Pott's disease 

is a presentation of extrapulmonary tuberculosis that affects the spine, a kind of

tuberculous arthritis of the intervertebral joints. It is named after Percivall Pott (1714–1788), a London
surgeon who trained at St Bartholomew's Hospital, London. The lower thoracic and upperlumbar
vertebrae are the areas of the spine most often affected. Scientifically, it is called
tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine. Pott’s
disease results from haematogenous spread of tuberculosis from other sites, often pulmonary. The
infection then spreads from two adjacent vertebrae into the adjoiningintervertebral disc space. If only one
vertebra is affected, the disc is normal, but if two are involved the disc, which is avascular, cannot receive
nutrients and collapses. The disc tissue dies and is broken down by caseation, leading to vertebral
narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and
superinfection is rare.

Contents
 [hide]

1 Signs and

symptoms

2 Diagnosis

3 Late

complications

4 Prevention

5 Therapy

6 Cultural

references

7 External links

[edit]Signs and symptoms

 back pain
 fever
 night sweating
 anorexia
 weight loss
 Spinal mass, sometimes associated with numbness, paraesthesia, or muscle weakness of the
legs
[edit]Diagnosis
 blood tests - elevated erythrocyte sedimentation rate
 tuberculin skin test
 radiographs of the spine
 bone scan
 CT of the spine
 bone biopsy
 MRI
[edit]Late complications

 Vertebral collapse resulting in kyphosis

 Spinal cord compression
 sinus formation
 paraplegia (so called Pott's paraplegia)
[edit]Prevention

Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis. Patients
who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking
medicines to prevent tuberculosis. To effectively treat tuberculosis, it is crucial that patients take their
medications exactly as prescribed.

[edit]Therapy

 non-operative - antituberculous drugs

 analgesics
 immobilization of the spine region by rod (Hull)
 Surgery may be necessary, especially to drain spinal abscesses or to stabilize the spine
 Richards intramedullary hip screw - facilitating for bone healing
 Kuntcher Nail - intramedullary rod
 Austin Moore - intrameduallary rod (for Hemiarthroplasty)
[edit]Cultural references
The fictional Hunchback of Notre Dame had a gibbous deformity (humpback) that is thought to have been
caused by tuberculosis. In Henrik Ibsen's play "A Doll's House," Dr. Rank suffers from "consumption of
the spine." Furthermore, Jocelin, the Dean who wanted a spire on his cathedral in William Golding's "The
Spire" probably suffered and died as a result of this disease. 18th-century English poets Alexander
Popeand William Ernest Henley both suffered from Pott's disease. Anna Roosevelt Cowles, sister of
president Theodore Roosevelt, suffered from Pott's Disease. Chick Webb, swing era drummer and band
leader, was afflicted with tuberculosis of the spine as a child, which left him hunchbacked.
The Sicilian mafia boss Luciano Leggio had Pott's disease and wore a brace. Morton, the railroad
magnate in Once Upon a Time in the West, suffers from the disease and needs crutches to walk.
Osteomyelitis (osteo- derived from the Greek word osteon, meaning bone, myelo- meaning marrow, and
-itis meaning inflammation) simply means an infection of the bone or bone marrow.[1] It can be usefully
subclassified on the basis of the causative organism (pyogenicbacteria or mycobacteria), the route,
duration and anatomic location of the infection. A bitevictim may incur osteomyelitis which can become
life threatening if untreated, whether or not the animal is carrying parvovirus or rabies virus.

Contents
 [hide]

1 Pathogen

esis

2 Cause

3 Diagnosis

4 Treatmen

5 See also

6 Reference

7 External

links

[edit]Pathogenesis

In general, microorganisms may infect bone through one or more of three basic methods: via
thebloodstream, contiguously from local areas of infection (as in cellulitis), or penetrating trauma,
including iatrogenic causes such as joint replacements or internal fixation of fractures or root-
canaled teeth.[1] Once the bone is infected, leukocytes enter the infected area, and, in their attempt
to engulf the infectious organisms, release enzymes that lyse the bone. Pus spreads into the bone's blood
vessels, impairing their flow, and areas of devitalized infected bone, known as sequestra, form the basis
of a chronic infection.[1] Often, the body will try to create new bone around the area of necrosis. The
resulting new bone is often called an involucrum.[1] Onhistologic examination, these areas of necrotic
bone are the basis for distinguishing betweenacute osteomyelitis and chronic osteomyelitis.
Osteomyelitis is an infective process which encompasses all of the bone (osseous) components,
including the bone marrow. When it is chronic it can lead to bone sclerosis and deformity.

Chronic osteomyelitis may be due to the presence of intracellular bacteria (inside bone cells).[2] Also, once
intracellular, the bacteria are able to escape and invade other bone cells.[3] In addition, once intracellular,
the bacteria becomes resistant to antibiotics.[4] These combined facts may explain the chronicity and
difficult eradication of this disease. This results in significant costs and disability and may even lead to
amputation. Intracellular existence of bacteria in osteomyelitis is likely an unrecognized contributing factor
to its chronic form.

In infants, the infection can spread to the joint and cause arthritis. In children,

large subperiosteal abscesses can form because theperiosteum is loosely attached to the surface of the
bone.[1]

Because of the particulars of their blood supply, the tibia, femur, humerus, vertebra, the maxilla, and

the mandibular bodies are especially susceptible to osteomyelitis.[5] Abscesses of any bone, however,
may be precipitated by trauma to the affected area. Many infections are caused by Staphylococcus
aureus, a member of the normal flora found on the skin and mucous membranes. In patients with sickle
celldisease the most common causative agent remains Staphylococcus aureus, but Salmonella species
become proportionally more common pathogens than in healthy hosts.

It has been noted that baseball Hall-of-Famer Mickey Mantle had osteomyelitis, as well as British
Singer/Songwriter Imogen Heap. During her tour in 2010 she devised an improvised track with the key
and tempo voted on by the audience. All proceeds went to the Great Ormond Street hospital, where a
surgeon had successfully performed an operation to save her leg.[6]

[edit]Cause

Age group Most common organisms

Newborns (younger than 4 mo) S. aureus, Enterobacter species, and group A and B Streptococcus species

S. aureus, group A Streptococcus species, Haemophilus influenzae,

Children (aged 4 mo to 4 y)
and Enterobacter species

Children, adolescents (aged 4 y S. aureus (80%), group A Streptococcus species, H. influenzae,

to adult) and Enterobacter species
Adult S. aureus and occasionally Enterobacter or Streptococcus species

Sickle Cell Anemia Patients Salmonella species

In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most
commonly affected.

Acute osteomyelitis almost invariably occurs in children. When adults are affected, it may be because of
compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or
other disease or drugs (e.g. immunosuppressive therapy).

Osteomyelitis is a secondary complication in 1–3% of patients with pulmonary tuberculosis.[1] In this case,

the bacteria, in general, spread to the bone through the circulatory system, first infecting
the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone.[1] In
tubercular osteomyelitis, the long bones and vertebrae are the ones which tend to be affected.[1]

Staphylococcus aureus is the organism most commonly isolated from all forms of osteomyelitis.[1]

Bloodstream-sourced osteomyelitis is seen most frequently in children, and nearly 90% of cases are
caused by Staphylococcus aureus. In infants, S. aureus, Group B streptococci (most common[7])
and Escherichia coli are commonly isolated; in children from 1 to 16 years of age,S.
aureus, Streptococcus pyogenes, and Haemophilus influenzae are common. In some subpopulations,
including intravenous drug users and splenectomized patients, Gram-negative bacteria, including enteric
bacteria, are significant pathogens.[8]

The most common form of the disease in adults is caused by injury exposing the bone to local
infection. Staphylococcus aureus is the most common organism seen in osteomyelitis seeded from areas
of contiguous infection, but anaerobes and Gram-negative organisms, includingPseudomonas
aeruginosa, E. coli, and Serratia marcescens, are also common. Mixed infections are the rule rather than
the exception.[8]

Systemic mycotic (fungal) infections may also cause osteomyelitis. The two most common
are Blastomyces dermatitidis and Coccidioides immitis.

In osteomyelitis involving the vertebral bodies, about half the cases are due to Staphylococcus aureus,
and the other half are due totuberculosis (spread hematogenously from the lungs). Tubercular
osteomyelitis of the spine was so common before the initiation of effective antitubercular therapy that it
acquired a special name, Pott's disease. The Burkholderia cepacia complex have been implicated in
vertebral osteomyelitis in intravenous drug users.[9]
[edit]Diagnosis

Diagnosis of osteomyelitis is often based on radiologic results showing a lytic center with a ring

of sclerosis.[1] Culture of material taken from a bone biopsy is needed to identify the specific pathogen;
alternative sampling methods such as needle puncture or surface swabs are easier to perform, but do not
produce reliable results.[10]

Factors that may commonly complicate osteomyelitis are fractures of the bone, amyloidosis, endocarditis,
or sepsis.[1]

[edit]Treatment

Osteomyelitis often requires prolonged antibiotic therapy, with a course lasting a matter of weeks or

months. A PICC line or central venous catheter is often placed for this purpose. Osteomyelitis also may
require surgical debridement. Severe cases may lead to the loss of a limb. Initial first line antibiotic choice
is determined by the patient's history and regional differences in common infective organisms. A
treatment lasting 42 days is practiced in a number of facilities.[11] Local and sustained availability of drugs
have proven to be more effective in achieving prophylactic and therapeutic outcomes.[12]

In 1875, American artist Thomas Eakins depicted a surgical procedure for osteomyelitis at Jefferson

Medical College, in a famous oil paintingtitled The Gross Clinic.

Prior to the widespread availability and use of antibiotics, blow fly larvae were sometimes deliberately
introduced to the wounds to feed on the infected material, effectively scouring them clean.[13][14]

Hyperbaric oxygen therapy has been shown to be a useful adjunct to the treatment

of refractory osteomyelitis.[15][16]

Open surgery is needed for chronic osteomyelitis whereby the involucrum is opened and the sequestrum
is removed or sometimes saucerization[17] can be done
Spinal cord injury (SCI) refers to an injury to the spinal cord. It can cause myelopathy or damage
to nerve roots or myelinated fiber tracts that carry signals to and from the brain.[1][2]Depending on its
classification and severity, this type of traumatic injury could also damage thegrey matter in the central
part of the cord, causing segmental losses of interneurons and motorneurons. Spinal cord injury can
occur from many causes, including:

 Trauma such as automobile crashes, falls, gunshots, diving accidents, war injuries, etc.

