBV, CMV, HIV, Mumps, VZV, HAV,
of pancreatitis (NEJM 2012;366:1414) HBV, HSV), bacterial (Mycoplasma, Legionella, Salmonella), fungal
- Autoimmune: IgG4, +ANA (rare) (Aspergillus), parasitic (Toxoplasma, Crypto, Ascaris)
- Hypercalcemia: Ca activates pancreatic enzymes - Ischemia: vasculitis (SLE, PAN), hypoTN/shock, cholesterol emboli
- Genetic - Tropical: pt from low SES in SE Asia, first bout as child
- Trauma: blunt, especially s/p MVA - Idiopathic (10-25%)
D I A G N O S I S / S E V E R I T Y / P R O G N O S I S (Revised Atlanta Classification: Gut 2013; 62:102, Pancreatology 2014; 14:324)
• Presentation: abd pain (90%) (band-like pain to back is specific but only 50%), n/v (90%), ileus, jaundice, flank/umbilical ecchymoses
• Diagnosis – need 2/3: 1) consistent clinical presentation, 2) lipase >3x ULN, 3) characteristic imaging
• Severity: mild: absence of organ failure and local or systemic complications; moderate: organ failure that resolved within 48 hours or
local/systemic complication; severe: organ failure >48 hours (22% mortality)
• Prognosis: many scoring systems; BISAP is quick. SIRS mortality. Ranson, APACHE II, & other organ failure scores less practical.
WORKUP
• History: prior episodes, EtOH/smoking, prior GI procedures (e.g. CCY, ERCP), meds, infx sx, autoimmune hx, FH
• Labs: lipase (Sn vs. amylase; no need to trend; false + in CKD, DKA, others), CBC (often Hct), BMP w/ Ca, LFTs ( ALT
>3.5ULN w/ 95% PPV for gallstone pancreatitis: AJG 1994; 89:1863), lipids (TGs)
• Imaging: CT if need to establish dx or to eval. for complications; RUQUS to r/o gallstones. MRI/MRCP can detect necrosis, stones.
M A N A G E M E N T (AGA Guidelines: Gastro 2018;154:1096)
• IV fluids: aggressive in first 24hrs: boluses + infusion 150-250/hr. LR>NS (SIRS, CRP; but avoid if Ca: CGH 2011;9:710). Goal-
directed: HR, Hct, BUN (Δ BUN a/w mortality: Gastro 2009;137:129), UOP 0.5-1cc/kg/hr. Generally aggressive resuscitation
after 24-48hr. Overresuscitation risk for abdominal compartment syndrome, need for intubation.
• Pain control: IV opioids | Abx: no role for prophylactic abx
• Nutrition: start PO (low fat) immediately once no n/v or abd pain. At 5-7d, if PO not tolerated start TFs (NG or NJ). Enteral > TPN:
maintains intestinal barrier, prevents gut flora translocation. TPN a/w risk of infections, organ failure/death (Cochrane Rev 2010)
• Reverse precipitants: treat Ca or TG (see below), stop culprit meds. For gallstone pancreatitis, urgent ERCP (24hrs) if cholangitis
or CBD obstruction. CCY ideally prior to discharge as biliary complications if CCY is delayed (AJG 2004;99:2417)
o HyperTG: insulin gtt (0.1-0.3U/kg/hr) + D5, q1h FSBG (initially), q12h TG. Goal TG <500 (may take several days). No good
evidence for apheresis so typically not done at MGH. Once can take PO, fibrates are first line. DC: lifestyle Δs, lipid clinic referral.
COMPLICATIONS (AGA Guidelines: Gastro 2020;158:67; NEJM 2016;375:1972)
Local Vascular Systemic
< 4 weeks > 4 weeks Thromboses: splenic, Abd. compartment
Acute peripancreatic fluid Pancreatic pseudocyst: fluid portal, SMV; AC if portal syndrome: intra-abd
Interstitial collection: w/o features of collection w/ well-defined wall. If vein or bowel ischemia pressure >20 w/ new organ
edematous pseudocyst; resolve dx unclear, EUS w/ FNA Pseudoanuerysm: erosion failure. bladder pressure
pancreatitis spontaneously w/o drainage (amylase). Drain if sx, rapidly , of GDA/splenic artery if in ICU.
infxn. (endo vs. perc/surg) bleeding into pseudocyst. ARDS: via phospholipase
Acute necrotic fluid Walled off necrosis: Suspect if Hgb, expansion degradation of surfactant
collection: intra- or encapsulated collection of of fluid collection,
extrapancreatic collection of necrosis. Drainage if sx or infected unexplained GIB. Metabolic: Ca, Glc, TG
Necrotizing fluid & necrosis (endo vs. perc) Dx: arterial phase CT. GIB: via pseudoaneurysm
pancreatitis Infected necrosis: initially sterile but 1/3 become infected, Tx: IR embo. prior to AKI
usually later in course; abx: (cefepime or cipro) + flagyl vs. drainage of fluid collection.
pip/tazo vs. carbapenem in critically ill. Necrosectomy – can DIC
delay 4wks if stable.
• Chronic pancreatitis (ACG Guidelines: AJG 2020;115:322): repeat acute attacks (esp EtOH & smoking; AJG 2019; 114:656) fibrosis &
loss of glandular tissue chronic abd pain, exocrine insufficiency ( steatorrhea, weight loss), endocrine insufficiency ( brittle
DM). Lipase/amylase may be early but nml/low as more tissue lost. ⊕ Fecal fat, stool elastase. CT/MRI pref. for dx: calcifications,
ductal dilation. Tx: pancreatic enzyme replacement (Creon), ensure vit ADEK replete, pain control. risk of pancreatic CA.
PANCREATIC MASSES (Curr Gastro Rep 2013;15:347)
• Solid: adenoCA (85-90%), autoimmune panc, neuroendocrine (1-5%), 1o lymphoma (<1%), mets (melanoma, RCC, etc)
• Cystic: inflammatory (pseudocyst, paraduodenal wall cyst), IPMN (mucinous cystic or serous adenoma or adeno Ca) (Guidelines
for dx & mgmt. of pancreatic cysts: AJG 2018;113:464; Gastro 2015;148:819)
• Imaging: CT abd pancreatic mass protocol; EUS with FNA allows biopsy (87% Se & 96% Sp); MRI useful in <2 cm lesions or
when vascular involvement needs to be delineated better); consider PET-CT, MRCP for malignancy in IPMN (70% Se, 92% Sp)
• Labs: CA 19-9 (⊕ in 80% of panc CA, 86% Sn / 87% Sp), CEA (mucinous lesions), ANA, IgG4 (if autoimmune panc suspected)
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Commonly used drugs that can cause hepatocellular injury: acetaminophen, allopurinol, amoxicillin-clavulanate (Augmentin),
amiodarone, aspirin, carbamazepine, clindamycin, fluconazole/ketoconazole, fluoxetine, glyburide, heparin, hydral, INH, labetalol, lisinopril,
losartan, methotrexate, niacin, nitrofurantoin, NSAIDs (some), phenytoin, protease inhibitors, statins, sulfa drugs, trazodone, valproic acid
Illicit drugs: anabolic steroids, cocaine, ecstacy, PCP. See livertox.nih.gov for full list. (APT 2007;25:1135, NEJM 2019;381:264)
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Prognosis: MELD score >30.5 = poor prognosis; King’s College Criteria – list for OLT if:
Acetaminophen-induced ALF:
consider liver transplant. King’s College Criteria also
Arterial pH <7.3 OR all 3 of: INR >6.5, Cr >3.4, grade 3-4 HE
used for prognosis – more specific but less sensitive All other causes of ALF:
vs. MELD. Poor prognosis for ALF due to HBV, INR >6.5 OR 3/5 of: age<10 or >40, Tbili ≥17, INR >3.5, time from jaundice to
Wilson’s, Budd-Chiari, autoimmune, drug injury. encephalopathy >7d, unfavorable etiology (seronegative hepatitis, DILI, Wilson’s)
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Alcohol-Related Hepatitis:
Presentation: varies from few sx to liver failure; jaundice, anorexia, fever, abd pain (tender hepatomegaly), malaise, weakness, nausea
• Can lead to portal HTN & its sequelae (EVs, ascites, HE) in the absence of cirrhosis due to hepatic swelling & portal venous obstruct.
Diagnosis: onset of jaundice w/in prior 8wks, ongoing heavy EtOH (F >40 g/d, M >60 g/d) for >6mo. with <60d abstinence before onset of
jaundice, AST moderate (50-400) w/ AST/ALT >1.5, Tbili >3 (Consensus Dx: Gastro 2016;150:785). Often WBC (<20k, PMNs), INR.
• Ddx: other etiologies of acute hepatitis/jaundice (viral, meds/herbs, ischemia, AIH, Budd-Chiari, biliary obstruct.), decompensated
cirrhosis (can be difficult to distinguish). HAV/HBV/HCV, U/S w/ doppler, ± others. Assess for signs of cirrhosis.
• Transjugular Bx: consider if atypical presentation and/or labs (e.g. AST or ALT >400), uncertain alcohol intake hx, confounding factors
such as use of hepatotoxic meds w/in last 30 days, possible ischemic insult (e.g. hypoTN, cocaine use) or other etiology
Exclude infection: BCx, U/A, UCx, diag. para if ascites, CXR ± sputum Cx if indicated. Some will have SIRS/fever due to inflamm., but
important to screen for infxn as at high risk (esp. if severe AH: 12-26% at admission), can be difficult to dx, and has tx implications.
Prognostic tools:
Tool Use Components Stratification
Maddrey Discriminant Initiation of steroids, PT, PT control (14.5 at ≥32 = severe 1mo. mortality 30-50%;
Function (MDF) prognosis MGH), Tbili start steroids (Gastro 1978:75:193)
Prognosis, consider >20 = 3mo. mortality 20%;
MELD Tbili, INR, Cr, Na
initiation of steroids consider steroids (Hepatology 2005;41:353)
≥0.45: Nonresponse stop steroids
Day 7 continuation or Day 0: Age, Albumin, PT, Cr
Lille <0.45: Response continue steroids
cessation of steroids Day 0 & Day 7: Tbili
(Hepatology 2007;45:1348)
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H E M A T O L O G I C A B N O R M A L I T I E S (AGA: Gastro 2019;157:33; NEJM 2011;365:147, CGH 2013;11:1064, Thromb Haemost 2018;118:1491)
• Cytopenias: multifactorial; thrombocytopenia (splenomegaly, TPO), leukopenia (splenomegaly), anemia (bleeding, spur cell
anemia); also may have BM suppression by EtOH/infection, nutritional deficiencies (e.g. folate), direct effect of HCV/HBV
• Coagulation abnormalities: coagulation factors (except for FVIII), anticoagulant proteins (C, S, ATIII), dysfibrinogenemia,
accelerated fibrinolysis (tPA) risk of both clotting and bleeding & patients not auto-anticoagulated; balance tends to favor
thrombosis in early stages vs bleeding in late stages of cirrhosis
o Labs: PT/INR, PTT, /nml fibrinogen (though does not function normally; if fulminant), /nml D-dimer (vs. in DIC),
factor VIII (vs. in DIC); note PT and PT/INR do NOT correlate with risk of bleeding or clotting
• Anticoagulation: (J Hepatol 2017;66:1313, JACC 2018;71:2162, Gastro 2019;157:33)
o VTE ppx: should not be withheld unless high risk of bleeding or plts<50
o Systemic AC: ok unless decompensated CPS C or high risk of bleeding. EGD for EVs prior to starting. VKA, LMWH, or DOAC all
options. VKA dosing can be c/b baseline PT/INR; LMWH can be c/b ATIII levels; DOACs relatively safe in stable pts though
all have some degree of hepatic metabolism – can use all except rivaroxaban w/ caution in CPS B, avoid all in CPS C
• Bleeding: consider role of coagulation factor deficiency, dysfibrinogenemia, hyperfibrinolysis, thrombocytopenia
o If suspect vitamin K deficiency, give vitamin K 10mg x3 days to correct nutritional component
o Transfuse pRBCs Hgb <7, platelets <50k, cryo for fibrinogen <100-120 (or if c/f dysfibrinogenemia)
o Persistent bleeding despite cryo or requiring many pRBCs can give FFP (though large volume portal pressures)
o Delayed bleeding or oozing from mucocutaneous sites c/f hyperfibrinolysis topical and/or systemic Amicar (3g PO QID or
4-5g IV over 1hr 1g/hr) or TXA (1g IV q6hr)
• Procedures:
o Platelets: >50k for surgery, TIPS, liver biopsy, or other procedure w/ high bleeding risk; TPO agonists can reduce need for peri-
procedural plt transfusions but take ~10d to plts (NEJM 2012;367:716; Gastro 2018;155:705).
o PT/INR: NO benefit to giving FFP pre-procedure to “correct” INR. volume can bleeding risk by portal pressures.
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STEPWISE WORKUP
1) History/exam: vitals (hyper/hypoTN), volume status, exposures (contrast, meds, see below), recent infection (IgA nephropathy 1-2d,
post-strep GN in 10-14d), active infection (sepsis can induce ATN independent of BP or RBF (JASN 2011;22:999), trauma/myalgias
(rhabdomyolysis), rashes (AIN, vasculitis)
2) Urinalysis (UA): See Urinalysis page
3) Urine chemistries:
o FENa: FENa< 1% c/w pre-renal AKI, >2% c/w ATN. Note this is ONLY verified in oliguric AKI; overall limited use except to rule
out HRS with elevated FeNa (J Hosp Med 2016;11:77)
o FEUrea: if on diuretics, FENa unreliable. Calculate FEUrea as above, <35% consistent with pre-renal (Kid Int 2002;62:2223)
o Urine Osm: >500 is consistent with a pre-renal etiology. Patients with ATN are only rarely able to concentrate to this degree.
o Urine protein: if proteinuria on UA, send serum albumin, urine total protein, urine microalbumin and urine Cr. Urine
albumin/protein ratio(APR) > 0.4 suggests glomerular > tubulointerstitial process (Sn 88% / Sp 99%) (Nephro Dial Trans
2012;27:1534)
4) Urine sediment: see Urinalysis page. Important if clinical history/above studies are not strongly suggestive or if AKI fails to respond to
initial management.
5) Eosinophilia/eosinophiluria: poor test for AIN. Urine eos >1% has Sn 31%, Sp 68% (J Hosp Med 2017;12:343)
6) Renal U/S: exclude hydronephrosis. In absence of a suggestive history, <1% of renal U/S for AKI showed post-renal etiology; can
provide evidence of chronic processes if no known hx (BMC Nephrol 2013;14:188).
7) Monitor Cr: what is the response to empiric treatment of presumed cause?
8) Next: if sediment or history suggests glomerular disease, broaden workup with C3/4, ANCA, anti-GBM, ANA, anti-dsDNA,
HBV/HCV/HIV, cryo, SPEP w/ IMFX/SFLC as per below. Consider biopsy if expected to change treatment.
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RENAL TRANSPLANT
• Listing: refer EARLY, pts can be listed when GFR <20; pt and graft survival are improved if transplant occurs PRIOR to starting HD
• Contraindications: short life expectancy, active malignancy, SUD, nonadherence; age/HIV/psych comorbidities NOT contraindications
• Allograft dysfunction: delayed graft function: <1wk (prerenal, ATN, thrombus, obstruction), early: 1-12 wks (prerenal, CNI tox, infxn
[BK virus, CMV], acute rejection), late acute: > 3mo (prerenal, CNI tox, noncompliance), late chronic: yrs (HTN, CNI toxicity, BK
virus, recurrence of original renal pathology, chronic allograft nephropathy
IMMUNOSUPPRESSION
Class Examples Mechanism of Action Adverse Events
Calcineurin Cyclosporine Inhibits calcineurin-mediated activation of Nephrotoxicity (long-term fibrosis), HTN,
inhibitor Tacrolimus (FK506) NFAT blocks T-cell cytokine production tremor, insomnia, hirsutism (CsA only)
Pulmonary edema, wound healing,
mTOR inhibitor Sirolimus (Rapamycin) Inhibits mTOR blocks IL-2 production
hyperTG
Mycophenolate
Inhibits de-novo purine synthesis N/V/D
Antimetabolite (Cellcept, Myfortic)
Azathioprine Purine analogue BM suppression, N/V/D, hepatitis
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Fractional Excretion
• Loop diuretics have a sigmoidal dose-response curve so double dose until adequate
of Sodium (%)
response is achieved
• Transient increases in serum Cr are common in diuresis. No association between
worsening renal function during diuresis and biomarkers of kidney tubule injury;
increased survival in HF (Circ 2018;137:2016)
Urinary Diuretic Concentration or
Excretion Rate (log value)
(via 5-oxoproline)
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HYPOtonic hyponatremia (SOsm < 300) ISOtonic hyponatremia (SOsm ≈ 300) HYPERtonic hyponatremia (SOsm > 300)
AKA “pseudohyponatremia” Hyperglycemia
Hyperproteinemia, Hyperlipidemia (True Na= SNa +[(Sgluc-100)/100])
✓ Uosm Osmolal gap (mannitol, sorbitol, IVIG)
ADH Absent States UNa < 30: RAAS active, Na avid UNa > 30: RAAS inactive, Na wasting
Overwhelming kidney’s ability to dilute effective art blood volume (EABV)
1° Polydipsia True hypovolemia ( TBW and EABV) Common: diuretics, Na-wasting nephritis, SIADH
Solute intake: Tea & Toast TBW but EABV cerebral Na wasting / pain / nausea , SSRIs
Beer Potomania 3rd spacing (pancreatitis, musc injury) Mineralocorticoid / glucocorticoid
CHF, cirrhosis, nephrotic syndrome Hypothyroidism (severe)
1° Polydipsia: restrict fluids, psych Hypovolemia: replete volume Correct underlying cause:
TREATMENT
eval, risk for overcorrection, avoid Pancreatitis: replete volume Hold diuretics, fix endocrinopathy
DDAVP CHF, Cirrhosis, Nephrosis: diuresis SIADH: restrict free H2O. Consider NaCl tabs (1g
Tea & Toast or Potomania: SLOW TID Na delivery thus H2O excretion). If UOsm >
introduction of solute, will correct Figure adapted from 2x SOsm or if UNa + UK > SNa consider Lasix
RAPIDLY, at VERY risk for Am J Med 2010;123:652. (10-20mg BID; cortico-medullary gradient).
overcorrection Consider vaptans (NEJM 2006;355:2099). Treat
pain.
Treatment: depends on acuity, severity, and etiology (JASN 2017;28:1340)
• Safest to assume hypoNa is chronic unless accurately known from labs/hx. Strict I/O, fluid restriction and monitor BMP frequently. In
general, do not give isotonic saline. Consult renal if starting hypertonic saline.
• Severe symptomatic hypoNa (seizures, AMS): 3% NaCl bolus (100mL up to 3x over 10min until sx resolve or Na 4-6 mEq/L)
• Severe asymptomatic hypoNa (Na<120): Goal Na 6 mEq/L in first 24h. 3% NaCl with rate based on Sodium Correction Rate,
usually 15-30mL/hr. Stop 3% NaCl when Na>125 or if correcting too fast. Consider DDAVP clamp (below).
• Mild/mod hypoNa (Na≥120): if not hypovolemic in etiology, fluid restriction <1.5L, +/- salt tablets 1g TID
• Overcorrection: ADH once euvolemic free water diuresis and rate of correction. Increased risk of osmotic demyelination
syndrome if Na ≤ 105, hypovolemic hypoNa, tea/toast, beer potomania, low K, EtOH, ESLD, malnourished
o Definition: Na > 8 mq/L in 24h or ≥ 18 mEq/L in 48h. If overcorrecting or UOP rises > 300cc/hr x 2h, consider DDAVP
“clamp”: 2mcg IV or SC q8h for 24-48h or until Na > 125; plus 3% NaCl based on Sodium Correction Rate. Augment with D5W
and 3% NaCl PRN to achieve above goal. (Am J Kidney Dis 2013;61:571)
• Concurrent hypokalemia: K and Na freely exchanged, giving 1 mEq of K = giving 1 mEq of Na; be aware of overcorrection
H Y P E R N A T R E M I A : free water loss in excess of NaCl loss (Crit Care 2013;17:206, NEJM 2015;372:55)
Etiologies: impaired access to free water or impaired thirst, urinary concentrating ability or DI ( production or efficacy of ADH)
• Renal losses: Uosm <700–800; either ADH not released or kidney unable to respond: post ATN diuresis, osmotic diuresis, DI, rarely
loop diuretic; elderly ( max concentrating ability)
• Extrarenal losses: Uosm >700–800; GI loss from NGT, vomiting, diarrhea, insensible losses, hypodipsia
Acute HyperNa (<48h, rare salt poisoning, acute DI crisis). BMP q2-4h.
• Goal: correct to normal Na within 24H with D5W IV at 3-6ml/kg/hr until Na 145, then reduce D5W to 1ml/kg/hr until Na 140.
Chronic HyperNa (>48h, most common). BMP q12-24h. Strict I/O, UOP.
• Goal: correct at rate of 10-12mEq/L/day to prevent cerebral edema, though risk is low (CJASN 2019;14:656).
1. Calculate free water deficit. Shortcut FWD = (Current Na – Goal Na)/3. Target Na should be 24h goal based on correction rate
(i.e. <10-12mEq/L/day). Obese patients will have decreased %TBW.
2. Account for ongoing losses: insensible losses (600-800cc/day), UOP, stool output, burn patients to avoid undercorrection
3. Calculate hourly rate of free water replacement, adding ongoing losses and provide as PO free water, enteric tube free water
boluses (e.g. 200-400mL Q6-8h) or IV D5W. If DI, may need DDAVP (See Pituitary Disorders in Endocrine section).
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HYPOKALEMIA
Signs and symptoms: usually with K+ < 2.5 cramps, ileus,
weakness (LEs > trunk/UEs > respiratory muscle paralysis),
rhabdo (Annals 2009;150:619)
• ECG: flat T waves, ST dep, U waves, QT, atrial or ventricular
ectopy VT, VF (esp if K+ <3, susceptible pts, or on digoxin)
• Etiologies:
o Lab artifact (pseudo-hypokalemia): WBC >100 WBC absorb K if sample sits out (check K on ABG+)
o Inadequate intake unlikely to be 1° cause, usually combined with another etiology
o Redistribution: pH, insulin, hypoK/thyrotox periodic paralysis, blood cell prod (e.g. s/p G-CSF), hypothermia, β-
adrenergic activity (e.g. albuterol, epi), refeeding syndrome, toxins (cesium, barium, chloroquine)
o Extrarenal losses: diarrhea (esp. if chronic, VIPoma, villous adenoma, laxatives), insensible losses, vomiting/NGT
o Renal losses (w/o HTN): urine flow (psych polydipsia, excess IVF), Mg++, meds (ampho B, ifosphamide, cisplatin, gent)
Acidemia: DKA, RTA (proximal and some distal)
Alkalemia: diuretics, UGI losses (2° hyperaldo), Bartter’s (~loop diuretic), Gitelman’s (~thiazide)
Other: urine excretion of anions (β-OH-butyrate in DKA, bicarb [e.g. UGI losses], toluene + PCN metabolites)
o Renal losses (with HTN):
1° hyperaldo: aldo. renin (e.g. adrenal adenoma); 2°: a, r (e.g. renin-secreting tumor, renal art. stenosis)
Other: glucocorticoid or ENaC activity (e.g. Cushing’s, Liddle’s syndrome, black licorice)
• Management: 10mEq raises K+ by 0.1 mmol/L; caution if Cr or if due to transcellular shifts
o Oral KCl (ER = pill, IR = powder) preferred for tx as SAFER, quick acting, retention of K+, and many pts are Cl depleted
o IV formulation KCl if unable to take PO or if severe / symptomatic max 10mEq/hr (floor), 20mEq/hr (ICU)
o Always replete Mg++, otherwise K+ repletion ineffective (JASN 2007;18:2649)
o Avoid dextrose-containing solutions can acutely worsen hypoK (dextrose insulin secretion K+ shifts into cell)
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MGH Albumin Policy (Ellucid): put in place to prevent non-evidence-based overuse (ASA Choosing Wisely)
Albumin 25% = 12.5g albumin in 50ml solution; Albumin 5% = 12.5g albumin in 250ml solution
Use to replace serum oncotic pressure. If you need volume, give crystalloid.
• SBP: improves renal outcomes. Dosing: albumin 25% at 1.5g/kg IV within 6hrs arrival, decrease to 1g/kg on Day 3.
• Large volume paracentesis in cirrhosis: only if >5L removed. Dosing: Albumin 25% at 6-8g/L ascites removed.
• Augmenting diuresis in ARDS: already on high dose loop diuretic AND Albumin <2.5 or Total Prot <6
Dosing: Albumin 25% at 25g IV q8h for 3 doses (requires attending approval; sop once alb >2.5. MAX 3 days).
• Hepatorenal syndrome: diagnosis and/or treatment by protocol. See Hepatorenal Syndrome in GI section.
• Other: chatter in ECMO/VADs, burns, nephrotic syndrome
ELECTROLYTE REPLETION – see Potassium Disorders, Magnesium & Phosphorus Disorders, and Calcium Disorders
(Endocrinology) for more specific guidelines
Potassium Magnesium Phosphorus Calcium
- CAD/arrhythmia: ≥4
- Replete if sx, long QTc,
- Everyone else: ≥3.5 - CAD/arrhythmia: ≥2 - Replete if sx or phos <1
Goal Ca <7.5, iCal
- Do not replete if on HD - Everyone else ≥1.7 - At risk for refeeding: >2
<1.15mmol/L
unless <3.0
IV if severe,
PO or IV? PO > IV IV > PO PO > IV
PO if mild
- KCl IR (powder): q4-6 hr
- Mg oxide 400mg (240 mg - K-Phos: 1 packet QID - Ca carbonate 1250 mg
PO repletion - KCl ER (pills): giant pills
elemental Mg) TID x1 day - Neutra-Phos: 1 packet QID PO BID
- If K <3.5, ≥20 mEq KCl IR
- Peripheral: 10 mEq/hr - Give 15-45 mmol Phos at a time - Ca gluconate 1-2gm IV;
IV repletion - Central: 20 mEq/hr w/ - Mg sulfate 2g IV - K-Phos (1.5 mEq K/mmol Phos) - CaCl2 used in codes,
telemetry monitoring - Na-Phos (1.3 mEq Na/mmol Phos) 0.5-1g q2-5 min
- Correct for low Alb and
- 10 mEq K serum K by 0.1 - 2g will serum Mg by 0.5
- IV Phosphate can precipitate Ca hyperphos first
Comments - Max 80 mEq re-check K - Mg can cause K and
causing hypocalcemia - 1g Ca gluconate
- Correct hypoMg Ca
serum Ca by 0.5
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Nephrology Urinalysis
URINE DIPSTICK – urine should be analyzed within 2-4 hr
Can help approximate urine osm: decimal of SG x 30 (e.g. SG 1.020 20 x 30 ~ 600mosms)
Specific SG < 1.010: post-ATN (concentrating defect), diuretics, DI, polydipsia, hypovolemic hypoNa after resuscitation
Gravity SG 1.010 – 1.025: normal
SG >1.025: prerenal, contrast (esp >1.030), EABV, glycosuria (DM), proteinuria, SIADH
Normal 4.5 - 8, but strongly depends on serum pH and dietary intake
pH If normal urine pH + metabolic acidosis, suspect distal RTA (kidney not secreting NH4+)
If pH ≥7, suspect urease-producing organisms (Proteus, PsA), strict vegetarians (low protein diet), type I RTA
LE Released from lysed PMNs; FP: pH or SG (lyses WBCs); FN: proteinuria, glucosuria. For UTI, Sn 80% / Sp low
Nitrite Indicates nitrate-reducing GNR (E. coli, Klebsiella, Proteus, PsA – NOT Enterococcus). For UTI, Sn 60% / Sp>90%
UTI; if sterile pyuria, consider AIN, GN, Chlamydia, Ureaplasma, urethritis, TB, foreign body, exercise, steroid use,
WBC
cyclophosphamide
Detects heme (glomerular, renal, or urologic); FP: hemoglobinuria (hemolysis), myoglobinuria (rhabdo), semen,
Blood
drugs (rifampin, chloroquine, iodine), peroxidase producing bacteria
Detects albumin when excretion >300mg/d: glomerular, tubular, and overflow causes; does NOT detect light chains
Protein Semiquantitative categories (trace, 1+, 2+, and 3+) are not reliable, vary with SG
Falsely elevated by high SG, heavy hematuria (heme protein), and iodinated contrast (w/in 24h)
Ketones Detects only acetoacetate, NOT β-hydroxybutyrate; yield decreases as collected urine sits
Reflects glomerular overflow (serum glucose >180mg/dl or SGLT-inhibitor/mutation) OR
Glucose
PCT failure (glucosuria w/ normal serum glucose consider Fanconi’s syndrome 2/2 MM, heavy metal, drugs, etc.)
