415

Spinal Cord Injury Rehabilitation

Chapter 16

SPINAL CORD INJURY REHABILITATION 

STEPHEN P. BURNS, MD*; BARRY GOLDSTEIN, MD, PhD†; JELENA SVIRCEV, MD‡; STEVEN STIENS, MD§; KENDRA 

BETZ, MSPT, ATP¥; JAMES W. LITTLE, MD, PhD¶; and MARGARET C. HAMMOND, MD**

INTRODUCTION

PATHOPHYSIOLOGY OF SPINAL CORD INJURY

NEUROLOGICAL ASSESSMENT AND CLASSIFICATION

INITIAL REHABILITATION

PREVENTING AND MANAGING SPINAL CORD INJURY COMPLICATIONS

ORGANIZATION OF A SPINAL CORD INJURY UNIT

SUMMARY

*Staff Physician, VA Puget Sound Health Care System, SCI (128), 1660 South Columbian Way, Seattle, Washington 98108; Associate Professor, Department of Rehabilitation Medicine, 1959 NE Pacific, Seattle, Washington 98195

†Associate Chief Consultant, Spinal Cord Injury/Disorders Services, Department of Veterans Affairs; VA Puget Sound Health Care System, SCI (128N), 

1660 South Columbian Way, Seattle, Washington 98108; Professor, Department of Rehabilitation Medicine, 1959 NE Pacific, Seattle, Washington 

98195

‡Staff Physician, VA Puget Sound Health Care System, SCI (128), 1660 South Columbian Way, Seattle, Washington 98108; Acting Instructor, Department of Rehabilitation Medicine, University of Washington, 1959 NE Pacific, Seattle, Washington 98195

§

Staff Physician, VA Puget Sound Health Care System, SCI (128), 1660 South Columbian Way, Seattle, Washington 98108; Associate Professor, Department of Rehabilitation Medicine, 1959 NE Pacific, Seattle, Washington 98195

¥

SCI Clinical Specialist, Veterans Health Administration, Prosthetic & Sensory Aids (113), 810 Vermont Avenue, NW, Washington, DC 20006

¶

Assistant Chief, VA Puget Sound Health Care System, SCI (128), 1660 South Columbian Way, Seattle, Washington 98108; Professor, Department of 

Rehabilitation Medicine, 1959 NE Pacific, Seattle, Washington 98195

**Chief Consultant, Spinal Cord Injury/Disorders Services, Department of Veterans Affairs; Chief, Spinal Cord Injury Service, VA Puget Sound Health 

Care System, SCI (128N), 1660 South Columbian Way, Seattle, Washington 98108; Professor, Department of Rehabilitation Medicine, 1959 NE Pacific, 

Seattle, Washington 98195
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Care of the Combat Amputee

INTRODUCTION

During World War II, the attitude of fatalism toward 

the spinal cord injured began to change. Advances in 

anesthesia, surgical techniques, blood transfusions, 

and antibiotics all contributed to increased survival. 

Teams of physicians, nurses, and therapists in Great 

Britain established SCI units and developed procedures for meticulous care and rehabilitation of the 

injured.7 These protocols not only allowed the injured 

to survive, but in many cases made it possible for them 

to return to their communities. 

At the conclusion of World War II, the US government, following the British model, established 

the first comprehensive SCI unit at Hines Veterans 

Administration Hospital in suburban Chicago. Over 

75% of the paraplegics from World War II were alive 

20 years later, and of the 2,500 American paraplegics 

from that war, over half returned to the job force. The 

first federally designated SCI care system center (part 

of the national Model SCI System) for civilians in the 

United States opened in 1970, and additional regional 

centers were developed through the 1970s. Fourteen 

centers are currently funded through the National 

Institute on Disability and Rehabilitation Research to 

provide comprehensive care for individuals with new, 

traumatic SCI; contribute data to the National SCI 

Statistical Center; and conduct SCI research.

With improved care, particularly of urologic and 

skin complications, late mortality (ie, after initial 

rehabilitation) from SCI also declined. Late mortality 

was 1.7 times higher for those injured in the 1940s than 

for those injured in the 1960s.8 For those injured at age 

20 and with minimal paralysis, life expectancy is only 

reduced by about 6 years. With more than minimal 

paralysis, life expectancy is progressively reduced 

across higher injury levels, with life expectancy of 

about 43 years for a person who becomes ventilator 

dependent at age 20 and survives for the first year 

following injury.9 As mortality has declined, the focus 

of SCI care has gradually shifted. Initially, the target 

was defining and adopting procedures and practices 

to control the often fatal sequelae. Now the focus also 

includes retraining individuals for independence, 

return to community, a lifetime of healthy behaviors, 

and full quality of life.

Spinal cord injury (SCI) among the US civilian 

population occurs at the rate of 11,000 new injuries 

per year. The most recent data from US National SCI 

Statistical Center indicate that young men are the most 

common demographic to sustain SCI (78% of the total 

injured are males). Although the most frequent age at 

injury is 19, the mean age at injury is 38. Impacts at 

high velocity are the most common cause of SCI. Motor 

vehicle collisions are responsible for 50%, falls for 24%, 

acts of violence for 11%, and sports for 9% of SCIs.1,2

Low-velocity gunshot injuries are responsible for most 

acts of violence that result in SCI; other penetrating 

injuries account for 0.9%, and blasts account for 0.1%.3

The most common SCI site is the cervical cord (54% 

of cases), followed by the thoracic cord (36%), and the 

lumbar cord (10%). The most common neurological 

category is incomplete tetraplegia (34.1% of all injuries; the term “tetraplegia” replaced “quadriplegia” to 

indicate a cervical neurological level, and “paraplegia” 

refers to a thoracic, lumbar, or sacral neurological 

level).1 About 253,000 Americans (roughly 0.1% of the 

US population) are traumatic SCI survivors.

The demographic profile of war-injured SCI survivors is less well documented. In Vietnam, 0.9% of those 

admitted to US Army hospitals had sustained SCI, and 

3.8% of those patients died during initial hospitalization.4

 In various Israeli wars, the percentage of those 

injured by gunshots to the spinal cord varied between 

0.2% during the War of Independence in 1948–1949 

and 1.1% in the Sinai Campaign of 1956.5 As of December 31, 2008, 432 active duty US service members 

serving during Operations Enduring Freedom and 

Iraqi Freedom sustained SCI and received treatment 

in Department of Veterans Affairs SCI units. Of these 

individuals, 141 were injured in theater.

From the time the first recorded description of SCI 

was written on Egyptian papyrus until World War 

II, SCI was viewed as “an ailment not to be treated.” 