 Tumor such as meningiomas, ependymomas, astrocytomas, and metastatic cancer.
 Ischemia resulting from occlusion of spinal blood vessels, including dissecting aortic
aneurysms, emboli, arteriosclerosis.
 Developmental disorders, such as spina bifida, meningomyolcoele, and others
 Neurodegenerative diseases, such as Friedreich's ataxia, spinocerebellar ataxia, etc.
 Demyelinative diseases, such as Multiple Sclerosis.
 Transverse myelitis, resulting from stroke, inflammation, or other causes.
 Vascular malformations, such as arteriovenous malformation (AVM), dural arteriovenous
fistula (AVF), spinal hemangioma, cavernous angioma and aneurysm.
Contents
 [hide]

1 Classification

2 Effects

o 2.1 The Location of the Injury

 2.1.1 Cervical injuries

 2.1.2 Thoracic injuries

 2.1.3 Lumbar and Sacral injuries

 2.1.4 Central Cord and Other Syndromes

3 Treatment

4 Spinal Cord Injury Implications and Occupational Therapy

5 How Occupational Therapy Can Help Address Occupational Performance

Issues

o 5.1 Phase 1: Acute Recovery

o 5.2 Phase 2: Acute Rehabilitation

o 5.3 Phase 3: Community reintegration

6 Epidemiology

7 See also

8 External links

9 References

[edit]Classification

The American Spinal Injury Association (ASIA) defined an international classification based on
neurological responses, touch and pinprick sensations tested in each dermatome, and strength of ten key
muscles on each side of the body, e.g. shoulder shrug (C4), elbow flexion (C5), wrist extension (C6),
elbow extension (C7), hip flexion (L2). Traumatic spinal cord injury is classified into five categories by the
American Spinal Injury Association and the International Spinal Cord Injury Classification System:

 A indicates a "complete" spinal cord injury where no motor or sensory function is preserved in the
sacral segments S4-S5.
 B indicates an "incomplete" spinal cord injury where sensory but not motor function is preserved
below the neurological level and includes the sacral segments S4-S5. This is typically a transient
phase and if the person recovers any motor function below the neurological level, that person
essentially becomes a motor incomplete, i.e. ASIA C or D.
 C indicates an "incomplete" spinal cord injury where motor function is preserved below the
neurological level and more than half of key muscles below the neurological level have a muscle
grade of less than 3, which indicates active movement with full range of motion against gravity.
 D indicates an "incomplete" spinal cord injury where motor function is preserved below the
neurological level and at least half of the key muscles below the neurological level have a muscle
grade of 3 or more.
 E indicates "normal" where motor and sensory scores are normal. Note that it is possible to have
spinal cord injury and neurological deficits with completely normal motor and sensory scores.

In addition, there are several clinical syndromes associated with incomplete spinal cord injuries.

 The Central cord syndrome is associated with greater loss of upper limb function compared to
lower limbs.
 Divisions of Spinal Segments

 The Brown-Séquard syndrome results from injury to one side

with the spinal cord, causing weakness and loss of proprioception on
the side of the injury and loss of pain and thermal sensation of the
other side.
 The Anterior cord syndrome results from injury to the anterior
part of the spinal cord, causing weakness and loss of pain and
thermal sensations below the injury site but preservation of
proprioception that is usually carried in the posterior part of the
spinal cord.
 Tabes Dorsalis results from injury to the posterior part of the
spinal cord, usually from infection diseases such as syphilis, causing
loss of touch and proprioceptive sensation.
 Conus medullaris syndrome results from injury to the tip of the
spinal cord, located at L1 vertebra.
 Cauda equina syndrome is, strictly speaking, not really spinal
cord injury but injury to the spinal roots below the L1 vertebra.
[edit]Effects

The effects of a spinal cord injury may vary depending on the type, level,
and severity of injury, but can be classified into two general categories: Segmental Spinal Cord Level
and Function
 In a complete injury, function below the "neurological" level is Level Function
lost. Absence of motor and sensory function below a specific spinal
C1-C6 Neck flexors
level is considered a "complete injury". Recent evidence suggests
C1-T1 Neck extensors
that less than 5% of people with "complete" spinal cord injuries
C3,C4, Supply diaphragm (m
recover locomotion.[citation needed] C5 ostly C4)
 In an incomplete injury, some sensation and/or movement below
Shoulder movement,
the level of the injury is retained. The lowest spinal segment in raise arm(deltoid);
flexion of elbow
humans is located at vertebral levels S4-5, corresponding to the anal C5,C6 (biceps); C6 externall
sphincter and peri-anal sensation. The ability to contract the anal y rotates the arm
(supinates)
sphincter voluntarily or to feel peri-anal pinprick or touch, the injury is
Extends elbow and wri
considered to be "incomplete". Recent evidence suggests that over
st(triceps and
C6,C7
95% of people with "incomplete" spinal cord injuries recover some wrist extensors);pronat
es wrist
locomotor function.[citation needed]
C7,T1 Flexes wrist

Supply small muscles

C7,T1
of thehand

Intercostals and trunk 
T1-T6
above the waist

T7-L1 Abdominal muscles
In addition to loss of sensation and motor function below the level of injury, individuals with spinal cord
injuries will also often experience other complications:

 Bowel and bladder function is regulated by the sacral region of the spine. In that regard, it is very
common to experience dysfunction of the bowel and bladder, including infections of the bladder and
anal incontinence, after traumatic injury.
 Sexual function is also associated with the sacral spinal segments, and is often affected after
injury. During a psychogenic sexual experience, signals from the brain are sent to spinal levels T10-
L2 and in case of men, are then relayed to the penis where they trigger an erection. A reflex erection,
on the other hand, occurs as a result of direct physical contact to the penis or other erotic areas such
as the ears, nipples or neck. A reflex erection is involuntary and can occur without sexually
stimulating thoughts. The nerves that control a man’s ability to have a reflex erection are located in
the sacral nerves (S2-S4) of the spinal cord and could be affected after a spinal cord injury.[3]
 Injuries at the C-1/C-2 levels will often result in loss of breathing, necessitating
mechanicalventilators or phrenic nerve pacing.
 Inability or reduced ability to regulate heart rate, blood pressure, sweating and hence body
temperature.
 Spasticity (increased reflexes and stiffness of the limbs).
 Neuropathic pain.
 Autonomic dysreflexia or abnormal increases in blood pressure, sweating, and other autonomic
responses to pain or sensory disturbances.
 Atrophy of muscle.
 Superior Mesenteric Artery Syndrome.
 Osteoporosis (loss of calcium) and bone degeneration.
 Gallbladder and renal stones.
[edit]The Location of the Injury
Determining the exact level of injury is critical in making accurate predictions about the specific parts of
the body that may be affected by paralysis and loss of function.

The symptoms observed after a spinal cord injury differ by location (refer to the spinal cord map on the
right to determine location). Notably, while the prognosis of complete injuries are generally predictable,
the symptoms of incomplete injuries span a variable range. Accordingly, it is difficult to make an accurate
prognosis for these types of injuries.
[edit]Cervical injuries
Cervical (neck) injuries usually result in full or partial tetraplegia (Quadriplegia). However, depending on
the specific location and severity of trauma, limited function may be retained.

 C3 vertebrae and above : Typically results in loss of diaphragm function, necessitating the use

of a ventilator for breathing.
 C4 : Results in significant loss of function at the biceps and shoulders.
 C5 : Results in potential loss of function at the shoulders and biceps, and complete loss of
function at the wrists and hands.
 C6 : Results in limited wrist control, and complete loss of hand function.
 C7 and T1 : Results in lack of dexterity in the hands and fingers, but allows for limited use of
arms. C7 is generally the threshold level for retaining functional independence.
[edit]Thoracic injuries

Injuries at or below the thoracic spinal levels result in paraplegia. Function of the hands, arms, neck, and
breathing is usually not affected.

 T1 to T8 : Results in the inability to control the abdominal muscles. Accordingly, trunk stability is
affected. The lower the level of injury, the less severe the effects.
 T9 to T12 : Results in partial loss of trunk and abdominal muscle control.
[edit]Lumbar and Sacral injuries

The effects of injuries to the lumbar or sacral regions of the spinal cord are decreased control of
thelegs and hips, urinary system, and anus.
[edit]Central Cord and Other Syndromes

Central cord syndrome is a form of incomplete spinal cord injury characterized by impairment in the arms
and hands and, to a lesser extent, in the legs. This is also referred to as inverse paraplegia, because the
hands and arms are paralyzed while the legs and lower extremities work correctly.

Most often the damage is to the cervical or upper thoracic regions of the spinal cord, and characterized by
weakness in the arms with relative sparing of the legs with variable sensory loss.

This condition is associated with ischemia, hemorrhage, or necrosis involving the central portions of the
spinal cord (the large nerve fibers that carry information directly from the cerebral cortex). Corticospinal
fibers destined for the legs are spared due to their more external location in the spinal cord.

This clinical pattern may emerge during recovery from spinal shock due to prolonged swelling around or
near the vertebrae, causing pressures on the cord. The symptoms may be transient or permanent.
Anterior cord syndrome is also an incomplete spinal cord injury. Below the injury, motor function, pain
sensation, and temperature sensation is lost; touch, proprioception (sense of position in space), and
vibration sense remain intact. Posterior cord syndrome (not pictured) can also occur, but is very rare.

Brown-Séquard syndrome usually occurs when the spinal cord is hemisectioned or injured on the lateral
side. On the ipsilateral side of the injury (same side), there is a loss of motor function, proprioception,
vibration, and light touch. Contralaterally (opposite side of injury), there is a loss of pain, temperature, and
deep touch sensations

[edit]Treatment

Treatment options for acute, traumatic non-penetrating spinal cord injuries include the administration of a
high dose of an anti-inflammatory agent, methylprednisolone, within 8 hours of injury. This
recommendation is primarily based on the National Acute Spinal Cord Injury Studies (NASCIS) I and II.
However, in a third study, methylprednisolone failed to demonstrate an effect in comparison to placebo.
Additionally, due to increased risk of infections, the use of this anti-inflammatory drug after spinal cord
injuries is no longer recommended.[4][5] Presently, administration of cold saline acutely after injury is
gaining popularity, but there is a paucity of empirical evidence for the beneficial effects oftherapeutic
hypothermia.

Scientists are investigating many promising avenues for treatment of spinal cord injury. Numerous articles
in the medical literature describe research, mostly in animal models, aimed at reducing the paralyzing
effects of injury and promoting regrowth of functional nerve fibers. Despite the devastating effects of the
condition, commercial funding for research investigating a cure after spinal cord injury is limited, partially
due to the small size of the population of potential beneficiaries. Despite this limitation, a number of
experimental treatments have reached controlled human trials[citation needed]. In addition, therapeutic
strategies involving neuronal protection and regeneration are also being investigated in
other neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, Amyotrophic
Lateral Sclerosis andMultiple sclerosis. There are many similarities between these conditions of the CNS
and spinal cord injuries, thus increasing the potential for discovery of a treatment after spinal cord injuries.

Advances in identification of an effective therapeutic target after spinal cord injury have been newsworthy,
and considerable media attention is often drawn towards new developments in this area. However, aside
from methylprednisolone, none of these developments have reached even limited use in the clinical care
of human spinal cord injury in the U.S.[citation needed]. Around the world, proprietary centers offering stem
celltransplants and treatment with neuroregenerative substances are fueled by glowing testimonial reports
of neurological improvement. It is also evident that when stem cells are injected in the area of damage in
the spinal cord, they secrete neurotrophic factors, and these neurotrophic factors help neurons and
vessels grow, thus helping repair the damage [6] [7] .[8] Independent validation of the results of these
treatments is lacking.[9]

[edit]Spinal Cord Injury Implications and Occupational Therapy

The signs and symptoms of spinal cord injury significantly impact everyday activities. Occupational
therapy plays an important role in the rehabilitation and management of SCI at all levels. An important
therapeutic goal is to assist the client to restore function, enabling clients to participate in the activities
and tasks that are important to them. The ability to participate in meaningful, everyday activities is
essential to an individual’s health and well-being.

Occupational therapists (OTs) focus on three life areas, which include self-care, productivity, and leisure.
[10]
 Self-care tasks include basic needs such as bathing, hygiene, feeding, and dressing. Productivity
includes activities such as paid work, volunteering, care-giving, or parenting. Leisure includes fun and
enjoyable activities activities typically done during spare time. Performing daily activities can be difficult
for an individual with a spinal cord injury. However, through the rehabilitation process individuals with SCI
can live independently in the community with or without full-time attendant care, depending on the level of
their injury.[11]

Occupational therapists work collaboratively with their clients to identify challenges in the performance of
daily tasks and activities related to self-care, productivity and leisure.[12] Informal and formal assessments
help OTs gain information that helps them to understand their clients' challenges.