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Virology/Epidemiology Transmission
Clinical Illness: Coronavirus Disease 2019, COVID-19 Main Route:
Virus: SARS-CoV-2, 2019 Novel Coronavirus, 2019-nCoV ● Person to person via (large) respiratory droplets + direct
● 4 genera of coronavirus exist, some cause common cold contact; aerosolization thought to only occur with specific
(or viral PNA in pts w/comorbidities). Genus procedures
Betacoronavirus includes SARS-CoV, MERS-CoV, and ● Median duration of viral shedding 20 days. Resp. viral
SARS-CoV-2 shedding highest early in course; evidence for pre-
● Source: zoonotic, reservoir unknown (Nature Med symptomatic transmission (JAMA 2020;323:1406); may
2020;26:450), original association with live animal market persist after sx resolution depending on illness severity.
in Wuhan, China No good evidence for late transmission. Peak
● Host entry: Viral S spike binds ACE2 receptor (Cell infectiousness around 1 day before symptoms
2020;181:271) on type 2 alveolar cells & intestinal epithelia Extra-pulmonary transmission:
(same as SARS). ACE2 also in olfactory epithelium, liver, ● Fomites: droplet lives hours to days on surfaces (NEJM
kidney, endothelium, & myocardium (Cardiovasc Res 2020;382:1564)
2020;116:1097) ● Viral RNA also detected in stool in pts with GI sxs (NEJM
● Epidemiology: 2020;382:929; no known fecal-oral transmission, but could
o R0 estimate 2-4; decrease to 1 with control measures have direct contact transmission since ACE2 receptors in
(Lancet ID 2020;20:553) oropharynx), conjunctiva (Acta Ophth 2020), serum (Emerg
o Symptomatic CFR 1-2%, though varies with age and Microbes ID 2020;9:469; more common in critically ill pts),
comorbidities; Incubation 4-24d (median 5.1d, 1/100 and very rarely urine.
develop sxs after 14d; Annals 2020;172:577) ● Vertical transmission: recent evidence of IgM in newborns
o True # cases may be much higher than reported is suggestive (JAMA 2020;323:1848 & 1846), no viral
(Science 2020;368:489) shedding in breast milk. Placental infxn may cause
miscarriage (JAMA 2020)
Symptoms (NEJM 2020;382:1708)
Prevention:
● No universal symptom; can vary widely
● Social distancing; CDC Patient Guidance
● Constitutional: fatigue (23-70%), myalgia (15-35%),
● Hand washing soap > alcohol; don’t touch face; wipe
anorexia (40-78%). Fever: 80%-96% throughout the
surfaces w/alcohol, bleach, EPA-approved disinfectant
course, but not always present on admission. May be low
grade (i.e. 99.5F/37.5C)
● Respiratory: dry cough: (41-79%), sputum production (10-
45%), dyspnea (11-80%), rhinorrhea (5-15%), sore throat,
anosmia and ageusia
● GI: (e.g. n/v/d): 10-50% (Gastro 2020)
● Skin: localized or widespread urticaria, petechial rash
Laboratory Findings: for frequency and indications for testing, refer to MGH guidelines
Labs Findings/Notes
Leukopenia & lymphopenia (60-80%), AKI in ~3-9% (more common later
Basic labs: CBC w/ diff, BMP, LFTs
in course), AST/ALT/Tbili (Lancet RM 2020;8:475)
Inflammatory markers and acute phase reactants:
All may be elevated
CK, ferritin, CRP, ESR, LDH
Coagulation studies: PT/PTT, fibrinogen, D-dimer D-dimer (associated with mortality), fibrinogen can be or
Viral serologies: HBsAg, HBsAb, HBcAb, HCV Ab, 20% of COVID-19 cases have abnormal LFTs, want to r/o other causes,
HIV) may influence treatment choice (esp. remdesivir and lopinavir/ritonavir)
Only if c/f bacterial infection (note: rate of co-infection with bacterial PNA
Bacterial infection studies: BCx, procalcitonin, Strep
thought to be low. Procal initially low in COVID-19 but may rise after ~10
pneumo + legionella urinary Ag
days of infxn, even w/o superimposed bacterial infxn)
Extended infectious studies: Tspot, sputum Please refer to MGH guidelines for testing indications. DO NOT obtain
AFB/fungal Cx, pneumocystis DFA, 1,3-BDG, IgG induced sputum due to risk of aerosolization
Troponin troponin in some cases (see Complications below)
β-hCG Women of childbearing age
UA + spot urine protein:Cr If AKI
IL-6 If category 2 or 3 risk factors
Risk Factors (for severe COVID-19)
● Category 1 – epidemiological: age>65, BMI >30, underlying pulmonary disease, CKD, DM with A1c>7.6, HTN, CVD,
immunosuppression (s/p transplant or on biologics), HIV with CD4 count <200 or unknown CD4 count.
● Category 2 – vital signs: RR >24, HR>125, SpO2 ≤93% on RA, P:F<300
● Category 3 – labs: D-dimer>1000, CPK> 2x ULN, CRP >100, LDH >245, elevated troponin, admission absolute lymphocyte
count <0.8, ferritin >500
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Complications and Critical Care Management (see MGH Critical Care Guidelines; NEJM 2020)
● Suspect 5-15% of hospitalized COVID-19 patients will develop critical illness; low threshold to call Sr On if concerned
o Sr On will work with ICU Triage intensivist to decide whether needs ICU transfer
o Note: RICU needs ~10min to don PPE for intubation. Can call RICU attending (via x63333 – STAT vs. non-STAT) to
discuss concerning pts (generally >4LNC or rapidly O2 requirement ≥1L NC/hr). Confirm Code Status before calling.
● ARDS may develop ~8-9 days after initial sx.
o Warning signs for deterioration:
worsening hypoxemia (P:F < 300,
room air O2 saturation <93%),
progressive lymphopenia,
increasing lactate and CRP,
worsening CXR
o Consider proning (MGH protocol)
as a rescue therapy for floor pts
requiring supplemental O2 (esp.
escalating levels)
o Note: early intubation is for lung
protection from barotrauma (due
to large spontaneous tidal
volumes/transpleural pressures;
avoiding HFNC/NIPPV is NOT
just about aerosol generation)
● Septic shock less common. If shock
worsens, consider myocarditis or
cardiomyopathy cardiogenic shock
(JAMA 2020;323:1612)
● Cardiac injury: elevated troponin
associated with increased risk of
death (HR 4.26; JAMA 2020)
● Coagulopathy: MGH Heme Guidelines
o Clotting: venous: PE/DVT seen in
7-27% of pts; arterial: reports of
large vessel strokes (NEJM 2020);
microvascular: lung, kidney, and
liver (rates of clotting are higher
in critically ill patients)
o Bleeding: 2-5%
o As many as 21% of pts with severe COVID may meet criteria for DIC (JTH 2020;18:1094)
● Causes of death: 53% respiratory, 33% combined respiratory/cardiac, 7% cardiac, 7% unattributed (ICM 2020;46:846)
Disclaimer: this page is updated in real time as more data emerge – for the most recent version, please refer to the White Book App
(https://mghwhitebook.app/). The management guidelines are also actively evolving, so these are linked within this page.
Clinical features: frequency, urgency, dysuria (premenopausal); malaise, incontinence, nocturia, suprapubic
tenderness (Infect Dis Clin NA 2014;28:1)
Fever, other s/sx of systemic illness e.g., chills/rigors, flank pain, CVA tenderness, pelvic or perineal pain (men)?
No Yes
Uncomplicated UTI (JAMA 2014; 312:1677) Complicated UTI
• Diagnosis: clinical; U/A can be used to confirm; pyuria (>10 • 30% w/ UTI and fever are bacteremic (usually older, flank /
WBC) has NPV>PPV, sensitivity (nearly 100%) >> specificity suprapubic pain, CRP, BP) (JAMA 2018;378:48)
o Women: if dysuria and frequency without vaginal • Pyelonephritis is a complicated UTI, & may itself be
discharge/irritation, >90% likelihood of UTI. In outpatient, complicated by perinephric or renal abscess
U/A unnecessary unless immunocompromised or w/ risk o WBC casts on U/A are suggestive of pyelo
factors for complicated UTI • Microbiology: same as UTI plus Serratia, Morganella,
o In outpatient, get UCx only if male, atypical sx, persist Providencia, Pseudomonas, Citrobacter. Gram-positives still
48-72 hr after abx initiated, or recur w/in 3 mo. of tx rare. If S. aureus, think bacteremia. Increasingly resistant
o Nitrites: only positive with Enterobacteriaceae (convert organisms (especially to FQ, TMP/SMX)
urinary nitrate to nitrite) • Dx: UCx in all; imaging if ill, suspect. obstruction, persistent sx
o Only test for pyuria if dipstick shows +LE • Treatment: Outpt: CPO 500mg BID OR LVO 750mg x 5-7d
• Differential diagnosis: vaginitis, urethritis, structural OR T/S DS BID x 7-10d. Can give 1x IV CTX prior to oral tx.
abnormality, PID, nephrolithiasis Inpt: CTX OR CEFE OR P/T; CBPN if c/f ESBL. Narrow to
• Microbiology: E. coli, Klebs, Proteus, S. Saprophyticus. oral agent if improving. Add Vanc / Linezolid if GPC on urine
Enterococcus rarely causes true infection. G/stain. Duration for inpt: depends on clinical course & oral
• Treatment: NFT 100mg BID x5d OR T/S DS BID x 3d OR agent chosen (5-7d for FQ; 7-10d for T/S; 10-14d for β-
fosfomycin 3g x1; alternatives: oral β-lactam (e.g. Augmentin lactam).
500mg BID, Cefpodoxime 100mg BID) x7d o Avoid NFT & fosfomycin (poor soft tissue penetration)
o Avoid NFT if CrCl < 30 o Remove/replace coated urologic devices
o Avoid empiric T/S if resistance >20% (E. Coli resistance o Prostatitis: FQN preferred for better penetration; tx
28% at MGH) duration up to 6 weeks
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hemodialysis, HIV, athletes, prisoners, military, LTC facility residents): add empiric PO/IV MRSA coverage (T/S or doxy)
‡ Systemic signs of infection include: T >38C or <36C, tachycardia (HR >90), tachypnea (RR >24), WBC >12 or <4
NB: erythema may worsen initially; should improve w/ 72h of abx. Take pictures and draw margin lines to track progress.
o Additional coverage: anaerobes (if necrosis, putrid smell, crepitus, certain diabetic infections [see below], animal bite); GNRs
(cirrhosis w/ severe infection, immunocomp, certain diabetic infections [as below]); PsA (neutropenic, trauma, post-op)
o Specific associations: gas gangrene (myonecrosis) C. perfringens; dog/cat bite Capnocytophaga, Pasteurella; human
bite/IVDU Eikenella; water exposure Aeromonas (freshwater); saltwater Vibrio vulnificus (esp. in cirrhosis)
o IVDU: discuss safe injection practices with patient. Links to printable patient resources: (CDC 1, CDC 2, HRC)
o Emerging data on long-acting injectables: oritavancin, dalbavancin, & telavancin (OFID 2018;5;S118; DIC 2018;7;1)
NECROTIZING FASCIITIS (NEJM 2017;377:2253)
• Microbiology: Type I: polymicrobial (mixed aerobes/anaerobes), risk factors include DM, immunosuppression, PVD; Type II:
monomicrobial (usually GAS, less often other Strep or Staph, Vibrio, Aeromonas), associated with TSS; myonecrosis (i.e., gas
gangrene); caused by C. perfringens, presents with gas in tissues, severe pain, toxin-mediated shock
• Risk factors: immunosupp., DM (esp. Fournier’s), cirrhosis, neutropenia, EtOH, trauma (even minor), skin/mucosal breach
• Clinical manifestations: pain out of proportion to exam, bullae, induration (risk of compartment syndrome), tissue anesthesia,
rapid skin changes (purple-red blue-grey), crepitus (suggestive of myonecrosis); systemic toxicity, CK, lactate, Cr, WBC
• Diagnosis: early suspicion and involvement of a surgeon for surgical exploration and ID is critical
o LRINEC score ≥ 6 raises high suspicion for nec fasc; 90% Sn / 95% Sp (CCM 2004;32:1535)
• Treatment: urgent surgical debridement + Abx: (vanc or linezolid) + (pip/tazo or penem) + clinda for toxin inhibition
DIABETIC FOOT INFECTIONS ( D F I ) (IDSA Guidelines: CID 2016;63:944)
• Severity: mild (superficial ulcer, no involvement of deeper structures, erythema <2 cm); moderate (ulcer with involvement of
deeper structures or erythema >2 cm); severe (moderate + systemic signs of infxn)
• Initial evaluation: cleanse, debride, probe, culture. Check pulses/sensation, ABIs (40% will have PAD), consider XR/MRI
• Diagnosis: wound culture. Most polymicrobial w/ GPCs>GNRs, anaerobes. For mod-severe infxn: add blood Cx + ESR/CRP
o Osteomyelitis: risk if: visible bone/probe to bone (Sn 87%/Sp 83%), ulcer >2 cm2, ulcer >1-2 weeks, ESR >70mm/h
(JAMA 2008;299:806, CID 2008;47:519)
o If suspicious for osteo, obtain plain films ± MRI ± surgical consult for bone/tissue biopsy ± ID consult
• Treatment: definitive tx based on deep cx obtained PRIOR to the initiation of abx. Appropriate wound care is critical.
o Mild: oral target GPCs (cephalexin, amox/clav, diclox, levoflox); TMP-SMX or doxy for MRSA; 1-2 weeks tx
o Moderate/severe: IV target GPCs, GNRs, ± anaerobes: (CTX or FQ) + flagyl; or amp/sulb. MRSA coverage w/ vanc,
linezolid, or dapto if: severe infxn, prior MRSA infxn/colonization, other RFs (see above). PsA coverage w/ cefepime or
pip/tazo if: severe infxn, immunocomp, neutropenic, water exposure, burn/puncture, nosocomial.
o If improved, may de-escalate IV to highly bioavailable PO regimen to complete course
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Treatment: Empiric Tx
• Antibiotics (tx based on culture data, see table) Vancomycin + GNR coverage (typically ceftriaxone 2g
o Delay empiric tx until Bx if pt HD stable, no q24). Include PsA coverage (cefepime) for IVDU
neurologic compromise or epidural abscess
Organism-Specific Tx
o Common organisms: MSSA/MRSA, coag-neg staph,
Nafcillin 2g IV q4h; cefazolin 2g IV q8h
strep, enterococci, aerobic GNRs. Other: Brucella, MSSA
(not if a/w CNS infxn).
Mycobacteria, Fungal.
o Can consider adding rifampin if Staph + hardware MRSA or CoNS Vancomycin; daptomycin
(for biofilm) (Arch Intern Med 2008;168:805) Pen G 4 mill U IV q4h; Ampicillin 2g q4;
PCN-S Strep
o Duration: usually ≥4-6 wks, PO may be adequate CTX 2g q24; Vanc.
but discuss w/ ID (OVIVA trial). If using PO, FQ + Pen G 4 mill U IV q4h; Ampicillin 2g q4
Enterococci
rifampin most commonly used (NEJM 2019;380:425) +/- CTX 2g q24; Vanc; Dapto.
o If no residual infected bone (i.e. amputation), short CTX 2g q24h; Cipro 750 PO BID;
course abx 2-5d up to 10-14 if associated soft GNR Levoflox. 750mg PO/IV q24; Cefepime
tissue infection. 2g IV q12h, q8h if PsA
o Consider rechecking ESR/CRP; if elevated at end of abx course, consider further w/u (NB: routine repeat MRI NOT
done b/c MRI findings take weeks to months to resolve)
• Surgical debridement: indicated if failure to respond to medical therapies, chronic osteomyelitis, complications of
pyogenic vertebral osteo (e.g., early signs of cord compression, spinal instability, epidural abscess), or infected prosthesis
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Clinical Manifestations
• Features: watery diarrhea (≥3 loose stools in 24/hrs) +/- mucus/occult blood; fever, abd pain, isolated WBC (CID
2002;34:1585); ileus in severe infection
• Ddx: non-C. diff abx-associated diarrhea, infectious diarrhea, postinfectious IBS, IBD, microscopic colitis, celiac disease
• Severity: see table below; severe colitis may be c/b hypovolemia, AKI, marked leukocytosis, lactic acidosis, protein-losing
enteropathy; fulminant colitis characterized by hypotension/shock, ileus, or toxic megacolon & has high mortality
Diagnosis
• MGH protocol: see algorithm to right. NB: indeterminant results can be
2/2 asymptomatic (non-toxin-producing) colonization.
o GDH: enzyme produced by all C. diff strains; assay sensitive but
cannot distinguish toxigenic & non-toxigenic strains
o Toxin A/B: assay detects toxin production; high Sp. but poor Sn.
o NAAT/PCR toxin gene: high Sn. but can be ⊕ even in the absence of
active infection (strain may have toxin gene but not produce it)
• DO NOT retest within 7d w/o significant clinical change & DO NOT test for
“cure” (stool assays may remain ⊕ for up to 6w in pt w/ resolution of sx).
• CT A/P: if severe illness or fulminant colitis to assess for complications
warranting surgical intervention (e.g. toxic megacolon, bowel perf)
• Flex sig: in rare cases when alt dx suspected and need visualization/bx
Other Considerations
• Prophylaxis: mixed data but secondary ppx w/ PO vanc (standard or reduced dose 125-250mg BID) may recurrence in
pts w/ prior CDI receiving systemic abx (AJG 2016;111:1834, CID 2016;63:651, ICHE 2019;40:662). May also be effective as
primary ppx in high-risk patients (older, recent systemic abx) w/ 125mg daily dosing (CID 2019).
• Probiotics: insufficient evidence & therefore not in guidelines; some evidence however does support use w/ abx to
reduce abx-associated diarrhea (JAMA 2012;307:1959) and potentially prevent CDI (Gastro 2017;152:1889)
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Diagnostic Testing
Fungal markers:
• 1,3-β-D Glucan (BDG) (CID 2011;52:750): cell wall
polysaccharide, detects Candida, Aspergillus,
Pneumocystis (PCP/PJP), Fusarium, Trichosporon,
Histo, Coccidio; CANNOT detect Mucor, Rhizopus,
Blasto, Crypto; Sn 77%, Sp 86% w/ cut-off of 80
o False ⊕ w/ IVIG, albumin, HD, meds (cefepime)
• Galactomannan (GM) (Cochrane Rev 2015): detects
Aspergillus cell wall component; Sn 65-80% for serum
test (BAL 90-95%), Sp 88%. Can be used to monitor tx.
o False ⊕ w/ some TPN formulations
• Histo urine/serum Ag: UAg Sn 90% if disseminated (vs.
serum Ag 80%); Sp limited by cross-reactivity
• Crypto Ag: serum Ag Sn & Sp > 90% if disseminated,
less so for pulm. disease only
• Blastomycoses: urine > serum Ag; high Sn, but modest
Sp due to cross-reactivity
Culture: Candida grows in blood/urine Cx but Sn if deep
tissue infxn; if high concern for Coccidio, alert lab (biohazard) Notes: [1] Variable utility, e.g., sens for Histo but not Blasto. [2] 91% of MGH C.
Antibody detection: clinically most useful if testing for Coccidio glabrata is fluc-S. [3] Only approved for invasive aspergillosis/mucor. [4] In aspergillosis
vori + mica not superior to vori alone. [5] Covers all invasive fungi w/ rare exceptions,
e.g., C. lusitaniae. Always order AmphoB w/ pre & post hydration AND BMP, Mg BID.
Pathogen-Specific Information Adapted from JA Freed and AJ Hale, IDModules.com
Invasive Opportunistic Fungi
Risk factors: neutropenia, immunocompromised, TPN, IVDU, CVC, prior abdominal surgery
Spectrum of illness: sepsis (25% mortality), macronodular skin lesions (10%), endophthalmitis, endocarditis, osteo
Diagnostics: blood cultures (Candidemia never a contaminant in blood); obtain ophtho exam & ID consult
Candida Treatment: micafungin 1st line/empiric, transition to fluc if albicans, high dose fluc/vori if glabrata/krusei (or AmphoB for resistant
strains); Duration: 2 weeks after 1st neg Cx and no dissemination in candidemia, longer for deep-seated infxn
Source: non-neutropenic: lines most likely source (remove early); neutropenic: GI most likely source
Prophylaxis: fluconazole, posaconazole or micafungin (for SOT, SCT, neutropenic)
Risk factors: immunocompromised, liver disease, HIV, but can occur in immunocompetent (IDSA guidelines: CID 2010;50:291)
YEAST
Prophylaxis: consider posaconazole in grade III-IV GVHD (NEJM 2007;356:348), vori in lung transplant w/ h/o aspergillus.
Risk factors: DKA, iron overload, heme malig, prolonged neutropenia, immunocomp. (Semin Respir Crit Care Med 2015;36:692)
Spectrum of illness: rhino/orbital/cerebral invasion, pulmonary, GI, renal; black eschars over ulcers, rapidly progressive
Mucor Diagnostics: culture, wet prep (non-septating hyphae with wide-angle branches), CT with reverse halo sign
Treatment: DEBRIDEMENT, AmphoB, consider posaconazole or isavuconazole (for salvage therapy or if renal disease)
Endemic Fungi
Endemic areas: Houston, OH/MS river valleys, Central America, Asia, Africa (CID 2007;45:807)
Spectrum of illness: PNA, meningitis, mediastinal disease, disseminated disease
Histoplasmosis Diagnostics: Ag from urine/serum/BAL, Cx; NB: chest imaging may appear similar to sarcoid
Treatment: itraconazole (mild-mod) or ampho B (severe), followed by itraconazole; Duration: 6-12 weeks
Prophylaxis: for both Histo and Blasto (below), consider itraconazole ppx for HIV+ with CD4 <150 in hyperendemic areas
Endemic areas: OH/MS river valleys)
Spectrum of illness: fever, PNA, ARDS in severe, ulcerated skin lesions, prostatitis, CNS
Blastomycosis Diagnostics: wet prep (broad-based, budding yeast), culture, urine > serum Ag, never a colonizer
Treatment: itraconazole (mild-mod) or ampho B (severe), followed by itraconazole; Duration: 6-12 mos
Endemic areas: SW and S US
Spectrum of illness: fever, cough, rash, HA, eosinophilia, meningitis, osteo.
Coccidiomycosis Diagnostics: serologies, cx, spherules on bx/aspirate
Treatment: fluconazole or itraconazole, consider amphoB if severe; Duration: 3-12 mos
Prophylaxis: fluconazole for 1° ppx ONLY for transplant recipients in endemic areas, not in HIV; use fluconazole for 2° ppx
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Send brushings, washings, BAL, sputum for AFB smear, NAAT/PCR (Xpert) and culture; +/- transbronchial
Bronch
biopsy. Obtain post-bronch induced sputum to increase yield.
Ascites or pleural Adenosine deaminase (ADA): if >39 units/L high Sn/Sp; free IFN-gamma (if elevated, high Sn/Sp); AFB
fluid smear, NAAT/PCR (Xpert), & culture (poor sensitivity, helpful if positive)
At least 3 large vol (10-15cc) serial LPs if possible ( dx yield). Cell counts w/ glucose, protein,
CSF
lymphocyte predominance; ADA useful adjunct. Send smear, Cx, and NAAT/PCR (Xpert)
Wound/Tissue AFB-positive staining and caseating granulomas; if cytopenic, consider bone marrow biopsy
Urine UA shows “sterile” pyuria; send first AM void (large vol -50cc) for culture x3 days
Blood Can send mycobacterial cultures (isolators) for AFB
Patient Isolation: clinical decision based on likelihood of active TB
• When: cough, dyspnea, or hemoptysis + ≥1 risk factor (HIV+, foreign born, substance use disorder, homeless, recent
incarceration, prior TB or exposure). First obtain CXR; if CXR normal (and HIV- or CD4>200), TB less likely. If CXR
abnormal/equivocal (or HIV+ and CD4<200), maintain isolation and obtain 3 sputum samples for AFB smear and mycobacterial
culture as above. Consider ID c/s.
• Discontinue: if alt dx OR AFB smear neg x3 w/ very low suspicion OR on TB tx x2wks + AFB smear neg x3 + clinical improv.
Approach to Treatment (ATS/CDC/IDSA Guidelines: Clin Infect Dis 2016;63:e147; NEJM 2015;373:2149)
• Prior to starting treatment:
o General: check baseline LFTs/Cr, visual acuity/color discrimination, screen for HIV, Hep A/B/C, DM, EtOH use, pregnancy
o Before treating latent TB: need to rule out active TB (obtain relevant history, CXR)
o Before treating active TB: obtain ID consult, send TB for drug sensitivity testing
• Treatment regimens:
o Active TB: isoniazid (INH) + rifampin (RIF) + pyrazinamide (PZA) + ethambutol (EMB) x2mo., followed by INH+RIF x4mo.
o Latent TB: INH+rifapentine (RPT) qweek x12 (DOT no longer required) OR RIF x4mo. OR INH+B6 x6-9mo (less preferred)
(CDC Tx Table; CDC Tx Specifics; NEJM 2011;365;11; NEJM 2011;365;2155)
o Quinolones: 1st line w/ MDR-TB, avoid in bacterial PNA if suspicious for active TB ( dx yield & risk of resistance)
• Drug-resistant TB: suspect if previously treated, treatment failure, from prevalent area (India, China, Russia, S. Africa), or
known exposure. Treatment regimen depends on drug susceptibility profile; usually for 12-24 month tx course. 80% mortality
• HIV co-infection: if CD4<50 or CD4>50 with severe clinical disease but not meningitis, start ART within 2 weeks after starting
TB therapy. Discuss with ID.
• Extrapulmonary TB: highly variable presentation/therapy, duration depends on site of infection & response. For meningitis,
glucocorticoids confer 25% short term RR reduction in mortality (Cochrane Rev 2016)
• Medication side effects: hepatotoxicity (INH, RIF, PZA), optic neuritis (EMB), peripheral neuropathy (INH add pyridoxine [B6]
with initiation of treatment), orange bodily fluids (RIF), numerous drug-drug interactions (especially RIF)
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Virus
derived HHV 6,7 HPV, JC/PML, PTLD
VZV
CMV, community-acquired
Aspergillus Aspergillus
Fungus
Candida Endemic fungi Crypto
Mucor PCP Mucor
Bact.
related TB, non-TB mycobacteria
Toxo, leishmaniasis
Para.
HSCT Prophylaxis (J NCCN 2016;14:882) Strongy, T. cruzi
Adapted from Am J Transplant 2017;17:856
- Candida: fluconazole 400mg PO (d0-365 at MGH)
- HSV/VZV: famciclovir 250mg PO BID or acyclovir (d0-365)
- PJP: TMP/SMX SS QD or DS TIW; also covers Toxo, Nocardia, Listeria; alternative: atovaquone, dapsone (d0-180 or 365)
- High-risk HBV reactivation: entecavir, tenofovir, or lamivudine (duration varies)
- CMV: pre-emptive monitoring of VL in high-risk pts & initiate tx (valganciclovir or ganciclovir) when vs. ppx in high-risk pts. Letermovir
(CMV-specific; no activity against HSV) can be considered for ppx in select cases (NEJM 2017;377:2433)
Select Transplant-Associated Infections
Pathogen Clinical Syndrome Diagnosis/Treatment Additional comments
Dx: serum PCR +/- bx involved organ (GI
Most common infxn s/p solid tx.
bx, BAL, CSF). Serum PCR may be ⊝ in
P/w fever, leukopenia, +/- Highest risk: D+/R- in SOT and D-/R+ in
colitis (15%).
hepatitis, colitis/esophagitis, HSCT. May rejection and
CMV Tx: c/s ID. PO valganciclovir vs. IV
pancreatitis, retinitis, susceptibility to OIs. Repeat VL testing
ganciclovir. Consider resistance testing if
meningoencephalitis should be at least 7d apart (t1/2 of CMV).
not improving (UL97, UL57).
VL not comparable between labs.
Alt Tx: foscarnet or cidofovir
Dx: BAL PJP stain/PCR +/- TBBx, LDH, 1-
In contrast to HIV, there is limited data
Subacute dyspnea, hypoxemia, 3-β-D-Glucan
PJP to support the routine use of
fevers. Tx: TMP-SMX (15-20 mg/kg/day of TMP IV
glucocorticoids
in divided doses q6h)
Nephritis w/ AKI, ureteral Dx: BK PCR +/- biopsy
BK Virus Mainly in renal tx and HSCT pts
stenosis, hemorrhagic cystitis. Tx: immunosuppression
Hyperinfection syndrome:
fever, n/v/d, cough / wheeze /
Ivermectin 200 ug/kg/day until stool ⊝ x2 Identify at-risk individuals and treat pre-
Strongyloides hemoptysis, no eos with
weeks transplant
hyperinfection; 2° polymicrobial
bacteremia (e.g., GNRs)
Symptom-Driven Diagnostics
CXR, CT chest w/ contrast, induced sputum (GS/Cx, consider AFB stain, MB Cx, PJP stain), legionella urine Ag (Sn 70-
SOB 90% / Sp 100%), viral resp panel. If cavitating or nodular lesions: β-D-glucan/galactomannan, crypto Ag, urine/serum
histo Ag, early bronch w/ BAL. NB: engraftment syndrome, cryptogenic organizing PNA also on DDx
Stool Cx, O+P (consider micro add-on for: Cryptosporidium, Isopora, Cyclospora, Microsporidia), C. diff, CMV PCR. If high
Diarrhea
suspicion for viral colitis (e.g., CMV, adeno), c/s GI re: colo w/ Bx. In HSCT, consider typhlitis and GVHD.
CT head, LP (OP, GS/Cx, glucose, TP, HSV PCR, crypto Ag, save extra for additional tests). NB: fludarabine, cytarabine
AMS/HA
and calcineurin inhibitors (via PRES) can also lead to encephalopathy
Rash GVHD, medication allergy, HSV, cellulitis, fungal infection
Leukopenia CMV PCR, EBV PCR, consider tick-borne illnesses during the correct season or if frequent blood transfusions
If post-HSCT, consider viral (HAV, HBV, HCV, EBV, CMV, adenovirus + more rarely enterovirus and HHV6), Candida, and
Hepatitis
non-infectious (GVHD, iron tox., meds, hepatic sinusoidal occlusion syndrome)
AKI UA/UCx, renal U/S, BK PCR if renal transplant. Consider med toxicity and check levels (tacro, cyclosporine)
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Painful genitals/perianal ulcer 5-7d Usually clinical with negative Azithro 1g or CTX 250mg IV; PCN
Chancroid post-exposure w/ inguinal LAD +/- syphilis/HSV; also gram stain, Cx, PCR often also given empirically for
(H ducreyi) drainage in tropics in some labs syphilis; evaluate partners as well
Discharge Symptoms Diagnosis Treatment
♀: mucopurulent cervicitis, urethritis, ♀: vaginal swab NAAT (Sn >65%) > Ceftriaxone 250mg IM +
Gonorrhea PID (abd pain, adnexal/cervical urine NAAT (Sn >57%) azithromycin 1g PO
(N gonorrhoeae), tenderness, +/- fever), frequently asx
♂: dirty catch urine NAAT NB: consider Cx to test for
♂: dysuria + purulent discharge, All: consider pharyngeal/anal swab resistance- Asia (EID 2018; 24:381);
Chlamydia
epididymitis based on hx (pts can self-swab) Doxy not alternative to azithro but
(C trachomatis)
All: pharyngitis (BMJ Open 2019;9) used in PID to treat C trachomatis
Suspect in pts who fail tx for GC/CT Testing unavailable in USA, but: If failed tx for GC/CT & trich:
Mycoplasma ♀: cervicitis, PID, often asymptomatic ♀: vaginal swab NAAT moxifloxacin 400mg x7d (CID
genitalium ♂: dysuria + purulent discharge, ♂: urine NAAT 2015;60)
proctitis
♀: purulent malodorous discharge, Wet mount vaginal swab NAAT Metronidazole 2g PO or tinidazole
Trichomoniasis pruritus, dysuria, frequency, 2g PO +/- GC/CT tx; treat partner
(T vaginalis) dyspareunia
♂: usually asymptomatic
TRAVEL MEDICINE
Pre-Travel Evaluation
• Patient: medical conditions (immunosuppressed?), allergies (esp. vaccines), pregnant/planning to get pregnant, immunization hx,
prior travel history (experience with malaria prophylaxis/prior travel related illlnesses), med list
• Trip: place, duration, season, purpose of a trip, itinerary (urban vs. rural, cruise ship, exposure to animals, cave / water exposure)
• Counsel re: safety: sunscreen (SPF 50+), seatbelt/helmet, sexual practices etc. Provide patient with CDC Travel Tips.