Death following SCI commonly ensued from uncontrollable urinary tract infections (UTIs) and pressure 

ulcers. During the Balkan Wars of 1912–1913, 95% of 

soldiers with SCI died within a few weeks. During 

World War I, 80% of overseas American troops with SCI 

died before they could return to the United States.6

PATHOPHYSIOLOGY OF SPINAL CORD INJURY

The two primary types of traumatic SCI mechanisms 

are penetrating and nonpenetrating injuries. Penetrating injuries typically result from a bullet, fragment, or 

knife blade directly lacerating the spinal cord. Penetrating injury accounts for only 17% of traumatic SCI in 

the civilian population, and nearly all of these are due 

to gunshots. Nonpenetrating injuries commonly result 

from bone or herniated disk material compressing the 

spinal cord or cauda equina, or from traction from spinal dislocation. In the civilian population, automobile 
417

Spinal Cord Injury Rehabilitation

and motorcycle crashes, falls, and sports injuries are the 

primary causes of nonpenetrating SCI. Blast injuries 

cause SCI through secondary effects (eg, fragments 

that penetrate the spinal canal) or tertiary effects (eg, 

nonpenetrating injuries from acute angulation or 

loading of the spine due to blast wind, structural collapse, or deceleration after being thrown by a blast).10

Penetrating and nonpenetrating SCI may involve vertebral fracture with displacement of bony fragments 

into the spinal canal, or ischemia due to disruption in 

the blood supply to the cord. Nonpenetrating injuries 

often result in ligament disruption, with instability and 

resulting vertebral malalignment. Individuals with 

narrow spinal canals, either congenital or acquired due 

to degenerative changes, are at greater risk for cord 

injury, even from relatively minor trauma. 

Penetrating and nonpenetrating injuries may 

compromise gray matter, white matter, and nerve 

roots. Gray matter contains motor neurons that provide output to muscles and interneurons that receive 

descending motor and segmental reflex input. Gray 

matter is thought to be more vulnerable to mechanical 

trauma than white matter because it is relatively more 

vascular. Gray matter damage typically extends one 

or two segments rostral and caudal to the cord injury, 

but may be more extensive if the cord blood supply 

has been disrupted. All segments involved compose 

the “zone of injury.” Damage to gray matter causes 

segmental changes with denervation, muscle atrophy, 

and impaired reflexes. White matter is comprised of 

ascending and descending fibers at the periphery of the 

cord. Pathologic studies of cord trauma show greater 

gray than white matter involvement.11–13 Damage to 

white matter is more disabling because it results in 

loss of motor control and sensory input at and below 

the injury site, and hypertonia and hyperreflexia accompany weakness and sensory loss with such white 

matter involvement. Nerve root injury often results in 

an asymmetric level of injury.

Spinal cord damage can also arise indirectly from 

vascular disruption. Thus, cross clamping of the thoracic aorta or disruption of the artery of Adamkiewicz 

or a vertebral artery can result in cord ischemia or 

infarction.14–16 Another type of ischemic cord injury is 

decompression sickness, in which hyperbaric exposure 

(as in underwater diving) followed by sudden decompression results in gas bubble formation and bubble 

emboli that occlude blood vessels.17,18

In the majority of cases, the spinal cord is not completely transected anatomically, and secondary processes contribute to the degree of neurological deficit. 

These processes include ischemia, edema, hematomyelia, demyelination, persisting mechanical pressure, 

lactic acidosis, intracellular influx of calcium, increase 

of lipid peroxidation, and free radical formation.19–22

Various early treatments, such as hyperbaric oxygen, 

cord cooling, naloxone, thyrotropin-releasing hormone, 

and osmotic diuretics, have been proposed to minimize 

this secondary neurologic injury.22 Methylprednisolone 

has been investigated in three multicenter trials as a 

neuroprotective agent following acute SCI,23–25 and it 

may modestly improve neurological outcomes when 

given within 8 hours of nonpenetrating SCI. However, 

trial findings have been questioned,26 and there are 

concerns about increased infection rates with use of 

methylprednisolone. GM-1 gaglioside showed promising results as a neuroprotective agent in an early 

trial, but a multicenter trial with 760 subjects failed to 

show any benefit in the primary neurologic outcome.27

Another intervention to promote recovery is late (ie, 

1–12 months after SCI) anterior decompression. This 

procedure reportedly allowed functional recovery in 

subjects with incomplete SCI, and residual cord or root 

compression for those whose recovery had plateaued 

for 4 weeks or more.28

Animal models of incomplete SCI demonstrate 

that much of the spontaneous neurologic recovery is 

mediated by spared white matter axons that substitute 

for those pathways that have degenerated, rather than 

by resolution of conduction block, remyelination or 

resolution of ischemia, or edema. The mechanisms that 

allow for this substitution of function by spared pathways likely include rapid-acting denervation supersensitivity and slower-acting synaptogenesis. When 

spared, descending white matter pathways and spinal 

reflex pathways undergo trauma-induced reactive synaptogenesis, which may result in both motor recovery 

and spinal hyperreflexia. The slow pace of this motor 

recovery and the gradual onset of spasticity may be 

explained by the slowness of synaptogenesis. Because 

neural activity seems to be a necessary condition for 

such recovery, one way to enhance this process may 

be to increase the activity in the spared neural pathways.29 In animal models of stroke, administration of 

central nervous system stimulants (eg, amphetamine), 

combined with exercise, has enhanced recovery. These 

observations suggest that remobilization of the patient 

and active exercise are essential factors in optimizing 

recovery of function after SCI.

Medications and growth factors are unexplored 

methods of regulating activity in the cord’s spared neural pathways. The optimal treatment for minimizing 

developing spasticity during this period of recovery is 

also unresolved. With stroke patients, some advocate 

reflex facilitation during strengthening exercises to 

enhance motor recovery; however, this may result in 

greater spasticity. Alternatively, aggressive early treatment with medication and physical modalities may 
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Care of the Combat Amputee

suppress the development of spasticity, but it may not 

optimize recovery of motor function. Resolving these 

issues will allow more effective rehabilitation of acute, 

incomplete SCI in the future.

In contrast to white matter or long-tract recovery, 

zone-of-injury recovery involves recovery of lower 

motor neurons (gray matter recovery) and roots at the 

site of injury.30,31 Mechanisms to explain zone-of-injury 

recovery include resolution of conduction block, reactive synaptogenesis by descending pathways in the 

spinal cord, motor axon sprouting by lower motor neurons,32 and muscle fiber hypertrophy. These recovery 

mechanisms mitigate upper and lower motor neuron 

weakness, both of which can be identified electrophysiologically.33 The optimal rehabilitation interventions 

for these two types of weakness are not yet known.

NEUROLOGICAL ASSESSMENT AND CLASSIFICATION

The methods described in the International Standards for Neurological Classification of Spinal Cord Injury 

are the most widely used ways of classifying SCI.34,35

Commonly referred to as “the American Spinal Injury 

Association (ASIA) classification,” this assessment 

requires manual muscle testing of 10 key muscles 

bilaterally (Table 16-1), sensory testing for light touch 

and sharp/dull discrimination in all dermatomes, and 

a rectal exam for sensation and presence of voluntary 

anal contraction. These tests are used to classify injury 

levels and ASIA Impairment Scale (AIS) grade (Figure 

16-1). The sensory level is the most caudal level with 

normal light touch and sharp/dull discrimination 

(provided that all rostral levels are normal), and is 

defined separately for the right and left sides. Motor 

level is defined as the most caudal level that is grade 3 

or greater with all rostral levels normal (grade 5), and 

it is also defined separately for the right and left sides. 