[edit]How
Occupational Therapy Can Help Address Occupational
Performance Issues
When an individual receives occupational therapy, they are referred to as a client. The role of
occupational therapy in SCI rehabilitation is to assist clients in regaining abilities and roles that are
important and meaningful.[13] After identifying areas that the client feels challenged with, the OT and client
work together to prioritize and set goals. Together, they create plans that address the performance issues
in order to encourage participation in everyday activities. An important feature of occupational therapy is
the use of ‘therapeutic activities’ to achieve this goal. Finally, reassessment is done to measure the
outcome of the effectiveness of the therapy plans.

Pallastrini et al. [13] emphasize the importance of early occupational therapy, started immediately after the
client is stable. During these early stages, OTs evaluate what the client is able to do and what the client is
having difficulty with. Occupational therapists then work one-on-one with the client on skills required for
daily living. The client is shown new ways of doing things and may be given assistive devices or
equipment. Occupational therapists also help their clients develop coping skills, and implement exercises
and routines that strengthen muscles.[13]
Occupational therapists use the information gained from formal and informal assessments to guide their
intervention plans. When considering the role of OT in SCI, it is helpful to think about what interventions
are commonplace during different phases of recovery, namely acute, acute rehabilitation and community
phases. During the rehabilitation process, assessments are re-administered to evaluate progress and the
effectiveness of therapy interventions. When considering assessments and interventions, consideration
must also be given to age, gender, and a multitude of client-specific factors.

[edit]Phase 1: Acute Recovery

During acute recovery, the focus is on support and prevention. The OT helps the client gain a sense of
control over a situation in which the client likely feels little independence.[11] The OT may make splints to
prevent deformities in the hands. Additionally, daily arm and hand exercises are performed to maintain
normal function. Fitting and selecting the most appropriate temporary wheelchair to enable mobility is
important in this stage. Finally, teaching the client and care providers appropriate positioning in bed and in
the wheelchair is critical for the prevention of pressure sores.[11] Education regarding pressure sore
prevention continues into the rehabilitation phase. See self-care skills.

[edit]Phase 2: Acute Rehabilitation

During acute rehabilitation, OT interventions focus on support, education for the client and
family/caregivers, meaningful activities, choosing equipment and restoring the client’s self esteem and
confidence.[11] It is particularly important to consider the client’s discharge environment (i.e. home,
community and social setting) in order to prepare for community living. With the client, the OT creates an
individual program to meet the client's needs. The following are key areas of intervention common to
numerous rehabilitation settings [14] :

Assessment and treatment of the upper limbs.

Early in the rehabilitation phase, the OT and/or Physical Therapist evaluates the client’s strength and
sensation in the upper extremity (UE) and lower extremity (LE). The OT makes use of therapeutic
activities to both strengthen muscles and improve hand function. Custom-made splints are commonly
used to help position the hands in a functional position and assist in preventing deformity.[14] Individuals
who retain wrist function are taught to use tenodesis grasp (extending the wrist to bring the thumb and
index finger together and flexing the wrist to separate the thumb and index finger) for picking up and
releasing light objects.[11] Using meaningful activities to build strength, endurance, and coordination helps
to differentiate the work of occupational therapists from physical therapists.

Self care retraining.

Obtaining competency in self-care tasks contributes significantly to an individual's sense of self

confidence and independence. The focus is on feeding, grooming, bathing, dressing and bowel/bladder
management.[11] Assistive devices and specialized equipment are prescribed by the OT to help the client
achieve greater competency and independence in their activities of daily living. Depending on the level
and severity of the injury, independence in feeding, grooming, UE dressing and bathing may be achieved
with the assistance of adaptive equipment for dressing and bathing the LE.[15] Examples of commonly
prescribed equipment include: dressing and bathing aids for the LE, a padded transfer tub bench, shower-
commode chair, or hand-held shower. Adaptive devices may also be required to assist with bowel and
bladder management. A key role for the OT is to educate both the client and the client's caregiver(s) in
the proper care and use of the adaptive aids/equipment. Practice sessions under the supervision and
guidance of the OT are provided until the client feels competent using the adaptive aids and techniques.

Pressure sores are secondary complications of SCI. Educating clients about the risks that lead to
pressure sores and strategies for prevention is important to health and well-being.[14] For example, an
important part of the prevention strategy includes teaching clients about the importance of maintaining a
good position in bed and in any seating aids (e.g. wheelchair). In addition, the OT teaches the client about
the importance of shifting their weight regularly in both lying and seated positions. Clients who lack
strength in their upper extremity can achieve a weight shift by tilting their chair in space. Tilting the
wheelchair takes pressure off the buttocks area, which is one area at high-risk for pressure sore
development. In addition to education, the therapist assesses the client for the best pressure relieving
surfaces (i.e. cushion and mattress) to aid in pressure sore prevention.

Transfer skills.

Transfers are a key area of education and skill development.[14] Examples of different transfers include:
moving from bed to wheelchair, from wheelchair to toilet or tub, and from wheelchair to driver’s seat.
Strength in the upper extremities makes it possible to transfer independently from one surface to another
either with the aid of a sliding transfer board or by utilizing grab bars. Frequent practice under the
guidance of the OT assists clients with the necessary skill development.

Bed mobility.

Occupational therapists teach their clients bed mobility skills required for many daily tasks, such as
getting dressed, moving out of bed, and correct positioning in bed for skin protection and comfort.[14]

Mobility skills.

Not being able to move around without help is the largest restriction to participating in activities of daily
living. The wheelchair that a person uses can significantly affect their quality of participation. A key area
for the OT is to assist clients with the selection of the most suitable mobility aid in accordance with their
needs, finances, abilities, preferences and available technology.[16] A proper fitting wheelchair is critical for
good posture and comfort. Creating an ideal match between the client's needs and the equipment
available is challenging. The client's level of funding and the high cost of equipment adds further
complexity.[16]

The level and severity of a clients SCI determines the most suitable mobility aid. For example, some
clients require a power wheelchair both indoors and outdoors while others can manage on both terrains
using a manual wheelchair. If a client requires assistance with uneven outdoor surfaces, the OT may
prescribe both a power and manual wheelchair to allow for flexibility according to their needs. This
involves fitting clients for both wheelchairs and selecting the best pressure relieving surfaces/cushions
and backrests. In addition, power and manual wheelchair training assists clients in developing skills both
indoors and outdoors.

Home assessment and modifications.

Discussing the client's housing situation is an important part of rehabilitation planning. Where possible,
the OT will make a home visit to assess the need for changes and adaptations to the home. Examples of
common adaptations include: adding ramps or lifts to get into the home, widening doorways, adapting the
bathroom and kitchen for wheelchair accessibility, placing electrical switches at wheelchair level, and
choosing wheelchair-friendly flooring. Involving the client and family in determining solutions and making
decisions is very important. Assessing the need for specialized equipment (i.e. hospital bed or pressure
relieving mattress) also takes place during rehabilitation. The client will be encouraged to try different
pieces of equipment in relation to self-care, communication, and other activities of daily living. With
guidance from the OT, the client will decide on the most appropriate items of equipment to suit their
needs.

Domestic retraining.

During rehabilitation, opportunities are provided for clients to practice a variety of domestic skills. For
example, clients can practice cooking in a wheelchair-accessible kitchen. They can trial different pieces of
equipment that can enhance independence in this area. A variety of adaptive aids for the kitchen address
limitations in grip strength.[13] Occupational therapists teach adaptive strategies for carrying out domestic
chores (i.e. childcare, cleaning, laundry) that are adjusted to suit the client's needs and abilities. It may be
necessary to hire a community home care support worker to assist with domestic chores. The amount of
additional outside support depends on the level and severity of the client's SCI and can vary from 24
hours per day to just a few hours per day.[11]

Assistance with return to driving/transportation.

Clients who are able to transfer independently from their wheelchair to the driver’s seat using a sliding
transfer board, are candidates for returning to driving. Complete independence with driving also requires
the ability to load and unload one’s wheelchair from the vehicle.[11]Clients capable of driving are referred
by the OT to the 'Return to driving program' within the Driver Assessment and Rehabilitation Unit at the
hospital. The goal of the program is to provide education and retraining to help clients return to driving.
Assistance with selecting an appropriate modified vehicle that will meet the client’s needs and budget are
part of the program. For clients who do not wish to return to driving, alternate transportation options are
also addressed (i.e. accessible parking, taxi subsidy vouchers, modified vehicle for passenger transit and
public transportation).

Community living skills.

Clients may be involved in a support group, which addresses skills that prepare clients for returning home
and to the community. As previously mentioned, driving and wheelchair mobility skills are important for
accessing the community. Community outings are commonly organized to help transition the client into
the community.[14] (See community reintegration for more details.)

Leisure and recreation skills.

Part of rehabilitation involves investigating options for returning to previous leisure/recreation interests as
well as developing new pursuits. In addition, the OT can assist the client in finding ways to cope with
physical and social issues that may get in the way of leisure participation.[15]

Work/study skills.

Addressing the client's career and educational goals is very important. If appropriate, a work site/school
visit may be arranged to assess for accessibility. Otherwise, a referral to a community based work/school
assessment service may be indicated.[15]

Sexual Health.

Exploring concerns related to sexual health and function should form an integral part of each client's
treatment plan. The OT can assist their client by providing information and identifying alternate resources
and adaptive devices as needed.[15]

[edit]Phase 3: Community reintegration

Following rehabilitation, the client begins the process of community reintegration. Community participation
is an important aspect in maintaining quality of life.[17] During community reintegration, the focus of
occupational therapy is on restoring client roles at home and in the community, and promoting social
participation and life satisfaction.[17] Ongoing education of the client, family and caregivers continues
throughout this stage. Referrals can be made to an outpatient clinic or community therapist to continue
with treatment and progress made during rehabilitation. Outpatient programs teach clients how to use
new movement and they offer training for activities of daily living as clients continue to gain strength
during the first year after injury. In addition, the OT and client work on goals and skills that encourage the
client towards community integration (i.e. driving, vocational evaluation and training, participation in
leisure interests). Additionally, the therapist identifies transitional services such as support groups and
transitional living centres if required.