Immunizations
• Ensure routine vaccinations are up to date then use MGH developed “Pre Travel PREP” or CDC site to get country-specific recs
• Common travel vaccines: Yellow Fever, HAV, Typhoid, Japanese Encephalitis, pre-exposure rabies, Cholera
Malaria Prophylaxis (typically South/Southeast Asia, Africa, Central/South America)
• Vector avoidance: DEET, permethrin, mosquito nets, cover exposed skin
• Rx per CDC tool based on resistance pattern. Start ~1 week before travel and up to 4 weeks after. Daily Rx: atovaquone-proguanil
(Malarone), doxy, primaquine. Weekly meds: mefloquine, chloroquine
Traveler’s Diarrhea
• Common pathogens: ETEC > C. Jejuni, Shigella & Salmonella spp, Giardia, E. histolytica, Strongyloides
• Tx: mild / moderate: loperamide/bismuth; severe (fever, interference w/ activity, dysentery): azithro 1g x1 > FQ (CDC Yellow Book)
Infections in a Returning Traveler
• Assess if life threatening illness or if transmissable via respiratory droplets, contact, etc (isolate pts)
• Broad ddx, consider geography, exposure risk, pt vulnerability, incubation periods. Common culprits: Malaria, dengue, TB, STIs, tick-
borne, typhoid fever, regular infections (CAP/UTI etc.) (NEJM 2017;376:548)
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Infectious
sinusitis, prostatitis, TB (miliary), tick-borne
valve disorders, recent procedure/hospitalization, changes in weight/anorexia infections, endemic fungi (e.g.
• Exam: assess for dental caries/thrush, sinus and temporal artery tenderness, cocci/histo/paracocci), malaria, cat-scratch
thyromegaly, CV murmur, abd tenderness, HSM; inspect eyes, fundi; perform disease, toxoplasmosis, Q fever (Coxiella),
complete lymph node, skin/nails, rectal, and joint exam brucellosis, Bartonella, salmonella, typhus,
mellioidosis, schistosomiasis, visceral
Diagnostic Testing leishmaniasis, Whipple’s disease,
• Initial: CBC w/ diff, BMP, LFTs, ESR/CRP, UA/UCx, BCx x3 (diff. sites), CXR lymphogranuloma venereum
(AJM 2015:128;1138e1) Lymphoma, leukemia, MM, myeloproliferative
Malig.
• Inflammatory markers: disorders, RCC, HCC, pancreatic, cervical,
o ESR: measure of chronic inflammation. Falsely elevated in ESRD (can mets, myxoma
be very high), paraproteinemia, anemia, obesity, and advanced age. Cryo, PMR/GCA/TA, RA, Adult Still’s
Correct for age (age / 2) for males and (age / 2) + 10 for females.
Rheum.
(JRA)/MAS, SLE, dermato/polymyositis,
o CRP: rises more acutely than ESR; may be falsely low in cirrhosis sarcoid, HSP, PAN, Kikuchi’s, Takayasu’s,
• Other labs to consider: IGRA, HIV Ab/Ag/PCR, RPR, LDH, TFTs, Behcet’s, GPA/MPA/EGPA
SPEP/SFL, ANA, ANCA, RF/CCP, cryo, CK/aldolase, EBV serologies, CMV Drug fever, serotonin syndrome, NMS,
PCR, ferritin, blood smear, HBV/HCV DVT/PE/hematoma, hypothalamic dysfunction,
• Imaging (Arch Intern Med 2003;163:545): CT C/A/P (19% Sn / 71% Sp), LENIs, pheo, thyroiditis, alcoholic hepatitis, cirrhosis,
Other
TTE, FDG-PET/CT (Sn 50-100% / Sp 46-90%), tagged WBC scan (Sn 60- IBD, factitious, HLH, familial periodic fever
75% / Sp 82-92%), maxillofacial CT syndromes (FMF, Hyper-IgD Syndrome,
• Tissue diagnosis: biopsies of LN, liver biopsy (14-17% yield), BM (low yield Schnitzler’s, TRAPS)
at 0-2%), temporal artery biopsy (GCA), kidney (RPGN), consider LP in *bold = common causes (AJM 2015;128:1138e1)
patients with CNS findings
Treatment
• Try to avoid empiric antibiotics and observe (unless hemodynamic instability or immunocompromised)
• Discontinue possible offending medications
• If high suspicion for GCA/vasculitis, strongly consider empiric steroids (prior to biopsy) to prevent vision loss / end-organ damage
• If extensive workup is negative, prognosis is usually good and most cases defervesce (AJM 2015:128;1138e1)
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Hematology Thrombocytopenia
THROMBOCYTOPENIA (Hematology 2012;2012:191) Anti-infectives:
Definition: platelet count < 150k. Risks: <50k w/ surgery, <20k spont. bleed (less so in ITP), <10k severe bleed TMP/SMX
SEQUESTRATION / Vancomycin
PRODUCTION DESTRUCTION
POOLING / DILUTIONAL Penicillin
- Infxn: late HIV/HCV, parvo, sepsis - Infxn: early HIV/HCV, H. pylori > - Splenomegaly (e.g. Ampicillin
- Nutrition: B12/folate/Cu, EtOH HSV/VZV/CMV/EBV, tick-borne illness cirrhosis & portal HTN): may Piperacillin
- Drugs: see list in margin - Immune: ITP (+AIHA=Evan’s), SLE/APS, sequester 90% of circulating
Ceftriaxone
- Malignancy: leukemia, MDS, PMF, RA, CLL, CVID, post-transfusion platelets
aplastic anemia, infiltrate - Drugs: immune (see list; NEJM 2007;357:580) - Massive transfusion 10U Rifampin
- Congenital: Bernard Soulier, vWD - MAHA: DIC, TTP/HUS, mHTN, HELLP pRBC plt by 50% Ethambutol
(specific types), other rare causes - Shearing/aggregation: CVVH, CPB, IABP; - Hypothermia Quinine
vasculitis, hemangioma (Kasabach-Merritt) - Gestational (in tonic water,
Workup: initial labs: CBC w/ diff (Δ other cell lines), review special slide (schistos, other), HIV, HCV (if not recently) bitter lemon)
• If c/f hemolytic anemia (Hgb & Plts) also LDH / hapto / bili, DAT (AIHA), retic count Quinidine
• If schistocytes on slide also coags, D-dimer, fibrinogen (eval for DIC vs. TTP/HUS), consider heme consult
• Consider ANA (SLE), ACL/LA (APLS) if appropriate based on other clinical signs/symptoms Anti-epileptics:
• If >60 yo, splenomegaly, or systemic sx consider BMBx to r/o MDS, AA, leukemia, infiltrate Cabamazepine
• Rule out pseudo-thrombocytopenia platelet clumping 2/2 EDTA (can order Platelet Count, Citrated) Phenytoin
Valproic acid
PRIMARY IMMUNE THROMBOCYTOPENIA (ITP) (ASH: Hem 2018;2018:568, Blood 2017;129:2829, NEJM 2019;381:945)
Pathophys: thrombocytopenia d/t auto Ab-mediated megakaryocyte destruction and plt production Anti-platelets:
Presentation/Dx: p/w mucocutaneous bleeding (or asx); defined by isolated plt <100k, dx of exclusion; 10% have ITP Abciximab
+ AIHA = Evans Syndrome. BMBx only done if atypical; anti-plt Ab not useful. Screen for H. pylori (tx may plts in ITP)
Eptifibatide
Management: treat if <30k, but 20-30k w/ no/mild bleeding (i.e. skin only) can be observed; response = >30k & 2x
• Severe bleeding: plts, IVIG, methylpred 1g/d IV x3d (or dexamethasone 40mg/d x4d), consider romiplostim. Tirofiban
o If no response in plts, consider Amicar (0.1g/kg/30min0.5-1g/hr) / tranexamic acid / activated FVII
Others:
• 1st line: dexamethasone 40 mg/d x4d (or prednisone 1 mg/kg/d PO x2-3wk taper) +/- IVIG 1 g/kg/d IV x 2d
Heparin (HIT)
• No response/recurrence: romiplostim (Nplate) / eltrombopag / avatrombopag, rituximab, splenectomy (after 6mo-
1y) Ranitidine
Simvastatin
HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) (Blood Adv 2018;2:3360, Blood 2017;129:2864, NEJM 2015;373:252) Haloperidol
Pathophys: anti-PF4-heparin complex Ab binds & activates plts, thrombin hypercoag. state, plts Amiodarone
Presentation: 5-10d after exposure, plt >50%, nadir 40-80K, thrombosis in 30-50% (skin necrosis, DVT/PE, arterial) Oxaliplatin
• risk w/ UFH; major surgery restarts the clock; consider rapid-onset HIT if <24hrs with prior exposure <1-3mo.;
Irinotecan
delayed-onset can present up to 3wks after heparin is discontinued
Acetaminophen
Diagnosis: calculate 4Ts Score. If ≥4, D/C heparin and anti-PF4. If high prob 4T w/ any degree of ⊕PF4 or int. prob
4T w/ mod/strong ⊕PF4, serotonin release assay. Otherwise, if neg PF4 or int. prob 4T w/ only weakly ⊕PRA, HIT Naproxen
unlikely, ok to resume heparin. 4T of ≤3 has high NPV (99%). Ibuprofen
Management: D/C all heparin products & add to allergy list. C/s heme, start alternative AC (NEJM 2013;368:737). Do Furosemide
NOT transfuse platelets unless severe hemorrhage. Needs AC until plt >150k if ⊝ thrombosis, ≥3mo. if ⊕. OTC/herbal
• Fondaparinux (synthetic, IV or subQ): for stable non-surgical patients, contraindicated if GFR <30, irreversible
• Argatroban (DTI, IV): monitor w/ chromogenic Xa (goal 20-40%), preferred in renal failure & surgical pts Direct BM:
• Bivalirudin (DTI, IV): only approved for HIT undergoing PCI, preferred in liver failure Linezolid
• DOACS for non-urgent AC: apixaban, edoxaban, rivaroxaban, dabigatran Thiazide
• VKA: not until plt >150K for 2 consecutive days Chemo/XRT
EtOH
THROMBOTIC MICROANGIOPATHIES (TMAs) (NEJM 2014;371:654)
Pathophys: small-vessel irregularities microthrombi MAHA (Hb, LDH, haptoglobin, +schistos, -DAT), plt
(aggregation, consumption), ischemic end-organ injury (vascular occlusion)
Diagnosis: special slide, CBC w/ diff, coags, D-dimer, fibrinogen, LDH, haptoglobin, retics, Cr, LFTs
Secondary etiologies: DIC, infxn, malignancy, SLE, APLAS, HELLP syndrome, scleroderma, severe HTN, post-HSCT
Primary etiologies: in addition to below, also metabolism-mediated (B12 metab. d/o) & coag.-mediated; rare & typically present in infants
• TTP (plt <30K): inherited/acquired ADAMTS13 def. vWF multimers. S/Sx: fatigue, purpura, GI sx, neuro sx in 60%; fever
uncommon, AKI rare, pentad rare. Dx: PLASMIC score if mod/high prob., ADAMTS13 (<10% = TTP). Tx: plasma exchange,
steroids, ritux. Caplacizumab may be option (NEJM 2019;380:335). No plts unless bleeding. (Blood 2017;129:2836, NEJM 2019;381:1662)
• HUS (plt >30K): Shiga-toxin-mediated bloody diarrhea w/ abd pain (O157:H7 E. coli, Shigella). S/Sx: severe AKI; severe neuro sx
(SZ, coma, hemiparesis) rare. Dx: stool⊕ for organism or toxin; Tx: supportive, often w/ HD, unclear role for Abx (Blood 2017;129:2847)
• Complement-mediated (“atypical HUS”): S/sx: severe AKI + 20% w/ extra-renal sx (CNS, cardiac, pulm hemorrhage, panc.); Dx:
complement genotyping, anti-complement Ab. Tx: plasma exchange; eculizumab (NEJM 2013;368:2169; Blood 2017;129:2847)
• Drug-induced: 1) Immune-mediated (gemcitabine, oxaliplatin, quetiapine, quinine) acute f/c, abd pain, n/v/d, AKI
2) Dose-dependent (gemcitabine + other chemo; tacrolimus, CSA + other IS; cocaine) subacute fatigue, HTN
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Hematology Eosinophilia
OVERVIEW (Am J Hematol 2017;92:1243, Hematology 2015;2015:92)
• Eosinophilia: AEC >500. Hypereosinophilia: AEC >1500. Hypereosinophilic syndromes (HES): AEC >1500 + organ dysfunction.
o Eosinophils are quickly eliminated by steroids eosinophilia may be unmasked as pts taper off chronic glucocorticoids.
• Either primary and due to clonal expansion (HES/leukemia) or secondary (reactive) due to infection, atopy, meds, rheum dz, etc.
Helminth: Strongyloides, toxocariasis, shistosomiasis, ascaris, filariasis, trichinellosis. Fungal: Aspergillus (ABPA),
Infections
coccidiomycosis, histoplasmosis. Protozoal: isospora. Viral: HIV, HTLV1/2.
Malignancy Primary HES (PDGFRA-assoc.), eosinophilic leukemia, CML, NHL, HL, mastocytosis; less common with solid tumors
Autoimmune EGPA (see Vasculitis), PAN, eosinophilic fasciitis, RA, IBD, IgG4, sarcoidosis, GVHD, blistering disease
Allergic Drugs, DRESS Syndrome, asthma/atopy, ABPA, hyper IgE syndrome, AIN, episodic angioedema (Gleich syndrome)
Misc Adrenal insufficiency, cholesterol emboli syndrome, acute arterial thrombosis.
WORKUP (Br J Haematol 2017;176:553, J Allergy Clin Immunol Pract 2018;6:1446, Hematology 2015;2015:92)
• Hx: meds/supplements (<6 wks), diet, travel, occupational exposures, atopy, infxn, malignancy, rheumatic dz, full ROS
• Exam: assess for rashes, cardiac/pulmonary abnormalities, nasal/sinus involvement, LAD, hepatosplenomegaly, neuropathy
• Initial diagnostics: CBC w/ diff (repeat), special slide, BMP, LFTs, LDH, ESR/CRP
o If AEC 500-1500: check troponin, B12/tryptase, CXR if clinically indicated
o If AEC >1500, assess for HES: check U/A, CK, troponin, EKG, CXR, PFTs, CT C/A/P (for adenopathy, organomegaly, masses,
organ infiltration), tissue biopsy of affected organs; also obtain B12, tryptase, serum Ig levels
• Additional diagnostics (as clinically indicated): Strongyloides serology & stool O&P, other serologies if potential exposure; ANCA if
?EGPA; ANA, RF, CCP if ?rheum dz; IgE levels + allergy testing if ?allergic; imaging/bronch, serologies (e.g. aspergillus IgE) if
?pulm. dz; imaging/endoscopy if ?GI dz; TTE/CMR if ?cardiac dz; periph. flow +/- BMBx if ?MPD or >1500 & no obvious 2° cause
TREATMENT (Hematology 2015;2015:92)
• Urgent Tx: if cardiac, neuro, or thromboembolic complications, AEC >100,000/rapidly rising, or s/sx of leukostasis 1mg/kg to 1g
solumedrol (+empiric ivermectin 200mcg/kg if potential Strongyloides exposure); obtain HES diagnostics above prior to initiating
• Non-urgent Tx: symptomatic or evidence of end-organ damage but does not need urgent Tx; see below for Tx by condition
• No Tx: if asymptomatic, no organ involvement, & no identified cause to treat, can monitor for resolution & organ damage
DRUGS: can be isolated Eos or accompanied by systemic illness (DRESS, hepatitis, AIN, etc). In hospital, PCNs/cephalosporins
common culprits. Suspect DRESS if new drug 2-6w prior, fever, rash, facial edema, LAD, abnml LFTS, ± organ involvement, atyp. lymphs.
ORGAN-SPECIFIC PATHOLOGY
Cardiac: (JACC 2017;70:2363, Immunol Allergy Clin North Am 2007;27:457)
• Eosinophilic endomyocarditis: necrosis thrombus formation ( embolic events) fibrosis restrictive CM, valve involvement
o May be due to hypersensitivity myocarditis, parasitic infections, malignancy, idiopathic HES
o Dx: TTE (LV/RV apical dysfunction, signs of restriction, intracardiac thrombi) and cardiac MRI (+subendocardial LGE)
o Tx: high dose steroids (≥1mg/kg pred) & remove culprit med (if hypersensivity), treat underlying disorder (parasite, HES)
• Eosinophilic coronary arteritis: rare complication of EGPA; may mimic ACS
Pulmonary: (Clin Microbiol Rev 2012;25:649, Chest 2014;145:883, J Allergy Clin Practice 2014;2:703)
• Acute eosinophilic PNA: <7d fever, cough, SOB; a/w smoking; periph. Eos often absent at presentation; Dx: BAL Eos ≥25%
• Chronic eosinophilic PNA: subacute fever, cough, SOB, wt loss; a/w asthma; Dx: BL periph/pleural infil, UL-predom; BAL Eos≥25%
• Allergic bronchopulmonary aspergillosis (ABPA): asthma/CF c/b recurrent exacerbations w/ fever, malaise, brown mucus plugs; Dx:
Eos, total IgE, Aspergillus IgE & IgG, imaging w/ central bronchiectasis, UL/ML consolidations; Tx: steroids + itraconazole
Loeffler syndrome: transient/migratory pulm. opacities, Eos 2/2 helminth larvae; Dx: larvae in resp secretion (stool usually ⊝)
GI: (AGA EoE: Gastro 2020;158:1776; NEJM 2015;373:1640; Clin Rev Allergy Immunol 2016;50:175)
• Eosinophilic esophagitis (EoE): dysphagia, food impaction, GERD-like sx/refractory GERD, assoc w/ allergic conditions; Dx: EGD w/
bx, exclude other causes (GERD, motility d/o, Crohn’s, infxn, CTD, etc.); Tx: dietary Δs, PPI, topical steroids (MDI/neb, PO liquid)
• Eosinophilic gastroenteritis (EGE): stomach/duod. +/- esoph., colon; Sx: n/v/d, abd. pain, ascites; Tx: dietary Δs, PO steroids
Others: neuro (peripheral neuropathy, encephalopathy, CVA/TIA from thromboemboli), thrombotic complications, skin Δs
PRIMARY HYPEREOSINOPHILIC SYNDROMES (HES) (Am J Hematol 2017;92:1243, Hematology 2015;2015:92)
• Myeloproliferative HES (~20% of HES in US): acute/chronic eosinophilic leukemia, PDGFRA-associated MPN clonal expansion
of Eos; 80% pts have FIP1L1-PDGFRA fusion gene; remainder have PDGFRA, FGFR1, JAK2 rearrangements
o Dx: anemia, thrombocytopenia, tryptase, B12, special slide (dysplastic eosinophils), flow cytometry (PDGFRA, BCR-ABL1,
JAK2, FGFR1, KIT), BM Bx (fibrosis, hypercellularity)
o Tx: if PDGDR+, imatinib; if JAK2+, JAK2 inhibitor; if FGFR1+, chemo; 2nd line or no rearrangment: hydroxyurea, IFN-α, other
TKI/empiric imatinib
• Lymphocytic HES: clonal T-cell expansion IL-5 Eos. Often p/w skin/soft tissue involv., polyclonal hyper-IgG, IgE. Episodic
angioedema (Gleich syndrome) is very rare subset of L-HES. Up to 25% risk of progression to lymphoma.
o Dx: flow cytometry for CD3, CD4 (clonal IL-5-secreting CD3- CD4+ T-cells)
o Tx: steroids; 2nd line: IFN-α, hydroxyurea, mepolizumab (anti-IL-5; NEJM 2008;358:1215), alemtuzumab
• Idiopathic HES: eosinophilia without identified cause and evidence of end-organ damage consider ANCA-neg EGPA (50% cases)
o Tx: steroids; 2nd line: hydroxyurea, IFN-α, imatinib, mepolizumab, alemtuzumab
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DIC: massive activation of coag cascade consumption of coag. factors (bleeding), microvascular thrombosis (MAHA, organ
ischemia). 2/2 various inflamm. etiologies (sepsis, CA, trauma, pancreatitis). Dx: PT/PTT, D-dimer, fibrinogen, plts, +schistos,
LDH, hapto. NB: often normal coags in chronic DIC. Can differentiate DIC from liver dz w/ FVIII (in endothelium, not liver). DIC score.
Tx: underlying cause, transfuse plts if <10k (or serious bleeding <50k), cryo if fibrinogen <100, FFP if INR >2. Amicar generally contraind.
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PARENTERAL AGENTS
Agent Dosing/Monitoring Bridging/Switching Reversal Other
Heparin (UFH) - ACS: 60U/kg 12U/kg/hr; PTT 63-83 - To LMWH: give LMWH & - Protamine: 1 mg per - Preferred in renal
- Binds & activates - VTE: 80U/kg 18U/kg/hr; PTT 70-100 UFH at same time 100U heparin or 1mg failure (CrCl <30),
ATIII inactivates - PPX: 5,000U SC q8-12h - To warfarin: UFH LMWH (max 50mg). peri-procedure, poor
Xa & IIa - Monitoring: PTT; anti-Xa (goal 0.3-0.7) if once therapeutic ≥2d 60% reversal for absorption, pregnancy
- t1/2 60-90min baseline PTT or high doses; ACT if ) LMWH, most effective
Enoxaparin - ACS/VTE: 1mg/kg BID; QD if GFR <30 - To UFH: LMWH & if last dose within 8 hr - Acute VTE: LMWH >
(LMWH, Lovenox) - PPX: 40mg SC QD; 30mg BID if risk; start UFH w/o bolus 1-2h - Do NOT give FFP UFH (Cochrane Rev
- Binds & activates 30% if BMI ≥40; 30mg QD if GFR <30 before LMWH dose due (has ATIII, which 2017)
ATIIIinact. Xa>>IIa - Monitoring: not routine; can anti-Xa 4h - To warfarin: LMWH potentiates A/C effect) - Prolonged t1/2 in renal
- t1/2 4.5-7hrs after 4th dose, goal 0.5-1.0 once therapeutic INR ≥2d failure
Fondaparinux - VTE: <50kg 5mg QD | 50-100kg - To warfarin: fonda. - No reversal agent - aPTT at
(Arixtra) 7.5mg QD | >100kg 10mg QD once therapeutic INR ≥2d therapeutic doses
- Binds & activates - PPX: 2.5mg SC QD - To UFH: start UFH (no - If CrCl 30-50,
ATIIIinact. Xa only - CrCl <30: contraindicated bolus) 1-2hrs before due consider Δ to different
- t1/2 17-21 hrs - Monitoring: not routine; can 4hr anti-Xa - From UFH: start 1hr after agent
UFH
Argatroban - HIT: 1-2mcg/kg/min - To warfarin: once - No reversal agent - Only dabigatran (PO)
- Direct IIa (thrombin) - Monitoring: PTT, goal 1.5-3x baseline PTT chromogenic factor Xa is has antidote
inhibitor - Caution in critically ill, cardiac dysfunction, 20-40% (argatroban (idarucizumab)
- t1/2 45min liver disease INR)
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Annabelle Anandappa
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Annabelle Anandappa
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Vinayak Venkataraman
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• Complications: (1) DIC (if presentstrong suspicion for APL, see below); (2) febrile neutropenia; (3) TLS allopurinol, fluids,
consider rasburicase if uric acid >10; (4) leukostasis hydroxyurea, fluids, consider leukapheresis
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Oncology Lymphoma
Lymphadenopathy (LAD) Evaluation (Am Fam Phys 2016;94:896)
• Generalized LAD DDx: HIV, EBV, mycobacteria (TB), SLE, medications (e.g. phenytoin), sarcoid, lymphoma/malignancy
• Localized LAD DDx: cervical (EBV, CMV, toxo, TB, lymphoma), supraclav (malignancy), axillary (infxn, breast CA), inguinal (STDs)
• Hx: exposures, travel, meds, B Sx (fevers/drenching night sweats, >10% unintentional wt loss in 6 mo), other s/sxs of infxn or malig
• Exam: localization (think about area of nodal drainage), size (abnormal >1 cm), consistency, fixation, tenderness (inflammation)
• Labs: CBC, HIV (RNA if acute), LDH, HBV/HCV, PPD/TSpot, RPR, ANA, heterophile Ab; consider HTLV and EBV serologies
• Imaging: CT C/A/P (I+), PET (can define node size and distribution, more helpful for monitoring of disease treatment/progression)
• Biopsy: consider if large node (>2cm), persistence 4-6 wks, or increase in size, with immunophenotyping and cytogenetics
o Excisional (open) biopsy: reveals abnormal cells and nodal architecture (THIS IS THE PREFERED METHOD)
o Core needle biopsy: tissue for molecular studies, alternative to open if node inaccessible; ask IR to use large-bore needle
o FNA: can be used as initial screening test for LAD, not diagnosis; no info on tissue architecture, high false neg rate
General Lymphoma Staging: for Hodgkin lymphoma (HL), add “B” if presence of B symptoms
Stage I: ≥ 1 LN in a single LN group, or single extralymphatic organ Stage III: LN groups above and below diaphragm
Stage II: ≥ 2 LN groups on same side of diaphragm Stage IV: disseminated ≥ 1 extralymphatic organs
BM biopsy, PET (except in HL stage IA/IIA w/ favorable features, CLL by flow cytometry), labs above, HBV serologies if Rituximab needed
Hodgkin Lymphoma: Reed-Sternberg cells (CD15+ CD30+ CD20-) in inflammatory background; bimodal age distribution (Lancet
2012;380:836)
• WHO classification (classical HL, separate from NLPHL): Hodgkin Lymphoma
o Nodular Sclerosis (70%): mediastinal mass, good prognosis International Prognostic Score (IPS)
o Mixed Cellularity (25%): periph LAD, HIV/EBV, poor resource areas 1 point per factor (JCO 2012;30:3383)
o Lymphocyte Rich (5%): periph LAD, good prognosis Age >45 Points 5y PFS
o Lymphocyte Depleted (<1%): worst prognosis (late stage @ pres) Male 0 88%
• Treatment: note risk of late effects – cardiotox, 2° malignancy, pulm tox Stage IV 1 84%
o Stage I-II: ABVD + XRT (curative intent) Albumin <4 2 80%
o Stage III-IV: ABVD x 6 cycles vs. escalated BEACOPP ± XRT Hb <10.5 3 74%
o Refractory/relapsed: salvage chemo + auto-SCT, followed by WBC ≥15,000 4 67%
maintenance Brentuximab; PD1/PD-L1 blockade (JCO 2018; 36:1428) Lymphocytes <600 or <8% ≥5 62%
Non-Hodgkin Lymphoma (NHL): a/w immunosupp (e.g. HIV, txp), autoimmune disease (e.g. Sjogren), infection (e.g. H. pylori, HCV,
HTLV1, EBV) (Lancet 2012;380:848)
• Indolent: incurable but better prognosis, follicular lymphoma international prognostic index (FLIPI) (Blood 2004;104:1258)
• Aggressive: higher chance of cure but worse prognosis, aggressive NHL revised international prognostic index (IPI) (Blood
2007;109:1857)
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Zandra Walton
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T I M E L I N E (NEJM 2006;354:1813)
(1) Mobilization and harvest of stem cells: few weeks prior to transplant admission
o Stem cells mobilized using G-CSF ± chemotherapy ± plerixafor (CXCR4 inhibitor)
(2) Conditioning: day -8 to -3; varies based on conditioning regimen and donor type (Blood 2014;124:344)
o Goal: (i) eradicate/debulk tumor (ii) produce adequate immunosuppression to allow donor cell engraftment
o Types: myeloablative, reduced-intensity/nonmyelablative regimens of chemotherapy / radiation
(3) Transplantation: day 0, infusion of stem cells
(4) Engraftment (count recovery): day +7 to +28 varies based on stem cell source
o Defined as persistent ANC > 500 & Plt > 100k after nadir (nadir occurs 3-6d after conditioning)
o G-CSF (neupogen/filgrastim) accelerates neutrophil engraftment by a few days: 10 mcg/kg/d (Day +1 until ANC > 500)
o Transfusions (irradiated & leukoreduced), Hct>25, Plt>10K (>50K if bleeding), attending-dependent
Check post-transfusion CBC in 15-60 min
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TOXICITIES (NCCN 1.2020 Guidelines; Nat Rev Clin Oncol 2018;15:47) CRS Grade Therapy
• Cytokine-release syndrome (CRS) If >3 days, consider tx
o Most common toxicity. Typically 2-3d post-infusion, lasts 7-8d. 1 Fever
as in grade 2.
Fulminant cytokine release (IL‐2, sIL2R, IFNγ, IL‐6, GM‐CSF) Tocilizumab q8h PRN
triggered by CAR-T engagement of antigen and T cell Fever w/: hypotension
up to x4. Add steroids
proliferation. risk in bulky disease and specific constructs. 2 not requiring pressors
per below if still BP
o Signs/Sx: fever, BP, HR, pO2, malaise, anorexia, myalgia. or hypoxemia on NC
after 1-2 doses. Fluids.
Can affect any organ (CV, lung, GI/liver, renal, CNS) w/ Fever w/: BP
arrhythmia, ARF, capillary leak, HLH/MAS. requiring pressors or Tocilizumab as above.
o Diagnosis: monitor for 14 days post infusion (inpt or possibly 3 pO2 requiring HFNC / Dexamethasone 10 mg
close outpt); vitals, basic labs, ferritin, coags, CRP, TLS labs. face mask / Venturi / IV q6h (or equiv.).