If the sensory level falls in a segment where there are 

no corresponding limb muscles to test (levels C2–C4, 

T2–L1, or S2–S4/5), the motor level is assumed to be 

the same as the sensory level. A single neurological 

level can be derived from the four levels (right and 

left motor, right and left sensory) by taking the most 

rostral of the four; however, motor level is more closely 

associated with functional capacity. 

The AIS grade is a measure of the completeness of 

SCI. A complete injury is one in which no sensory or 

motor signals traverse the entire zone of cord injury. 

Because sparing of sensation or motor is most likely 

to occur in the sacral segments, the classification has 

been standardized to examine neurologic function in 

this region for the purpose of classifying injury completeness. An AIS score of A indicates a complete SCI 

and is defined as the absence of sensory and motor 

function in segments S4–5. AIS B is an incomplete SCI, 

with preservation of sensory function but not motor 

function below the injury level (patients may have 

some motor function in the segments adjacent to the 

neurological level, but it does not extend more than 

three segments below the neurological level). AIS C

indicates an incomplete SCI, with motor function preserved below the neurological level and the majority 

of muscles below the neurological level having less 

than grade 3 strength. AIS D indicates an incomplete 

SCI, with motor function preserved below the neurological level and at least half the muscles below the 

neurological level with muscle grade 3 or greater. AIS 

E indicates the patient had an SCI but made a complete 

neurologic recovery for all sensory and motor functions used in this classification. The exam required 

for this classification system does not involve deep 

tendon reflexes or muscle spasticity, and the muscles 

selected for the examination are not necessarily those 

TABLE 16-1

NEUROLOGIC EVALUATION: MYOTOMAL 

LEVELS

Level Area of Sensation

C-1,-2,-3 Trapezius, SCM, upper cervical 

paraspinals, prevertebral neck muscles

C-4 Diaphragm

C-5 Biceps brachii, brachialis

C-6 Extensor carpi radialis longus

C-7 Triceps brachii

C-8 Flexor digitorum profundus (3rd digit)

T-1 Abductor digiti minimi, 1st dorsal 

interosseus

T-6,-7,-8,-9,-10 Beevor’s sign*

L-2 Iliopsoas, hip adductors

L-3 Quadriceps femoris

L-4 Tibialis anterior

L-5 Extensor hallucis longus, hip abduction

S-1 Gastrocnemius, soleus

S-2,-3,-4 Anal sphincter

*Beevor’s sign represents upward movement of the umbilicus when 

the patient attempts a sit-up from supine lying.

SCM: sternocleidomastoid

The italicized muscles are the standard muscles used by the American Spinal Cord Injury Association for classifying injury level.1

 These 

muscles are innervated by more than one root level, but reduction 

to a representative level is useful for injury classification. 

(1) American Spinal Injury Association. International Standards for 

Neurological Classification of Spinal Cord Injury. Chicago, Ill: ASIA; 

2000.
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Spinal Cord Injury Rehabilitation

Figure 16-1. Standard neurological classification of spinal cord injury worksheet produced by the American Spinal Injury 

Association.

Reproduced with permission from: American Spinal Injury Association. International Standards for Neurological Classification 

of SCI. Chicago, Ill: ASIA; 2002.
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Care of the Combat Amputee

of the most functional importance. 

It has been reported that early neurological classification reliably predicts the classification of civilian SCI 

at follow up. Earlier studies focused on the examination 3 to 7 days after injury, but it appears the initial 

emergency department examination has high predictive value when distracting facts, like intoxication or 

brain injury, have been removed.36 For example, of 

patients with initial AIS A injuries and no distracting 

factors, 6.7% converted to AIS B and none converted 

to AIS C or D at 1 year following initial examination. 

In the presence of factors affecting the exam reliability, 

17.4% of those with initial AIS A scores converted to 

AIS B, and 13% converted to AIS C. Sparing of sharp/

dull discrimination in sacral dermatomes is favorable 

for motor recovery to a degree that allows ambulation, 

possibly due to a similar location of corticospinal and 

spinothalamic tracts within the spinal cord.37 The prognosis for improvement in AIS grade is much better for 

those initially classified AIS B, with 54% converting to 

AIS C or D. Patients initially classified AIS C or D often 

show large improvements in neurologic function; a 

trace of toe movement in the first few days after injury 

is highly favorable for functional recovery. Motor function typically descends at least one level between the 

acute exam and 1-year follow-up. Nearly all muscles 

near the injury level that initially show grade 1 on 

manual muscle test will regain at least grade 3 strength 

by follow-up.31

Various SCI clinical syndromes have been described 

(Table 16-2).38 Several relate to the presumed extent 

of the cord injury in the transverse plane, such as 

Brown-Séquard, central cord, and anterior cord syndromes. Brown-Séquard syndrome is attributed to a 

cord hemisection and is often the result of a penetrating injury, such as a knife or gunshot wound. The 

prognosis for return of functional ambulation and 

voluntary bladder control following Brown-Séquard 

syndrome is good.39,40 Central cord syndrome is a 

cervical-level, motor-incomplete injury with greater 

weakness in upper versus lower limbs. Central cord 

syndrome often occurs from a cervical hyperextension 

injury in the presence of an underlying narrow cervical canal, either from congenital or acquired stenosis. 

Bony fractures or instability are often absent. Anterior 

cord syndrome typically results from a cervical burst 

fracture or disk herniation, impinging on the anterior 

spinal artery, anterior cord, or both. It is not known 

whether direct mechanical pressure or disruption of 

arterial blood flow is the major cause. The likelihood 

of a return of lower limb function in anterior cord 

syndrome is reduced.