Occupational therapists are also involved with advocacy on behalf of their clients. Advocacy can take
many forms and apply in areas that impact the client's ability to fully participate within their community.
This includes helping to address barriers to employment, and leisure at a policy level. Examples of large
barriers involving physical structures are playground designs, city planning, and accessible buildings. An
OT can address decision makers, argue in favour of their client's needs and bring important information
and perspectives to others who may be causing a barrier for the client. Occupational therapists can
promote awareness, and lobby on behalf of their clients. Finally, OTs address issues such as social
stigma by advocating on their client's behalf. Stigma can be addressed: (a) by challenging others to think
differently, (b) by making others aware of marginalization, and (c) by helping others understand the loss of
privileges that can occur at both the societal and policy level.[18]

[edit]Epidemiology

One can have spine injury without spinal cord injury. Many people suffer transient loss of function
("stingers") in sports accidents or pain in "whiplash" of the neck without neurological loss and relatively
few of these suffer spinal cord injury sufficient to warrant hospitalization. In the United States, the
incidence of spinal cord injury has been estimated to be about 40 cases (per 1 million people) per year or
12,000 cases per year .[19] In China, the incidence of spinal cord injury is approximately 60,000 per year.[20]

The prevalence of spinal cord injury is not well known in many large countries. In some countries, such as
Sweden and Iceland, registries are available. According to new data collected by the Christopher and
Dana Reeve Foundation, in the US, there are currently 1.3 million individuals living with spinal cord
injuries- a number five times that previously estimated in 2007. 61% of spinal cord injuries occur in males,
and 39% in females. The average age for spinal cord injuries is 48 years old. There are many causes
leading to spinal cord injuries. These include motor vehicle accidents (24%), work-related accidents
(28%), sporting/recreation accidents (16%), and falls (9%)
Normal Structure And Function

The intervertebral disc is the largest avascular structure in the body. It arises from notochordal cells
between the cartilaginous endplates, which regress from about 50% of the disc space at birth to about 5%
in the adult, with chondrocytes replacing the notochordal cells. Intervertebral discs are located in the
spinal column between successive vertebral bodies and are oval in cross section. The height of the discs
increases from the peripheral edges to the center, appearing as a biconvex shape that becomes
successively larger by about 11% per segment from cephalad to caudal (ie, from the cervical spine to the
lumbosacral articulation). A longitudinal ligament attaches to the vertebral bodies and to the intervertebral
discs anteriorly and posteriorly; the cartilaginous endplate of each disc attaches to the bony endplate of
the vertebral body.

Images of herniated nucleus pulposus are provided below:

Hyaluronan long chains form a backbone for attracting electronegative or hydrophilic
branches, which hydrate the nucleus pulposus and cause a swelling pressure within the
annulus to allow it to stabilize the vertebrae and act as a shock absorber. Deterioration
within the intervertebral disk results in loss of these water-retaining branches and
eventually in the shortening of the chains.

Nuclear material is normally contained within the annulus, but it may cause bulging of the
annulus or may herniate through the annulus into the spinal canal. This commonly occurs in
a posterolateral location of the intervertebral disk, as depicted.

The spinal nerves exit the spinal canal through the foramina at each level. Decreased disk
height causes decreased foramen height to the same degree, and the superior articular
facet of the caudal vertebral body may become hypertrophic and develop a spur, which then
projects toward the nerve root situated just under the pedicle. In this picture, L4-5 has loss
of disk height and some facet hypertrophy, thereby encroaching on the room available for
the exiting nerve root (L4). A herniated nucleus pulposus within the canal would embarrass
the traversing root (L5).

The disc's annular structure is composed of an outer annulus fibrosus, which is a constraining ring that is
composed primarily of type 1 collagen. This fibrous ring has alternating layers oriented at 60° from the
horizontal to allow isovolumic rotation. That is, just as a shark swimming and turning in the water does not
buckle its skin, the intervertebral disc has the ability to rotate or bend without a significant change in
volume and, thus, does not affect the hydrostatic pressure of the inner portion of the disc, the nucleus
pulposus.

The nucleus pulposus consists predominantly of type II collagen, proteoglycan, and hyaluronan long
chains, which have regions with highly hydrophilic, branching side chains. These negatively charged
regions have a strong avidity for water molecules and hydrate the nucleus or center of the disc by an
osmotic swelling pressure effect. The major proteoglycan constituent is aggrecan, which is connected by
link protein to the long hyaluronan. A fibril network, including a number of collagen types along with
fibronectin, decorin, and lumican, contains the nucleus pulposus.

The hydraulic effect of the contained, hydrated nucleus within the annulus acts as a shock absorber to
cushion the spinal column from forces that are applied to the musculoskeletal system. Each vertebra of
the spinal column has an anterior centrum or body. The centra are stacked in a weightbearing column
and are supported by the intervertebral discs. A corresponding posterior bony arch encloses and protects
the neural elements, and each side of the posterior elements has a facet joint or articulation to allow
motion.

The functional segmental unit is the combination of an anterior disc and the 2 posterior facet joints, and it
provides protection for the neural elements within the acceptable constraints of clinical stability. The facet
joints connect the vertebral bodies on each side of the lamina, forming the posterior arch. These joints are
connected at each level by the ligamentum flavum, which is yellow because of the high elastin content
and allows significant extensibility and flexibility of the spinal column.

Clinical stability has been defined as the ability of the spine under physiologic load to limit patterns of
displacement so as to avoid damage or irritation to the spinal cord or nerve roots and to prevent
incapacitating deformity or pain caused by structural changes.1 Any disruption of the components holding
the spine together (ie, ligaments, intervertebral discs, facets) decreases the clinical stability of the spine.
When the spine loses enough of these components to prevent it from adequately providing the
mechanical function of protection, surgery may be necessary to reestablish stability.

Recent studies

 Tomasino et al presented radiologic and clinical outcome data on patients who underwent single-
level anterior cervical discectomy and fusion (ACDF) for cervical spondylosis and/or disc
herniation using bioabsorbable plates for instrumentation. Overall, at 19.5 months
postoperatively, 83% of the patients had favorable outcomes based on the Odom criteria. The
authors found that absorbable instrumentation provides better stability than the absence of a
plate but that graft subsidence and deformity rates may be higher than those associated with
metal implants. In this study, the fusion rate and outcome were found to be comparable to the
results achieved with metallic plates, and the authors concluded that the use of bioabsorbable
plates is a reasonable alternative to metal, avoiding the need for lifelong metallic implants.2
 Buchowski et al performed a cross-sectional analysis of 2 large prospective, randomized
multicenter trials to evaluate the efficacy of cervical disc arthroplasty for myelopathy with a single-
level abnormality localized to the disc space. The authors found that patients in both the
arthroplasty and arthrodesis groups had improvement following surgery, with improvement being
similar and with no worsening of myelopathy occurring in the arthroplasty group. The authors
noted that although the findings at 2 years postoperatively suggest that arthroplasty is equivalent
 to arthrodesis in these cases, they did not evaluate the treatment of retrovertebral compression
as occurs with ossification of the posterior longitudinal ligament.3
 Carragee et al compared progression of common degenerative findings between lumbar discs
injected 10 years earlier with those same disc levels in matched subjects who were not exposed
to discography. The authors found that in all graded or measured parameters, discs exposed to
puncture and injection had greater progression of degenerative findings than the control
(noninjected) discs. Progression of disc degeneration was 35% in the discography group,
compared to 14% in the control group, with 55 new disc herniations occurring in the discography
group and 22 in the control group. The study also found significantly greater loss of disc height
and signal intensity in the discography discs. They noted, therefore, that careful consideration of
risk and benefit are necessary in regard to disc injection.4
 McGirt et al performed a prospective cohort study with standardized postoperative lumbar
imaging with CT and MRI every 3 months for a year, then annually, to assess same-level
recurrent disc herniation. Improvement in all outcome measures was observed 6 weeks after
surgery. At 3 months after surgery, 18% loss of disc height was observed, which progressed to
26% by 2 years. In 11 (10.2%) patients, revision discectomy was required at a mean of 10.5
months after surgery. According to the authors, patients who had larger anular defects and
removal of smaller disc volumes had increased risk of recurrent disc herniation, and those who
had greater disc volumes removed had more progressive disc height loss by 6 months after
surgery. The authors suggested, based on the findings, that in cases of larger anular defects or
less aggressive disc removal, concern for recurrent herniation should be increased and that, in
such cases, effective anular repair may behelpful.5
 Fish et al performed a retrospective single-center study to analyze whether MRI findings can be
used to predict therapeutic responses to cervical epidural steroid injections (CESI) in patients with
cervical radiculopathy. Patients were categorized by the presence or absence of 4 types of
cervical MRI findings: disc herniation, nerve root compromise, neuroforaminal stenosis, and
central canal stenosis. The authors found that only the presence, versus the absence, of central
canal stenosis was associated with significantly superior therapeutic response to CESI. They
therefore concluded that the MRI finding of central canal stenosis is a potential indication that
CESI may be merited.6
 Hirsch et al did a systematic review of the literature to determine the effectiveness of automated
percutaneous lumbar discectomy (APLD). According to the authors, based on United States
Preventive Services Task Force (USPSTF) criteria, the indicated evidence for APLD is level II-2
for short- and long-term relief, indicating that APLD may provide appropriate relief in properly
selected patients with contained lumbar disc prolapse. However, the authors noted that there is a
paucity of randomized, controlled trials in the literature covering this subject.7

Degeneration: Process And Models

Low back pain (LBP) is ubiquitous, with 60-80% of people having an activity-limiting episode at least
transiently in their lifetime. Genetic factors appear to have a dominant role, with LBP starting at an earlier
age than previously suspected on the basis of subsequent structural changes; men begin having LBP
about a decade earlier than women.8

The water-retaining ability of the nucleus pulposus, or the inner portion of the intervertebral disk, declines
progressively with age. The decline in the mechanical properties of the nucleus pulposus is associated
with the degree of proteoglycan deterioration and the decrease in hydration, which lead to excessive
regional peak pressures within the disk. As the hyaluronan long chains shorten and swelling pressure
decreases as a result of this deterioration, the mechanical stiffness of the intervertebral disk decreases,
which causes the annulus to bulge, with a corresponding loss of disk and foramina height.9

The etiology of back pain for a particular individual cannot be determined because of the multiplicity of
potential sources. Although periosteal disruption causes pain with fractures, bone itself is devoid of pain
receptors (eg, asymptomatic compression fractures commonly are seen in the thoracic spine of elderly
individuals with osteoporosis). However, the degenerating intervertebral disk is known to have
neurovascular elements at the periphery, including pain fibers. Disk deterioration and loss of disk height
may shift the balance of weightbearing to the facet joint; this mechanism has been hypothesized as a
cause of LBP through the facet joint capsule, as well as through other tissues attached to and between
the posterior bony elements.

When the annulus in animals is incised, a degenerative cascade is initiated that mimics the natural aging
process observed in humans, thus providing a model of disk deterioration.10 As the use of discography has
increased for various clinical applications, similar annular tears are seen routinely that are associated with
the degeneration of the intervertebral disk, even in patients who are asymptomatic. Annular tears may
simply be the result of aging and the degenerative cascade.

Pathology studies of young patients who died as a result of trauma reveal a surprising degree of articular
surface damage in the facet joints; magnetic resonance imaging (MRI) routinely reveals disk deterioration
in individuals in the second or third decade of life. Injection of chymopapain into the intervertebral disk
causes a repeatable and predictable degenerative cascade in the facet joints, illustrating the coupling
between the disk and facet joints. Immobilization by facet fusion posteriorly leads to disk deterioration;
this avascular structure is solely dependent upon motion to facilitate the diffusion of nutrients into it.
Whether the deterioration of the disk or that of the facet comes first has not been determined; however,
deterioration is known to occur in both.

Dehydration results from shortening of the hyaluronic chains, deterioration of the state of aggregation,
and decreases in the ratio of chondroitin sulfate to keratan sulfate, leading to the disk bulging and disk
height loss. The consistency of the nuclear material undergoes a change from a homogeneous material to
clumps, which leads to the altered distribution of pressures within the disk and resistance to the flow of
nuclear material; the nuclear material thereby becomes mechanically unstable.11 The clumping of the
degenerating nuclear material can be likened to a marble held between 2 books—that is, it is difficult to
contain.

These clumps may be lateral to the posterior longitudinal ligament and, therefore, may have the least
resistance to herniating through the corner of the intervertebral disk and into the spinal canal or foramen.
Surgical removal of the herniated fragments is achieved by grasping them with a pituitary rongeur. This
method of surgical removal is not possible with normal, homogeneous material, which is encountered
when healthy interverterbral disks are excised anteriorly in patients having surgery because of deformity
or trauma. Using the pituitary rongeur technique to perform a microdiscectomy on a herniated fragment
necessitates a preexisting state of deterioration; the weakened areas in the annulus provide a path of
least resistance for the nuclear material to egress.