When suspect: admit, tele, r/o infection. NRB
o Therapy: if plan to treat CRS with steroids or anti-IL6, first get Fever w/: BP Tocilizumab + dex as
clear approval by the treating attending requiring multiple above. If refractory,
Broad-spectrum abx if fever or neutropenic until r/o infxn 4
pressors or pO2 consider methylpred
MGH: tocilizumab (anti-IL6R) 8 mg/kg IV over 1h (max 800 requiring NIPPV / MV 1g/d IV x 3d w/ taper
mg); siltuximab (anti‐IL6) also exists; 2nd line: steroids
• CAR-T-cell-related encephalopathy syndrome (CRES) Immune Effector Cell-Associated Encephalopathy
o Etiology is unclear; passive cytokine diffusion into brain (IL-6, IL- (ICE) Assessment Tool
15 a/w neurotoxicity) vs. CAR-T trafficking into CNS AAOx3 (4 pts), naming x3 (3 pts), follows
Max score:
o Timing: typical onset 4-10d post-infusion, duration 14-17d, commands (1 pt), writes sentence (1 pt),
10
variable. Can be concurrent w/ CRS or after (more severe) serial 10s from 100 (1 pt)
o S/Sx: toxic encephalopathy. See ICE tool and ICANS ASBMT Immune Effector Cell-Associated Treatment
grade. Neurotoxicity (if CRS, add
o Diagnosis: neuro consult, ICANS (or CARTOX‐10) Syndrome (ICANS) Grade tocilizumab)
score. If ≥ grade 3: MRI brain w/wo contrast + EEG ± Grade 1 ICE = 7-9 Supportive
LP. Funduscopic exam. ICE= 3-6, or does not awaken Dex 10 mg IV x1. If
o Therapy: Ppx: if CAR-T known to cause neurotoxicity, Grade 2 spontaneously worsens, advance.
start seizure ppx on day of infusion (levetiracetam ICE = 0-2, or awakens only to Dex 10 mg IV q6h
500-750 mg q12h for 30d). Tx per chart. Grade 3 tactile stimulus, or focal edema on PRN or methylpred
o Prognosis: generally reversible, rare fatal cases neuroimaging 1 mg/kg IV q12h.
• CAR-T-cell-related hemophagocytic ICE = 0, difficult to arouse,
lymphohistiocytosis (HLH) / macrophage activation prolonged seizure >5m or w/o Methylprednisolone
syndrome (MAS) Grade 4 return to b/l, or deep focal motor IV 1g/d x 3d or
o Profound systemic inflammatory state characterized weakness (e.g. paresis), or equivalent w/ taper.
by cytotoxic T cell hyperactivation (IFNγ) diffuse cerebral edema or ICP
macrophage activation (IL-6), lymphohistiocytic tissue infiltration, and multiorgan failure; develops in ~1% of patients treated with
CAR‐T. S/Sx: fever, cytopenias, multiorgan dysfunction
o Criteria for considering: rapidly rising ferritin >5K with cytopenias in context of CRS, especially if any: oliguria or Cr >4 or 3x
b/l, or pulmonary edema, or AST or ALT 5x ULN, or Tbili 1.5x ULN; hemophagocytosis in bone marrow or other organs.
o Dx: labs resemble HLH. CBC w/ diff, ferritin, sIL2R, LDH, fibrinogen, TGs, LFTs, Cr. BMBx rarely critical (low Sn/Sp).
o Tx: high mortality, do not delay diagnosis, escalate therapy aggressively. Manage as per CRS with addition of steroids. If no
improvement in 48h, consider etoposide or intrathecal cytarabine for neurotoxicity.
See Anemia & Pancytopenia for further details on HLH.
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Leon Pappas
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Sara Khosrowjerdi
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IMMUNE-RELATED ADVERSE EVENTS (irAEs) (NEJM 2018;378:158, Ann Oncol 2017;28:iv119, J Immunother Cancer 2017;5:95)
• Definition: systemic autoimmune or inflammatory events due to immune system activation by ICIs
• Risk factors:
o Combination immunotherapy (anti-CTLA-4 + anti-PD-1): associated w/ earlier, higher incidence, and severity; significantly less
with anti-PD1 compared with anti-CTLA-4
o No predictors of who will develop irAEs. Patients with pre-existing autoimmune disease can flare (see above).
• Timing: highly variable based on organ system involved, drug target, Timing of irAE after ipilimumab
monotherapy vs combination. Can present over weeks to years. (adapted from Ann Oncol 2017;28:iv119)
• Clinical presentation: dermatologic toxicity (rash, vitiligo), hepatitis, Rash, pruritus
thyroiditis, colitis, myocarditis, pneumonitis, DM1, neurotoxicity (aseptic Liver toxicity
Diarrhea, colitis
meningitis, encephalitis, transverse myelitis, neuropathy/mononeuritis, Hypophysitis
Toxicity grade
Additional reading: hepatitis Oncologist 2018;23:991; pneumonitis: Chest 2017;152:271, JCO 2017;35:709
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Rahul Nayak
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Opioids
• Opioid-tolerant defined as total daily dose (TDD) x7 days: morphine 60 mg/oxycodone 30 mg/hydromorphone 8 mg/fentanyl 25 mcg/h
• Patients on suboxone or methadone for OUD consult ACT for assistance with pain management
• No max dose. Goal is to find minimum dose needed to
control sx w/ minimal SE __________________Converting Opioids____________________
Ex: Pt takes morphine ER 60 mg PO q12h and uses two morphine IR
• Avoid using combo pills (limits titration flexibility)
15 mg PO breakthrough doses per day
• Treat constipation prophylactically
• Rotate opioids if side effects, dose reduce by 25-50% Step 1) Calculate total daily opioid requirement
TDD = (60 mg x 2 doses) + (15 mg x 2 doses) = 150 mg
morphine per day
Opioid Equianalgesic Doses Step 2) Convert TDD to equivalent dose of new opioid
Drug PO (mg) IV (mg) 30 mg morphine 150 mg morphine
Morphine 30 10 = x = 100 mg oxycodone
20 mg oxycodone x
OxyCODONE 20 n/a
HYDROcodone 20 n/a Reduce dose by 25-50% to account for incomplete cross-tolerance
HYDROmorphone 7.5 1.5 ~60 mg oxycodone total daily dose
FentaNYL* n/a 0.1 (100 mcg) Step 3) Divide TDD by number of doses per day
Fentanyl patch (mcg/hr) Morphine PO (mg/day) - If initiating or converting to long-acting opioid, divide TDD into ER
25 50 doses and add breakthrough dose (10-20% of TDD of ER opioid)
*Use caution converting to Fentanyl (short duration of action) Final dose: oxyocodone ER 30 mg q12h with 10 mg oxycodone q4h
prn breakthrough
Route Onset (min) Peak Effect (min) Duration of Effect (hr) Clearance/Metabolites
IV 5-10 10-30 3-5
Morphine AVOID in renal disease
PO 15-60 90-120 4
IV 5-20 15-30 3-4
HYDROmorphone Safer in renal disease
PO 15-30 90-120 4-6
OxyCODONE PO 15-30 30-60 4-6 2nd line for renal disease
HYDROcodone PO 30 90 3-4 AVOID in renal disease
FentaNYL IV <1 5-7 45 min to 2+ hr Safest in renal and liver disease
IV 10-20 60-120 4-6
Methadone Safest in renal disease
PO 30-60 90-120 4-12
Pain Crisis Management: severe worsening of pain; while treating, pursue reasonable diagnostic workup for etiology (e.g., bowel
perforation/peritonitis, procedural complication, bleeding). Goal is reduction in pain score by >50%.
1) Opioid-naïve: give morphine IV 2-5 mg or hydromorphone IV 0.2-0.4 mg bolus dose
Opioid-tolerant: convert usual breakthrough PO dose or 10-20% of total daily ER dose to IV and administer
2) Assess for response after 15 min:
o No pain relief and no side effects increase dose by 50-100%
o Minimal relief and no side effects (<50% reduction in pain score) repeat the same dose
o Pain reduced >50% and no side effects reassess in 2-3 hours, use this dose as new breakthrough dose
o Side effects with no pain relief rotate to different IV opioid (no dose reduction if uncontrolled pain)
Uptitration: if pain only moderately controlled with scheduled doses (not in pain crisis), total daily dose by 30-50%
• If taking ER opioid and needing >3-4 rescue doses daily, ER dose by 50-100% of total rescue dose used in past 24 hrs
Patient-Controlled Analgesia (PCA): appropriate for patients who are alert & oriented and able to use equipment. Families may NOT use
PCA by proxy at MGH.
• Quickest relief if episodes sudden and severe (pain onset to drug administration; don’t have to call/wait for RN to pull medication).
• PCA and/or continuous infusion, when implemented safely, reduce burden on nursing for patients who need frequent administration of
pain medications (generally q1-2h is the most frequent a PRN can be ordered on the floor)
• Medicine residents can order “General PCA” (for opioid-naïve patients) or “High Risk PCA” (BMI >40, hx OSA, RAAS -2 to -5, age
>65). If opioid-tolerant, requiring continuous infusion, or pain difficult to control, consult Palliative Care or Pain.
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Geriatrics & Palliative Care Adv Care Planning & Code Status
Serious Illness Conversations
● When? Preferred early in disease course as outpatient, but in the inpatient setting some scenarios include:
o New or progressive serious medical illness such as advanced cancer, ESRD, ESLD, HF, COPD
o Prognosis trigger: “Would I be surprised if this patient died in the next year?” (J Palliat Med 2010;13:837)
o Indicator of life expectancy <6 months (calculator, J Palliat Med 2012;15:175)
o Age > 80 and hospitalized; see Geriatrics: Frailty
● Why? Ascertain how the patient wants to live, what they value; more than just end of life care preferences
● How? Often best to plan patient or family meeting (NEJM 2014;370:2506)
Preparation
● Identify time and location to accommodate all meeting participants in an appropriate manner
● Include patient and their preferred participants, primary team, RN, SW, and other providers as appropriate
● If complex decisions/psychosocial issues/family conflict, consider a palliative care consult
● Pre-meet with team to decide meeting leader, discussion goals, unified assessment of clinical scenario, treatment
options, and team recommendation
Serious Illness Conversation: suggested outline / prompts (adapted from Ariadne Labs SICG)
Step Suggested Prompts
Open the conversation “I’d like to talk about what is ahead with your illness. Would that be ok?”
“What is your understanding of your illness?”
Assess prognostic awareness “Looking to the future, what are your hopes about your health?”
“What are your worries?”
“Would it be ok if we talked more about what lies ahead?”
“I hear you’re hoping for ____ and I’m concerned the decline we’ve seen will
Share hope and concerns
continue” or “I’m concerned something serious may happen in next (time
window: weeks, months, years)”
Align “I wish we didn’t have to worry about this”
“If your health worsens, what is most important to you?”
Explore what’s important
“How much do your family or friends know about your priorities and wishes?”
“It sounds like ____ is very important to you”
Close the conversation
“Given what’s important to you, I would recommend______”
**Note: some patients may respond better to being asked about their “health” rather than their illness--especially those
who are semi-stable in clinic but have frailty or multimorbidity
Next Steps:
● Debrief with team: How did that feel? What went well? What could have gone better?
● Document Serious Illness Conversation in Epic:
o Patient ID banner (top of chart): click “Code: ___” “Advance Care Planning Activity” “Serious Illness
Conversation” in left tab; fill out SIC form “Close”
o Write ACP note: Within “Advance Care Planning Activity” “ACP Notes” “Create ACP Note” type
.ACPSICDOCUMENTATION; write rest of the note if relevant
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Geriatrics & Palliative Care Adv Care Planning & Code Status
Code Status Discussions
General Considerations
● Ideally code status should be confirmed in Epic at time of admission
● Confirm directly with the patient/HCP, MOLST, and/or prior documentation by outpatient providers
● Readdress if a patient’s clinical status changes, or if code status is deemed inappropriate for the clinical setting, but do
not need to routinely readdress on admission if has been addressed by outpatient providers
● Code status should reflect a patient’s values and preferences and is not equivalent to ACP (it is a specific medical
procedure for which harms/benefits should be weighed given clinical context)
Survival Outcomes (Circulation 2019;139:e56)
● Out-of-hospital cardiac arrest: survival to hospital discharge 10.4%; survival with good neurologic function 9.9%
● In-hospital cardiac arrest: survival to discharge 25.6%; survival with good neurologic function 22%
o Favorable outcomes: ACS, drug overdose, drug reaction (up to 40% survival)
o Unfavorable outcomes: age >80 (<10% survival), multiorgan failure, sepsis, advanced cancer, ESRD, ESLD,
dementia
o Post-arrest complications: hypoxic-ischemic brain injury, rib fractures, pulmonary contusion, prolonged ICU care
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DEATH PRONOUNCEMENT
PRONOUNCEMENT. Introduce yourself to the family, explain what you are doing, express condolences
• FEEL for pulse, LISTEN for heart sounds/breath sounds (> 60 sec), SHINE light to determine absence of pupillary light reflex, and
NOTE time at the end of your exam, which becomes the time of death
QUESTIONS FOR NEXT OF KIN (Not HCP, but Next of Kin (NOK): Husband/Wife > Children > Other Family)
• If no NOK in room, call NOK to notify of patient’s death.
• Ask the family if they would like to see a CHAPLAIN or SOCIAL WORK AUTOPSIES are free and do not delay funerals
(can still have open casket). In addition to
• Ask if family would want an AUTOPSY?
helping determine cause of death, they can be
• If family accepts autopsy, ask about DISPOSITION OF ORGANS. Consider
instrumental in advancing research.
recommending the option of MGH retaining organs for further testing,
education, research (if not, value of/info from autopsy lower)
• Are there OTHER FAMILY MEMBERS they would like you to inform?
• Will anyone else be COMING TO VIEW THE BODY prior to morgue?
• What you can tell family: body is kept at MGH until the funeral home calls MGH (path: 617-726-2967) and arranges for pick-up.
Ask family if they plan to contact funeral home or if they have a preferred funeral home they want notified.
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Emily Moin
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ANA first
C3/C4, anti-Sm, anti-
Work-up RF, anti-CCP, ANA dsDNA, anti-Scl70, ANCA, Limited role for ACE,
anti-histone, anti- cryoglobulins can send IgG4
U1RNP, anti-Ro/La,
antiphospholipid Abs
Treatment* NSAIDS/Glucocorticoids
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Rheumatology Arthritis
Approach to the Patient with Arthritis
Jacquelyn Nestor
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Rheumatology Arthritis
Chronic Arthritis Syndromes
tocilizumab)
- 5 patterns (distal - 70% with psoriasis - Clinical dx - NSAIDs (1st line)
DIP, asymm oligo, - Extra-articular: - ESR/CRP - If mod/severe, MTX > SSZ,
symm poly, arthritis synovitis, enthesitis, (40%) leflunomide
Psoriatic mutilans, dactylitis, nail - HLA-B27 - If severe/erosive, TNFα inhibitor
arthritis spondyloarthritis pits/onycholysis, uveitis - CASPAR criteria infliximab, adalimumab, golimumab
[sacroiliitis]) (91% Sn / 99% (ACR Guideline 2018)
- axial (spine) Sp)
involvement (42%)
- Spine & SI joints - Gradual onset - Sacroiliitis (XR - NSAIDs (1st line)
- AM stiff >30min or MRI) - No steroids
- Pain in low back, - Impaired spine - DMARDs not effective
buttock, ankle, TMJ mobility - TNFα inhibitor (2nd line)
Ankylosing
- Extra-articular: - ESR/CRP infliximab, etanercept, adalimumab
spondylitis synovitis (mono or - HLA-B27 (90%
oligo), enthesitis, Sn/Sp)
dactylitis, uveitis,
psoriasis, IBD
NON-
NO RMA L I NFL AM MATOR Y S E P TI C H EMORR HAG IC
INFLAMMATORY
Clarity Transparent Transparent Transparent-opaque Opaque Bloody
Color Clear Yellow Yellow to opalescent Yellow to green Red to brown
Viscosity High High Low Variable Variable
WBC (per mm3) < 200 0 - 2,000 2,000 - 100K 50 - 150K 200 - 2,000
PMNs (%) < 25 < 25 ≥ 50 ≥ 75 50 - 75
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Cody Cichowitz
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Rheumatology Vasculitis
D I A G N O S T I C O V E R V I E W (Arthritis Rheum 2013;65:1)
• Classified by size and type of blood vessel involved. Large vessels (aorta and its branches) vs. medium-sized vessels (main visceral
arteries = named) vs. small vessels (vessels without names such arterioles, capillaries, venules)
STEP 1 – SUSPECT VASCULITIS
Overview:
• No “typical” presentation but consider in
constitutionally ill patient with evidence of
multisystem organ involvement and
evidence of inflammation
• LARGE vessel: aorta/branches, e.g.
external carotid, temporal, ophthalmic
limb claudication, bruits, asymmetric BP,
absent pulses, HA, visual loss
• MEDIUM vessel: renal/hepatic/mesenteric
arteries, etc. cutaneous nodules,
“punched out” ulcers, livedo racemosa,
digital gangrene, mononeuritis multiplex
(e.g. foot/wrist drop), renovascular HTN
• SMALL vessel: vessels of skin, small
airways, glomeruli palpable purpura,
glomerulonephritis, alveolar hemorrhage,
mononeuritis multiplex, scleritis
General testing:
• Inflammation? CBC w/ diff (ACD, thrombocytosis, neutrophilia, eosinophilia), ESR, CRP
• Organ involvement? BMP, LFTs, stool guaiac, CXR, brain MRI (if neurologic symptoms), CTA (if GI/claudication)
Presentation-specific testing (i.e. small-vessel s/sx): difficult to discern clinically
• Immune complex formation? complement levels (C3, C4), ANA, RF/Cryoglobulins
o ANA/RF are NOT positive in 1° vasculitis; ⊕RF could suggest cryoglobulinemia or endocarditis (in addition to RA)
o C3/C4 in cryoglobulinemia, SLE, and 25% of PAN; normal complement levels in all other vasculitides (rarely low in HSP)
• ANCA-associated? send ANCA for IIF; will reflex to MPO (p-ANCA) and PR3 (c-ANCA) antibody ELISA if positive
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Rheumatology Vasculitis
L A R G E – V E S S E L V A S C U L I T I S (NEJM 2003;349:160)
GIANT CELL ARTERITIS: inflammation of the aorta & its extracranial branches (i.e. spares ICA), often involves temporal artery (TA), most
common primary systemic vasculitis. Age >50, 2:1 M:F. Rare <50 yo = consider alternative diagnoses, mimics.
• Sx: constitutional (low grade fevers, fatigue, wt loss, anorexia), new/different HA, abrupt visual disturbance (amaurosis fugax, blindness,
diplopia), jaw claudication (most specific sign; fatigue with chewing, NOT PAIN)
• Exam: asymmetric BP/pulse; tender, thickened or pulseless TA; jaw claudication (r/o TMJD)
• Dx: a combination of 2-3+ symptoms and exam findings should prompt doppler U/S and rheum consult. Gold standard = temporal
artery biopsy. ESR (ESR usually high but <50 in 10%), CRP (correlates with disease activity) IL-6
o TA biopsy: start w/ unilateral; if ⊝, consider bilateral ( yield by 5%); up to 30-45% of bx may be false neg due to “skip areas”
o If concern for large-vessel GCA (e.g. aorta, subclavian): pursue imaging (CTA vs. MRA)
• Rx: start prednisone 1mg/kg/d immediately (up to 60mg) if high suspicion; NEVER delay Rx for Bx
o Steroid sparing regimens include tocilizumab, MTX
POLYMYALGIA RHEUMATICA: seen in 50% of GCA pts; 10% develop GCA, peak age 70-80
• Sx: symmetrical AM stiffness/pain (+/- weakness) in neck, shoulders/prox arms, hips/prox thighs
• Rx: prednisone 12.5-20 mg/day with slow taper, consider addition of MTX if refractory (Ann Rheum Dis 2015;74:1799)
TAKAYASU ARTERITIS: “pulseless disease,” inflammation of thoracoabdominal aorta & branches. Age <40, 8:1 M:F, Asians
• Sx: inflammation (fever, arthralgias/myalgias, weight loss, night sweats), vessel inflammation (carotidynia, limb claudication), vascular dz
(TIA/stroke, HF, CAD, mesenteric ischemia)
• Exam: unequal pulses and BPs (lower > upper extremities), pulses, bruits, formal eye exam
• Dx: MRA or CTA; arteriography will show occlusion, stenosis, aneurysms; consider carotid ultrasound/Doppler studies
• Rx: prednisone 1mg/kg/d; 50% of patients will need 2nd agent for chronic sx (MTX, tocilizumab, TNFi)
MEDIUM–VESSEL VASCULITIS
POLYARTERITIS NODOSA: kidneys, skin, muscles, nerves, GI, joints (almost always spares lung). Age 40-60, associated with HBV
• Sx: mononeuritis multiplex (in up to 70% of pts), GI distress (mesenteric ischemia), myalgias, AKI (GN suggests alternate etiology),
testicular/ovarian pain (>10%), seizures
• Exam: HTN, skin lesions (erythematous nodules, purpura, livedo reticularis, ulcers, bullous eruption, palpable purpura), neuropathy
• Dx: gold standard = biopsy; HBV/HCV serologies, C3/C4, CTA/MRA showing focal stenosis or microaneurysm (renal/mesenteric vessels)
• Rx: prednisone 1mg/kg/d ± CYC 2 mg/kg/d PO or IV pulse (if mod-severe or steroid-refractory); antivirals if HBV-related
THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE): segmental inflammation of small-med arteries and veins of extremities; occlusive
intravascular thrombi. Age ≤ 45, 70-90% ♂, strongly associated with tobacco use, Raynaud’s in 40% of pts
• Dx: clinical - 1) age 2) tobacco use 3) distal ischemia 4) arteriographic findings 5) exclusion of autoimmune, thrombophilia, DM, embolism
• Rx: smoking cessation! Iloprost (PG analog) for pain, CCB (for Raynaud’s), intermittent pneumatic compression (painful ulcers)
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Familial Mediterranean Fever (FMF): autoinflammatory disorder due to mutations in MEFV gene, autosomal recessive
inheritance, characterized by recurrent bouts of fever and serosal inflammation
• Epi: most common in Jews, Armenians, Turks, and Arabs. Onset <10 yo (65% pts), <20 yo (90% pts)
• Sx: recurrent acute attacks (1-3d, resolves spontaneously) of fever associated w/ peritonitis (often mistaken for surgical
abdomen), unilateral pleuritis, arthritis (monoarticular, sterile joint), or skin lesions (erysipelas-like).
o Other manifestations include: exertional myalgia, pericarditis, testicular pain, and aseptic meningitis.
o Long-term complications: secondary (AA) amyloidosis: renal disease (major cause of mortality), SBO, infertility
• Dx: During acute attack: WBC, ESR/CRP. Check UA for amyloidosis (proteinuria). Genetic testing for confirmation.
o Diagnostic criteria: requires 1 major or 2 minor criteria (Arthritis Rheum 1997; 40:1879)
• Rx: colchicine 1-3 mg/day (to prevent acute attacks and progression to amyloidosis). 5-10% colchicine resistant, add on
IL-1 inhibitors (Ann Rheum Dis. 2016;4:644)
Adult Onset Still’s Disease (AOSD): systemic inflammatory disorder characterized by fevers, arthritis, and rash. Can present
as single episode (wks-mos), multiple flares, or be persistently active.
• Epi: F=M, bimodal (15-25 yrs old and 36-46 yrs old)
• Sx: fever; arthralgias; evanescent, salmon-colored maculopapular rash that coincides w/ fever, usually on the trunk,
may be precipitated by trauma (Koebner phenomenon); pericarditis; pleural effusions; macrophage activation
syndrome (rheum-associated HLH; see Hematology)
• Dx: Yamaguchi criteria requires ≥5 features, including ≥2 major criteria (J Rheumatol 1992;19:424)
o Major: fever ≥39ºC for ≥1 week, arthralgias/arthritis ≥2 weeks, salmon-colored rash, WBC (≥10K + ≥80% PMN)
o Minor: sore throat, LAD, HSM, AST/ALT, LDH, negative ANA/RF
o Other labs (not part of criteria): ESR/CRP, ferritin >3000 ng/mL (if >10,000, consider MAS spectrum), plt, Hgb
• Rx:
o Mild: NSAIDs
o Severe: prednisone 0.5-1mg/kg/d (may not respond). If uncontrolled: MTX, anti-TNF, anti-IL6R, anti-IL1
Fibromyalgia: NOT a rheumatic disease. Chronic widespread musculoskeletal pain, often w/ fatigue, sleep disturbance, and
multiple somatic symptoms.
• Epi: F>M, 20-55 yo. Can coexist with other inflammatory diseases like SLE, RA. Often psychiatric comorbidities.
• Sx: widespread MSK pain, fatigue, cognitive disturbance (decreased attention & ability to perform complex tasks),
psychiatric sx (depression), headache, parasthesias, IBS. Pan-positive ROS not uncommon.
• Dx: clinical diagnosis, > 3 months duration of sxs, multiple tender points. Newer criteria involve widespread pain index
(WPI) and symptom severity (SS) scale (J Pain 2019;6:611)
o Labs: normal ESR, CRP, TSH, CBC, BMP
• Rx:
o Initial therapy: patient education, exercise program
o Pharmacologic therapy: 1st line includes amitriptyline, duloxetine, or milnacipran; also may consider
cyclobenzaprine, gabapentin, and pregabalin (monotherapy > combo therapy). Avoid narcotics.
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Rheumatology Autoantibodies
Antibody Antigen ANA pattern Disease Comments
Inflammatory polyarthritis
RA (50-75%), - Nonspecific despite name: RA, CTD, cryoglobulinemia, chronic infxn (e.g.
Sjogren’s (30%), HCV, SBE).
RF (IgM) Fc gamma negative Cryoglobulinemia - Positive in 10% of healthy patients
(90%), chronic - RA: “seropositive”, a/w erosive and extraarticular manifestations (nodules,
infection scleritis, ILD, pleuritis, rare rheumatoid vasculitis)
- Most specific test for RA, positive in 50-75% (“seropositive RA”), a/w
Citrullinated
CCP negative RA (50-75%) erosive dz & extraarticular manifestations
proteins
- Used for dx only, NOT marker of dz activity
Connective tissue diseases (SLE, Sjogren’s, SSc, MCTD, UCTD, DM/PM)
- ANA = antinuclear antibodies (specific ANA Abs listed below). Low titer ≤1:160 are often false positive. If ⊕, order specific
autoantibodies guided by clinical presentation
ANA - ⊕ ANA: MCTD (100%), SLE (98%), scleroderma (90%), drug-induced lupus (90%), Sjogren’s (60%), PM/DM (50%)
- Ddx for ⊕ ANA: Autoimmune: autoimmune hepatitis, PBC, IBD, myasthenia gravis, Graves’, Hashimoto’s; ID: malaria, SBE,
syphilis, HIV, HSV, EBV, HCV, parvo-B19; Systemic inflammation: lymphoproliferative disorders, IPF, asbestosis
- Specific for SLE, a/w SLE activity and lupus nephritis, consider TNF
dsDNA ds/mtDNA homogeneous SLE (40-60%)
inhibitor drug-induced lupus
SLE, drug-induced - Sensitive, but not specific for drug-induced lupus (DIL)
Histone histones homogeneous lupus (90%), - Common meds: procainamide, hydralazine, phenytoin, lithium
Felty’s
U1-snRNP MCTD (100%), - MCTD: high-titer anti-U1 RNP
RNP speckled
SLE (30%)
Smith snRNP speckled SLE (30%) - Specific for SLE, not indicative of dz activity
- Can be seen with myositis
Sjogren’s (75%),
SS-A/Ro Ro52, Ro60 speckled - In SLE, a/w skin disease and congenital heart block
SLE (40%),
- 2% SLE pts have ⊝ ANA but ⊕ anti-Ro Abs
Sjogren’s (40%), - In SLE a/w congenital heart block
SS-B/La La speckled
SLE (10-15%)
- A/w limited systemic sclerosis, risk of PAH, risk of ILD, esophageal
ACA CENP A-F centromere lcSSc (15-40%)
disease
Scl-70 topo-I speckled dcSSc (10-40%) - A/w diffuse systemic sclerosis; risk of ILD, scleroderma renal crisis
RNA pol III RNA pol. III nucleolar dcSSc (4-25%) - A/w scleroderma renal crisis, rapidly progressive skin disease, cancer
Fibrillarin U3-RNP nucleolar dcSSc (<5%) - A/w PAH, pulmonary fibrosis, and myositis, esp. in African-Americans
- A/w limited systemic sclerosis, risk of pulmonary and renal dz, risk
PM-Scl exosome nucleolar SSc (5-10%)
inflammatory myositis
Myositis
PM/DM (30%), - Antisynthetase syndrome: myositis (DM/PM), ILD (70%), polyarthritis,
Jo-1* tRNA (His) cytoplasmic anti-synthetase mechanic’s hands, Raynaud’s, fever
syndrome (~20%)
homogenous/ - More likely in acute DM, good prognosis
Mi-2* Mi-2 DM (15-20%)
speckled
MDA-5* MDA-5 negative DM - Clinically amyopathic dermatomyositis, rapidly-progressive ILD
TIF1g* TIF1g fine speckled Juvenile DM - A/w malignancy in adult DM
signal recog. - Immune-mediated necrotizing myopathy (degenerating, regenerating, and
SRP* cytoplasmic PM
particle necrotic cells on bx), rapidly progressive disease course
- Immune-mediated necrotizing myopathy, 70% with statin exposure (at any
HMG CoA
HMGCR negative myositis time in past), ≠ statin myopathy (does not respond to discontinuation of
reductase
statin), very high CPK, often steroid-refractory, good response to IVIG
Vasculitis
PR3 - Poor correlation of titer with disease flare/remission
proteinase 3 negative GPA (90%)
(c-ANCA) - Antibody frequency lower in GPA without renal involvement
MPA (70%), - Poor correlation of titer with disease flare/remission
MPO myelo- EGPA (50%), - Drug-induced vasculitis (DIV): high-titer positive for MPO (hydral, PTU,
negative
(p-ANCA) peroxidase Renal-Limited, minocycline)
DIV (95%) - Levamisole vasculitis 2/2 cocaine use: MPO or PR3/MPO
Cryo- Cryoglobulinemic - HCV > HBV, HIV, CTDs, lymphoproliferative disease
Fc gamma negative
globulins vasculitis - A/w low C4, glomerulonephritis, +RF
* ordered as part of myositis panel
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AAV (ANCA-associated vasculitis), AOSD (Adult-onset Still's disease), APLAS (anti-phospholipid antibody syndrome), AS (ankylosing
spondylitis), DM (dermatomyositis), EGPA (eosinophilic granulomatosis with polyangiitis), GCA (giant cell arteritis), GPA (ranulomatosis
with polyangiitis), IBD (inflammatory bowel disease), IMNM (immune-mediated necrotizing myopathy), JRA (juvenile rheumatoid
arthritis), MAS (macrophage activation syndrome), MPA (microscopic polyangiitis), PM (polymyositis), PsA (psoriatic arthritis), RA
(rheumatoid arthritis), SLE (systemic lupus erythematosus), UC (ulcerative colitis)
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Insulin Supplies
• Needles: come as universal pen needles, or attached to syringes, made by many companies. 32G 4mm is less painful (higher gauge
= thinner and shorter needle), but obese patients and high insulin doses often require deeper/wider needle.