Cauda equina syndrome results from injury below 

the termination of the spinal cord (levels L-1–L-2), 

damaging the anterior and posterior roots, but sparing 

the cord itself. Midline lumbar disk herniations and 

major trauma (eg, gunshot wounds or seatbelt injuries) 

are common causes of cauda equina injury. Prognosis 

for functional recovery is good because the roots are 

less vulnerable to mechanical trauma than the spinal 

TABLE 16-2

SPINAL CORD INJURY CLINICAL SYNDROMES

Clinical Features Prognosis

Central Cord Common; greater weakness of upper limbs than lower Often recover bladder and bowel function/

limbs control and ambulation

Brown-Séquard Common; unilateral impaired pain and temperature Usually recover bladder and bowel 

sensation contralateral to the more paretic side; function/control and ambulation

unilateral impaired vibration and position sense 

ipsilateral to the paretic side

Anterior cord Uncommon as pure syndrome; loss of motor, pain, and Functional recovery uncommon

temperature, with preserved vibratory and 

proprioception

Posterior cord Rare; absent position and vibratory sensation; intact Usually recover bladder and bowel 

pain and temperature sensation function/control and ambulation

Cauda equina About 10% of all cord injuries; often motor incomplete Commonly recover bladder and bowel 

and with asymmetric deficits function/control and ambulation

Conus medullaris Mixed upper motor neuron and lower motor neuron May recover ambulation; less likely to 

findings through lumbar and sacral myotomes recover bladder and bowel control
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Spinal Cord Injury Rehabilitation

cord. In addition, motor axons have some capacity for 

regeneration to proximal muscles and to the bladder.41

Conus medullaris syndrome involves damage to the 

spinal cord at the lumbar or sacral segments, resulting 

in bowel, bladder, and sexual dysfunction, with some 

upper motor neuron findings present due to sparing 

of the terminal portion of the conus, and lower motor 

neuron findings due to root injury or direct compression of lower motor neuron cell bodies. In cases where 

the entire conus has been injured at its termination at 

level L-1 or level L-2, the clinical findings are identical 

to cauda equina syndrome. 

“Spinal shock” represents depressed spinal reflexes 

and weakness caudal to an SCI. This is likely caused 

by loss of normal tonic descending facilitation because 

a block of conduction in suprasegmental pathways 

results in hyperpolarization of cord neurons.42 Spinal 

reflexes gradually return over days to months, typically becoming hyperactive leading to spasticity, flexor 

and extensor spasms, and hypertonia.43,44 Some reflex 

activity may return as early as 24 hours after complete 

SCI, such as the bulbocavernosus reflex or the tibial 

H-reflex, even though tendon reflexes usually return 

weeks or months later in patients with complete injuries. In those with incomplete SCI, tendon reflexes and 

spasticity may appear within days of the injury.45 Spinal shock is not observed if the myelopathy develops 

gradually, as is often seen with a cord tumor, cervical 

stenosis, or syringomyelia. Presumably, hyperactive 

reflexes, such as a Babinski sign and ankle clonus, 

develop before overt weakness because mechanisms 

of neuroplasticity (such as sprouting by reflex afferents 

and spared descending pathways) mediate hyperreflexia and spared voluntary movement.

INITIAL REHABILITATION

Functional Outcome

Rehabilitation goals vary according to the level of 

injury and the extent of damage to the spinal cord. 

When the injury is motor-complete (AIS A or B), the 

functional outcome depends to a large degree on the 

level of injury. The lower the injury is on the cord, 

the more voluntary movement is preserved and the 

greater the expectations for independence. Expected 

functional outcomes for the average person with SCI 

may be found in recent clinical practice guidelines.46

Mobility

Mobility is essential to resuming life outside the 

hospital. In teaching mobility, self-care, and other 

functional tasks, the following general principles apply: (a) start with the simple and move toward the 

more complex; (b) break tasks down into components, 

beginning with discrete units that can be learned 

separately and then combined into completed units; 

and (c) teach patients to substitute for weakened or 

absent muscles with head motions, momentum, and 

preserved muscles. The expected optimal outcome for 

a given patient, based on the level and the completeness of the injury, dictates how and which muscles 

should be trained (Table 16-3).46

Mobility encompasses a spectrum of movement, 

including bed mobility (ie, turning from side to side, 

moving from supine to sitting), sitting balance, wheelchair transfers (ie, from wheelchair to bed, wheelchair 

to car, and wheelchair to floor), standing balance, 

and ambulation (wheelchair or walking). Each task is 

mastered in physical therapy.

Wheelchair Use

One of the first objectives of therapy for the spinal 

cord injured is to get the patient sitting upright, a task 

usually attended to by physical therapists and nurses. 

During this procedure, the patient is monitored closely 

for orthostatic hypotension (OH), a common condition 

brought on by prolonged bed rest and the deficient 

vasoconstriction that accompanies disruption of the 

sympathetic nervous system. Tilt tables and reclining 

wheelchairs can aid in achieving upright posture. Progressively increasing the verticality of a tilt table challenges the cardiovascular system, which eventually 

improves systolic blood pressure and cerebral blood 

flow in the upright sitting and standing positions. For 

expected wheelchair users, the same can be achieved at 

the bedside in a reclining wheelchair with elevating leg 

rests; therapy staff can immediately recline the chair if 

a patient develops symptomatic hypotension.

As the patient regains mobility, spinal alignment and 

neurologic status may be affected. If this is suspected, 

frequent radiographs and neurologic examinations are 

required to be certain that gravity, postural changes, 

and muscular forces do not compromise alignment. 

The wheelchair is a patient’s key to mobility, and 

helping the patient select the correct chair is a complex 

task. The chair should be custom fit according to the 

user’s pelvis width, trunk height, and leg, thigh, and 

forearm length. A clinician must review the wheelchair setup and make appropriate adjustments to 

ensure proper posture and seating. The chair should 

be efficient, appropriately stable, maneuverable, and 

matched to the strength and coordination of the user; 

a manual wheelchair that is configured to allow one 
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Care of the Combat Amputee

patient to negotiate a curb with a “wheelie” may put 

another at risk for a dangerous fall. Extra features to 

consider include antitip devices, lap trays, arm rests, 

and foot and leg supports. Aesthetics and cost must 

be considered as well. Proper training is essential for 

long-term protection of the upper extremities.47

An individual with tetraplegia as high as the C-5 

level may be able to propel a manual wheelchair. Propulsion for individuals with C-5 level cervical injuries 

is possible by using the biceps brachii, brachialis, and 

anterior deltoid muscles in a closed kinetic chain to 

convert the regular elbow–shoulder flexion to elbow 

extension when the hand is fixed on a wheelchair handrim by friction. The benefits to operating a manual 

wheelchair include greater upper limb and cardiovascular exercise, having a backup means of mobility in 

the event that a power wheelchair malfunctions, and 

the ability to travel in a passenger car without a wheelchair lift or ramp. Despite this, most C-5 level manual 

wheelchair users will require a power chair for outdoor 

mobility involving distances, rough terrain, or grades. 