Natural History
Much has been written concerning the process of spinal deterioration or spondylosis, which occurs over a
lifetime.Intervertebral disk deterioration leads to decreased stiffness of the disk, as well as diminished
stability, resulting in episodic pain that is common and may be temporarily severe. However, continued
deterioration ultimately leads to restabilization of the spine by collagenization, which stiffens the disk.
Patients in their 50s and 60s customarily have stiffer spines but less pain than patients in their 30s and
40s who are undergoing initiation of the degenerative cascade. Patients who ask if they have to live with
this pain "for the rest of their lives" can be reassured to some extent by this natural history. Furthermore,
spontaneous recovery from an acute pain episode routinely occurs, so any treatment must be
demonstrated as effective by positively altering the expected course without treatment.

In general practice, the overall incidence of herniated nucleus pulposus (HNP) in patients who have new
LBP onset is less than 2%. Therefore, most of these patients have deterioration of the intervertebral disk
and dysfunction of the functional segmental unit. They will have LBP, and some will have associated leg
pain but without sciatica (an intractable, radiating pain, below the knee) or radiculopathy. A disk fragment
that is no longer contained within the annulus but is displaced into the spinal canal has decreased
hydration and deteriorated proteoglycan that can be expected to undergo further deterioration and
consequent annular desiccation, essentially like a grape being transformed into a raisin.

Spontaneous resolution of sciatica may result from shrinkage of a herniated fragment, aided by
macrophages and the evoked inflammatory reaction, but practitioners too often attribute this clinical
improvement to their favorite treatments. Intractable symptoms of sciatica from intervertebral disk
displacements may benefit dramatically from surgical intervention. Within 20 years of Mixter and Barr's
1934 report, Friedenberg compared operative treatment with nonoperative treatment.12,13 Nonoperative
treatment yielded 3 groups of results: pain free, occasional residual pain, and disabling pain. Proportions
of these groups remained similar after 5 years. Friedenberg concluded that even recurrent severe
episodes may resolve without surgery; the problem was and remains patient selection.

Weber presented a randomized, controlled study (marred by dropouts in the surgery control group
because of severe pain) and concluded that patient results were the same whether treated operatively or
conservatively, except that those who were treated operatively had better results at 1 year.14 The Spine
Patient Outcomes Research Trial (SPORT) observational cohort is similarly limited in its conclusions by
crossovers: 50% of the surgery arm had surgery within 3 months and 30% of the nonsurgical group had
surgery, but at long-term follow-up, both groups again were not statistically different.15

Herniation

Nuclear material that is displaced into the spinal canal is associated with a significant inflammatory
response, as has been demonstrated in animal studies. Disk injury results in an increase in the
proinflammatory molecules interleukin-1 (IL-1), IL-8, and tumor necrosis factor (TNF) alpha. Macrophages
respond to this displaced foreign material and seek to clear the spinal canal. Subsequently, a significant
scar is produced, even without surgery, and substance P, which is associated with pain, is detected.
Acute neural compression is responsible for dysfunction; compression of a motor nerve results in
weakness, and compression of a sensory nerve results in numbness. Radicular pain is caused by
inflammation of the nerve, which explains the lack of correlation between the actual size of an
intervertebral disk herniation or even the consequent degree of neural compression and the associated
clinical symptoms.16
Furthermore, intervetebral disk degeneration may result in radial tears and leakage of the nuclear
material, which leads to neural toxicity. The subsequent inflammatory response often results in neural
irritation causing radiating pain without numbness, weakness, or loss of reflex, even when neural
compression is absent.

Several factors seem to influence the occurrence of herniated nucleus pulposus. Smoking is a risk factor
in the epidemiology of lumbar disk herniations and has been documented to decrease the oxygen tension
in the avascular disk dramatically, presumably by vasoconstrictive and rheologic effects on blood. Lumbar
disk herniationmay result from chronic coughing and other stresses on the disk. For example, sitting
without lumbar support causes an increase in disk pressures, and driving is also a risk factor because of
the resonant coupling of 5-Hz vibrations from the road to the spine. People who drive signifcant amounts
have increased spinal problems; truck drivers have the additional risk of spinal problems from lifting
during loading and unloading, which, unfortunately, is done after prolonged driving.

Studies have shown that peak stresses within a deteriorated intervertebral disk exceed those from
average loads on a normal disk, which is consistent with a pain mechanism. Further repetitive stress at
physiologic levels did not produce a herniation after prolonged testing, contradicting the concept of injury
accumulation with customary work activities. However, after a simulated injury to the annulus (cutting), a
lower mechanical stress did result in disk herniation, consistent with intervertebral disk degeneration and
with clinical experience on discography.

The presumed traumatic cause of disk herniations has been questioned scientifically in the literature,
particularly with the increased availability of genetic information.17,18 

The pathologic state of a weakened annulus is a necessary condition for herniation to occur. Many cases
involve trivial trauma even in the presence of repetitive stress. An annular tear or weak spot has not been
demonstrated to result from repetitive normal stress from customary activities or from physically stressful
activities.

Mixter and Barr first recognized that the cartilaginous masses in the spinal canal of their patients were not
tumors or chondromas.12 They proposed that herniation of the nucleus pulposus and displacement of
nuclear material caused neural irritation, inflammation, and pain. They showed that excising a disk
fragment was effective, but their recommendation to perform this procedure with a fusion was
necessitated by relatively aggressive laminectomy. This procedure has been replaced by techniques that
are less invasive, such as microdiscectomy.

Clinical Evaluation

Obtaining pertinent patient historical information should begin with an analysis of the chief complaint.
Does the patient's complaint concern dominant leg pain, dominant back pain, or a mixture of significant
problems with both? Next, is the onset acute, subacute, or chronic? Under what circumstances does
onset occur? What is the patient's prior history, particularly regarding similar symptoms or treatment
response?

Identify risk factors, obtain a pertinent medical history, and specifically exclude red flags, such as
nonmechanical pain, which causes pain at night without activities because pressure in the pelvic veins
may be increased upon reclining. Nonmechanical pain may be indicative of a tumor or infection. A
progressive neurologic deficit or cauda equina syndrome is considered a surgical emergency because
irreversible consequences may result if these are left untreated.
Obtaining a thorough history of activity intolerance requires some time and attention to the details of
specific examples and the positions or actions that cause problems. Also, it is helpful to determine which
activities the patient is unable or less able to perform and which activities exacerbate or moderate the
pain. An assessment of the physical demands of the patient's occupation and daily activities provides the
perspective for the described activity intolerance. A pain drawing can be very helpful in assessing the
pattern of pain, such as a dermatomal distribution, or in assessing the organicity of the complaints.

Physical examination classically involves range-of-motion (ROM) testing of the lumbar and cervical spine,
but these findings may be more reflective of aging or deterioration in the intervertebral disks and joints
than any quantifiable assessment of impairment. The remainder of the examination is essentially a
neurologic assessment of weakness, dermatomal numbness, reflex change, and, most important, sciatic
or femoral nerve root tension in the lumbar spine.

Numerous examination maneuvers (eg, Lasegue classic test, Lasegue rebound sign, Lasegue differential
sign, Braggard sign, flip sign, Deyerle sign, Mendel-Bechterew sign, well leg test or Fajersztajn sign, both-
legs or Milgram test) are available but cloud the issue, because the sciatic nerve root tension or straight-
leg raising test is the basis for nearly all of them. They are essentially modifications for subtle differences,
but the provocation of radiating pain down the leg is of a neural compressive lesion and compression of
the sciatic nerve root, if it goes below the knee. Furthermore, the provocation of radiating pain down the
leg is the most sensitive test for a lumbar disk herniation.

For a higher lumbar lesion, reverse straight-leg raising or hip extension that stretches the femoral nerve is
analogous to a straight-leg raising test. The Spurling test in the cervical spine is used to detect foraminal
stenosis (Kemp's test is used in the lumbar region) rather than specifically for intervertebral disk
herniation or nerve root tension. Careful hip, rectal, and genitourinary examinations help exclude
complications of those organ systems in the diagnosis of higher lumbar lesions.

After obtaining plain radiographs, further imaging studies (eg, MRI, computed tomography [CT] scanning,
CT myelography) may be indicated to assess degenerative disk disease, loss of disk height, and facet
deterioration, such as sclerosis or hypertrophy. MRI clearly provides the most information, perhaps too
much, as it has a 25% false-positive rate (asymptomatic herniated nucleus pulposus [HNP]). An HNP that
is noted on imaging studies must be correlated with objective examination findings; otherwise, it must be
presumed to be an asymptomatic HNP if there is no correlation between the imaging findings and pain or
clinical symptoms. Therefore, imaging studies should perhaps be reserved for cases in which positive
physical findings have been documented.

Other causes of significant back pain in the absence of neurologic findings should be considered. Sciatic
nerve irritation may result from sacroiliac dysfunction or degenerative joint disease caused by the
proximity of the sciatic notch to the sacroiliac joint or peripheral entrapment, including piriformis
syndrome. Careful examination with an adequate differential for the diagnosis may prevent prolonged
ineffective empirical care for presumed lumbar disk disease.

The facet syndrome has been controversial, but neurophysiologic studies have shown discharges from
the capsule consistent with pain, as well as inflammation and degenerative joint disease.19 However, large
numbers of patients have reported significant relief after facet joint injections for nonspecific LBP; as a
result, the facet syndrome has become more widely accepted. Clinically, patients usually have pain only
to the knee, not below, as would be expected from an HNP.
Conservative Treatment

Spontaneous improvement of low back discomfort has allowed ineffective treatments to perpetuate,
because benefits have been ascribed to them when they are prescribed while the patient is still
symptomatic but otherwise improving. Hippocrates expected improvement in sciatica in 40 days, and the
customary and contemporary guideline is 6 weeks. An often-quoted study suggests near-resolution
improvement of 90% of patients within 6 weeks, but this study has been faulted because the criterion for
patient recovery was failure to return to the observing physician.20 The prevalence of back problems is
consistent with the failure of a subgroup of patients to improve and to have periodic recurrent episodes of
disability.

Analysis of the effectiveness of treatments and attempts to restrict treatment to those modalities that have
demonstrated efficacy are evidence-based medical practice. Bedrest has a long history of use but has not
been shown to be effective beyond the initial 1 or 2 days; after this period, bedrest is counterproductive.
All conservative treatments are essentially efforts to reduce inflammation; therefore, only a very short
period of rest is appropriate, anti-inflammatories are of some benefit (because the pain is from
inflammation of the nerve), and warm, moist heat or modalities may be helpful. Activities should be
resumed as early as tolerated. Exercises and physical therapy mobilize muscles and joints to facilitate the
removal of edema and promote recovery. Muscle relaxants may offer symptomatic relief of the acute
muscle spasms but only in the early stages; however, all are central acting, there is no direct relaxation of
skeletal muscle, and they are also sedating.

For back pain without radiculopathy, chiropractic care has high patient satisfaction when performed within
the first 6 weeks, and it has been shown to have good efficacy acutely from an evidence-based
standpoint.21 Injections (eg, epidural) may be particularly helpful in patients with radiculopathy by providing
symptom relief, which allows the patient to increase activities and helps facilitate rehabilitation.22,23 Any
nuclear material that is herniated may shrink as the proteoglycan deteriorates, loses its water-retaining
ability, and turns from a grapelike object to a raisinlike object.