• Syringes: boxes of 100. Long-acting insulin only = 1 box/3 mo. Use this barrel size… With this dose range…
Basal/bolus insulin = 4 syringes/day (4 boxes/3 mo). Choose smallest 3/10 mL 30 units or less
syringe that will hold the dose (smaller barrel clearer scale 1/2 mL 31-50 units
markings). 1 mL 51-100 units
• Alcohol swabs (or patients can wash hands/skin with soap and water)
• Glucometer & test strips: Many choices (insurance dependent), each with own strip brand. Most test strips come in boxes of 50-100.
• ** All durable medical equipment including test strips and glucometers requires an ICD-10 code on the script itself **
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Endocrinology DKA/HHS
DIABETIC KETOACIDOSIS (DKA)
Pathophysiology: think about each element of Diabetic Keto-Acidosis
• Diabetes: insulin & opposing hormones (glucagon, catechols, cortisol) hyperglycemia osmotic diuresis hypovolemia
• Ketones: insulin lipolysis free fatty acids ketones (acetoacetate, β-hydroxybutyrate, acetone [fruity breath])
• Acidosis: β-hydroxybutyrate and acetoacetate, and contraction alkalosis with total body HCO3 deficit (NEJM 2015;372:546)
Precipitants (the “I’s”): infection (30-40% of cases), initial presentation of DM (20-25% of cases), insulin non-adherence, inflammation
(pancreatitis – but amylase / lipase in DKA even w/o this), ischemia/infarction (MI, CVA, gut), intoxication (EtOH, cocaine), iatrogenesis
(e.g. SGLT2 inhibitors, steroids, thiazides, dobutamine/terbutaline, atypical anti-psychotics), infant (pregnancy)
Presentation: dehydration, polyuria/polydipsia, n/v/abd pain, weakness, AMS, Kussmaul’s respirations, fruity breath (acetone)
Dx: BG 250-800, pH <7.3, AG >10, urine/serum ketones. Consider euglycemic DKA in pt on SGLT2i, EtOH liver dz, pregnancy.
• Check BMP, CBC w/ diff, UA, Sosm, serum β-hydroxybutyrate, ABG/VBG. Consider hs-trop, EKG, BCx/UCx, CXR, lipase/amylase.
• Na correction use absolute sodium value when calculating anion gap. Use corrected value to assess for underlying hypotonic
hypoNa add 1.6 mEq/L to Na for every 100 mg/dL of serum glucose >100 mg/dL (e.g. if glucose 300 mg/dL, add 3.2 mEq/L to Na)
• UA ketone does not test for β-hydroxybutyrate, which is the predominant ketone in DKA (must measure from serum)
Management: prioritize ABCs, volume status, identifying precipitant THEN electrolytes (especially K+) THEN glucose
Labs: BMP q2h until AG closes, then q4h until normal K+; VBG, β-hydroxybutyrate q2-4h; FSBG q1h while on insulin gtt
Step 1: volume resuscitation (typically 5-8L deficit)
o Bolus NS 15-20cc/kg/hr for initial resuscitation in first 1-4 hours (unless CHF, ESLD, ESRD, hypoxemia)
o Corrected Na if low, start NS±K+ at 250-500cc/hr; if normal/high or hyperCl acidosis, start ½NS±K+ at 250-500cc/hr
o Add D5 to IVF once BG<200 (DKA) or <300 (HHS)
Step 2: potassium repletion and management
Potassium Action K+ may be normal/elevated at presentation, but total body K+
K<3.3 Give 20-40 mEq KCl IV per hour + hold insulin! actually low. Multifactorial causes: solute drag of K+ into
3.3≤K≤5.3 Add 20 mEq K to IVF extraceullar space, osmotic diuresis, insulin not driving K+
into cells. Aggressive K+ repletion is critical: HYPOkalemia
K>5.3 Continue to monitor q2h will limit your ability to administer the necessary insulin
Step 3: insulin therapy (Diab Care 2009;32:1335)
o The #1 goal of insulin therapy in DKA is to stop ketogenesis and close the AG; glucose correction is secondary
o Don’t start insulin until you have control of K+
o Don’t stop the insulin gtt unless true hypoglycemia (<65 mg/dL) or hypokalemia (<3.3 mEq) occurs
o Initial: bolus 0.1 U/kg regular insulin, then start 0.1 U/kg/hr IV regular insulin gtt; OR no bolus and start 0.14 U/kg/hr IV gtt
Goal is to BG by 50-75 mg/dL each hour
For mild DKA, subcutaneous insulin regimens may be used instead of IV (Cochrane Rev 2016)
o Titrating insulin drip: MICU insulin gtt protocol is for general glycemic management, NOT for DKA
If BG does not by 50-75 mg/dL in the first hour, re-bolus (DKA) or double the gtt (HHS)
No evidence for hourly titration of the insulin infusion rate in DKA while BG>200
Once BG <200 (DKA) or <300 (HHS), gtt to 0.02- For BG < 150 ∆ Insulin gtt and glucose source
0.05 U/kg/hr and add D5 to fluids
BG 91-149 gtt by 25% + D5 gtt by 50 cc/hr
Goal is to maintain BG at 150-200 (DKA) or 250-300
BG 66-90 gtt by 50% + ½ amp D50 + continue D5 gtt
(HHS)
BG ≤ 65 hold insulin + 1 amp D50 + continue D5 gtt
Other electrolytes:
• HCO3: no proven benefit w/ pH > 6.9. If pH <6.9, give 2 amps HCO3 dissolved in 400mL sterile water w/ 20mEq KCl over 2h
• Phos: total body deficit but serum phos may be / nml; will w/ insulin; only replete if < 1.0 to prevent cardiac dysfunction
Transitioning to SQ insulin: start if BG < 200 and pt is able to eat and two of the following are met: AG<12, HCO3≥15, pH>7.3. Start
basal regimen w/ either: home glargine dose OR glargine at 0.25-0.4 U/kg/d OR glargine at (# units on IV gtt over past 6h x 4 x 0.7). Start
bolus regimen w/ either: 0.25-0.4 U/kg/d divided (if T1DM or unknown) OR ISS only (if T2DM). Overlap IV gtt/SQ insulin by 2-4h.
Ketosis-prone diabetes: characterized by DKA w/ hx T2DM or atypical substrate for T1DM (older age, overweight). Patients should be
discharged on insulin and see an endocrinologist for antibody (GAD65, IA2) and β-cell function (C-peptide levels) testing to determine
diabetes subtype (antibody +/-, β-cell function +/-). Patients may not require long-term insulin therapy.
HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)
Pathophysiology: hyperglycemia osmotic diuresis volume depletion; ketogenesis suppressed by low (but present) insulin levels
Precipitants: same as DKA (note: pts w/ T2DM and burnt-out pancreas can also present with DKA)
Presentation: AMS (25-50%), obtundation, seizure, focal neuro def, volume depletion, evolves over days-weeks (vs hours-days in DKA)
Dx: glucose >600 mg/dL (frequently >1000), osmolality >320 mOsm/kg, pH >7.3, absent or minimal ketones
Management: as above for DKA w/ modifications: more aggressive IVF (~8-10 L deficit); goal glucose 250-300 mg/dL (in DKA, 150-200);
transition to SQ insulin when BG<300 and mental status improved and patient is able to eat. Mortality >> DKA (Diab Care 2014;37:3124)
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- Hypoparathyroidism (surgical,
autoimmune, infiltrative dz, radiation) PO4 PO4
- Hypomagnesemia (causes PTH - Vitamin D deficiency - CKD (2° HyperPTH)
suppression/resistance) - Pancreatitis - Tumor lysis
- Drugs (bisphosphonate, - Rhabdo (early)
phenytoin, cinacalcet) - Pseudohypoparathyroidism
- Critical illness
- Transfusions (citrate)
Management:
• Replete magnesium (hypoCa can be hard to correct without first correcting hypoMg causes PTH resistance and secretion)
• IV Ca repletion: if severe (corrected Ca < 7.5, iCa < 1), symptomatic, or prolonged QT
o 1-2g IV Ca gluconate or CaCl2 (in codes: via central line, risk of skin necrosis if extravasates) over 10-20 min
o IV therapy serum levels for only 2-3h (chase w/ gtt or PO); can do sliding scale repletion in ICU
o Telemetry recommended as arrhythmias may occur
• PO Ca repletion: if Ca > 7.5 or asymptomatic: 1-2 g elemental Ca QD in divided doses (Ca citrate better absorbed vs CaCO3 esp. if pt
on PPI)
• Vitamin D repletion: 800-1000 IU Vit D3 daily (if severely deficient trial 50,000 IU Vit D2 or D3 qweek x 6-8wks and measure 25(OH)D
level in 3-4mos). In patients w/ poor conversion of 25(OH)D (e.g. hypoparathyroidism, CKD) use calcitriol (start w/ 0.25mcg PO QD)
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Endocrinology Osteoporosis
Definitions:
• Osteoporosis: history of fragility fracture or T-score ≤ -2.5 on DXA. Osteopenia: T-score -2.4 to -1.
o T-score: SD compared to mean for normal, healthy young adults
o Fragility fracture: fracture from a fall from standing height or less or with no trauma, particularly spine, hip, wrist, rib, and
pelvis
Etiology:
• Primary osteoporosis is the most common. Risk factors: age ≥65, low body weight (<57.6 kg), FH osteoporosis or fractures,
smoking, early menopause, excessive EtOH intake
• Secondary osteoporosis caused by: renal disease, liver disease, hyperthyroidism, hyperPTH, vit D deficiency, hypogonadism,
glucocorticoids (≥5mg prednisone for >3mos), myeloma, malabsorption (celiac, IBD), RA, SLE, COPD, drugs (PPI, AED, long-
term heparin, leuprolide, aromatase inhib, MTX, GnRH agonists)
Diagnosis:
• Screen women with DXA scan at age 65 or younger if RF or high risk as determined by FRAX (USPSTF guidelines)
• Screen men ≥70 or age 50-69 who have RF (low body weight, prior fracture, smoking) (Endocrine Society Guidelines)
• Labs for secondary causes: CBC, BMP, LFTs, 25(OH)D, TSH, PTH, SPEP
Management:
• Inpatient following fragility fracture: assess need for surgical treatment, consult Fracture Liaison Service (p25656), can start
medical management (bisphosphonates); zoledronic acid has been shown to decrease mortality post-hip fracture (HORIZON
trial)
• Lifestyle measures: weight-bearing exercises 3-4x/week, smoking cessation, decrease EtOH intake, RDA 800-1000 IU
vitamin D (goal level >30), calcium 1200 mg ideally from diet
• Pharmacologic therapy:
o Bisphosphonates: must have normal vit D and calcium levels prior to initiating therapy
Indicated for: all patients with osteoporosis, osteopenia in men and postmenopausal women with FRAX 10-yr
risk >20% for any fracture, >3% for hip; consider when initiating long-term glucocorticoids in pts with med-high risk of
fracture.
PO alendronate 75mg or PO risendronate 35mg weekly for 5-10 yrs. Avoid if GFR <30. Provide strict instructions to
prevent pill esophagitis: take on empty stomach w/ full glass of water, sit upright and wait 30 min prior to taking other
meds or food.
- If contraindication to PO bisphosphonate (e.g. GI intolerance, roux-en-Y gastric bypass), IV zoledronic acid
Re-evaluate q3-5yrs and if low-moderate risk consider a “bisphosphonate holiday” (JCEM 2019;104:1592)
o Denosumab (monoclonal antibody with affinity for RANKL): option for patients with renal dysfunction or other
contraindication to bisphosphonates, 60 mg SQ q6mo; treat with teriparatide first if severe osteoporosis. FREEDOM trial
showed denosumab improves fracture risk and bone mineral density compared to placebo
o Anabolic agents (teriparatide: recombinant PTH; abaloparatide: PTHrP analog): VERO trial
For severe osteoporosis or for patients with contraindications to bisphosphonates, daily SQ injection
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HYPOTHYROIDISM
• Definition: elevated TSH with low T4 (primary) or low/normal TSH with low T4 (secondary/central)
• Signs/symptoms: general (fatigue, cold intolerance, constipation, dry skin, myalgias), neuro (depression, cognitive
dysfunction, carpal tunnel), CV (bradycardia [severe dz], diastolic HTN)
o Exam: delayed relaxation phase of DTRs, non-pitting edema, lateral TSH FT4
eyebrow thinning, macroglossia, froggy voice Primary
• Labs: LDL, triglycerides, macrocytic anemia, Na Secondary /normal
o Check other pituitary axes if concern for central hypothyroidism Subclinical Normal
• Workup: TSH with reflex, anti-TPO ab. No role for thyroglobulin or anti-thyroglobulin ab (only useful for monitoring thyroid Ca)
• Causes:
o 1°: Hashimoto’s (most common, +TPO Ab), infiltrative disease (hemochromatosis, sarcoid), transient thyroiditis
(lymphocytic, granulomatous, postpartum), drugs (lithium, amio, TKIs, contrast), iatrogenic (thyroidectomy, radiation),
iodine deficiency
o 2°: see Pituitary Disorders
o T4 requirement: pregnancy, estrogen ( THBG), weight gain, malabsorptive states (e.g. celiac disease), nephrotic
syndrome ( excretion), rifampin, phenytoin, carbamazepine, phenobarbital
• Treatment: levothyroxine (T4) starting dose ~1.6 mcg/kg/d PO (use 25-50 mcg QD for elderly or comorbidities); IV = 50-75%
PO
o Take on an empty stomach 1h before food/meds; several hrs apart from PPI, aluminum hydroxide, iron, cholestyramine
o Check TSH q6 weeks and adjust by 12-25 mcg until normal TSH
MYXEDEMA COMA
• Manifestation of severe hypothyroidism, STAT endocrine consult
• Mortality >30%, most common cause of death is hypercarbic respiratory failure
• Precipitants: infection, MI, cold exposure, surgery, administration of sedative drugs (esp opioids) in a poorly controlled
hypothyroid pt
• Signs/symptoms: AMS (lethargy/obtundation, not always coma), hypothermia, hypotension, bradycardia, ventricular
arrhythmias, hypercarbic resp failure, seizures
o Exam: puffy hands and face, swollen lips, enlarged tongue
• Labs: Na (be careful with IVF), Glu, T4
• Treatment: do not wait to start tx for lab confirmation
o Test and empirically treat adrenal insufficiency: give hydrocortisone 50-100mg BEFORE T4 (if concomitant AI,
replacing thyroid hormone first will catabolize residual cortisol and cause HoTN/death). Draw serum cortisol before
initiating therapy.
o Levothyroxine (T4) 12.5-50mcg IV QD in elderly or at risk for MI, up to 200mcg if sick and young.
o Liothyronine (T3) (5-10mcg Q8H) only given if pt is critically ill (T4 conversion to T3 takes several days), give only with
endo guidance, can cause rebound hypermetabolism
o Recheck FT4 in 3-7d; if giving T3, monitor peak levels
o Patients are hypometabolic: use lower drug doses at lower frequency, avoid MS-altering meds.
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THYROID STORM
• Manifestation of severe thyrotoxicosis, STAT endocrine consult
• Mortality rate 10-30%, most common cause of death is cardiovascular collapse
• Precipitants: surgery (thyroid or other), trauma, infection, iodine load, irregular use or discontinuation of antithyroid drugs
• Signs/symptoms: AMS (agitation, delirium, psychosis, coma), hyperthermia, tachycardia, atrial arrhythmias, CHF
o Exam: goiter, tremor, warm/moist skin, exophthalmos (Graves’)
• Labs: T4/T3, TSH
• Dx: Burch-Wartofsky Point Scale (BWPS) >44 highly suggestive
• Treatment:
o βB: only propranolol decreases T4T3 conversion, may require high doses (2g/day). Titrate to sx and HR (i.e. <80).
o Anti-thyroid meds: only stop formation of new hormone, not release of stored hormone.
Methimazole (20mg q4h-q6h) is preferred unless pt is critically ill. PTU (200mg q4h-q6h) decreases T4T3 but
higher rates of fulminant hepatic necrosis.
o Iodine (100-250mg q6h-q8h) blocks release of thyroid hormone, must be given at least 1hr after thionamide; can cause
Jod-Basedow in toxic adenoma and Wolff-Chaikoff in Graves.
o Hydrocortisone (300 mg loading dose then 100 mg Q8H) to reduce T4T3
o Patients are hypermetabolic and will clear drugs quickly
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- Rheumatoid disorders
Infancy/childhood Bacteria: S aureus, PsA, ANC
Phagocytic - Oral, anorectal, SSTI Serratia, Klebsiella, non-TB Oxidative burst via DHR/NBT test
(10%) - Unusually severe infections mycobacteria for CGD
- Granulomas, poor wound healing Fungi: Candida, Aspergillus
T cell subset Infancy Bacteria: Mycobacteria Flow cytometry
defects (5%) - Oral thrush Fungi: Candida Anergy/proliferation tests
>6 mos, can present in adulthood Bacteria: H flu, Strep, Staph, SPEP, flow cytometry
- Recurrent sinusitis, PNA, viral URI Moraxella cat, PsA, Vaccine response
- Chronic GI malabsorption, diarrhea mycoplasma pneumoniae Polysaccharide PPSV23 titers:
- Autoimmune disease (29% in Virus: Enterovirus (esp with IgA ≥70% of serotypes ≥1.3 =
B cell /
CVID) (Blood 2012;119:1650) deficiency) adequate. If not, give PPSV23 &
Antibody (65%)
- Post-vaccination paralytic polio Parasites: Giardia repeat titers in 4-6 wks
ADAPTIVE
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Neurology Delirium
DELIRIUM or “Acute Brain Failure”: an acute disturbance of attention with fluctuating severity over the course of the day or
week & concomitant disturbance in cognition, neither of which are better explained by pre-existing/evolving neuro-cognitive
disorder or newly developed reduction in arousal. Presentation is a direct consequence of a medical condition, intoxication, or
withdrawal (DSM-5)
• Risk factors: Hx delirium/TIA/CVA/dementia, long hospitalization, EtOH, age >65 (~50% have delirium inpatient), infection,
visual/hearing impairment, comorbidity/severe illness, depression, HIV, h/o TBI
• Associated with mortality (JAMA 2010;304:433), institutionalization (Lancet 2014;383:911), cognition (NEJM 2012; 367:30)
• Both HYPERactive and HYPOactive delirium warrant treatment
Management:
• Behavioral management (see top of page)
• Identify & treat UNDERLYING CAUSE w/ special attention to life-threatening conditions (see Altered Mental Status)
• Daily EKG to monitor QTc (goal <550ms); Daily repletion of K>4 & Mg>2 (in anticipation of pharmacotherapies)
Medical Management (for dangerous behavior ONLY, i.e. if pt is a danger to self or others)
1:1 sitter (re-orients) >> meds >> restraints (deliriogenic)
• For HYPERactive delirium/AGITATION start PRN, escalate to scheduled (Nat Rev Neur. 2009; 5:210)
o Haloperidol 2-5mg IV q3h PRN vs. 0.5-1mg PO q4h PRN vs. IM q1h PRN (NB: can lead to EPS, acute dystonias in
Parkinsonism)
o Quetiapine 12.5-50 mg PO q6-12h PRN
o Olanzapine 2.5-10 mg SL/PO/IM qd-q4h PRN
• If continued severe agitation consider Psych/Geri consult:
o Haloperidol PRN: double PRN dose q20 min till effective, ~5-20 mg IV, consider standing or gtt (ICU)
o Quetiapine PRN: standing 25-50 mg TID, extra dose HS
o Olanzapine PRN: standing 2.5-10 mg BID, extra dose HS
• QTc severity: haloperidol > quetiapine > olanzapine; ∆ tx if QTc by 25-50%, QTc>500, ⊕U-wave/T-wave flattening
• Discontinue when able, avoid benzos. Prolonged antipsychotic use in elderly can increase mortality.
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Neurology Dementia
INITIAL EVALUATION: should almost always be in outpatient setting where can assess over time without acute illness or delirium
• Obtain collateral, determine symptom onset, ADLs/IADLs, assess safety, screen for depression
• Review medications for those with cognitive s/e’s (e.g. analgesics, anticholinergics, psychotropic medications, sedative-hypnotics)
• Assess cognitive impairment (MOCA >> MMSE), track score at subsequent visits
• Labs: CBC, TSH, BMP, B12; consider: tox, RPR, Lyme, HIV, UA, metals, ESR, LFT, folate, B1, B6 (Amer Fam Phys 2005;71:1745)
• Neuroimaging: NCHCT or MRI brain (preferred) to r/o structural lesion (tumor), assess atrophy pattern, eval for vascular dementia
and microhemorrhages (CAA). PET can be considered if dx unclear but often unnecessary.
• Formal neuropsych testing: pattern of deficits can suggest particular dementia syndrome; also helpful to r/o comorbid psych disease
• Inpatient evaluation should be considered for any rapidly progressing dementia syndrome or a new dementia diagnosis in pts <55
(consult Neuro for ?LP, consider RT-QuIC >14-3-3 [CJD], ACE [sarcoid], autoimmune encephalitis [only after d/w Neuro]), new focal
neurologic deficits (?stroke), fall with head trauma or LOC
• Outpatient Neurology referral to Memory/Cognitive clinic
DEMENTIA SYNDROMES (Prog Neurol Psych 2012;16:11, BMJ Neurol, Neurosurg, & Psych 2005;75:v15, Annals of Neurol 2008;64:97)
Syndrome Presentation Exam Imaging Treatment
Gradually Progressive
• Amnesia earliest sx; • Normal neuro exam (excluding Hippocampal (+/- • AChE-inhibitors
Alzheimer also language and MS) global) volume loss; (mild-severe dz)
Dementia visuospatial deficits • Neuropsych: amnesia w/ short ?microhemorrhages • NMDA-inhibitors
• Apraxia in later stages memory span, alexia, agraphia (CAA) (mod-severe dz)
• Fluctuations in • Parkinsonism: resting tremor Global volume loss • AChE-inhibitors
attention/alertness (can be absent), cogwheel (specifically
• Visual hallucinations rigidity, bradykinesia, rivastigmine) for
• REM behavior d/o stooped/shuffling gait – named memory sx
Lewy Body • Falls/syncope Parkinson’s dementia if • Carbidopa/levodopa
Dementia • Neuroleptic intolerance movement sx present for >1 yr trial for motor
• Memory problems late before dementia deficits
• Neuropsych: fluctuations w/ • Sx management of
intrusions and confabulation, autonomic dysfxn
visuospatial impairment
Behavioral variant most • May have frontal release Atrophy predominantly • Management of
common: signs (non-specific) in frontal and temporal behavioral sx (low
• Changes in personality • 15-20% get motor neuron dz lobes threshold c/s psych)
Frontotemporal (disinhibition, apathy) • Neuropsych testing: poor • AChE-inhibitors not
Dementia • Stereotyped behaviors impulse control, difficulty in helpful
• Lack of insight organization • Avoid NMDA-
Primary Progressive inhibitors
Aphasia variant
Stepwise Progressive
• Abrupt focal sx, • Focal deficits (depending on Cortical or subcortical • Secondary stroke
stepwise progression stroke location), can include: punctate lesions, prevention and risk
Vascular
• Depression common weakness, dysarthria, ataxia, white matter disease, factor modification
Dementia
• Hx: CVA, HTN, HLD, AF gait changes and volume-loss • AChE-inhibitor for
• Often look older than age memory deficits
Rapidly Progressive
• Rapidly progressive sx • Myoclonus, exaggerated MRI: cortical • No tx
Prion Diseases in memory, startle response ribboning on DWI, • Death w/in 1 year
(Sporadic, concentration, judgment • EPS: bradykinesia, nystagmus, subcortical (median disease
Variant • Mean onset age ~60 for ataxia hyperintensity on FLAIR duration 6 mo.)
Creutzfeldt- sporadic, 28 for variant • UMN signs (hyperreflexia, EEG: 1-Hz periodic
Jacob Disease) • Younger pts: more sig ⊕Babinksi, spasticity) epileptiform discharges
psychiatric sx • LP: RT-QuIC>>14-3-3
• Sx evolve days-weeks • Prominent psych features MRI: FLAIR • Immunotherapy:
Limbic (more indolent possible) • Dyskinesias, rigidity hyperintensity or steroids, IVIG,
Encephalitis • Short-term memory sx • Autonomic instability contrast enhancement PLEX, rituximab,
(Autoimmune, • Psych sx: agitation, • LP: lymphocytic pleocytosis, (esp in temporal lobe) cyclophosphamide
Paraneoplastic) delusions, hallucinations oligoclonal bands, EEG: extreme delta • Tumor resection
• Focal seizures autoantibodies (CSF + serum) brush very specific
TREATMENT: treat sx but do not slow the progression of disease
• AChE inhibitors: donepezil (first line), rivastigmine (patch), galantamine. Small effect on cognition, ADLs.
Major side effects: GI (n/v/d); less common bradycardia and heart block (increased vagal tone)
• NMDA inhibitors: memantine. Can precipitate agitation and exacerbate neuropsychiatric sx (caution in pts with sig behavioral sx)
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Episodic Ongoing
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CARDIOEMBOLIC STROKE
SUSPECT WHEN: DX WORKUP:
• ACA/MCA/PCA occlusion w/o sig vascular dz • TTE (w/ bubble if < 60 yo) - if PFO, r/o venous thrombus (LENIs/
• Infarcts in multiple territories or cerebellar stroke MRV pelvis), can consider closure (RESPECT NEJM 2017;377:1022)
• Known risk factors (LA/LV thrombus, AFib, • Inpatient telemetry followed by 30-day MCOT vs. LINQ at discharge
LVEF<25%, aortic disease, intracardiac shunt) (unless known AFib)
• Hypercoagulability/hyperviscosity (solid organ or ACUTE MANAGEMENT CONCERNS:
heme malignancy, HbSS, cryo, clotting d/o) • Avoid immediate AC unless known intracardiac thrombus or
mechanical valve. Transition to long-term AC in 2-4 weeks.
SYMPTOMATIC CAROTID STENOSIS
SUSPECT WHEN: ACUTE MANAGEMENT CONCERNS:
• Carotid stenosis present on ipsilateral side • If >50% carotid stenosis causing stroke/TIA, consider carotid
• H/o amaurosis fugax revascularization (stent/angioplasty/endarterectomy) – ideally w/in 2
DIAGNOSTIC WORKUP: weeks of sx (NASCET II NEJM 1998;339:1415)
• CTA vs. MRA head & neck usually sufficient • Consider temporary anticoagulation (d/w neurology)
• Alternatives: carotid US - typically need carotid • Consider induced HTN if symptoms fluctuate with BP
U/S prior to carotid endarterectomy (CEA)
INFECTIVE ENDOCARDITIS
SUSPECT WHEN: ACUTE MANAGEMENT CONCERNS:
• Unexplained fever w/ stroke or pt with valvular dz • Immediate antibiotics; caution with tPA
DIAGNOSTIC WORKUP: • Early cardiac surgery if small non-hemorrhagic stroke; delayed cardiac
• Blood cultures, TTE followed by TEE if neg surgery (2-4 wk) if large or hemorrhagic stroke
• CTA head to identify mycotic aneurysms (↑risk • Avoid anticoagulation or antiplatelet w/o a separate indication
bleeding)
• If CTA negative, may need conventional angio
(CTA not as sensitive for mycotic aneurysms)
CAROTID AND VERTEBRAL DISSECTIONS
SUSPECT WHEN: ACUTE MANAGEMENT CONCERNS:
• <60 yo or posterior circulation stroke in pt w/o RFs • Goal of tx is to prevent stroke: highest risk in first few days
• Neck pain, HA, or Horner’s syndrome • Anticoagulation vs antiplatelet. Prefer antiplatelet if: sx onset >3d
• Trauma (vertebral fx), chiropractor, coughing spells ago, dissection extends intradurally (no AC due to risk of SAH), large
DIAGNOSTIC WORKUP: infarct (risk of hemorrhage) (CADISS Lancet Neurol 2015;14:361)
• CTA vs. MRA with T1 fat saturation • High rate of recanalization Tx 3 months then re-image vessel
• Consider comorbid conditions (Marfan’s, FMD)
CEREBRAL VENOUS SINUS THROMBOSIS
SUSPECT WHEN: ACUTE MANAGEMENT CONCERNS:
• Positional HA, vomiting, papilledema, vision Δ • Immediate anticoagulation even in presence of hemorrhage
• P/w seizure (common, may be difficult to control) • AEDs if seizures (not indicated for ppx)
DIAGNOSTIC WORKUP: • IV fluids, avoid dehydration, modify risk factors (smoking, OCPs)
• NCHCT: hyperdensity in torcula (dense delta sign)
• CTV vs. MRV to assess intracranial venous system
• Consider hypercoagulable workup
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Cord Compression: high level of suspicion in cancer patients with back pain, urinary sx or LE weakness
• Etiologies: subacute (tumor/mets, abscesses) vs acute (disc herniation, trauma, hemorrhage)
• Symptoms: back pain, motor weakness, hyperreflexia below lesion if chronic (*can be hyporeflexic in acute injury or w/cauda equina),
⊕Babinski, loss of sensation (assess level), bowel/bladder incontinence OR retention, loss of rectal tone, saddle anesthesia
• Tests: STAT whole spine MRI w/contrast (cord compression protocol), call ED MRI (x63050) or inpt MRI (x64226)
• STAT page NSGY/Ortho spine +/- Rad Onc (x68652) for possible XRT if tumor related
• Dexamethasone (10mg IV x1 then 8mg IV BID), esp in malignancy. Solumedrol in acute cord injury 2/2 trauma is controversial
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Neurology Seizures
Definitions (Epilepsia 2014;55:475, Epilepsia 2015;56:1515, Continuum 2019;25:306, MGH Status Epilepticus Treatment Protocol)
• Epilepsy: ≥2 unprovoked seizures >24h apart or 1 unprovoked seizure + recurrence risk ≥60% over the next 10 yrs
• Status epilepticus: at least 5 mins of continuous seizure or 2+ seizures w/ incomplete recovery of consciousness in between
• Non-convulsive status epilepticus: non-convulsive electrographic seizure ≥10s or rhythmic EEG responsive to seizure treatment
• Tonic: persistent flexion/extension; Clonic: limb jerking; Atonic: loss of postural tone; Myoclonic: sudden brief muscle contraction
• Psychogenic Non-Epileptic Seizures (PNES): important to distinguish from epileptic events. Common features: waxing and waning
movements or fluctuating course, long duration of events, eye closure, ictal crying, gradual onset, asynchronous movements, pelvic
thrusting, recall during the period of apparent unresponsiveness, and hyperventilation (Ann Neurol 2011;69:997)
• Classification (Epilepsia 2017;58:522)
o Focal: unilateral, occuring in one hemisphere +/- impaired awareness (formerly simple partial, complex partial)
o Generalized: occuring in and rapidly engaging b/l distributed networks
Etiology: provoked vs not? Primary epilepsy, vascular (stroke/ischemia/hemorrhage), withdrawal (EtOH/BZDs), mass lesions (tumor,
abscess), trauma, metabolic ( glc, CO2, O2, Ca), meds, infection (systemic, CNS), HTN or HoTN, high fever, eclampsia, PRES
• Ddx: syncope, TIA, migraine, PNES (~30% also have epilepsy), myoclonus, dystonia, cataplexy, tremor
• H&P: previous sz history, prodrome (palpitation, sweating, N/V, aura), med list (many lower sz threshold), triggers (exertion,
pain/fatigue/emotional stress, cough/urination/defecation), tongue biting, incontinence, lateralizing signs, alcohol. GET COLLATERAL.