For many of these individuals, power wheelchairs are 

the only feasible means of mobility. Fit and function 

should be considered when selecting power chairs as 

TABLE 16-3

EXPECTED FUNCTIONAL OUTCOME FOR COMPLETE SPINAL CORD INJURY

Cord Level Preserved Muscle Eating Dressing Transfers Mobility Writing

 Indoor Outdoor

C-1, -2 Trapezius, sternocleidomastoid D D D lift or pivot I I I

 Power WC Computer

 Sip and puff Sip and puff

C-3, -4 Diaphragm, neck flexor/extensor D D D lift or pivot I I I

 Chin control Mouth stick

C-5 Deltoid, biceps I cuff D D lift or pivot I I I

 Power WC cuff

C-6 Serratus anterior, extensor I I? I? loops I I? I

carpi radialis sliding board (+/– power WC)

C-7 Triceps I I reachers I I I I

adapted Manual WC

clothes

C-8 to T-1 Hand intrinsics I I I I I I

 Manual WC

T-2 to T-6 Intercostals, paraspinals I I I I I I

 Manual WC

T-7 to T-12 Abdominals I I I I I I

 Manual WC

L2 Iliopsoas I I I I I I

 (+ manual WC)

L-3 Quadriceps I I I I I I

 (+/– manual WC)

L-4, -5 Tibialis anterior, extensor I I I I I I

hallucis longus Crutches AFOs

L-5 to S-1 Hamstrings, gluteus medius I I I I I I

 AFOs AFOs

S-1, -2 Gluteus maximus, I I I I I I

gastrocnemius-soleus

S-3, -4 Anal/urethral sphincters I I I I I I

AFO: ankle-foot orthosis I: independent pivot: quad pivot transfer

cuff: universal cuff I?: possibly independent WC: wheelchair

D: dependent lift: hydraulic lift transfer
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Spinal Cord Injury Rehabilitation

well, as should the method of control (eg, manual joystick, chin, sip-and-puff straw, mouth stick, or tongue; 

Figure 16-2). For these patients, reclining mechanisms 

are essential to minimize the risk of skin breakdown. 

Two such mechanisms are the zero-shear mechanism 

and the tilt-in-space recline. The latter is less likely to 

elicit extensor spasms (Figure 16-3).

Walking

Some patients will progress from sitting to walking. Ambulation goals differ depending on the level 

of the SCI and whether the cord injury is complete or 

incomplete. For motor-complete SCI in the absence 

of lower limb movement, the goals are exercise and 

short-distance mobility on level surfaces. Those with 

complete injuries at the T-6 level or below with no other 

major medical complications are the usual candidates 

for this training. Contraindications include limited 

lumbar spine extension or limited hip, knee, and ankle 

joint motion. Initially, patients are taught to stand between parallel bars and maintain balance without arm 

Figure 16-2. A chin joystick controller can be mounted on a 

boom attached to the chair frame (as shown) or on a plastic 

yoke placed over the sternum. In addition to driving the 

power wheelchair, it can be used to operate a tilt-in-space 

mechanism or environmental control unit.

support, using temporary knee-ankle-foot orthoses. 

They then learn to walk with a swing-through gait, 

using the parallel bars for support. With this gait, 

upper body center of gravity must be behind the axis 

of rotation of the hip joint to maintain hip extension 

(Figure 16-4). The energy expended for this type 

of walking can be as much as 800% of that of ablebodied walking and manual wheelchair propulsion.48

Swing-through walking also requires considerable 

motor coordination and can place excessive loads 

across the upper limb joints. Previously, this form 

of ambulation was considered a goal for all young 

patients with new paraplegia, but that has changed 

in recent years because most patients did not continue to ambulate after discharge from the hospital. 

Only those who demonstrate progress and sustained 

motivation with temporary bracing should be fitted 

with custom knee-ankle-foot orthoses and proceed 

to learning a swing-through gait, which requires use 

of forearm crutches.

For individuals with some preserved lower limb 

movement, the goals vary from assisted standingpivot transfers to long-distance ambulation, depending on the extent of motor and proprioceptive 

function and the degree of spasticity. For those with 

considerable sparing and rapid recovery, therapy is 

primarily the reconditioning of muscles that have 

atrophied from disuse. Those with little sparing and 

slow recovery require months of spontaneous healing, strengthening, and functional training. For the 

latter, recovery is less complete and spasticity often 

interferes with movement, although extensor spasms 

can aid standing.

Activity-Based Therapy

In past years, there has been a relatively static view 

of neuroplasticity and neurologic recovery following 

SCI. Most interventions were pharmacologic and surgical, with the intention of minimizing the primary 

injury and secondary effects, such as edema. As general knowledge of plasticity and remodeling in the 

central nervous system has grown, there is renewed 

interest in developing therapies to stimulate these 

processes and enhance functional recovery. Physical 

rehabilitation strategies have recently been employed 

for these purposes.

Activity-based therapy is now advocated by many 

rehabilitation centers throughout the world. The 

general approach is to use neuromuscular activity 

below the level of an incomplete SCI to stimulate 

neuroplasticity and promote recovery of function. 

Locomotor training is the most well-developed 

activity-based therapy.49,50,51 Bodyweight support 
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Care of the Combat Amputee

and a treadmill, overground ambulation with upper 

limb aids, electrical stimulation during walking to 

activate the neuromuscular system, and functional 

electrical stimulation bikes are used for locomotor 

training. 

Spinal Cord Injury Complicated by Concomitant 

Traumatic Amputation

Review of data from Operations Iraqi Freedom and 

Enduring Freedom reveals that the incidence of SCI 

and amputation is low, albeit with a high functional 

impact. In addition to managing the multitude of 

medical issues associated with both SCI and amputation, specific attention must be directed toward 

identifying and managing heterotopic ossification 

(HO), which is a known complication after SCI52 and 

combat amputations.53

The functional impact of SCI complicated by 

amputation depends on the level of SCI, AIS grade, 

and the anatomic location of the amputation. When 

amputation level can be elected, consideration should 

be given to preserving length in individuals without 

SCI. An individual with SCI who will be a full-time 

Figure 16-3. Power wheelchair with tilt-in-space mechanism 

for relieving pressure on the skin near the ischial tuberosities. 

The chair is driven using a joystick controller. (a) The seat 

elevation feature can be used to allow a user to reach high 

objects. (b) Seat tilt and recline help prevent pressure ulcers, 

reduce discomfort, and lower swelling in the legs.

wheelchair user will be affected differently by an 

amputation than an individual with SCI presentation 

consistent with partial or full-time ambulation. For 

the wheelchair user, a lower limb amputation must be 

considered relative to the prescribed seating system because a unilateral amputation is likely to cause postural 

compromise. Specific modifications may be needed 

to provide postural support and skin protection. The 

functional impact of lower extremity amputation can 

be minimized for wheelchair users who acquire compensatory techniques to optimize balance and stability 

while performing self-care tasks and mobility skills. 

For individuals with SCI who can stand and walk, the 

impact of lower limb amputation is a greater challenge 

because the individual may desire to use a prosthetic 

leg despite impaired neuromuscular function in the 

residual limb and trunk. Given the known significant 

physical requirements for prosthetic limb use and 

the additional demands resulting from SCI-related 

impairments, part-time or intermittent wheelchair 

use should be considered. Upper limb amputation in 

individuals with SCI creates significant self-care and 

mobility challenges and indicates a high risk for upper limb pain and injury due to repetitive strain of the 

intact arm. Clinical interventions and patient education 

must be targeted toward optimizing functional skills 

while preserving remaining upper limb function, as 
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Spinal Cord Injury Rehabilitation

supported by published clinical practice guidelines.47

This may be partially addressed by providing a power 

wheelchair with power seat functions. Regardless of 

level of SCI, AIS, or amputation location, maintaining 

normal range of motion across all joints, maximizing 

strength of innervated muscles, developing efficient 

mobility skills, and learning joint preservation techniques are critical to optimize functional outcomes 

and long-term quality of life. 