Arbitrary time schedules for improvement are inappropriate in any patient who continues to improve and
whose function is relatively maintained. Traction in the acute setting may help muscle spasms, but it does
not reduce the HNP and has no good evidence of efficacy. The use of traction does not justify hospital
admission, as it is not cost-effective and can be administered on an outpatient basis.

Long-term use of physical therapy modalities is no more effective than hot showers or hot packs are at
home. A transcutaneous electrical nerve stimulation (TENS) unit may be subjectively helpful in some
patients with chronic conditions. Encourage patients to essentially compensate for intervertebral disk
incompetence, as possible, by muscular stabilization, and to maintain flexibility by initiating life-long
exercise regimens, including aerobic conditioning, particularly swimming, which allows gravity relief.

Assess the body mechanics of every patient who is disabled from work. Educate all patients about body
mechanics, and discuss the risk factors for faulty body mechanics, so that applications can be
incorporated into individual work settings, including appropriate seating (eg, lumbar support). The lumbar
facet joints are oriented relatively vertically, thus allowing forward flexion, but the joints impact each other
when a person bends and then rotates. Repetitive bending and twisting have been noted to be
epidemiologic problems in workers, and may be associated with chronic pain and disability.24 Attention to
lifting techniques and ergonomic modification at workstations may be very appropriate.
Surgical Intervention

The classic presentation of an herniated nucleus pulposus includes the complaint of sciatica, with
associated objective neurologic findings of weakness, reflex change, and dermatomal numbness. Various
surgical procedures have been reported and share the common goal of decompressing the neural
elements to relieve the leg pain. These procedures are most appropriate for patients with minimal or
tolerable back pain, with an essentially intact and clinically stable disk. However, the hope of permanently
relieving the back pain is a fantasy, a false hope.

The most common procedure for a herniated or ruptured intervertebral disk is a microdiscectomy, in
which a small incision is made, aided by an operating microscope, and a hemilaminotomy is performed to
remove the disk fragment that is impinging on the nerves.

Many patients who undergo microdiscectomy can be discharged with minimal soreness and complete
relief of leg pain after an overnight admission and observation. Same-day procedures are in the process
of cautious development; patients with dominant back pain have a different problem, even if HNP is
present, and would require stabilization by fusion if unresponsive to well-managed appropriate therapy or
arthroplasty (if there is an isolated level with good facet joints).

Minimally invasive techniques have not replaced this standard microdiscectomy procedure but can be
summarized in 2 categories: central decompression of the disk and directed fragmentectomy.

Central decompression of the disk can be performed chemically or enzymatically with chymopapain, by
laser or plasma (ionized gas) ablation and vaporization, or mechanically by aspiration and suction with a
shaver such as the nucleotome or percutaneous lateral decompression (arthroscopic microdiscectomy).

The Food and Drug Administration (FDA) initially released and then withheld chymopapain for injection
into lumbar disks because of adverse allergic reactions in patients; skin tests subsequently were used to
determine sensitivity. However, the procedure continued to induce severe muscle spasms that could be
far worse than those of an open operation and thus required hospitalization and bedrest for up to 50% of
patients.25 This morbidity must be considered a contradiction to the assertion by proponents that the
enzyme is limited to the disk in the chemical digestion of the nucleus pulposus, because the muscles are
severely affected, which would not be expected if the enzyme were contained. In addition, severe scarring
in the spinal canal is noted routinely after this procedure.

The nucleotome and laser central decompressions have been shown only to equal placebo in
effectiveness, and their use has declined. Further development of alternatives, such as nucleoplasty, and
efforts to reduce disk pressure remain under study.

Directed fragmentectomy is similar to an open microdiscectomy and has demonstrated greater

effectiveness than placebo. This procedure uses an arthroscopic approach and a probe that directs a
flexible pituitary rongeur from the center of the intervertebral disk toward the posterior annulus.
Endoscopic techniques to perform a directed fragmentectomy and to minimize disruption of normal
structures continue in development, but superiority has not been demonstrated despite this minimally
invasive approach.

Concerning the cervical spine, HNP customarily is treated anteriorly, because the pathology is anterior
and manipulation of the cervical cord is not tolerated by the patient. The posterior approach is reserved
for disk herniation that is confined to the foramen and for foraminal stenosis. An alternative to the anterior
cervical spine approach is minimal disk excision; clinical stability following this procedure is dependent
upon the residual disk, which is also true in cases where there is lumbar spine involvement with back
pain. Removal of neural compression dramatically relieves radiculopathy; however, residual axial neck
pain may result in significant impairment.

Anterior cervical interbody fusion is another intervention. Proponents of discectomy alone assert
equivalent results, but the adequacy of follow-up in those case reports is a significant concern. Patients
with more severe disk degeneration, particularly myelopathy, would more uniformly undergo fusion.
Anterior instrumentation is being used more commonly, and interbody cages are under consideration as a
means of attaining more rapid rehabilitation and more consistent results.

Controversies And Outcomes

The diagnosis of an internal disk derangement is controversial. The classic patient presents with back
pain without imaging abnormalities except for varying degrees of the black disk, which is the converse of
the asymptomatic patient with an intervertebral disk herniation. Patients without a disk herniation have a
favorable course and long-term outcome with conservative treatment or surgery. However, some patients
with prolonged limitations and limited job skills benefit from surgical intervention for segmental instability
or clinical instability as we earlier discussed. A positive discogram properly done and carefully interpreted
in context may raise the expectation of success for surgical treatment in this patient population. The
greatest controversy is over the effectiveness of fusion surgery. Unfortunately, there is no clear objective
criterion; clinical judgment is mandatory and is not perfect; clearly, good patients do well, and patient
selection is paramount.

Patients with "broad-based" intervertebral disk herniations generally have a deterioration of the disk or a
failure of clinical stability with associated back pain, rather than isolated sciatica. These patients are not
appropriate candidates for microdiscectomy alone. Lumbar fusion is being used increasingly in these
cases, and arthroplasty is also being considered; however, this treatment remains controversial because
it is, again, based inevitably on subjective patient pain and clinical judgment without objective
determination.

With a discectomy, patients with dominant leg pain have excellent results, with 85-90% returning to full
function. However, up to 15% of patients have continued back pain that may limit their return to full
function, despite the absence of radiculopathy. Patients who undergo surgery do not necessarily show
better results than patients who defer surgery.26

Intervertebral disk degeneration that causes clumping of the nuclear material and relative mechanical
instability is the necessary preceding condition for HNP. However, it is impossible to tell which patients
will do well after microdiscectomy for a herniation and which will have continued problems, of varying
severity, from the disk degeneration. Significant deterioration and accompanying LBP increasingly are
being treated with stabilization, via either an anterior lumbar interbody fusion (ALIF) or a posterior lumbar
interbody fusion (PLIF) in association with posterior decompression (when necessary) and
instrumentation. Results are not yet available, as techniques are still evolving, but experience is
accumulating.

Multimedia
 Media file 1: Hyaluronan long chains form a backbone for attracting
electronegative or hydrophilic branches, which hydrate the nucleus
pulposus and cause a swelling pressure within the annulus to allow it to
stabilize the vertebrae and act as a shock absorber. Deterioration within the
intervertebral disk results in loss of these water-retaining branches and
eventually in the shortening of the chains.

(Enlarge Image)

Media file 2: Nuclear material is normally contained within the annulus, but it
may cause bulging of the annulus or may herniate through the annulus into
the spinal canal. This commonly occurs in a posterolateral location of the
intervertebral disk, as depicted.

(Enlarge Image)

Media file 3: The spinal nerves exit the spinal canal through the foramina at
each level. Decreased disk height causes decreased foramen height to the
same degree, and the superior articular facet of the caudal vertebral body
may become hypertrophic and develop a spur, which then projects toward
the nerve root situated just under the pedicle. In this picture, L4-5 has loss of
disk height and some facet hypertrophy, thereby encroaching on the room
available for the exiting nerve root (L4). A herniated nucleus pulposus within
the canal would embarrass the traversing root (L5).

(Enlarge Image)

Keywords

herniated disc, HNP, herniated disk, disc herniation, disk herniation, bulging disk, bulging disc, back pain
 
Introduction

With the burden of musculoskeletal disease at the forefront of health care worldwide, the World Health
Organization (WHO) declared 2000-2010 the Bone and Joint Decade (USBJD).1 The USBJD comprises
over 100 professional and patient organizations, with the American Academy of Orthopaedic Surgeons
(AAOS) being one of the founding organizations. The campaign promotes initiatives throughout the world,
with particular support for activities in developing countries.2,3,4,5 

The USBJD campaign became increasingly relevant with the earthquake in Haiti on January 12th.
According to Joseph D. Zuckerman, MD, the AAOS President, "Historically, severe earthquakes cause a
high number of orthopaedic traumas. With the staggering number of reported injuries and deaths in Haiti,
we believe the need for any and all volunteer medical support is high and our members are responding in
sync with that need. We encourage all interested parties—doctors, nurses and medical staff—to go
to www.aaos.org/Haiti to view additional information as it becomes available. The AAOS will provide
whatever support we can to assist in the relief efforts."6 

The World Health Organization has created a "Health Action in Crises" Page that provides Technical
Guidelines, Situation Reports, Maps, and other information that includes the needs of the people in Haiti
during the current crisis.

Also responding to the need for information concerning patient care following the earthquake in Haiti, the
Centers for Disease Control and Prevention (CDC) has published 2 fact sheets on Emergency
Preparedness and Response7 :
  Emergency Wound Management for Healthcare Professionals
 After an Earthquake: Management of Crush Injuries & Crush Syndrome

Problem
A fracture is defined as a disruption in the integrity of a living bone, involving injury to the bone marrow,
periosteum, and adjacent soft tissues. Many types of fractures exist, such as pathologic, stress,8 and
greenstick fractures. When a fracture occurs, it is described radiographically and clinically in terms of the
following factors:

 Anatomy: The fracture is described with relation to the bones involved and the location within the
bone (diaphysis, metaphysis, physis, epiphysis).
 Articular surface involvement: Does the fracture have intra-articular involvement? Is there intra-
articular displacement or gapping?
 Displacement: Is the distal fracture fragment displaced compared with the proximal fragment? To
what degree or percentage is the fracture displaced?
 Angulation: The angular deformity is defined in degrees in terms of the distal fragment in relation
to the proximal fragment or with respect to the proximal apex of the distal fragment.
 Rotation: Rotational deformity is described both clinically and radiographically.
 Shortening: Has the fracture caused shortening of the involved bone? To what extent has
shortening occurred?
 Fragmentation: The Muller AO (Arbeitsgemeinschaft für Osteosynthesefragen [Association for
Osteosynthesis]) Comprehensive Classification of Fractures provides a standardized description
of fracture patterns, making communication regarding such injuries more precise and
understandable.
o A multifragmentary fracture is one that has several breaks in the bone, creating more
than 2 fragments.
o Wedge fractures are either spiral (low energy) or bending (high energy) and allow the
proximal and distal fracture fragments to contact each other.
o The complex multifragmentary fracture is a segmental fracture or one in which there is no
contact between the proximal and distal fragments without the bone shortening.
o Simple fractures are spiral, oblique, or transverse.
o Management of multifragmentary fractures may be more complicated than that for simple
fractures.
 Soft-tissue involvement: Is the fracture open or closed? Is associated neurologic and/or vascular
injury present? Is there muscle damage or is compartment syndrome (CS) evident? Gustilo et al
described a classification of open fractures comprising 3 types9 :
o Type I: The wound is smaller than 1 cm, clean, and generally caused by a fracture
fragment that pierces the skin (ie, inside-out injury). This is a low-energy injury.
o Type II: The wound is longer than 1 cm, not contaminated, and without major soft-tissue
damage or defect. This is also a low-energy injury.
o Type III: The wound is longer than 1 cm, with significant soft-tissue disruption. The
mechanism often involves high-energy trauma, resulting in a severely unstable fracture
with varying degrees of fragmentation. Type III fractures are also subdivided into the
following:
 IIIA: The wound has sufficient soft tissue to cover the bone without the need for
local or distant flap coverage.
  IIIB: Disruption of the soft tissue is extensive, such that local or distant flap
coverage is necessary to cover the bone. The wound may be contaminated, and
serial irrigation and debridement procedures are necessary to ensure a clean
surgical wound (see image below).