• Labs: FSBG, Tox, AED levels, lytes, CBC, LFTs, NH3, VBG, CK, INR, lactate, troponin, blood cx, b-hcg. Prolactin Sn ~50%
• Monitoring: tele ( risk for fatal cardiac arrhythmias during ictal/post-ictal period; ictal arrhythmias risk of sudden death)
• Neuroimaging: obtain in all w/ unprovoked 1st sz (MRI w/ con more sens) (Neuro 2015;84:1705) or if focal neuro exam, h/o trauma,
malignancy, HIV, or focal seizure (Neuro 2007;69:1772). Imaging changes management in ~10% (Neuro 2007;69:1996).
• LP/BCx: if febrile, HIV/immunocompromised, or if no clear etiology
• EEG: within 24h-48h if not seizing, emergent EEG if seizing: DO NOT wait to manage. If emergent, contact EEG fellow (p16834)
TREATMENT OF STATUS EPILEPTICUS
ABCs: VS, O2, EKG First 5-10 min (1st line): Correct reversible Concurrently: call neuro, RICU,
Assess pt safety Ativan 4 mg IV over 2 min causes: FSBG continuous EEG
Place 2 PIVs (BZD + repeat 4 mg x1 PRN in 5min (start IV thiamine + Check AED levels and rebolus if
PHT incompatible) If no IV, diazepam 20 mg PR or D50), lytes, fever, needed PHT, VPA, PHB 1 hr
midaz 10 mg IM/nasal/buccal O2 after load, FOS-PHT 2 hrs after
(RAMPART Trial) load (correct for albumin)
Persistent SZ (10-30 min, 2nd line): Refractory SZ (30-60 min, 3rd line):
Levetiracetam, VPA, fosphenytoin/phenytoin, phenobarb, +/- Intubate, continuous EEG
lacosamide (pre/post EKG to check PR) Midaz (if HD unstable) +/- propofol gtt
Seizure PPX: no AED in 1st seizure unless previous brain injury (Level A) OR abnormal EEG (Level A) OR significant abnormal imaging
(Level B). Early AED reduces short term recurrence (<2yr), not sustained remission (3+ yrs) (Neuro 2015;84:1705).
• ETOH seizure: Ppx not indicated when intoxication or withdrawal is the cause of seizure (Neuro 2006;67:s45)
• Brain tumor: no ppx (Cochrane 2008;CD004424). If seizures occur, start AEDs: Keppra > Lacosamide (fewer chemo interactions)
• Severe TBI: Keppra 500-750 mg BID x 7 days (Neurosurg Focus 2008;25:E3)
• ICH: AED only if clinical seizure or traumatic etiology, Keppra 500mg BID x 7days (Stroke 2016;47:2666)
• PNES: treatment with outpatient Cognitive Behavioral Therapy (CBT), psychiatry involvement. In acute setting it may be helpful to
educate patients about functional neurologic symptoms (http://www.neurosymptoms.org), and place social work consult.
• In MA, no driving for LOC event until 6 mos event free. Counsel pt and include in discharge summary. (Driving laws database)
AED Loading Dosing Goal Level Side Effects
60mg/kg No goal, level to Psychiatric sx (irritability, anxiety, depression, sedation,
Levetiracetam (Keppra) 1:1 PO:IV
Max 4.5g check adherence psychosis).
Teratogenic. Abnormal LFTs, weight gain, hair loss, N/V,
Valproic acid 20- 50-100 mcg/mL
1:1 PO:IV encephalopathy (NH3), pancreatitis, thrombocytopenia.
(Depakote) 40mg/kg (>1h post load)
Good for mood disorders.
10-20 mcg/mL, Teratogenic. Gingival hypertrophy, hair growth, rash, AMS,
Phenytoin (Dilantin), 20 pheny
1:1 PO:IV correct for alb, diplopia, ataxia, slurred speech, hypotension/arrhythmia (if
Fosphenytoin equiv/kg
(2h post load) run faster than 50mg/min; Fosphenytoin is less cardiotoxic).
Headache, diplopia, dizziness, nausea, hypotension. Obtain
Lacosamide (Vimpat) 200-400mg 1:1 PO:IV 10-20 mcg/mL
EKG prior and after load, and watch for PR prolongation.
Rash, SJS, nausea, somnolence, dizziness, ataxia. Good in
Lamotrigine (Lamictal) No Load Only PO 3-15 mcg/mL
mood disorders.
Weight loss, fatigue, teratogenic. Nephrolithiasis,
Topiramate (Topamax) No Load Only PO N/A
cognitive decline, anxiety, anorexia, tremor
Carbamazepine SIADH, N/V/D, rash, pruritis, fatigue, blurred vision, diplopia,
No Load Only PO 4-12 mcg/mL lethargy. Screening for HLA-B*1502 in Asians.
(Tegretol)
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Neurology Neuroprognostication
Neurological prognostication after cardiac arrest is challenging and uncertain (Seminar in Neurology 2017;37:040). The introduction
of therapeutic hypothermia alters the timeframe for neurological recovery and the interpretation of prognostic markers. Studies of
neurological prognostication are hampered by heterogenous patient populations and variable definitions of “coma”. We will discuss
the clinical predictors of recovery and available diagnostics – clinical exam, electrodiagnostic testing, and neuroimaging.
Therapeutic hypothermia: post-cardiac arrest patients are cooled within 6 hours of return of spontaneous circulation (ROSC),
to 32–34°C, where they are maintained for 24 hours via surface or endovascular cooling methods (Nat Rev Neurol 2014;10:190).
Targeted temperature management to 36°C, has equivalent efficacy (NEJM 2013;369:2197). During this period, patients can be
paralyzed with neuromuscular blocking agents to prevent shivering, and are commonly maintained on propofol, midazolam, fentanyl
and other sedatives. After completion of 24 hours of TH, patients are typically rewarmed in a controlled fashion over 8-12 hours, with
discontinuation of paralytics (if used) only once the shivering threshold—estimated at around 36°C—is passed; sedative-hypnotics
are continued while patients are paralyzed.
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PSYCHOSIS
• Characteristics: delusions, hallucinations (auditory>visual), thought disorganization
• Ddx: schizophrenia, schizoaffective, MDD w/ psychosis, bipolar w/ psychosis, malingering, substance-induced (cocaine,
amphetamines, MJ, bath salts, hallucinogens, EtOH), less frequently OCD/PTSD/borderline PD, intellectual disability,
dementia, due to another medical condition (delirium, epilepsy, AIP, paraneoplastic limbic encephalitis)
o New onset psychotic disorders in patients >50 is fairly rare. Medical cause of psychotic symptoms in this age group
(delirium, CNS pathology, dementia) is more likely unless known psych diagnosis.
• Labs: CBC, BMP, UA, Utox+VPAIN, serum tox including EtOH, UA, med levels, delirium workup (see neuro page)
• Refer to psych: outpatient = always, inpatient = if decompensated (can be associated with fear, agitation, aggression)
Treatment Basics: confirm home antipsychotics/mood stabilizers early in admission, continue only if patient reliably taking;
otherwise, dose reduce. Ask if patient on long-acting injectable medication/date of last injection, ask which PRN medications
work well for patient. Obtain Depakote, lithium, clozapine levels.
• Antipsychotics:
o Avoid multiple antipsychotics in 1 patient. If med list includes >1 antipsychotic, confirm before ordering as it’s unlikely
they’re taking all in outpatient setting.
o Continue home Cogentin (benztropine) if prescribed to reduce EPS sx (common in 1st gen antipsychotics)
o If on clozapine, consult psychiatry early to continue medication in house
• Mood stabilizers:
o Include lithium, Depakote, lamotrigine, some antipsychotics. Confirm compliance with lamotrigine given risk of SJS.
o Consider lithium toxicity in patients with n/v/d, tremor, ataxia, confusion, agitation seizures, nonconvulsive
status, encephalopathy if severe. Precipitating factors include dehydration, AKI, new medications (NSAID, ACE/ARB,
diuretics).
AGITATION IN DELIRIUM: (see Delirium in neuro section)
• Safety: #1 priority is patient and staff safety. LISTEN to nursing concerns. Very low threshold to page security.
o Can always page psychiatry (page APS resident after 6PM on weekdays/5PM on weekends)
o Offer oral medications early. Consider lorazepam 1st line if strong suspicion for stimulant intoxication or catatonia
o If patient requires restraints, ensure appropriate sedation as agitated patients are at risk of rhabdo/MSK injury
o 2nd generation antipsychotics carry a black-box warning for increased all-cause mortality in pts with dementia (who
commonly present with superimposed delirium) – goal is lowest effective dose for shortest time possible
• Treat underlying cause:
o Carefully review pts’ medications and assess risk/benefit of continuing anticholinergics & benzodiazepines. If opiates
are required, use PO oxycodone or IV hydromorphone if needed
• Management:
o Use behavioral strategies (including frequent re-orientation & light/physical activity (OOB/PT) cues) as first-line
o If medication is required for adults with QTc <550ms, can trial oral quetiapine (initial doses 12.5-25mg q6 hrs)
o If requires IV, trial IV haloperidol (initial dose 2.5-5mg, 1-2mg in elderly/frail). May be effective and is less associated
with dystonia than IM or PO dosing. Prefer early psych consultation for pts requiring higher/more frequent doses.
o Monitor QTc, replete Mg ≥2 and K ≥4 while using antipsychotics.
o AVOID antipsychotics in patients with Parkinsonian syndromes, catatonia, NMS
• IM medications: use only as a last resort in case of emergencies. Consult psychiatry for pts requiring IMs.
o IM haloperidol (5mg) should be co-administered with either IM diphenhydramine (25-50mg) or IM benztropine (0.5-
1mg) to reduce risk of dystonia although these medications may temporarily worsen delirium.
o IM olanzapine or thorazine may be given alone but should be used cautiously in elderly pts given risk of orthostasis
o IM olanzapine cannot be administered with IM benzos/barbiturates due to risk of cardiorespiratory depression
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Benzodiazepine Protocol:
• Use Epic Alcohol Withdrawal Order Set!
• Route: PO Ativan if able to take POs>IV Ativan>>Valium and Librium (long half-life, delayed toxicity, cleared by
the liver)
• PRN: use CIWA scale (only if patient can communicate), NOT HR, BP alone as poor predictors of DTs (JGIM
1996;11:410). PRN protocol inappropriate if AMS, DTs, or severe w/d. Consider switching to RAAS scoring.
• Standing: if likely to have severe w/d
• Beware paradoxical response, resistance (>6mg ativan/hr), or BZD toxicity (similar to DTs) w/ escalating dose
• Consider switch to phenobarb if CIWA consistently >16 and BZD dose <30mg Ativan equivalents
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ACUTE OPIOID WITHDRAWAL: agonist treatment with buprenorphine or methadone is first line treatment for opioid withdrawal and OUD.
Should be offered to every patient. Long-term agonist therapy decreases mortality and morbidity (BMJ 2017;357:j1550)
• Sx: dysphoria, restlessness, irritability, yawning, piloerection, mydriasis, rhinorrhea, lacrimation, mylagias/arthralgias, n/v/d, abdominal
cramping. Onset: 6-12h after short-acting opioids, 24-48 hours after last methadone use, variable with fentanyl analogs
• Medications:
o Buprenorphine (Suboxone): high affinity partial agonist with less risk of respiratory depression/OD than methadone
Wait until Clinical Opioid Withdrawal Scale (COWS) >10, usually 10-12h after last heroin use/short acting opioids. Avoid
precipitated withdrawal—rapid, intense withdrawal due to displacement of full agonist by partial agonist.
First dose: 4mg/1mg (1/2 of an 8mg/2mg Suboxone tablet)
Second dose: if continued withdrawal sx, give another 4mg/1mg after 45-60 minutes
Third dose: if recurrent withdrawal sx, give another 4mg/1mg after 6-12 hours
Maximum dose for Day #1 is 12mg buprenorphine
Prescribe total from Day 1 for Day 2, then reassess later in the day. Can give additional 4mg/1mg for withdrawal symptoms,
but max dose for Day #2 is 16mg buprenorphine
o Methadone: long-acting full agonist. Check and trend EKG for QTc, use with caution with other QTc-prolonging meds
Day 1 Initial dose: 10-20mg x1. COWS q2h: If <6 observe; if 6-12 5mg dose x1; if ≥ 12 10mg dose x1.
REQUIRED to call ACT if ≥40 mg daily dose.
Day 2 Stabilization: day 1 dose if COWS <6, increase by 20% if COWS 6-12.
If not planning to transition to methadone maintenance, decrease dose by 20% per day.
o If unable to initiate suboxone/methadone, offer symptomatic medications and short-acting opioids for pain:
Autonomic dysregulation: clonidine 0.1-0.2mg TID PRN (monitor BPs; avoid w/ 1st Suboxone/methadone dose)
GI upset: Bentyl 10-20mg Q6H PRN abd cramps; promethazine 25-50mg IM PRN N/V; loperamide 2mg PRN diarrhea
Anxiety: hydroxyzine 25mg Q8H PRN or trazodone 50-100mg q8h PRN
• Discharge: ensure pts have insurance, PCP, provider who can prescribe suboxone/methadone, list of shelters/needle exchanges
o Last dose letter for patients on methadone maintenance (includes date/amount of last methadone dose)
o Prescribe naloxone and teach OD response. Emphasize that Narcan reverses OD for ~30m. After OD EMS to the ED.
o Bridge clinic: Call 617-643-8281 Mon-Fri 8am-4pm to schedule appt or present as walk-in
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Obesity Annual BMI refer for or offer comprehensive lifestyle program if ≥25 (overweight) [B]d
Diet Intensive behavioral counseling if CVD RF* [B]a
Exercise 150 min/wk mod exercise or 75 min/wk intense exercise & 2 days of muscle strengthening activityf
Universal Cancer Screening
Colorectal CA Start 10 years prior to age of affected family member at dx*** Colo Q10y, flex sig q5y, FIT q1y [A]a +/-***
Q1y low-dose CT if 30 pack-yrs & current
Lung CA
smoker or quit w/in last 15y [B]a
Skin CA Insufficient evidence for routine skin exams by clinicians [I]a
Infectious Disease Screening
HIV Screen at least once; repeat based on risk assessment [A]a
HCV Screen all 18-79 at least once; repeat based on risk assessment [B]a
HBV Born in endemic region, getting HD, or immunosuppression, HIV+, IVDU, MSM, close contact w/ HBV+ person [B]a
Latent TB Screen if born or lived in high risk country (see CDC website) or high risk setting (homeless, jail) in last 2 years [B]a
Psych/SUD/Social Risk Factor Screening
Depression Q1y [B]a; PHQ-2: in 2 wk how often (a) little interest/pleasure doing things & (b) down/depressed/hopeless
EtOH Misuse Screen regularly with AUDIT-C [B]a
Tobacco Every encounter [A] . Advise to quit, Assist doing so (plan, quit date, QuitWorks, meds), Arrange f/u.
a
Intimate
Screen regularly in women of reproductive age [B]a. HITS screen well- No data but consider ongoing IPV, elder abuse
Partner
validated. Assess immediate safety & consider HAVEN referral. screening
Violence
Fall Risk PT, Vit D [B]a
* If ASCVD borderline risk (5%-7.5%) or intermediate risk (7.5%-20%) use risk-enhancing factors (i.e. FHx, metabolic syndrome, CKD,
race/ethnicity, CKD, chronic inflammatory disease) or CA calcium scanning to guide decision about preventative interventions
δ history of previous GIB or PUD, or bleeding from other sites, thrombocytopenia, coagulopathy, CKD, and concurrent use of other
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Shoulder Pain
• Rule out neck etiology: neck pain, pain radiation beyond elbow, numbness, tingling
• History: trauma, acute vs chronic, constitutional sx, orthopedic history, day/night, provoking activity, loss of ROM, weakness
o Get precise pain location
Etiology History & Physical Exam Findings
Subacromial Bursitis Ref. pain to deltoid. Pain w/ arc 60°-120° abduction +/- impingement. Overuse, heavy lifting. No imaging.
Acute=trauma. Chronic=age, acromial spurring, overuse. Can be tendonopathy, partial or full thickness tears.
Rotator Cuff
Pain & weakness, ROM, ⊕ internal/external lag test, painful arc, impingement. Ortho referral, MRI if tear.
Glenohumeral OA / Aching, stiff; chronic loss of active and passive motion in all planes. OA: crepitus, age >60 yo.
Adhesive Capsulitis Capsulitis: risk with diabetes, thyroid disease, immobilization, often 40-60 yo. Plain films for OA
Young athletes. “Click, pop, catch.” Ant inferiorshot-blocking arm pulled back. Posteriorpush-up.
Labral Tears & Instability
SLAP (Superior Labrum Anterior Posterior) baseball pitching, swimming. Crepitus/catching w/ ROM. MRI
Young: traumatic sprain, fall with separation. Older: AC evolves into OA (can contribute to impingment)
AC Joint Pain
Pain, tenderness, swelling over AC joint, ⊕ cross arm test. Plain films (w/ “stress views” for trauma)
Shoulder Exam
Test Maneuver
Drop Arm (RTC) Ask patient to abduct arm at 90°. ⊕ if cannot smoothly adduct shoulder to waist-level.
Bring dorsum of patient’s hand against lumbar region of back. Take forearm and hand away from
Internal Lag Test (RTC)
the back (~20°). Ask pt to maintain position while supporting elbow. ⊕ if not maintained.
External Lag Test (RTC) Externally rotate shoulder 90°, flex elbow 90°. Ask pt to maintain position. ⊕ if not maintained.
Neer (subacromial/RTC) Fully pronate forearm (thumbs point backwards), bring shoulder to full forward flexion. ⊕ if pain.
Hawkins (subacromial/RTC) Forward flex shoulder to 90°, flex elbow to 90°, and internally rotate the shoulder. ⊕ if pain.
Ext. Rotation (teres minor & infraspin.) Flex elbow 90°. Pt externally rotates shoulder while examiner provides resistance. ⊕ if pain.
Empty Can (supraspinatus) Flex shoulder 90°, internally rotated forearm. ⊕ if pain w/ resistance of downward push
• Imaging: x-ray if h/o trauma c/f fracture or dislocation, gross deformity, exam concerning for RTC tear or joint involvement; true AP of
glenohumeral joint, axillary lateral, & “Y view” of AC joint. MRI w/o contrast in pts with ⊕ internal/external lag tests, r/o full thickness
RTC tear, previous abnormal radiograph, persistent pain despite 2-3 mos of conservative therapy (see below)
• Treatment: bursitis/capsulitis/tendinopathy/impingement/OA/partial thickness RTC tear: conservative therapy (e.g. activity avoidance,
NSAIDs, PT/home exercises +/- steroid injections short-term); surgery for refractory instability, labral/full RC tear, AC joint seperation
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Incidental Pulmonary Nodules (<3cm) (Radiology 2017;284:228, Chest 2013;143:e93S, Thorax 2015;70 Suppl 2:ii1)
NB: these guidelines are for incidental findings; recommendations for f/u of nodules found on LDCT for lung cancer
screening are different as that population is high risk (see Lung-RADS classification tables online)
• Ddx: malignant (primary, met, carcinoid) or benign (majority; infectious granuloma, hamartoma, AVM, inflammatory)
• Is it malignant? Pt characteristics: risk w/ h/o smoking, emphysema, pulmonary fibrosis, extra-thoracic cancer,
asbestos exposure, age. Nodule characteristics: density (part-solid/ground glass>solid), larger size, faster rate of growth
(increase >2mm on repeat CT), borders (irregular/spiculated>smooth), location (upper>lower lobe).
• Is it benign? demonstrates fat (pulmonary hamartoma) or characteristic calcification pattern (granuloma, hamartoma) or if
it is stable on CT for a defined period of time (>2 years for solid and >5 years for subsolid nodules)
• Follow up: tailored to patient and type of nodule. Subsolid (entirely ground glass): if <6 mm, no routine f/u. If >6 mm, CT at
6-12 months, then CT every 2 yrs until 5 yrs. Part solid: if <6mm, no routine f/u. If >6 mm, CT at 3-6 mos, then annual CT
for 5 yrs if unchanged and solid component <6 mm. Solid nodules: see below.
Nodule type < 6 mm 6-8 mm > 8 mm
Single solid nodule
CT at 6-12 months, then consider CT Consider CT at 3 months, PET/CT,
Low risk No routine follow up
at 18-24 months or tissue sampling
CT at 6-12 months, then CT at 18-24 Consider CT at 3 months, PET/CT,
High risk Optional CT at 12 months
months or tissue sampling
Multiple solid nodules
CT at 3-6 months, then consider CT CT at 3-6 months, then consider CT
Low risk No routine follow up
at 18-24 months at 18-24 months
CT at 3-6 months, then at 18-24 CT at 3-6 months, then at 18-24
High risk Optional CT at 12 months
months months
• Consider referral to the Pulmonary Nodule Clinic: refer in Epic or call x38728 for appointment
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No/unknown Yes
Operative Risk without Adjustment for Patient Factors
Intermediate
High Risk >5% Low Risk <1% Utilize RCRI and
Risk 1-5% Proceed to surgery
- Emergent major - HEENT, CEA - Superficial, Gupta surgical
risk calculators to
surgery, especially - Intrathoracic, cataract, breast assess clinical
in elderly intraperitoneal, - Endoscopy risk factors,
- Aortic, peripheral, prostate - Ambulatory consider stress
or major vascular - Orthopedic testing, and
reduce risk
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Consultants Dermatology
Before Consulting Dermatology: Upload photo of rash (ideally pretreatment) to media tab of EPIC using Haiku
• If consulting for drug rash, note exact timing of rash development and administration of suspect medications
Quick Steroid Guide MGH topical steroid formulary by level of potency
• Face/intertriginous areas: hydrocort. 2.5% Super-potent clobetasol 0.05%, betamethasone dipropionate 0.05%
cream, hydrocort. valerate 0.2% cream Potent fluocinonide-emollient 0.05%
• Body: fluocinolone 0.025% cream if mild, Upper-mid strength betamethasone valerate ointment 0.1%
clobetasol 0.05% ointment if severe mid Mid-strength fluocinolone ointment 0.025%
strength to super potent depending on Lower mid-strength fluocinolone cream 0.025%, betamethasone valerate
severity cream 0.1%
• Scalp: 0.01% fluocinolone scalp solution or Mild hydrocortisone valerate 0.2%, fluocinolone scalp oil
oil (dermasmoothe); oil better for dry scalp 0.01%
Counsel patients: Use daily x2 wks then 1 wk Least potent hydrocortisone 2.5%, hydrocortisone ointment 1.0%
“off”, avoid face (risk = skin thinning) Over the counter hydrocortisone cream 0.5%, 1.0%
Consultants Dermatology
o Zoster ophthalmicus: urgent ophtho consult if c/f ocular involvement (“Hutchinson sign” = vesicle on nasal tip).
o Post-herpetic neuralgia: risk w/ early antiviral treatment (<72 hr); if higher risk (>50yo w/ mod-to-severe acute pain) consider
preventive tx w/ gabapentin 300mg PO QD, titrate up to 3600mg QD, divided TID as tolerated.
o Consider high lysine, low arginine diet + post-episode vaccination to prevent HSV recurrence.
• Erythema multiforme: target lesions (well-defined, circular erythematous macules/papules w/ 3 distinct color zones + central bulla or
crust) on palms/soles +/- mucosal involvement occurs within 24-72 hours; persist for 2wks;
o 90% triggered by infection (HSV, mycoplasma, GAS, EBV); less commonly drug rxn
o Tx: treat underlying infxn, NSAIDs, cool compresses, topical steroids, antihistamines; systemic steroids only if severe
• Erythroderma: diffuse redness >90% BSA.
o Causes: psoriasis, atopic derm, cutaneous T-cell lymphoma (incl. Sezary), pityriasis rubra pilaris (islands of sparing), drugs
o Work-up: detailed med rec, +/- HIV. Tx: derm c/s; liberal emollients, mid-potency topical steroids, antihistamines; fluids/lytes;
monitor for 2º infections; d/c offending meds.
• Purpura fulminans: “DIC in skin” = true emergency; consult Hematology for possible factor replacement;
o Microvascular skin occlusion w/ platelet-fibrin thrombi retiform purpura
o Causes: infection (Strep, Staph, H. flu, N. meningitidis, Capnocytophaga, VZV, CMV, Babesia); catastrophic APLAS, CTD,
malignancy, protein C/S deficiency
o Work-up: DIC labs, blood cultures, skin bx w/ GS and culture. Tx: broad-spectrum abx + supportive care.
• Stasis dermatitis: LE compression (ACE wraps, stockings) with elevation; mid-strength to super potent corticosteroid ointment BID x
1-2wks +/- occlusion with plastic wrap; mupirocin ointment BID x1-2wks to erosions; intensive moisturization (hydrated petrolatum);
can be unilateral or bilateral
• Psoriasis: depends on severity; Short-term tx includes topical steroids, calcipotriene, intense moisturization +/- occlusion w/ plastic
wrap; Long-term tx includes phototherapy, acitretin, MTX, biologics w/ outpt derm f/u (JAAD 2011;65:137)
• Seborrheic dermatitis: Face: least potent to lower mid-strength topical steroid BID x 1wk and/or ketoconazole 2% cream BID x4wks,
then 1-2x/wk for maintenance; Alternative: pimecrolimus cream, tacrolimus 0.03 or 0.1% ointment. Scalp: ketoconazole 2%
shampoo QHS
• Tinea pedis: “moccasin distribution”; apply topical imidazole (econazole 1% cream QD or clotrimazole 1% cream BID x 2-4 wks) or
allylamine (terbinafine 1% cream BID x 2 wks) to entire foot and webbed spaces between toes
Allergic Contact
Calciphylaxis Erythema Multiforme HSV Purpura fulminans
Dermatitis
Drug Eruptions
• Step 1: Make timeline to determine time course of drug initiation and development of rash
• Step 2: Discontinue offending agent. Common drugs for each eruption listed, but any drug can be a culprit at any time
Consultants Dermatology
Solitary sharply demarcated
round red-brown patch or
edematous plaque recurring
Abx (sulfa, TMP,
in same location each time
FQs, TCNs), -Topical steroids if
Fixed Drug Minutes-hours drug ingested. Can evolve to
NSAIDs, symptomatic
Eruption bullae. Oral/anogenital
barbiturates
mucosa common sites but
can occur anywhere.
Usually asx.
Pruritic, erythematous
4-14d (if prev. macules/papules. Start on Abx (PCN, sulfa), -Topical steroids,
exposed to trunk, spread centrifugally to allopurinol, antihistamines
Exanthematous/ the drug, symmetric extremities. May phenytoin, (Note: may take 7-
Morbilliform could be lead to erythroderma. requires repeat 14d after stopping
sooner) +/- low grade fever exposures drug to resolve)
Consultants Surgery
See Calling Consults for details on how to call the appropriate surgical service.