Driver’s Training and Community Mobility

Automobiles usually provide the greatest convenience and flexibility for accessing the community and 

participating in vocational and avocational activities. 

Some patients with motor-complete (AIS A or B) injuries as high as level C-5 can learn to drive with hand 

controls, although even at the C-6 level, a specialized 

van with sensitized steering and braking is often 

required. Those with SCI at level C-7 or lower can 

often use a passenger car with hand controls, provided they have the ability to transfer themselves 

and stow their wheelchairs independently. Vision, 

including visual scanning (the absence of which 

can sometimes be compensated for with panoramic 

and side mirrors), reaction time, absence of seizures, 

adequate spasm control, cognitive awareness, hand 

function, transfer skills, and a financial source for the 

necessary equipment and insurance are additional 

factors determining whether or not a patient is a 

candidate for driver’s training. Adaptations may 

include hand controls for brakes and gas, steering 

wheel attachments, power seats, and vans with 

wheelchair lifts or ramps.

Self-Care

Along with increasing mobility, minimizing the 

need for assistance in self-care is a major step toward 

independence for those with SCI. Self-care includes 

feeding, bathing, dressing, grooming, and toileting. 

Those with motor-complete injuries at the C-7 level or 

below can usually achieve independence in all of these 

activities. Occupational therapists and rehabilitation 

nurses work with patients to master new techniques 

for accomplishing these tasks. Alternate strategies, 

such as using a tenodesis grip (which uses wrist extension to passively flex fingers) for holding eating 

utensils or writing implements, must be learned and 

mastered. A wrist-driven, flexor-hinge splint improves 

Figure 16-4. Swing-through gait.
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Care of the Combat Amputee

the strength of a tenodesis grip. Other special equipment such as reachers, universal cuffs, built-up handles 

on utensils, and tub benches also aid independence. 

Tendon transfers54 or implantable functional electrical 

stimulators55 may achieve a more functional pinch, 

but costs and training time are considerable. Full independence and self-management of the neurogenic 

bladder and bowel is a goal for patients with a motor 

level of C-7 or caudal.

Partial independence may be achieved with level C-6 

or level C-5 motor-complete injury. For those tasks that 

require assistance, the patient is shown how to teach 

others to complete the task and a caregiver is instructed 

in how to help with the activity. For example, the assistance needed for self-feeding may include fitting a 

universal cuff and utensil on a patient, positioning food, 

opening containers, and cutting meat. With similar 

assistance, some grooming and hygiene tasks, such as 

combing hair, brushing teeth, shaving, and washing 

face and upper body, may be mastered. With motorcomplete injury at a C-4 level or rostral, a person will 

typically be dependent for all self-care activities.

Living Skills

Living skills (eg, meal preparation, shopping, check 

writing, housekeeping, etc) are necessary tasks of 

everyday life and must be relearned and adapted to a 

patient’s needs. These skills are often reacquired with 

the help of occupational therapists. Again, reachers 

and other specialized equipment are used as aids and 

spared muscles substitute for paretic muscles, a motor 

learning task that requires practice. These tasks can 

usually be managed by patients with injuries sparing 

level C-7 or more. Those with higher injuries need 

assistance, including environmental control systems 

and computers. These can be accessed via mouth stick, 

sip-and-puff, tongue touch pads, eye movements, or 

voice. Environmental control systems allow the use of 

telephones, appliances, sound equipment, intercoms, 

televisions, lights, and door openers—all items that 

can be accessed by remote control. The complexity 

of the system will vary according to the extent of the 

impairment and the patient’s financial resources. The 

use of a computer, accessed through the keyboard 

using hand or mouth sticks, head controls, or voice 

activation, allows a degree of control and a range of 

communication, vocation, and recreation options.

Vocational and Avocational Pursuits

Tools to help patients explore available vocational 

and avocational opportunities include psychological 

testing, vocational counseling, assessing physical 

capacities, vocational remediation and training, identifying sources of financial assistance to support training and education, peer counseling, and job-seeking 

guidance. Rehabilitation staff can also communicate 

with potential employers. Hiring an individual with 

a disability can raise issues about physical accommodations for a disabled person and the psychology of 

responding to someone who is permanently disabled. 

Providing technical assistance for workspace modifications and information about disability can also aid 

patients in their employment pursuits.

Healthcare providers should organize and encourage outings for SCI patients, such as attending sporting 

and cultural events, eating at restaurants, and shopping. Many individuals with SCI will want to return 

to a form of physical exercise or sport, although they 

may initially be apprehensive. They should be made 

aware that numerous activities have been successfully 

pursued by people with SCI (Exhibit 16-1).

Patient and Family Education

Families are critical to helping patients adjust to 

disability. Initially, the concerns of the patient and 

family often center on prognosis for neurological and 

functional recovery. Response to these concerns should 

respectfully acknowledge the uncertainty and difficulty a patient may have in accepting new limitations. 

EXHIBIT 16-1

EXAMPLES OF ACTIVITIES AVAILABLE 

TO INDIVIDUALS WITH SPINAL CORD 

INJURIES 

	 •	 archery

	 •	 boating

	 •	 football

	 •	 camping

	 •	 hunting

	 •	 flying

	 •	 golf

	 •	 scuba diving

	 •	 swimming

	 •	 sailing

	 •	 basketball

	 •	 table tennis

	 •	 weight lifting

	 •	 tennis

	 •	 horseback riding

	 •	 wheelchair racing

	 •	 wheelchair dancing

	 •	 sit skiing
427

Spinal Cord Injury Rehabilitation

Hope, even if based on an improbable outcome, helps 

patients cope with the initial grief that accompanies 

disability. Acceptance of the new reality generally 

comes with time. Patients and their families can be 

convinced of the need to learn alternate methods of 

mobility and self-care.

The focus during rehabilitation is to educate the 

patient, family, and caregivers on the nature of SCI, 

maximizing health, and accessing community resources. Educational topics include the following:

	 •	 level and completeness of the SCI, which

determine the anatomic and physiological 

correlates;

	 •	 prognosis for motor recovery and spasticity;

	 •	 current research on spinal cord regeneration

and new technology;

	 •	 care of neurogenic bladder and bowel;

	 •	 prevention of skin breakdown;

	 •	 management of autonomic dysreflexia (AD),

if applicable;

	 •	 psychological adjustment to disability;

	 •	 attendant care management;

	 •	 sexuality,impairedsexualfunction,andfertility;

	 •	 vocational and educational options;

	 •	 avocational outlets, such as wheelchair

sports;

	 •	 finances; and

	 •	 housing.