Gustilo type IIIB open fracture.

 IIIC: Any open fracture associated with an arterial injury that requires repair is
considered type IIIC. Involvement of vascular surgeons is generally required (see
image below).


Angiographic evidence of vascular injury after traumatic injury

(Gustilo type IIIC open fracture).

The soft-tissue injury component of trauma has become increasingly important with respect to fracture
treatment outcomes. The Gustilo classification has been shown to have only moderate intraobserver and
interobserver reliability in terms of fracture classification.10 The Tscherne11 and Hanover fracture scales are
classification systems that allow for a greater evaluation of the soft-tissue injury relative to wound size,
area of skin loss, and underlying soft-tissue damage.12 

The use of a classification system is important as it facilitates communication among clinicians, as well as
assists clinicians in the following: decision making, anticipating potential problems, suggesting treatment
options, predicting patient and surgical outcomes, and documenting cases.12

Frequency
Trauma causes more than 140,000 deaths per year in the United States, is the leading cause of death for
those aged 1-34 years, and causes more years of lost productivity before age 65 years than coronary
artery disease, cancer, and stroke combined.13 Each year, more than 50 million Americans undergo
medical treatment for an injury.13 The estimated lifetime cost of these injuries is over $400 billion.

Fracture incidence is multifactorial and often complicated by such factors as the patient's age, sex,
comorbidities, lifestyle, and occupation. In the United States, 5.6 million fractures occur each year,
corresponding to a 2% incidence.14 Almost 6000 fractures were treated in an orthopedic trauma unit in
Edinburgh, Scotland, in one year.15 The overall fracture incidence in the Scottish case series was 1.13% in
men and 1.16% in women. Interestingly, there was a bimodal distribution of fractures in males, with a high
incidence in young men and a second rise in men starting at the age of 60 years. In women, there was a
unimodal distribution of fractures, with a rise around the time of menopause. For a study of tibial shaft
fractures among Canadian orthopedia trauma surgeons, see Busse et al.16 For frequency of hip fractures,
see Gjertsen et al; Parker; and Holt et al.17,18,19

Etiology
Fractures occur when the force applied to a bone exceeds the strength of the involved bone. Both intrinsic
and extrinsic factors are important with respect to fractures.20 Extrinsic factors include the rate at which the
bone’s mechanical load is imposed and the duration, direction, and magnitude of the forces acting on the
bone. Intrinsic factors include the involved bone’s energy-absorbing capacity, modulus of elasticity,
fatigue, strength, and density.

Bones can fracture as a result of direct or indirect trauma. Direct trauma consists of direct force applied to
the bone; direct mechanisms include tapping fractures (eg, bumper injury), penetrating fractures (eg,
gunshot wound),21 and crush fractures. Indirect trauma involves forces acting at a distance from the
fracture site such as tension (traction), compressive, and rotational forces.

Pathophysiology
The 5 phases of fracture healing are the following22 :

1. Fracture and inflammatory phase

2. Granulation tissue formation
3. Callus formation23
4. Lamellar bone deposition
5. Remodeling

Actual fracture injuries to the bone include insult to the bone marrow, periosteum, and local soft tissues.
The most important stage in fracture healing is the inflammatory phase and subsequent hematoma
formation. It is during this stage that the cellular signaling mechanisms work through chemotaxis and an
inflammatory mechanism to attract the cells necessary to initiate the healing response. Within 7 days, the
body forms granulation tissue between the fracture fragments. Various biochemical signaling substances
are involved in the formation of the granulation tissue stage, which lasts approximately 2 weeks.

During callus formation, cell proliferation and differentiation begin to produce osteoblasts and
chondroblasts in the granulation tissue. The osteoblasts and chondroblasts, respectively, synthesize the
extracellular organic matrices of woven bone and cartilage, and then the newly formed bone is
mineralized. This stage requires 4-16 weeks.
During the fourth stage, the meshlike callus of woven bone is replaced by lamellar bone, which is
organized parallel to the axis of the bone. The final stage involves remodeling of the bone at the site of
the healing fracture by various cellular types such as osteoclasts. The final 2 stages require 1-4 years.

Patient factors that influence fracture healing include age,24 comorbidities,25 medication use,26 social

factors,27and nutrition28 (see the table below). Other factors that affect fracture healing include the type of
fracture,29 degree of trauma,30 systemic and local disease, and infection.31

Patients who have poor prognostic factors in terms of fracture healing are at increased risk for
complications of fracture healing such as nonunion (a fracture with no possible chance of healing),
malunion (healing of bone in an unacceptable position in any plane), osteomyelitis, and chronic pain.

Table. Patient factors that influence fracture healing.

Open table in new window

Factors Ideal Problematic

Age, y 24 Youth Advanced age (>40 y)
Comorbidities  25
None Multiple medical comorbidities (eg, diabetes)
Medications 26 None Nonsteroidal anti-inflammatory drugs (NSAIDs),
corticosteroids
Social factors 27 Nonsmoker Smoker
Nutrition 28, 32 Well nourished Poor nutrition
Fracture type 29 Closed fracture, neurovascularly Open fracture with poor blood supply
intact
Trauma 30 Single limb Multiple traumatic injuries
Local factors 31 No infection Local infection
Presentation
Single-limb injury 

A thorough history should be elicited for the mechanism of injury and for any accompanying or associated
events surrounding the injury; obtaining a history of any previous injury or fracture is mandatory. A
complete past medical and surgical history should also be obtained, including medications and allergies,
as well as a social (smoking and illicit drug use) and occupational history.

The physical examination must include a thorough inspection of the integument (with documentation). If
the fracture is open, a clinical photograph may be taken for documentation purposes. Distal neurologic
and vascular status must be assessed and documented. Palpate the entire limb—including the joints
above and below the injury—for areas of pain, effusions, and crepitus. Often, accompanying or
associated injuries may be present (eg, injuries to the spine with a jumping mechanism of injury).
Assessment of range of motion (ROM) may not be possible, but this should be documented.
Assessments for ligamentous injury and tendon rupture, as well as other noteworthy tests that surround a
special examination of the joints, should be completed and documented.

Multiple traumatic injuries

The initial assessment of a patient with polytrauma follows the advanced trauma life support (ATLS)
protocols33and includes the identification and treatment of life-threatening injuries.34 The first step is
evaluation of the individual's airway, breathing, and circulation. Immediate endotracheal intubation and
rapid administration of intravenous fluids may be necessary. Spinal precautions must be maintained until
injury to the complete spine can be excluded clinically and radiographically (with radiographs or computed
tomography [CT] scans). Once the patient is hemodynamically stable, the secondary survey, a complete
systems-based physical examination, is performed.

Initial management of fractures

The initial management of fractures consists of realignment of the broken limb segment and then
immobilizing the fractured extremity in a splint. The distal neurologic and vascular status must be clinically
assessed and documented before and after realignment and splinting. If a patient sustains an open
fracture, achieving hemostasis as rapidly as possible at the injury site is essential; this can be achieved
by placing a sterile pressure dressing over the injury site (see Open Fractures).

Splinting is critical in providing symptomatic relief for the patient, as well as in preventing potential
neurologic and vascular injury and further injury to the local soft tissues. Patients should receive adequate
analgesics in the form of acetaminophen or opiates, if necessary.

Management of open fractures 

The treatment goals for open fractures are to prevent infection, to allow the fracture to heal, and to restore
function in the injured limb. Once the initial assessment, evaluation, and management of any life-
threatening injury are completed, the open fracture is treated. Hemostasis should be obtained, followed
by  antibiotic administration and tetanus vaccination.

Cefazolin or clindamycin is adequate for type I and type II fracture injuries. If the wound is severely
contaminated (type III), an aminoglycoside (eg, gentamicin or tobramycin) should be added to
complement treatment. If the injury is a "barnyard injury" or water-type injury, penicillin should also be
added to provide prophylaxis againstClostridium perfringens. Tetanus prophylaxis and immunization
should be administered to patients who have not been previously immunized.

The prophylactic use of quinolones should not be used because of the rapid development of resistant
staphylococci and because quinolones are important drugs in the treatment of implant-related infections.35 

Urgent irrigation and debridement (I&D) of the wound in the operating room is mandatory. For type II and
type III injuries, serial I&Ds are recommended every 24-48 hours after the initial debridement until a clean
surgical wound is ensured. The wound is closed when it is clean and antibiotics are
generally continued until 2 days after the final I&D. 

Management of the open fracture depends on the site of injury and type of open fracture. The wound is
subsequently stabilized either temporarily or definitively. If soft-tissue coverage over the injury is
inadequate, soft-tissue transfers or free flaps are performed when the wound is clean and the fracture is
definitively treated.
Indications
Fracture management can be divided into nonoperative and operative techniques. The nonoperative
technique consists of a closed reduction if required, followed by a period of immobilization with casting or
splinting. Closed reduction is needed if the fracture is significantly displaced or angulated.36

If the fracture cannot be reduced, surgical intervention may be required. Indications for surgical
intervention include the following:

 Failed nonoperative (closed) management

 Unstable fractures that cannot be adequately maintained in a reduced position
 Displaced intra-articular fractures (>2 mm)
 Patients with fractures that are known to heal poorly following nonoperative management
(eg, femoral neck fractures)37
 Large avulsion fractures that disrupt the muscle-tendon or ligamentous function of an affected
joint (eg,patella fracture)
 Impending pathologic fractures
 Multiple traumatic injuries with fractures involving the pelvis, femur, or vertebrae
 Unstable open fractures or complicated open fractures
 Fractures in individuals who are poor candidates for nonoperative management that requires
prolonged immobilization (eg, elderly patients with proximal femur fractures)
 Fractures in growth areas in skeletally immature individuals that have increased risk for growth
arrest (eg,Salter-Harris types III-V)
 Nonunions or malunions that have failed to respond to nonoperative treatment

Contraindications

Contraindications to surgical reconstruction are as follows:

 Active infection (local or systemic) or osteomyelitis

 Soft tissues that compromise the overlying fracture or the surgical approach because of poor soft-
tissue quality due to soft-tissue injury or burns, previous surgical scars, or active infection
 Medical conditions that contraindicate surgery or anesthesia (eg, recent myocardial infarction)
 Cases in which amputation would better serve the limb and the patient
 The function of a cast is to rigidly protect an injured bone or joint. It serves to hold the broken
bone in proper alignment to prevent it from moving while it heals.

 Casts may also be used to help rest a bone or joint to relieve pain that is caused by moving it
(such as when a severe sprain occurs, but no broken bones).

 Different types of casts and splints are available, depending on the reason for the immobilization
and/or the type of fracture.

 Casts are usually made of either plaster or fiberglass material.