Abdominal Compartment Syndrome and Intra-Abdominal Hypertension (IAH): (Intens Care Med 2013;39:1190)
• Definition: IAH = IAP >12. Abdominal Compartment Syndrome = IAP > 20 AND clinical evidence of organ dysfunction (e.g. high
airway pressures, decreased venous return, elevated CVP/PCWP, UOP/AKI, elevated lactate, acidemia). IAP measured via
bladder pressure (most reliable if paralyzed, only done in ICU)
• Typically occurs after massive resuscitation in ICU patients with trauma, burns, s/p liver tx, severe ascites, pancreatitis, sepsis
• Tx: True Abdominal Compartment Syndrome (IAP >20, organ dysfunction despite medical management): surgical
decompression provides definitive management
o If IAP 12-20 w/o clinical instability:
Evacuate lumenal contents (NGT/rectal tube/enema)
Increase pain control/sedation (to level of paralysis if necessary)
Head of bed tilted up
LVP if ascites
Decrease tidal volume, permissive hypercapnia
Avoid over-resuscitation
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Consultants Urology
Symptomatic Urolithiasis (kidney stones)
• Evaluation/management:
o Imaging: CT Stone Protocol non-con (I–, O–): evaluates position, hydronephrosis, hints at composition
Alternative is KUB and ultrasound (requires both), with non-diagnostic studies prompting CT
o UA/UCx: in all patients except those with urostomies. If positive Cx, need decompression with stent by urology or percutaneous
nephrostomy (PCN) by IR
o Rehydration: NS @ 150 mL/hr if tolerated → ureteral peristalsis
o Alpha-Blockers: tamsulosin 0.4mg PO QD (hold for SBP < 90) → ureteral relaxation
o Analgesia: opioids preferred. NSAIDs/Ketorolac more effective but risk of bleeding and AKI
o Preoperative workup if requiring intervention: NPOpMN, EKG, Coags, T&S
• Consider urology consult: solitary or transplanted kidney, DM, immunosuppression, AKI, +UA/UCx, sepsis, inadequate pain control
• Urosepsis management: image ASAP, BCx/UCx, urgent Urology consult; IV abx to cover GNRs + enterococcus
• Clinical Pearl: patients with an acute abdomen lie still, pts with renal colic writhe in pain
Hematuria / Obstructed Catheter
• DDx: UTI, INR>3, traumatic catheter placement, bladder CA (5th most common neoplasm), upper urinary tract CA, prostate CA
• Workup: “The three C’s”: 1) hematuria protocol CT (3-phase: non-con, arterial phase, delays to assess ureters); 2) urine cytology
once hematuria clears (blood interferes with test); 3) outpatient cystoscopy
• Tx: If obstructed (can’t void or catheter not draining / “clot retention”) or significant hematuria: irrigate bladder via Whistle-Tip
catheter using a 60 cc catheter-tipped syringe – flush in and out with saline to remove clots until urine is clear. Then place 3-Way foley
on continuous bladder irrigation (CBI, AKA Murphy drip)
o Start CBI after clot extraction; titrate to keep urine cranberry juice color or lighter
Urinary Retention
• Urethral/bladder pathology:
o Etiology: BPH, UTI, constipation, neurogenic (MS, SC injury), DM, immobility, anticholinergics, opioids, benzos, pelvic surg
o Treatment (improvement may take 3-12 months):
Aggressive bowel regimen, treat UTI, minimize narcotics and anticholinergics, encourage ambulation
Alpha blockers (finasteride does not help acute retention, takes 4-6 months to work)
Clean intermittent catheterization (CIC) with bladder scans to ensure low residual volume vs chronic Foley/SPT
• Ureteral pathology: typically external compression on ureter by mass or LN hydronephrosis. Often due to underlying malignancy,
portends poor prognosis. Management depends on GOC, prognosis, GFR, need for nephrotoxic chemo. Options: PCN, ureteral stent.
Urinary Incontinence
• Classifications: stress (leakage w/ coughing, etc.), urge (proceeded by urgency), mixed (most common), overflow (PVR >150),
functional (neurologic, impaired mobility/cognition)
• Treatment:
o All types: lifestyle interventions, bladder training (timed voiding), Kegel pelvic floor exercises
o Stress: vaginal estrogen (post-menopausal women w/ vaginal atrophy), pessaries (mixed data), surgery (midurethral sling)
o Urge: antimuscarinics (oxybutynin, tolerodine, beware of side effects), beta agonists (mirabegron, avoid w/ uncontrolled HTN,
ESRD, liver disease), intravesicular botox
Tubes and Drains: see Tube Management for placement and management
• Foley catheter: externally placed tube which travels through urethra and into bladder
o Call urology if difficulty with placement
o Foley size: Hx instrumentation or urethral stricture small Foley (14 Fr or smaller). If elderly man/BPH or difficulty placement
large Foley (18 Fr Coudé or larger). Coudé catheter has a gentle upward curve to pass through the prostate
o Urethral trauma: leave catheter in for at least 5 days to allow for urethral healing
• Suprapubic tubes (SPT): externally placed tube which travels through the overlying skin and directly into the bladder
o Placed by GU IR. Once tract formed (after 1-2 changes by IR), change q6-12wks similar to Foley
o Staph aureus becomes a more common organism involved in infections
• Percutaneous nephrostomy tube (PCN): externally placed tube which travels through the overlying skin directly into the renal pelvis
o Placed by GU IR usually under local anesthesia. Cannot be coagulopathic, thrombocytopenic, or on ASA/Plavix
o Urine collects in external bag. If low UOP into bags, passage of blood or concern for malposition - obtain CT A/P, call GU IR
• Ureteral stent: internally placed stent which maintains ureteral patency from level of renal pelvis to bladder
o Placed by Urology in OR with general anesthesia, requires change every 3-6 months. May cause urinary urgency. Is NOT
changed in setting of infection
• Note: If stents/PCNs/Chronic Foley or SPT/ileal conduit or neobladder – UTIs should be treated only if symptomatic, NOT based on
UA/UCx
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Consultants ENT
To call an ENT consult: page the ENT consult resident p22220. To transfer a patient to MEEI: call MEEI ED at 617-573-3431.
Epistaxis (nosebleed)
• Acute management:
o Have pt lean forward, pinch nostrils, hold pressure for 20 min
Do not lean head back or hold bony part of nose
Hold over basin, measure blood loss as possible
Do NOT “peek” – hold continuous pressure for 20 min
Usually a patient will not pinch hard enough – best for RN/MD to
do so
o Afrin (oxymetazoline 0.025%) nasal spray (after gently clearing
clots)
o Control SBP (goal < 120) if much > baseline
o Correct coagulopathy if present
o Consult ENT if continued bleed
If bleed visualized, silver nitrate cauterization, nasal packing,
or Neuro IR embolization
YES NO
Nasal packing: risk of Toxic Shock very low but may prescribe prophylactic cephalexin or clindamycin; packing typically
removed after 5d by ENT (whether inpt or outpt)
• Location: most are anterior bleeds; posterior are more rare/serious/difficult to manage
• Hx: side, duration, EBL, prior episodes (and txs), trauma (fingers, fists, foreign body, etc), prior nasal surgery, nasal trauma hx, FHx or
PMHx coagulopathy, nasal tumors, HTN, anticoagulant meds, nasal steroid spray use
• Exam: rapidity of bleeding, inspect nasal septum and oropharynx for originating site; suction clots from OP to protect airway
• Tests: coags, CBC, type & screen; crossmatch pRBC if brisk bleed
• Epistaxis prevention: after resolution, x 2 weeks: petroleum jelly (or bactroban if cautery used) inside rims; no nose
blowing/touching, no exercise, keep head higher than heart (use pillows), sneeze with mouth open, use humidification (saline nasal
spray BID), oxymetazoline spray PRN if re-bleeding
Stridor
• Acute management:
o IV access, 100% O2 by non-rebreather
o Racemic epinephrine neb x1 STAT if concern for supraglottic source, 10 mg dexamethasone IV x1 STAT
o Consider IM/IV epinephrine and Benadryl if allergy suspected (see Angioedema & Anaphylaxis), consider Heliox
o If unstable Call RICU & trauma surgery (x6-3333) for possible surgical airway
o If stable Call ENT for airway evaluation
• Epinephrine dosing: if allergic reaction suspected: 0.3mg IM (1:1,000 solution) or 0.1mg IV (1:10,000 solution)
• Hx: timing/evolution, inspiratory/expiratory/biphasic, inciting events, prior episodes, evidence of infection, allergy, hx EtOH/tobacco
(cancer risks), hx of known cancer of head and neck, radiation
• DDx (in adults): iatrogenic/post-intubation (laryngeal/vocal cord edema/praxis of the recurrent laryngeal nerve from ET tube);
infectious (epiglottitis, laryngitis, laryngotracheitis [croup], bacterial tracheitis, Ludwig’s angina); allergic; tumor/mass of larynx or
trachea; neurological (vocal cord spasm or immobility); foreign body/trauma
• Imaging: if stable, CT with contrast of head/neck/chest to localize source
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Consultants Ophthalmology
Basic Eye Exam: “Ocular Vital Signs”
- Visual Acuity (e.g. 20/200, CF) - Extra Ocular Movements
- Pupils (4mm 2mm OD, No APD) - Intraocular pressure
- Visual Fields - Color vision testing (Ishihara cards)
Common Abbreviations:
APD Afferent pupillary defect NLP No light perception (VA)
AT Artificial tears NPDR Non-prolif. diabetic retinopathy
cc/sc With/without refractive corr. NS Nuclear sclerosis (i.e. cataract)
CE Cataract extraction OD/OS Right eye, left eye
Uvea = iris + ciliary body + choroid CF Count fingers (VA) OU Both eyes
CWS Cotton wool spot PDR Prolif. diabetic retinopathy
DES Dry eye syndrome PF Pred Forte gtt (prednisolone)
EOM Extraocular movement PFAT Preservative-free artificial tears
HM Hand motion (VA) PVD Posterior vitreous detachment
IOL Intraocular lens RD Retinal detachment
IOP Intraocular pressure SLE Slit lamp exam
LP Light perception (VA) SPK Superficial punctate keratitis/dry eye
MGD Meibomian gland dysfunction VA, VF Visual acuity, fields
To call an Ophtho consult: check vision using vision card and pupils prior to calling consult!
General inpatient consult: page 21004; can also call MEEI ED back desk 617-573-4063
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Consultants OB/GYN
How to Consult
• Obstetrics: if pt has pregnancy >20wk or has established MGH OB provider. If hCG⊕ but no confirmed intrauterine pregnancy,
should be followed on ectopic list
• GYN Onc: if pt has biopsy confirmed GYN malignancy or established GYN onc provider
• GYN: everyone else (e.g. pregnancy <20wk, undifferentiated ovarian mass)
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Consults – Weekdays
8am 12pm 5pm 7pm 8am
Cardiac CT Dodd XXXXXXXXXXXXXXXXXXXXXX
Chest Dodd ED
GI Dodd ED
Neuro Neuro Consult (730am – 430pm) Neuro ED
Vascular Dodd ED
Other Reading Room ED
• Life Images
o Upload images to lifeIMAGE and Epic: Partners Applications utilities MGH Upload Image to Radiology
(LifeImage) Access LifeImage find exam on CD/DVD upload images
o Send images to MGH PACS: upload to MGH request read
o Retrieve images from The Cloud: ISDrequests.partners.org file an urgent ticket
o Additional information:
Urgent reads: contact ISD (p34188, x30003)
Multiple body parts: interpretations only given for selected body parts
Multiple LifeImages of the same body part: upload all images request a read only on the most recent
Exams will not be read if: requisition was for a different body part than the uploaded images; study >6 months
old; a more recent LifeImage is available; US, fluoroscopy, or mammography
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o Phases of contrast:
Phase Time After Injection Structures Evaluated
CTPE 15 s Pulmonary arteries
Arterial (CTA) 30 s Aorta, systemic
arteries, renal cortices
Late arterial 60 s Routine chest
Portal Venous 70 s Routine abdomen
Nephrographic 100 s Renal medulla
Venous 120 s Peripheral veins
Delayed (Urogram) 10-15 min Ureters, bladder
o MRI safety:
Device compatibility: www.mrisafety.com
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Radiology Contrast
• Indications:
o IV: whenever possible, particularly for infection, tumors, and vessel imaging
o PO positive (hyperdense): bowel obstruction, bowel wall pathology, differentiate bowel from other abd. structures
o PO negative (hypodense): inflammatory bowel disease, GI bleed, mesenteric ischemia
o Rectal: appendicitis, penetrating abdominal trauma
• Pregnancy and breast feeding: (ACR 2020)
o Pregnancy:
Iodinated: no need to withhold contrast (no data to suggest potential harm to fetus)
Gadolinium: unknown risk to fetus consider noncontrast or alternative study
o Breast feeding: mother’s informed decision to “pump and dump” for 12-24 h after scan
• Renal function: (ACR 2020, MGPO 2020)
Contrast Induced Nephropathy Nephrogenic Systemic Fibrosis
Age >60 years, dialysis, kidney transplant, single
Dialysis, kidney transplant, single kidney, renal
Risk factors kidney, renal cancer, renal surgery, HTN on
cancer, renal surgery, HTN on medication, DM
medication, DM, metformin
Outpatient:
Screening
Outpatient: GFR within 30 d • GFR 45-59: GFR within 6 wks
(At risk pts
Inpatient: GFR within 24 h • GFR <45: GFR within 2 d
only)
Inpatient: GFR within 2 d
GFR ≥ 30: contrast per protocol (NO GFR ≥ 30: gadolinium per protocol
PREHYDRATION RECOMMENDED) GFR < 30: non-contrast or alternative study
Prevention
GFR < 30: non-contrast or alternative study • If necessary consult radiology and
• If necessary consult radiology nephrology, obtain informed consent
Dialysis pts HD within 72 h after scan Prompt post-scan HD (PD inadequate)
Decision is clinical and subjective No risk factors: proceed
Repeat studies
Insufficient evidence to hold contrast for 24 h At risk pts: consult radiology
GFR ≥ 30: continue metformin
Metformin No need to hold metformin
GFR < 30 or AKI: hold for 48 h after scan
• MGH prehydration protocol (prophylaxis only indicated when GFR < 30): (MGPO 2020)
o PO (preferred): 1-2 L PO non-caffeinated beverage 12-24 h prior to scan
o IV (outpatient): NS 250 mL IV bolus @ 1 h prior to scan
o IV (inpatient): NS 100 mL/h IV 6-12 h before and 4-12 h after scan (ACR 2020)
• Contrast reactions: (ACR 2020)
Allergic Physiologic Indications for Premedication
Limited urticaria N/V, flushing/warmth • Prior mild-moderate allergic reaction
Itchy throat HA/dizziness • None for prior physiologic reactions
Mild
Radiology Protocols
Ordering Studies:
• All cross-sectional studies are protocoled by radiology – simply provide the necessary information:
o Body part and modality
o Indication: clinical history relevant to the study (GOOD HISTORIES IMPROVE INTERPRETATIONS)
o Contrast: “per radiology discretion” unless specific reason otherwise
o Contraindications for contrast: kidney injury or prior allergic reaction (see Contrast)
o Questions: call the appropriate division or page the appropriate on-call radiologist (see Contact Information)
• Level of Urgency:
o Routine: order of interpretation depends on acquisition time
o Urgent: takes priority over routine studies
o STAT: means NOW, high acuity/life threatening emergencies
Patient must be ready for immediate transport
Patient must be accompanied by a responding clinician capable of providing emergency care
Responding clinician must be present for the entire exam
Radiology will provide preliminary read: phone call for XR/US, at the scanner for cross-sectionals
Overnight Reads:
• Studies with full interpretations overnight: all ED studies, STAT studies, and acute CT PEs
• Verbal preliminary reads:
o Typically done for ICU studies only
Inpatient studies are only reviewed overnight if there is an urgent clinical question (i.e. one that would alter
overnight management). Consider face-to-face consult in ED.
o After communication w/ the primary team, all verbalized prelim reads will be documented in the chart
o A full interpretation will be generated the following morning for all prelim reads
ED Protocols:
• Trauma: I+, single phase (arterial for chest, portal venous for abdomen/pelvis – images checked at the scanner by
radiology for possible delays)
o Blunt trauma: includes bone kernel reformats for improved visualization of bones
o Penetrating trauma: O+R+ for increased sensitivity of bowel injury
• Cervical spine: I-, need for CTA determined by radiology, bone kernel reformats in all 3 planes
o Images checked at the scanner by radiology only if IV contrast is required for another body part
• Appendicitis: I+ and O+/R+ (please specify PO or PR), kidneys through pelvis only
• Neuro ED: call reading desk @ x68188
Cardiovascular Protocols:
• DVT imaging: U/S (LENI) is initial test of choice (Cardiovascular Diagnosis and Therapy 2016;6:493)
o CTV/MRV: primarily used for central venous thrombosis when initial U/S is equivocal or non-diagnostic
• Arterial imaging:
o CTA: three phases (noncontrast, arterial, delays) stenosis, dissection, aneurysm
o Requisition: specify vessel of interest, field of view, and indication
• Coronary CTA:
o ECG-gated study of the heart only performed by CV CT on-call radiologist during normal hours
o Specify if body parts other than the heart should be imaged (thoracic aorta, CABG grafts, etc.)
• Other EKG-gated CTAs:
o Indications: any evaluation of the heart or ascending aorta
o EKG-gating is unnecessary for the descending thoracic aorta, abdominal aorta, and pulmonary arteries
• Noncontrast vascular studies:
o RP hematoma, pre-op aortic calcifications, coronary calcium score, follow-up aortic size
Thoracic Protocols:
• All chest CTs are high resolution – traditional “high res chest CT” is now the diffuse lung disease CT (see below)
• Routine chest vs CT PE vs CTA chest:
o Routine chest: single phase (late arterial) workhorse protocol
o CT PE: single phase (pulmonary arterial) pulmonary arteries
o CTA chest: three phases (noncontrast, arterial, delays) systemic arteries
• Double rule out studies:
o Clinical concern for PE and aortic dissection
o Contrast can only be optimized for one (must pick CT PE or CTA)
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Radiology Protocols
• Diffuse lung disease (a.k.a. misnomer “high res CT”):
o Indications: ILD, lung transplant, air trapping
o Inspiratory and expiratory images, plus prone images to differentiate between atelectasis and fibrosis
• Nodule follow-up: (Radiology 2017;284:228)
o Indications: incidental nodule on prior CT, age >35 y, AND no history of malignancy or recent infection
o Fleischner Society 2017 Guidelines
GI/GU Protocols:
• Stone protocol: I-O-, low dose
o Order contrast-enhanced CT if there is concern for ANYTHING else (stones may still be visualized)
• Routine abdomen/pelvis vs renal mass vs bladder cancer vs hematuria:
o Routine abdomen/pelvis: I+O+, single phase (portal venous) workhorse protocol
o Renal mass: I+O+, two phases (noncontrast, nephrographic), abdomen only renal masses or cysts
o Bladder cancer: I+O+, two phases (portal venous, delayed) workup or monitoring of GU malignancy
o Hematuria: I+O-, “three” phases (noncontrast, nephrographic, urogram) hematuria, hydronephrosis
• CT urogram vs CT cystogram:
o Urogram: antegrade filling of ureters and bladder with IV contrast (delayed phase)
o Cystogram: retrograde filling of bladder with contrast via Foley catheter evaluation of bladder rupture
• Arterially-enhancing tumors:
o MR CHIT: melanoma, RCC, choriocarcinoma, HCC, islet cell (neuroendocrine) tumors, thyroid
• Does my patient need to be NPO?
o IV contrast CT: 2 h Abdomen/pelvis CT: 8 h Non-contrast CT: no NPO
• Fluoroscopy protocols:
o Requisition: specify indication, h/o surgery or aspiration
o Barium swallow vs modified barium swallow vs UGI series vs SB follow-through:
Barium swallow: esophagus, GE junction, proximal stomach dysphagia, GERD
Modified barium swallow: mouth, pharynx, upper esophagus dysphagia, aspiration
UGI series: barium swallow plus stomach, pylorus, and duodenal bulb bariatric surgery
SB follow-through: small bowel, terminal ileum, and proximal LB +/- UGI series beforehand
Neuroradiology Protocols:
• Inpatients: page Neuro IP on-call radiologist @ p32535
• Acute stroke:
o Inpatients/ICU: page acute stroke consult fellow @ p21723
o ED: activate ED2CT via the group pager
• Head CT: typically noncontrast
o Indications for contrast-enhanced head CT: infection and/or tumor AND contraindication for brain MRI
• Spine MRI: for more than 1 segment, please order total spine and specify indication
o Separate MRIs should not be ordered prior to neurology/NSGY consult
• Fluoroscopy-guided LPs: performed by neuroradiology fellows, NOT neuro IR
o Indications: difficult anatomy, and only after LP is attempted on floor
Not to be used as an anesthesia service for unruly patients (typically performed without conscious sedation,
although this can be arranged if required for patient safety)
Musculoskeletal Protocols: if questions: page MSK IR on-call radiologist @ p36321
Nuclear Medicine Protocols:
• Overnight studies:
o Tagged RBC study: BRBPR (NOT guaiac positive stools, melena, or massive bleeding)
Requirements: consult IR first for possible angiogram if study is positive
o VQ scan: acute PE (NOT chronic PE), ONLY if results will alter management (i.e. AC tonight)
Requirements: CXR within 24 h, patient stable for duration of scan (~4 h)
o HIDA scan: acute cholecystitis, ONLY if results will alter management (i.e. OR tonight)
Requirements: NPO 4-24 h prior to study, no opiates 12-24 h prior to study, bilirubin <10
• PET:
o Fasting: hold everything but meds and water
Overnight is ideal, but AT LEAST 6 hours for non-DM patients
AT LEAST 4 hours for DM patients
- Continue long-acting insulin, hold short-acting insulin 4 h prior to scan
o Blood sugar thresholds: FDG-PET brain < 175 mg/dL, FDG-PET whole body < 250 mg/dL
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CT Chest MRCP
1. Lines and tubes (scout can be very helpful) 1. Choledocholithiasis: hypointense filling defect
2. Abdomen within CBD surrounded by hyperintense bile
3. Soft tissues
4. Bones
5. Heart and mediastinum: thyroid, lymph nodes, heart
and pericardium, major vessels, esophagus
6. Pleura: pleural effusion, pneumothorax
7. Lungs: secondary pulmonary lobule is the key
a. Radiology Assistant Lung HRCT Basics
CT Abdomen/Pelvis
1. Lung bases
2. Liver/gallbladder: focal lesions, biliary ductal dilatation
3. Spleen
4. Pancreas: focal lesions, pancreatic ductal dilatation
5. Adrenals
6. Kidneys/ureters: hydronephrosis, stones, focal lesions
7. Bladder/pelvic organs
8. Peritoneum: free air or fluid
9. Lymph nodes
10. Vessels
11. GI tract: bowel distension, bowel wall thickening
12. Soft tissues
13. Bones
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Transducer (probe): converts electricity into sound waves transmits sound wave into tissue receives sound waves echoed
back from tissue. Indicator (denoted by light or notch on probe) displays on left of the screen. Exception: echocardiography
indicator displays on right side. Ensure have probe positioned appropriately.
• PHASED-ARRAY (cardiac) probe: good for looking in small windows (i.e. between intercostal
spaces for cardiac or pulm imaging); low resolution, produces fan-like image. Cardiac Linear Curved
• LINEAR (vascular) probe: good for shallow structures (i.e. vascular, soft tissue). Uses high
frequency with good resolution, produces rectangular image.
• CURVED (abdominal) probe: good for deeper structures (i.e. intra-abdominal). Uses lower
frequency; combines linear and sector probe image qualities.
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• Central venous access: use LINEAR (vascular) probe. Reduces complications and
quality of placement compared to landmark approach (Crit Care 2017;21:225)
o In-plane (long axis): can view entire tip, but harder to keep needle in view
o Out-of-plane (short axis): easier to center needle, may underestimate depth
• Peripheral IV: use LINEAR (vascular) probe. Most of your time should be spent finding
the best vein to go for, often in the medial groove between biceps/triceps or anterior
forearm. Track along vessel length to determine trajectory, look for large, superficial,
compressible vessels that are not adjacent to pulsatile, non-compressible arterial vessels.
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Transverse Technique
NEJM 2012;366:e38: choosing a vein (8:45), transverse (10:05), longitudinal (12:28)
1) Setup: positioning is very important. Place U/S on opposite side of pts bed, adjust
bet to appropriate height, obtain seat if needed, abduct & externally rotate pts arm.
2) Place tourniquet: place tourniquet as proximal as possible, near axilla if possible.
Can stack two tourniquets for extra compression.
3) Confirm anatomy: use vascular probe on U/S at minimum depth to locate adequate
superficial veins.
o Find vessels: start at AC and move proximal and distal. Key is to find LARGE
vessels (>0.4cm) that are CLOSE to the surface (depth between 0.3cm –
1.5cm) (J Emerg Med 2010;39:70). Common veins: basilic, cephalic > deep
brachial
o Confirm venous circulation: gentle pressure differentiates veins (fully compressible, non-pulsatile) and arteries (pulsatile); color
doppler can confirm
o Trace vessel course: follow the vessel course proximally and distally; recognize and avoid branch points, diving veins, and
irregular coursing veins
4) Sterility: use alcohol pad or chlorhexidine swabs to sterilize proposed venipuncture site; clean U/S probe then cover with tegaderm;
use sterile lubrication (or sterile U/S gel) as conduction medium for probe
5) Orient ultrasound: center target vein on U/S screen, confirm with compression, confirm vein course is in line with proposed needle
course, stabilize probe by anchoring hand on patient
6) Insert angiocath: with bevel up, puncture skin and advance angiocath 2-3 mm at a 45° angle
o Angiocath needle tip should be centered on U/S probe – this will be directly over the
vein if vein is centered on screen
o Insertion site at skin is distal to the planned site of insertion into vein
o At insertion, eyes should be on the site of venipuncture, not on the U/S screen, though
after puncture, should be watching screen and not hand
7) Find tip and advance: as insert, needle tip (and shadow) should appear on screen
advance PROBE until you lose needle tip advance NEEDLE tip until it reappears on U/S
screen; continue to advance until tip is “tenting” the roof of the vein
8) Enter vein: a quick short jab will allow you to enter vein; visualize needle tip as “target sign”
9) Drop angle and advance: drop your hand to flatten needle angle; continue to advance as above, keep needle in center of vein.
10) Slide off catheter: once 3-5mm into vein, can slide catheter off needle into vein and hub, and retract needle.
Optional: continue to advance needle until angiocath is hubbed to skin
11) Flush: attach extension tubing, REMOVE TOURNIQUET, pull back on saline flush (ensure drawback), THEN FLUSH with saline
12) Secure: secure catheter and tubing with tegaderm; floor and ICU nurses may redress IV
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guide wire advances easily and syringe comes off needle easily
5)
6)
Locate IJ vein & carotid artery using ultrasound
Anesthetize with lidocaine; can make wheal & inject along tract (aspirate before injecting!)
ICA IJ
CA
7) Insert and advance the large bore needle bevel up, 45°, towards ipsilateral nipple, visualizing
tip with US; apply negative pressure. Once flash of blood is obtained stop advancing the
needle, continue to draw back venous flow (dark, non-pulsatile)
• If arterial flow seen, remove needle and compress ~10 min
• If air drawn back, suspect PTX STAT CXR, 100% FiO2, decompress if tension
8) Once flow obtained, stabilize needle with your non-dominant hand, remove syringe from
locator (occlude hub with thumb to minimize risk of air embolism in non-ventilated patients)
9) Feed the curved end of the wire into the needle (never feed the opposite end)
NEVER LET GO OF THE WIRE.
• If any resistance, remove wire, assess for flow w/ syringe; If good blood flow, try
twisting wire or flattening angle of needle
ICA RIJ
• For R-sided IJ feed ~25cm of wire (between two and three dark lines)
watch for ectopy (suggests wire in RV withdraw)
SCM
NB: catheter length = 14cm (usually), so need at least this distance of wire in vessel.
10) Remove needle
11) Confirm wire is in vein using U/S in transverse and longitudinal planes
12) Perform manometry confirmation advance angiocath from kit over wire, remove wire,
connect manometer tubing venous blood should be non-pulsatile, dark, and rise < 20cm (can directly visualize fill in tubing or
connect tubing to manometer) replace wire through angiocath, remove angiocath
13) Extend puncture site with scalpel by inserting along path of wire (face cutting edge away from wire to prevent cutting wire)
14) Thread dilator over wire (using twisting motion) until about 1/3 is inserted, then remove; goal is to dilate skin/subcutaneous tissue,
NOT the vessel itself (increased bleeding); ensure the wire moves back and forth freely while dilating (may otherwise be kinked)
15) Advance catheter over wire (wire comes out brown port, which is why it must be uncapped); remove wire
16) Draw back off all ports through caps using saline flush (only need to see small amount of flash), flush all lines clean, clamp ports
17) Secure with sutures; place Biopatch prior to securing with dressing
18) Order CXR (ASAP) to assess position, rule out PTX and hemothorax; look at the CXR yourself; catheters should terminate in
superior vena cava or cavo-atrial junction; may need to pull back if in RA ( ectopy). If adequate position, put in order “OK to use.”
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CVC Complications
Arterial puncture: hold pressure x 10 mins; compress 1 inch inferior (IJ) or 2 inches superior (femoral) to puncture mark
Dilation / line placement in an artery: consult vascular surgery BEFORE removing line; consider CT if pt stable
Pneumothorax (IJ & subclavian): suspect if hypoxemia, hypoTN, difficult stick; obtain STAT CXR thoracic surgery consult if PTX or
hemoTX; if tension physiology (shock) immediate decompression with 16G angiocath @ 5th ICS, mid-axillary line (enter above the rib)
Retroperitoneal bleed (femoral): suspect if hematoma or hypotension; STAT CT vascular medicine consult
Loss of wire or wire stuck in vessel: DO NOT use excessive force to pull out wire if it is stuck leave in place, hold pressure to prevent
exsanguination STAT KUB / CXR if wire loss vascular medicine consult
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Daily for ischemia (cool, white, purple) & infection (need for removal)
Troubleshooting and Alternatives
• If using Doppler, mark out course of artery with marking pen or indentations.
• If using U/S, can try advance needle/catheter under U/S guidance and once
firmly in vessel, advance catheter over wire (no guide wire; similar to PIV).
• If unable to thread guide wire AFTER ATTEMPTING TO SPIN during
insertion, consider micropuncture wire (cardiac cath lab or MICU med room).
May help with atherosclerotic arteries at the price of risk of perforation
• After multiple attempts, the artery may spasm. Pursue alternative site.