Various educational tools can be used, such as patient manuals for instruction and reference, weekly 

class discussions, peer interaction, and one-on-one 

instruction provided by each member of the rehabilitation team. Intake and discharge meetings with the 

rehabilitation team further complement instruction. 

The intake meeting defines specific goals for the hospitalization and addresses specific questions related 

to prognosis and course of treatment. The discharge 

meeting discusses plans for follow up, equipment 

needs, and accessing community resources. Family 

members and other caregivers of partially dependent 

patients need to be instructed in their roles. Onsite independent-living apartments allow patients and their 

caregivers to rehearse tasks, such as shopping, meal 

preparation, transfers, toileting, and bathing, with staff 

backup. Day and weekend passes can also be granted 

once a patient is medically stable and sufficiently 

trained in self care and mobility. Patients can practice 

their recently acquired mobility and self-care skills 

by participating in community outings organized by 

a recreation therapist. These outings typically include 

activities such as taking public transportation, visiting 

shopping malls, going to movies, grocery shopping, 

banking, and eating in restaurants.

Housing, Finances, and Community Reintegration

Social workers can help patients understand social 

security disability, Veterans Affairs and Medicare/

Medicaid benefits, separation from the military, accessible housing, housing modifications, advocacy groups 

for the disabled, and legal resources and protections. 

Occupational therapists can help patients understand 

accessibility features, such as ramp inclines and door 

widths.

PREVENTING AND MANAGING SPINAL CORD INJURY COMPLICATIONS

Mortality and morbidity due to SCI are higher in 

patients with tetraplegia than paraplegia and complete 

injuries compared to incomplete injuries, both acutely 

and chronically. Medical complications associated 

with SCI commonly occur during the first few months 

following the injury, and patients are frequently 

rehospitalized to treat acute medical conditions, particularly during the first year postinjury. Many need 

early diagnosis and treatment to minimize long-term 

sequelae. 

Some conditions occur more frequently in the first 

several years following injury, such as hydronephrosis, spasticity, and contractures. Suicides are also 

more common during this time. Other complications 

become more prevalent with increasing time (eg, 

musculoskeletal problems), and some complications 

are most closely associated with the patient’s age 

(eg, cardiovascular complications) or neurological 

classification (eg, pneumonia, AD). The most common causes of death after the first year following 

injury are respiratory disorders (22% of deaths), 

cardiovascular disorders (21%), cancer (11.9%), and 

sepsis (9.8%).9 More than 75% of respiratory-related 

deaths following SCI are due to pneumonia. Urologic 

causes, which were previously the leading causes 

of death following SCI, now account for only 2.3% 

of deaths. 

Pulmonary Complications

The inspiratory phase of breathing requires active muscle contraction and depends primarily on 

the diaphragm innervated at the C-3, C-4, and C-5 

levels. Resting expiration is passive and depends on 

the viscoelastic properties of the lung and chest wall; 

forced expiration is active, as in a cough for clearing 
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Care of the Combat Amputee

secretions from the lungs—an action requiring rapid 

contraction by the abdominal muscles innervated 

at the T-6 to L-1 levels and the thoracically innervated intercostals. If they are not paralyzed, the 

clavicular portion of the pectoralis major and the 

latissimus dorsi can contribute to active expiration.56

Impairment of the inspiratory phase of breathing 

and forced expiration cause most SCI pulmonary 

complications.57

Acute Respiratory Failure

The earliest pulmonary complication to manifest 

in SCI patients is acute respiratory failure. This condition develops most commonly in those with cervical 

cord injury at the C-5 level or rostral. It may appear 

immediately after the injury or develop over hours to 

days as respiratory muscles fatigue. Close monitoring 

is needed to detect muscle fatigue and avoid emergent 

intubation. Oxygen saturation may not be a sensitive 

marker for respiratory failure, especially in patients 

who are receiving supplemental oxygen, so the vital 

capacity and partial pressure of carbon dioxide need 

to be closely monitored. Attention must be directed to 

aggressive pulmonary toilet and early detection and 

treatment of atelectasis and pneumonia, which occur 

in 50% of all patients with motor-complete SCI during the first month following injury.58,59 The majority 

of patients who have initial ventilatory failure will 

eventually wean from the ventilator over a period of 

days to months. Forced vital capacities in patients with 

mid-cervical level tetraplegia typically improve over 

a period of months, presumably due to a combination 

of inspiratory muscle strengthening and changes in 

the stiffness of the ribcage. Tracheostomy is usually 

performed early if rapid weaning is not anticipated 

(prolonged endotracheal intubation has been associated with airway complications, such as subglottic 

stenosis). A tracheostomy tube can also allow for direct tracheal suctioning, oral intake of food, and leak 

speech, in which the tracheostomy cuff is deflated 

and larger ventilator volumes are delivered, enabling 

air to leak around the tracheostomy tube and upward 

through the larynx.60

Communication can be a major problem for intubated individuals. Initially, tongue clicking or exaggerated 

eye blinks can be used for “yes” and “no” signaling, 

but head nodding may not be possible because of spine 

instability or neck muscle paralysis with injuries at the 

C-1 or brainstem levels. Communication can also be 

pursued through lip reading, communication board, or 

computer. Eventually, as pulmonary status stabilizes, 

patients can use leak speech. Ventilator-dependent 

patients must always carry a suction device for clearing secretions and a self-inflating bag valve mask in 

the event of ventilator failure.

Atelectasis, Pneumonia, Aspiration, Impaired Cough 

Pneumonia is the leading cause of death for both 

acute and chronic SCI.61 Almost all SCI patients, with 

the exception of those with lesions at a low thoracic 

level or below, have impaired cough because of the loss 

of abdominal muscle strength. Those with tetraplegia 

and higher-level paraplegia have impaired inspiratory 

effort as well. Impaired cough and impaired inspiration predispose a patient to atelectasis. Mucous hypersecretion and hyperviscosity, along with impaired 

cough, contribute to mucous plugging. All of these 

factors predispose a patient to pneumonia; those most 

vulnerable are patients with high cervical cord injuries. 

The site of pneumonia during the acute phase is most 

often the left lower lobe, where the sharper angle of 

the left mainstem bronchus makes suctioning more 

difficult.59

The following strategies promote clearing secretions 

and reduce the risk of pneumonia: (a) turn the patient at 

least every 2 hours to promote gravity-assisted postural 

drainage; (b) offer incentive spirometry; (c) assist cough 

by manually compressing the abdomen in synchronization with the patient’s cough (ie, quad cough; this 

is contraindicated in the presence of an inferior vena 

caval filter); (d) consider use of a mechanical insufflatorexsufflator, which delivers + 40 cm H2

O pressure, then 

rapidly switches to – 40cm H2O pressure, producing 

an airflow that approximates a normal cough and mobilizes bronchial secretions. Fever, increased purulent 

sputum, altered auscultation of the lungs, and change 

in chest radiographs suggest pneumonia. Treatment for 

pneumonia involves more frequent and more aggressive 

pulmonary hygiene and antibiotics.