Fracture Types and Healing

 A fractured bone is the same as a broken bone. Most fractures happen because of a single and
sudden injury. The diagnosis of a fracture is usually made with an x-rayfilm. 

o A simple (or closed) fracture has intact skin over the broken bone.
 o An open fracture is also called acompound fracture. This means that a cut or wound
exists on the skin near the broken bone. If the cut is very severe, the edges of the bone may be
seen coming out from the wound. 

o A stress fracture can result from many repeated small stresses on a

bone.Microscopic fractures form and, if not given time to heal, can join to form a stress fracture.
These types of fractures are usually seen in athletes or soldiers who perform repetitive vigorous
activities.

o A pathologic fracture happens with minimal or no injury to an abnormal bone. This is

usually caused by an underlying weakness or problem with the bone itself, such
as osteoporosis or tumor.

 When a bone is fractured, it may require a reduction or realignment to put the ends of the
fracture back into place. A doctor will do this by moving the fractured bone into alignment with his or
her hands. If a bone has a fracture but is not out of position or deformed, no reduction is necessary.

 When the ends of the bone are aligned, the injured bone requires support and protection while it
heals. A cast or splint usually provides this support and protection.

 Many factors affect the rate at which a fracture heals and the amount of time a person needs to
wear a cast. Ask a doctor how much time the specific fracture will take to heal.

How Casts Are Applied

Many different sizes and shapes of casts are available depending on what body part needs to be
protected. A doctor decides which type and shape is best for each person. 

 Cast application 

o Before casting material is applied (plaster or fiberglass), a "stockinette" is usually

placed on the skin where the cast begins and ends (at the hand and near the elbow for a wrist
cast). This stockinette protects the skin from the casting material.
 o After the stockinette is placed, soft cotton batting material (also called cast padding or
Webril) is rolled on. This cotton batting layer provides both additional padding to protect the skin
and elastic pressure to the fracture to aid in healing.

o Next, the plaster or fiberglass cast material is rolled on while it is still wet.

o The cast will usually begin to feel hard about 10-15 minutes after it is put on, but it takes
much longer to be fully dry and hard.

o Be especially careful with the cast for the first 1-2 days because it can easily crack or
break while it is drying and hardening. It can take up to 24-48 hours for the cast to completely
harden.

 Plaster casts 

o A plaster cast is made from rolls or pieces of dry muslin that have starch or dextrose
and calcium sulfate added.

o When the plaster gets wet, a chemical reaction happens (between the water and the
calcium sulfate) that produces heat and eventually causes the plaster to set, or get hard, when it
dries.

o A person can usually feel the cast getting warm on the skin from this chemical reaction
as it sets.

o The temperature of the water used to wet the plaster affects the rate at which the cast
sets. When colder water is used, it takes longer for the plaster to set, and a smaller amount of heat
is produced from the chemical reaction.

o Plaster casts are usually smooth and white.

 Fiberglass casts 

o Fiberglass casts are also applied starting from a roll that gets wet.

o After the roll gets wet, it is rolled on to form the cast. Fiberglass casts also get warm
and harden as they dry.

o Fiberglass casts are rough on the outside and look like a weave when they dry. Some
fiberglass casts may even be colored.

Ice and Elevation

 A doctor may want the person to use ice to help decrease the swelling of the injured body part.
(Check with a physician before using ice.)

 To keep the cast from becoming wet, put ice inside a sealed plastic bag and place a towel
between the cast and the bag of ice.

 Apply ice to the injury for 15 minutes each hour (while awake) for the first 24-48 hours.

 Try to keep the cast and injured body part elevated above the level of the heart, especially for
the first 48 hours after the injury occurs.

 Elevation will help to decrease the swelling and pain at the site of the injury.

 Propping the cast up on several pillows may be necessary to help elevate the injured area,
especially while asleep.

Taking Care of Your Cast

 Always keep the cast clean and dry.

 If the cast becomes very loose as the swelling goes down, call the doctor for an appointment,
especially if the cast is rubbing against the skin.

 Cover the cast with a plastic bag or wrap the cast to bathe (and check the bag for holes before
using the bag a second time). Some drug stores or medical suppliers have cast covers—plastic bags
with Velcro straps to seal out water for protection during bathing. Avoid showers; use the bathtub and
hang the covered cast or injured body part outside of the tub while you bathe. Do not lower the cast
down into the water.

 If a fiberglass cast gets damp, dry it (make sure it dries completely). Because a fiberglass cast
allows air through it, a hairdryer on the cool setting should do the trick (do not try to dry it using a
hairdryer without a cool setting—you could burn yourself). If you have any trouble getting the cast dry,
call a doctor to find out if the cast needs to be replaced.

 If the cast gets wet enough that the skin gets wet under the cast, contact the doctor. If the skin is
wet for a long period of time, it may break down, and infection may occur.

 Sweating enough under the cast to make it damp may cause mold or mildew to develop. Call the
doctor if mold or mildew or any other odor comes from the cast.

 Do not lean on or push on the cast because it may break.

 Do not put anything inside the cast. Do not try to scratch the skin under the cast with any sharp
objects; it may break the skin under the cast. Do not put any powders or lotions inside the cast.

 Do not trim the cast or break off any rough edges because this may weaken or break the cast. If
a fiberglass cast has a rough edge, use a metal file to smooth it. If rough places irritate the skin, call
the doctor for an adjustment.
 An arm sling may be needed for support if the cast is on the hand, wrist, arm, or elbow. It is
helpful to wrap a towel or cloth around the strap that goes behind the neck to protect the skin on the
neck from becoming sore and irritated.

 If the cast is on the foot or leg, do not walk on or put any weight on the injured leg, unless the
doctor allows it.

 If the doctor allows walking on the cast, be sure to wear the cast boot (if given one by the
doctor). The boot is to keep the cast from wearing out on the bottom and has a tread to keep people in
casts from falling.

 Crutches may be needed to walk if a cast is on the foot, ankle, or leg. Make sure the crutches
have been adjusted properly before leaving the hospital or the doctor's office.

How a Cast Is Removed

 Do not try to remove the cast.

 When it is time to remove the cast, the doctor will take it off with a cast saw and a special tool. 

o A cast saw is a specialized saw made just for taking off casts. It has a flat and rounded
metal blade that has teeth and vibrates back and forth at a high rate of speed.

o The cast saw is made to vibrate and cut through the cast but not to cut the skin
underneath.

o After several cuts are made in the cast (usually along either side), it is then spread and
opened with a special tool to lift the cast off.

o The underlying layers of cast padding and stockinette are then cut off with scissors.

 After a cast is removed, depending on how long the cast has been on, the underlying body part
may look different than the other uninjured side. 

o The skin may be pale or a different shade.

o The pattern and length of hair growth may also be different.

o The injured part may even look smaller or thinner than the other side because some of
the muscles have weakened and have not been used since the cast was put on.

o If the cast was over a joint, the joint is likely to be stiff. It will take some time and
patience before the joint regains its full range of motion.

Complications

Many potential complications are related not only to wearing a cast but also to the healing of the
underlying fracture.

Immediate complications

 Compartment syndrome

o Compartment syndrome is a very serious complication that can happen because of a

tight cast or a rigid cast that restricts severe swelling.

o Compartment syndrome happens when pressure builds within a closed space that
cannot be released. This elevated pressure can cause damage to the structures inside that closed
space or compartment—in this case, the muscles, nerves, blood vessels, and other tissues under
the cast.

o This syndrome can cause permanent and irreversible damage if it is not discovered and
corrected in time.

o Signs of compartment syndrome

  Severe pain

 Numbness or tingling

 Cold, pale, or blue-colored skin

 Difficulty moving the joint or fingers and toes below the affected area.
 
o If any of these symptoms occur, call the doctor right away. The cast may need to be
loosened or replaced.
 
 A pressure sore or cast sore can develop on the skin under the cast from excessive pressure by
a cast that is too tight or poorly fitted.

Delayed complications

 Healing problems

o Malunion: The fracture may heal incorrectly and leave a deformity in the bone at the site
of the break. (Union is the term used to describe the healing of a fracture.)

o Nonunion: The edges of the broken bone may not come together and heal properly.

o Delayed union: The fracture may take longer to heal than is usual or expected for a
particular type of fracture.
 
 Children are at risk for a growth disturbance if their fracture goes through a growth plate. The
bone may not grow evenly, causing a deformity, or it may not grow any further, causing one limb to be
shorter than the other.

 Arthritis may eventually result from fractures that involve a joint. This happens because joint
surfaces are covered by cartilage, which does not heal as easily or as well as bone. Cartilage may
also be permanently damaged at the time of the original injury.

 alanced Suspension Traction

 Balanced suspension traction is used to stabilize fractures of the femur. It can be the skin or
skeletal type. If it is skeletal, a pin or wire is surgically placed through the distal end of the femur.
If it is skin traction, tape and wrapping or a traction boot of the kind described under Buck’s
traction is used.

 The patient is in the supine position, with the head of the bed elevated fro comfort. As the name
suggests, the affected leg is suspended by ropes, pulleys, and weights in such a way that traction
remains constant, even when the patient moves the upper body.

 Two important components of balanced suspension traction are the Thomas splint and the
Pearson attachment. The Thomas splint consists of a ring, often lined with foam, that circles and
supports the thigh. Two parallel rods are attached to the splint and extend beyond the foot. A
Pearson attachment consists of a canvas sling that supports the calf.

 Parallel rods lead from the pin sites on the distal and of the attachment for the rope. Traction to
the femur is applied through a series of ropes, pulleys, and weights. These weights hang freely at
the foot off the bed.

 The skin should be inspected frequently to identify problems early. The ring of the Thomas splint
can excoriate the skin of the groin. Special padding may have to be used. Again, the foot should
always be at a right angle on the footrest to prevent footdrop. If pins are used for fixation, aseptic
technique must be used around pin sites until they have healed. From then on, clean technique
can be used. The pin sites are cleansed carefully with soap and water and rinsed thoroughly,
unless this varies from policy. An antiseptic, such as povidone-iodine ointment, may then be
applied. Dressings are usually not required. You should, however, constantly assess for infection
at the pin sites. Indications include redness, heat, drainage, pain, or fever. Review your facility’s
policy on pin care.

 Skull Tongs Traction

 Skull tongs are used to immobilize the cervical spine in the treatment of unstable fractures or
dislocation of the cervical spine. Although Crutchfield tongs were used almost exclusively in the
past, Gardner-Wells skull tongs are in wide use. Some think these are less likely to pull out than
the Crutchfield tongs. The patient is prepared for either type with a local anesthetic to the scalp.
The tongs are surgically inserted into the bony cranium, and a connector half-halo bar is attached
to a hook from which traction can be applied.
 The patient is supine and is usually on a special frame instead of the regular hospital bed. If a
hospital bed is used, two or more people are required to assist the patient with any turning
movements. The head of the bed may be elevated to provide counter traction.

 Because patients remain in this type of traction for an extended period, observe the precautions
taken for the patient in other types of skeletal traction. Difficulties with the performance of
activities of daily living, infection at the tong sites, and restlessness and boredom are common. It
is useful to teach the patient range-of-motion exercises, provide good nutrition and suggest
recreational or occupational activities.

 Halo Traction

 Halo traction provides stabilization and support for fractured cervical vertebrae. The surgeon
inserts pins into the skull. A half circle of metal frame connects the pins around the front of the
head. Vertical frame pieces extend from a halo section to a frame brace that rests on the patient’s
shoulders. The halo traction allows the patient to be out of bed and mobile while stabilizing the
cervical vertebrae could injure the spinal cord.