• Femoral artery access can be considered in difficult cases. Use the long
catheter in the Arrow arterial line kit. Puncture must occur distal to the
inguinal ligament to prevent RP bleed. Too distal, however, and the femoral Proper femoral puncture site (Interventional Cardiac
artery will bifurcate into superficial and deep femoral vessels. The femoral Catheterization Handbook, 3rd Ed. 2013)
artery usually transverses the inguinal ligament ~1/3 distance from pubic
symphysis to the ASIS. Optimal point of skin puncture is 1-2 cm below the inguinal ligament at point where pulse is palpated (see
above)
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Procedures Paracentesis
Indications: Video: http://www.nejm.org/doi/full/10.1056/NEJMvcm062234
• Diagnostic: new-onset ascites, unknown etiology of ascites, rule out SBP. Low threshold for inpatients with cirrhosis and often helpful
to obtain concurrent RUQUS with Doppler to rule out hepatic or portal vein thrombosis
• Therapeutic: large volume paracentesis (>5L) performed for abdominal pain/discomfort, diuretic-refractory ascites, respiratory
compromise, abdominal compartment syndrome, adjunctive treatment of esophageal variceal bleeding (can lower portal pressures)
Contraindications: overlying infection (i.e. cellulitis), inability to demonstrate ascitic fluid on U/S, bowel obstruction/distention, acute surgical
abdomen, 2nd or 3rd trimester pregnancy
• INR / plts are NOT contraindications (INR in patients with cirrhosis is NOT reflective of the risk of bleeding). There is no need to
correct coagulopathy w/ FFP or platelets unless severe DIC (Hepatology 2013;57:1651)
Materials: sterile gloves, bouffant, face shield, chlorhex, sterile towels, ultrasound, 1% lidocaine (10cc syringe, SQ 25G needle, 1.5 inch 20-
22G needle), two 18G needles, 60cc syringe, diagnostic assay tubes as below, gauze, bandage or Tegaderm dressing
• Diagnostic: 20G two-way (pink box) angiocath or 18–22G 1.5-inch needle. In obese pts, may use angiocath from femoral art line kit.
Purple and green top tube, black top tube (for micro). Technically DO NOT need to inoculate blood culture bottles at the bedside.
• Therapeutic: safe-T-Centesis kit (preferred, pigtail minimizes perforation risk) or paracentesis kit (straight rigid needle), 1L vacuum
bottles, 25% albumin dosed 6-8g per liter of fluid removed if >5L (Hepatology 2013;57:1651)
Site Selection/Positioning:
• Position patient supine, turned slightly toward the side of the paracentesis, and angled upright at 30°
• Use abdominal probe to identify fluid pocket at least 2-3cm in all dimensions by rotating/fanning probe
and ensure absence of bowel loops
• Avoid superficial veins or prior surgical incisions and use vascular probe with Doppler to avoid SQ vessels 1 2 1
• Approaches:
o LLQ (1): more commonly used; LLQ risk of bowel perf, use caution if pt with splenomegaly; avoid
inferior epigastric vessels that run along lateral borders of rectus muscles
o Infraumbilical (2): midline, 2cm below umbilicus; lowest risk of bleeding but must ensure bladder empty
Instructions:
1. Identify best site with abdominal U/S probe and mark site with pen or round base of needle Approaches
2. Open sterile OR towels package and use light blue covering as sterile field to drop sterile supplies. Don sterile protective equipment
(technically only need gloves, mask, bouffant cap) and clean skin vigorously with chlorhexidine. Create sterile field over patient with
OR towels or open kit and use dressing provided
3. Anesthetize overlying skin using ~0.5cc lidocaine (SQ 25G needle) to make a wheal. For LVP, use 1.5 inch 20-22G to anesthetize
deeper tissues with lidocaine in 10cc syringe. Use Z-line technique (below) and aspirate while advancing needle. Once ascitic fluid
begins to fill syringe, stop advancing the needle & inject remainder of lidocaine to anesthetize the highly sensitive parietal peritoneum
Z-line technique: reduces risk of ascites leak. With non- Therapeutic paracentesis instructions:
dominant hand, pull skin ~2cm caudad to deep abdominal wall a) Prepare Safe-T-Centesis kit: place catheter on needle,
while para needle is being slowly inserted attach syringe, and prep tubing
b) Use scalpel to make small superficial incision (enlarge PRN)
Diagnostic paracentesis instructions:
c) Advance needle/catheter while pulling back on syringe until
a) Insert 20G two-way (pink) angiocath through wheal at same
ascitic fluid return is visualized, then advance 0.5 cm
angle as U/S probe and advance until slightly past when flash seen
d) Advance catheter until hubbed (only with Safe-T Centesis
b) Advance the catheter without moving the needle
kit!), hold rigid needle in place
c) Retract needle, attach 60cc syringe, and fill syringe
e) Retract needle, attach 60cc syringe for dx sample PRN
d) Withdraw the catheter and apply pressure with sterile gauze
f) Connect tubing to catheter and puncture vacuum bottles
e) Apply dressing using folded gauze under Tegaderm
g) Withdraw catheter and apply gauze/Tegaderm dressing
f) Attach 18G needle to 60cc syringe and fill diagnostic tubes
h) Give 25% albumin (6-8g/L removed) if >5L removed
Diagnostic Assays:
Tube Lab Tests
Green top Chem Fluid albumin (send serum albumin to calculate SAAG), fluid total protein (to determine need for SBP ppx)
Purple top Heme Fluid cell count
Blood culture bottles Micro Can send for aerobic & anaerobic fluid culture, clean top with alcohol and inoculate at bedside for max yield
Black top Micro Gram stain and culture plates
Other tests to consider: glucose, amylase, LDH, bilirubin, triglyceride, AFB smear, mycobacterial culture, adenosine deaminase, pH, cytology
Complications:
• Flow stops/slows: roll patient slightly to side of para, rotate catheter, slightly withdraw catheter, flush catheter, new vacuum container
• Flash of blood in catheter: use vascular probe to avoid SQ vessels withdraw & insert new catheter at different site
• BRB return: injury to mesentery or inferior epigastrics stop, assess for hematoma w/ U/S, IR or surgery consult if HD unstable
• Hypotension: likely vasovagal or fluid shift (>1500cc tap) Trendelenburg, hydrate, and consider 25% albumin
• Bowel perforation: may lead to polymicrobial bacterascites/sepsis surgery consult for potential laparotomy
• Fluid leak: prevent with Z-line technique apply pressure dressing, seal w/ Dermabond or single stitch (4-0 non-absorbable suture)
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Procedures Arthrocentesis
Indications
Diagnostic: evaluation of inflammatory mono/oligoarthritis or uncharacterized joint effusion. A single inflamed joint should always have
diagnostic aspiration to differentiate septic arthritis, crystalline arthopathy, inflammatory arthritis, and hemarthrosis
• Avoid if overlying cellulitis or periarticular infection; prosthetic joints should prompt Ortho/Rheum consult; safe to perform if on
warfarin (Am J Med 2012;125:265) or DOAC (Mayo Clin Proc 2017;92:1223) but consider smaller needle
• Ultrasound may be used to guide needle insertion and can also offer diagnostic information with complexity of fluid
• Hip joint aspiration should be performed by interventional radiology
Therapeutic: injection of corticosteroid/anesthetic in autoimmune arthritis (RA/JIA, spondyloarthropathies) or single-joint gout flare
(especially when systemic therapy is contraindicated); drainage of large effusion, pus, or blood
• Avoid if overlying cellulitis, periarticular infection, septic arthritis, periarticular fracture, joint instability
• Use of intra-articular steroids in OA is falling out of favor due to progressive cartilage damage (JAMA 2017;317:1967)
Complications: iatrogenic infection (1/3500, >48h after procedure, may see systemic signs of infection), post-injection flare (mirrors
infection and occurs within 24-48h of procedure), hemarthrosis, leakage of joint fluid, local or systemic steroid effects
Positioning/Approach: position the knee in extension or 15-20° flexion. Approaches described below:
• Lateral (see image): 1cm lateral and 1cm superior to the superior 1/3 of the lateral patella. Angle the needle approximately 45°
toward the feet and insert behind the patella at a 45° angle to the skin. More likely to yield fluid in difficult cases
• Medial: 1cm medial to the superior 1/3 of the medial patella. Angle the needle perpendicular to the leg and at a 45° angle to the skin
Lateral Approach
Protocol:
• Identify landmarks as above and mark point of entry with the base of a needle
cap or pen. Sterilize the site. A sterile field is not technically required but may
drape the area w/ a sterile sheet or towels. Prep needles and syringes.
• Anesthetize overlying skin using ~0.5cc lidocaine (SQ 25G needle, 5cc syringe)
to make a wheal. May use remaining lidocaine along procedure tract.
• Attach 18-20G needle to 30cc syringe and position needle according to approach.
Advance needle slowly (avg 1-1.5 in) and aspirate while advancing.
• Once fluid is visualized, aspirate joint fluid to fill syringe. May attach a 2nd 30cc
syringe to drain additional fluid for sx relief pending size of effusion.
• Withdraw needle and apply bandage. Fill diagnostic tubes (purple top
for cell count/diff and crystal eval, aerobic/anaerobic cx bottles).
Diagnostic Assays: cell count/diff, crystal analysis, gram stain/culture AND blood cultures (Am Fam Physician;2003;68:1)
• Septic arthritis: most common locations: knee > hip > shoulder > elbow
o If patient HDS, hold antibiotics prior to tap; 70% Staph, 17% Strep, 8% GNR (H. flu child > adult)
o WBC count usually 50-150K but can be lower (e.g. <20K in disseminated gonorrhea); WBC = risk of infection
o Presence of crystals does not rule out septic arthritis (up to 5% of pts with crystals also have septic joint)
o Gram stain: sens 75% for Staphylococcus, 50% for GNR, < 25% for Gonococcus
o Joint cx usually positive but only 50% sensitive in gonococcal arthritis (swab genitalia & pharynx for diagnosis)
• Gout: negatively birefingent needle-shaped urate crystals (yellow) on polarized microscopy (Sn 63-78% / Sp 93-100%)
• Pseudogout: positively birefringent CPPD rhomboid crystals (blue) on polarized microscopy (Sn 12-83% / Sp 78-96%)
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Diagnostic Assays
Tube Lab Tests
1 (1 mL) Heme CSF cell count
2 (1 mL) Chem Total protein, glucose
Gram stain/culture. Consider HSV PCR, VZV PCR, cryptococcal antigen, viral culture,
3 (3-5+ mL, depending
Micro AFB stain, VDRL. Ask lab to save extra CSF. If you may need flow cytometry, DO NOT
on number of tests)
FREEZE CSF!
4 (1 ml) Heme CSF cell count (should have fewer RBCs than tube 1 unless hemorrhage)
Additional tests: cytology & flow cytometry (meningeal carcinomatosis), oligoclonal bands (multiple sclerosis), paraneoplastic
antibodies, 14–3–3 & RT-QuIC (prion disease); may want to collect extra black top tubes for these purposes; if c/f prion disease,
contact materials management for instruction on special disposal of materials (highly contagious!)
Complications
Cerebral herniation (acute AMS, Immediately replace stylet and do not drain more CSF beyond what is in manometer. STAT
fixed pupils, BP, brady, arrest) consult neurosurgery and treat with ICP-lowering agents (e.g. mannitol)
Shooting pains during procedure usually transient. Withdraw slightly and adjust position away from
Nerve root injury
direction of pain. Consider dexamethasone if pain is persistent.
Post-LP headache (10-30% Onset 72h, lasts 3-14 days. Give pain meds that do not affect plt. No evidence for bed rest. If
incidence; likely 2/2 dural leak) persistent, c/s anesthesia for epidural blood patch (65-98% success, usually immediate relief).
Spinal hematoma Suspect if on AC w/ persistent back pain or neuro sx urgent MRI IV dexamethasone +
NSGY c/s
Procedures Thoracentesis
Indications
Diagnostic: to establish etiology of ≥1cm pleural effusion visualized by U/S (not necessary for small effusions w/ probable alternative dx)
• NB: pleural effusions are visible on CXR when > 200mL of fluid is present
Therapeutic: large effusions resp compromise or sx (e.g., dyspnea), hemothorax, empyema, complicated parapneumonic effusion
Contraindications (relative, not absolute) (Chest 2013;144:456)
• Consider reversing coagulopathy (INR >1.5, recent LMWH) or thrombocytopenia (plt < 50k), but no data to support
• Skin infection (cellulitis or herpes zoster) over site of entry risk of pleural space infection
• Positive pressure ventilation risk of PTX by 1-7% but is not a contraindication (Crit Care 2011;15:R46)
Preparation
• Materials: skin cleansing agent, gauze, sterile gloves/drape, hemostat, 1-2% lidocaine, 10mL syringe with 22 & 25 gauge needle,
thoracentesis kit with 18-20g over-the-needle catheter, 60cc syringe, 3way stopcock, drainage tubing, specimen tube, evacuation
container, occlusive dressing
• Attending MUST be present for thoracentesis: page IP (p23710), pulm, or call MICU x68048 to see who is on service
Management Overview: if in doubt about management, page the cardiology team that placed the drain
• Pericardiocentesis does not completely evacuate a pericardial effusion. A pericardial pigtail catheter is often left in for 24-
72h to allow for serial drainage, preventing re-accumulation and repeated procedures.
• Frequency of drainage depends on chronicity and size of the effusion, usually q6-q12h. Recommendations are often
found in the report from the cath lab when the drain was initially placed.
• Give cefazolin 1g q8h (or vancomycin if PCN allergy) for prophylaxis while drain is in place.
• Monitor effusion resolution and recurrent tamponade. Check serial hemodynamics/pulsus paradoxus.
• If >100cc output/day for 3 days s/p drain placement, aggressive therapy may be indicated (i.e. pericardial window,
sclerosing agents, etc.)
• Consider removal of pericardial drain if <50cc output over 24 hours. Obtain approval from cardiology prior.
Materials:
• Sterile technique: gloves, mask, hat
• Sterile towels
• Chlorhexidine swabs (at least 3)
• 60cc Leur lock (screw-on) syringe (x2-3 if high output)
• New blue cap for 3-way stopcock
• Heparin (10U/mL) pre-mixed syringe (in MICU/CCU med rooms)
Technique:
1. Put on, gloves, mask and hat (gown is optional). Open supplies onto sterile field.
2. Ask RN/assistant to lift catheter off skin by flush port. Sterilize distal exposed catheter and stopcock with chlorhex swab.
Holding the sterilized area, take catheter from RN and sterilize remaining portion
3. Place sterile towels around and underneath distal catheter and stopcock, and lay the now-sterilized catheter down
4. Ensure the stopcock is turned towards the catheter. This means the catheter line is closed.
5. Remove and throw away one blue cap (doesn’t matter which).
6. Sterilize open stopcock tip with iodine or chlorhex swab.
7. Hold up flush port; RN will connect heparin syringe (syringe itself is not sterile) to open/sterilized tip. Turn stopcock toward
the remaining capped valve (opens flush port/catheter), and infuse 2cc heparin.
8. Turn stopcock back towards catheter, remove (do not discard) heparin syringe, and connect 60cc Luer lock syringe.
9. Turn stopcock to the remaining capped valve and slowly withdraw pericardial fluid. This may require significant negative
pressure. Consider different patient positions (Trendelenberg, lateral decubitus, etc.) to mobilize pericardial effusion.
Patient may experience chest discomfort. Monitor hemodynamics
10. Save/transfer pericardial fluid if needed for analysis. Otherwise discard.
11. Can stop draining once fluid flow diminishes/ceases. Turn stopcock back towards catheter and remove syringe.
12. Ask RN to re-attach heparin syringe and infuse another 2cc heparin. Again close stopcock to the patient.
13. Remove heparin syringe and attach new blue cap to open flush port.
14. Consider re-sterilizing distal exposed catheter and stopcock with chlorhex swab.
15. Write procedure note. Be sure to deduct the 2-4cc infused heparin when calculating amount of fluid removed.
Fluid Studies:
• Gram stain and bacterial/fungal culture
• Specific viral studies/PCR
• Cytology
• AFB stain, mycobacterial culture, adenosine deaminase, IFN-gamma, or lysozyme (if considering TB pericarditis)
• Protein, LDH, glucose, red/white cell count are not helpful for fluid characterization
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NGT Placement:
• Assess patency and symmetry of nares by direct visualization TYPES OF NGTs & USES
• Consider topical anesthetic (e.g. 4% lidocaine) pre-treatment
• Position patient in upright “sniffing” position with neck flexed and chin to chest • Dobhoff: PO formula, meds
• Estimate distance of NGT insertion by measuring from xiphoid processearlobenose tip • 14, 16 Fr: Decompression
• Apply lubricant / ice to tip of NGT and/or apply viscous lidocaine directly into the nares
• Insert NGT into nares along floor & apply pressure posterior & slightly inferiomedial, not upward
• After passage of NGT into oropharynx (will feel curve & resistance), have patient swallow water via straw while advancing rapidly
o If patient excessively coughs, gags, has change in voice or dyspnea, or increased resistance, STOP (never force) and
suspect improper location (in airway or coiled) and immediately withdraw. Look in posterior oropharynx for coiling.
• Advance to predetermined depth. Can insufflate air w/ 60cc syringe while auscultating over stomach for rush of air. May also see
return of gastric contents. Inspect oropharynx to ensure no coiling before securing tube w/ tape or bridle if risk removal (AMS)
• Confirming position: MUST confirm placement with KUB prior to feeding/meds given risk of placement in trachea/lungs.
KUB will show NGT sideport below diaphragm. Optional for KUB if bilious return when NGT for decompression (bile = stomach).
Dobhoff tube / Enteroflex: thinner, more flexible; more comfortable but risk of placement into lung
• Requires 2-step 2-CXR placement method
1. Measure from nose to earlobe to mid-sternum insert tube this distance secure obtain CXR
2. If CXR shows tip (1) past carina & (2) midline advance into stomach repeat CXR remove stylette once confirmed
General Troubleshooting:
• If tube coiling repeatedly in oropharynx on insertion, soak tip in ice water to make tube more rigid prior to insertion.
• NGT to suction should “sump” – air should audibly enter blue port and exit main port; if not: (1) flush blue port with air (never
fluids), (2) flush main port with water (not NS, does not need to be sterile), (3) aspirate from main port if not able to withdraw
flush, NGT needs to be advanced vs. withdrawn (KUB can guide)
• To prevent clogging or adherence to gastric wall, NGTs should be flushed with 30cc water & air Q8hr. If clogged, can try methods
to unclog tube as below in “Gastrostomy Tubes”
Complications ( with longer duration):
• GI: malposition, coiling, knotting anywhere along course of tube, nasal/GI tract perforation. risk acid/stomach content reflux and
aspiration consider PPI. Chronic suction gastritis/pressure necrosis: consider removal if grossly bloody
• Pulm: intubation of lung inadvertent med, contrast, TF administration PNA, pulm abscess, tracheal perforation, PTX, death
• HEENT: nasal irritation, epistaxis, intracranial placement, skin erosion, sinusitis, alar necrosis, tracheoesophageal fistula/perf
Removal:
• If for ileus/SBO, consider removal when passing flatus or resolved n/v. Alternatively, may remove when NGT output <1L over 24
hours. Consider clamp trial before removing (clamp 4 hours, then check residual. Remove if <150 cc)
• Remove tape. Flush tube w/ 10mL air or NS. Turn OFF suction & clamp. Fold Chux around tube insertion site. Gently remove tube
FOLEY CATHETER
Choosing Catheter: (order from Central Supply, ED, or Ellison 6 if not on floor) Special Circumstances:
• Many contain Latex, use silicone if allergy; silicone also risk CAUTI • Artificial Urinary Sphincter (AUS):
• 2-way Foleys (drainage & balloon ports): men s/p prostatectomy c/b sig. urinary
16F (stock), 12F if stricture or device, 18F/20F Coudé if BPH or high bladder neck incontinence. DEACTIVATE device
insert curve up / nub on hub pointed toward umbilicus prior to placing foley. Place smallest
• 3-way Foleys (drainage, balloon, irrigation ports): 20F/22F used for continuous catheter possible (12F) and remove
bladder irrigation (CBI) in gross hematuria ASAP.
Troubleshooting:
Placement:
• Difficulty in female patient: likely
1. Lay patient flat, prep, hold penis upright (keep on stretch while advancing)
poor positioning. Place sheets under
2. Instill 10cc 2% viscous lidocaine (“UroJet”) into urethra
hips & place pt in Trendelenburg
3. Insert Foley catheter to the hub
• Urethral trauma: blood at meatus.
4. As catheter reaches bladder neck, keeping penis on stretch, point phallus down
Leave catheter ≥3-5d
towards toes (to mimic natural curve urethra).
• Foley is leaking:
5. After urine return AND catheter hubbed, fill balloon w/ 10cc sterile H2O
o Bladder spasms 2/2 infection,
6. Gently withdraw catheter to bladder neck
mucosal irritation, overactive
7. Verify position by flushing with 60cc fluid (catheter in bladder) and withdraw.
bladder. Start anticholinergic
Inability to withdraw suggests:
(oxybutynin 5mg TID PRN)
a. Bladder empty and sucking against bladder mucosa (instill 60 cc)
o Foley obstructed 2/2 sediment,
b. Catheter in urethra or false passage
kinked, dome of bladder, clot.
c. Catheter outside bladder (undermined bladder neck in pt s/p
Flush catheter & bladder US
prostatectomy/TURP)
o Urethra patulous (women w/
8. Don’t forget to reduce foreskin (if not, may cause paraphimosis = urologic
chronic indwelling catheters)
emergency)
Suprapubic Tubes:
Continuous Bladder Irrigation (CBI): consult urology to initiate
• Many types, usually standard Foley
• Indications: gross hematuria (when you cannot see your hand through the foley due
catheter
to presence of blood) +/- with clots
• Know type & size catheter, who
• Titrate flow to “fruit punch” colored urine (should be able to see through)
exchanges, how exchanged, how
• When d/c’ing, usually start with clamp trial to ensure resolution before removal
frequently
Bladder Pressure: only done in the ICU • Is this a new tract (<7d, ask urology to
Indications: concern for intra-abdominal hypertension (≥12mmHg) or frank abdominal replace) or established (years, you can
compartment syndrome (>20mmHg) try and replace)?
1. Ensure patient position correlates between measurements (head position as flat as • If need to reinsert, decompress balloon
possible) and pressure transducer set-up is arranged and remove indwelling SPT tube. Use
2. Drain bladder and clamp drainage tube of foley foley kit, prep area, apply lubricant to
3. Inject 25cc of NS into aspiration port, wait 30-60s (allows detrusor muscle relax.) new tube, insert through tract (may
4. Connect pressure transducer to aspiration port of foley and measure pressure at have to use some force) until urine
end-expiration return, inflate balloon and ensure tube
is mobile, attach to foley bag
INR Guidelines for Cardiac Catheterization: VAD Peri-Procedural Cardiac Catheterization Guidelines:
Planned Access Site INR INR goal 1.8-2.5; continue warfarin
Femoral artery or vein ≤ 1.8 PTT goal ≤ 80; continue UFH pre-, intra-, & post-procedure
Internal jugular vein ≤ 1.8
Radial artery ≤ 2.0 Cangrelor and Antiplatelet Agents:
Subclavian vein ≤ 1.5 • See Cardiology: ACS for switching/bridging P2Y12 inhibitors
Brachial or basilic vein ≤ 2.0 • Generally, prasugrel is held on day -7, clopidogrel/ticagrelor on day -5,
Pericardiocentesis ≤ 1.5 & cangrelor is started on day -3. Cangrelor is held 1-6hrs pre-
procedure.
IR Procedures
• NPO guidance: NPO (no solid food; ok to take medications with sip of water) for 8hrs if will receive sedation (e.g. port placement,
biopsies, tube placement) or if a patient-specific need for sedation.
• Low bleeding risk procedures: para., thora., chest tube, PleurX, PICC, non-tunneled central catheter, transjugular liver biopsy, IVC
filter placement & simple removal, catheter/tube exchange, dialysis access interventions, superficial bx/aspiration (thyroid, LN, breast,
superficial bone), embolization for bleeding control
o AC goals: INR <3, plt >20k; if cirrhosis: INR <3, plt >20k, fibrinogen >100 (if cirrhosis). No need to hold AC.
• High bleeding risk procedures: tunneled central access catheter placement/removal, G- or J-tube placement, nephrostomy tube
placement, biliary interventions, TIPS, solid organ/deep tissue biopsies, LP/spine procedures, arterial interventions/angiography,
intrathoracic venous interventions (SVC/IVC), portal vein interventions, catheter-directed lysis, complex IVC filter removal
o AC goals: INR <1.8, plt >50k; if cirrhosis: INR <2.5, plt >30k, fibrinogen >100. AC management per table below.
Medication Hold Pre-Procedure** Resume Post-Procedure
Heparin Therapeutic: 4-6hrs; Prophylactic: 6hrs 6-8hrs
Enoxaparin (Lovenox) Therapeutic: 24hrs / 2 doses; Prophylactic: 12hrs / 1 dose 12hrs
Dalteparin 24hrs / 1 dose 12hrs
Fondaparinux CrCl ≥50: 2-3 days; CrCl <50: 3-5 days 24hrs
Bivalirudin 2-4hrs 4-6hrs
Argatroban 2-4hrs 4-6hrs
Day after procedure; bridge
Warfarin 5 days or INR ≤1.8
if high-risk
Apixaban, edoxaban CrCl ≥50: ≥2 days / 4 doses; CrCl <50: ≥3 days / 6 doses 24hrs
Rivaroxaban CrCl ≥30: ≥2 days / 2 doses; CrCl <30: ≥3 days / 3 doses 24hrs
Dabigatran CrCl ≥50: ≥2 days / 4 doses; CrCl <50: ≥3-4 days / 6-8 doses 24hrs
**See “MGH Interventional Radiology Periprocedural Management” guidelines on Ellucid for further details.
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Special Cases
• Hospice:
o Criteria: pt must have a terminal illness with prognosis of ≤6 months as certified by a physician. Depending on the
hospice agency, pt may need to forego curative treatments (i.e., chemo, expensive antibiotics, etc.)
o Home hospice: fully funded by Medicare. RNs visit, but patients need full-time caregiver support in the home, which
can be a barrier to home hospice discharge
o Inpatient hospice (SNF or dedicated inpatient hospice facility): room & board (~$400 per day) only covered by
MassHealth, but not other insurers
o GIP (in-hospital hospice care): fully funded by Medicare, patient must quality discuss with Pall Care
• Long-term care:
o Patients residing in nursing homes with stably poor functional status and who require assistance with ADLs/IADLs,
but do not require post-acute level care
o Private pay or covered by MassHealth, but not funded by Medicare
• Patient/family refusal of SNF/rehab: recommend higher-quality SNFs in Partners Skilled Nursing Facility Network
• Alternative programs: if patient is in Partners ACO, discuss additional home-based care options with case manager
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Logistics Formulas
Recommended websites for formulas: Osmolality
www.mdcalc.com Plasma Osmolality:
www.nephromatic.com glucose (mg/dL) BUN (mg/dL) EtOH (mg/dL)
calc osm = 2 × Na (mEq/L) + + +
18 2.8 4.6
Drug Dosing and Body Weights Osmolar Gap:
Actual Body Weight (ABW): actual weight recorded on OG = Posm – calc osm (normal: < 10)
admission (most commonly used weight for dosing)
Stool Osmol Gap:
Ideal Body Weight (IBW): SOG = Osmstool – 2 × (Nastool +Kstool)
Male: 50.0kg + 2.3kg for every inch over 5 feet >125: suggests osmotic diarrhea; <50: suggests secretory
Female: 45.5kg + 2.3kg per inch over 5 feet diarrhea
Cardiac Output: CO = HR x SV
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Logistics Formulas
Bazett Formula: QTc = QT / √RR (♀ < 460 ms; ♂ < 440 ms)
UCr (mg/dl)× Uvolume (ml/min)
CrCl =
Friedewald Formula: LDL = TC – HDL – (TG / 5) serum Cr (mg/dL)
Maximum Heart Rate: Max HR = 220 – age (if unable to eGFR: use CKD-EPI equation (if black, multiply by 1.159)
achieve >85% max HR, suggests chronotropic incompetence)
Hematology
Pulmonary Physiology
Absolute Neutrophil Count: ANC = WBC x (% PMN + %
Transpulmonary and Diastolic Pulmonary Gradient: bands)
TPG = mPAP – PCWP; >12-15 suggests pre-cap pulm HTN
DPG = PAd – PCWP; >7 mmHg suggests pre-cap pulm HTN Reticulocyte Production Index (RI) (normal: 2-3):
Alveolar-arterial (A-a) Oxygen Gradient:
RI = %retic ×
Hct / maturation factor (MF)
patient' s normal Hct
Calculated A-a gradient = PAO2 − PaO2
PaCO2 PaCO2
where PAO2 = FiO2 × (Patm − PH2O) − ≈ FiO2 × 713 −
R 0.8 MF: 1.0 (Hct > 36), 1.5 (Hct 26-35), 2.0 (Hct 16-25), 2.5
FiO2 = 0.21 on RA; add 0.03 for each extra L O2/min cannula (Hct < 15)
Patm = atmospheric pressure (mmHg) = 760
PH2O = alveolar pressure of water (mmHg) = 47 RI: <2 in hypoproliferative state; >3 in hyperproliferative state
R = respiratory quotient = VCO2/VO2 ≈ 0.8
Statistics and Epidemiology
**Normal A-a gradient = 2.5 + (0.21 x age)** Sensitivity = TP / (TP + FN)
Shunt Fraction (normal: 3-8%, but ↑ 5% for every 100 mmHg Specificity = TN / (FP + TN)
drop in PaO2 below 600 mmHg):
Qs 0.0031 × (PAO2 - PaO2) Positive Predictive Value = TP / (TP + FP)
=
Qt [0.0031 × (PAO2 - PaO2)] + (Ca - vO2)
Negative Predictive Value = TN / (FN + TN)
where Qs = shunt flow, Qt = total flow, Ca-vO2 assumed 5%.
FiO2 must be 1.0 in this calculation Positive Likelihood Ratio = Sensitivity / (1 – Specificity)
R becomes 1.0 after breathing 100% O2 for 20 minutes
because of N2 wash-out Negative Likelihood Ratio = (1 – Sensitivity) / Specificity
> 15% = pathologic shunt
Number Needed to Treat = 1/absolute risk reduction (ARR)
Minute Ventilation (VE) (volume per unit time): VE = RR x Vt
Vd PaCO2-PetCO2
=
Vt PaCO2
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Cardiac Studies
ECG 6229
Echo 6231 / 2665
ETT or Nuclear Stress 5375 / 6229 /
6087
Ancillary Staff
Nursing Supervisor p57711
Pharmacy 6012
Respiratory Therapy 6213
Phlebotomy 5903
Speech Language Pathology 6548
Infection Control 6282
Case Management/Social Work 6695
Chaplain 6634
Interpreter Services 6698
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