An additional pulmonary problem is aspiration. 

Those with SCI at level T-10 or above are less able to 

cough effectively and clear their airways if they aspirate. Major risk factors for dysphagia in patients with 

recent SCI include tracheostomy and recent anterior 

cervical surgery.62,63 Precautions to minimize aspiration 

risk include restricting oral intake, gastric decompression by nasogastric tube for those with gastroparesis 

or ileus, upright or side-lying for eating, and avoiding 

assisted coughing by manual abdominal compression immediately after meals. Patients with suspected 

aspiration should have a swallowing evaluation that 

compares the effects of various consistencies, amounts, 

and techniques and develops optimal feeding strategies. 

Hyperextension of the neck in a cervical brace can make 

it easier for a patient to aspirate. Family members and 

caregivers should be trained to perform the Heimlich 
429

Spinal Cord Injury Rehabilitation

maneuver on someone who is lying down or sitting.

Certain interventions should be taken to reduce 

the long-term risk of respiratory complications in 

individuals with SCI, including smoking cessation 

and pneumococcal and annual influenza vaccination. 

When a patient has achieved a stable neurological 

exam and is free of acute respiratory disease, pulmonary function tests should be performed to establish 

a baseline. For patients with reduced vital capacity, 

an arterial blood gas test should also be performed as 

part of the baseline assessment.

Cardiovascular Complications

A variety of cardiac complications can compromise 

acute and chronic health for the spinal cord injured. 

Cervical and upper thoracic cord lesions disrupt 

sympathetic outflow to the heart and blood vessels, 

and the heart is influenced by unopposed parasympathetic activity. Abnormalities in sympathetic outflow 

manifest as arrhythmias (including bradycardia and 

asystole), postural hypotension, and AD. Loss of tonic 

arteriolar vasoconstriction results in vascular pooling 

and a lower baseline blood pressure; the expected 

blood pressure for a person with tetraplegia is around 

90/60 mmHg. In addition, decreased muscle activity 

in the lower extremities leads to venous stasis and the 

compromise of venous return. Reduced physical function as a result of motor paralysis and lipid dysfunction contribute to long-term cardiovascular risk. 

Bradycardia and Cardiac Arrest

Bradycardia that leads to cardiac arrest is a serious early complication of SCI; its incidence in those 

with tetraplegia is greatest in the first 5 weeks after 

injury.64,65 Tetraplegic injuries impair cardiac sympathetic outflow arising at the T-1 to T-4 levels, which 

normally accelerates the heart. The remaining cardiac 

innervation is parasympathetic; vagal input slows 

heart rate. If deceleration is severe, cardiac arrest may 

result. Tracheal suctioning or hypoxemia can trigger 

such a bradyarrhythmia, presumably via a vagovagal 

reflex. Oxygen and atropine can be administered prior 

to suctioning to inhibit the cholinergic receptors of the 

vagal efferents to the heart. Patients may occasionally 

require transvenous cardiac pacing.

Succinylcholine is a depolarizing paralytic medication rarely given as an adjunct to general anesthesia, 

but in patients with recent SCI, it can result in profound 

hyperkalemia with cardiac arrest because the neuromuscular junction is hypersensitive to cholinergic 

agents.66 Succinylcholine is contraindicated in SCI 

patients.

Deep Venous Thrombosis, Pulmonary Embolus

Another common and potentially fatal complication of acute SCI is deep venous thrombosis (DVT) 

with consequent pulmonary emboli. More than 50% 

of individuals with acute SCI develop DVT if they 

do not receive prophylaxis. DVT usually develops 

within the first 3 months following injury, peaking 

at 10 to 14 days; it occurs less commonly thereafter. 

Known predisposing factors are venous stasis, a hypercoagulable state following trauma, and venous 

intimal damage. All of these factors are commonly 

present in SCI patients. Preventive measures include 

performing a baseline venous Doppler examination to 

exclude early DVT, prescribing subcutaneous heparin 

(typically using low-molecular–weight heparin) and 

applying venous sequential compression pumps to 

the lower extremities.67,68,69 In patients whose thromboprophylaxis has been delayed for more than 72 hours 

after injury, tests should be performed to exclude the 

presence of DVT prior to applying venous sequential 

compression pumps. D-dimer has limited utility as 

a screening test in this population because of a high 

false-positive rate. Regular thigh and calf circumference measurements aid early detection of DVT. If a 

sudden increase or asymmetry in lower extremity 

circumference develops, or if a patient experiences 

unexplained low-grade fever or sudden onset dyspnea 

or chest pain, DVT or pulmonary embolism must be 

suspected and prompt action taken.70 The differential 

diagnosis for lower limb findings can include lower 

extremity fracture or hemorrhage, HO, dependent 

edema, or cellulitis. DVT can be diagnosed with 

ultrasound and, if inconclusive, contrast venogram. 

DVT is treated with low-molecular–weight heparin, 

transitioning to oral warfarin for at least 3 months. 

Bed rest, without lower extremity range-of-motion 

exercises, is recommended for 48 to 72 hours, until 

medical therapy is implemented.67 If anticoagulation 

therapy is contraindicated or if pulmonary emboli 

occur despite anticoagulation, an inferior vena cava 

filter should be considered. The routine placement 

of inferior vena cava filters in all patients with SCI is 

discouraged because their placement precludes the 

practice of quad coughing and their presence may 

lead to long-term complications. For patients with 

short-term contraindications to anticoagulation, a 

temporary filter can be placed and then removed once 

anticoagulation has been started.

Autonomic Dysreflexia

AD is a delayed sequela of high thoracic or cervical cord injury.71 This unique manifestation of SCI at 
430

Care of the Combat Amputee

or above the T-6 level presents after the resolution of 

spinal (neurogenic) shock, typically no sooner than 8 

weeks after injury. AD occurs in response to a noxious 

stimulus below the level of injury, most often due to 

overdistension of a hollow viscus, such as a bladder 

or bowel. Loss of supraspinal control results in unmodulated norepinephrine release and exaggerated 

vasoconstriction of arterioles receiving sympathetic 

innervation from below the level of the cord injury. 

Resultant blood pressure elevation may be moderate 

(140–160/90–100 mm Hg) or severe (> 180/110 mm 

Hg). In order to compensate for the elevated blood 

pressure, parasympathetic stimulation to the heart is 

increased via the vagus nerve and often causes bradycardia.72 Symptoms of AD include pounding headache, 

flushing, and diaphoresis. Severity varies among 

patients; in some, there are no manifestations besides 

these symptoms, while in others, hypertension can lead 

to retinal or intracerebral hemorrhage, seizures, and 

death.73,74 These symptoms result from high and potentially life-threatening systolic hypertension. To treat 

the condition, the head of the patient’s bed should be 

promptly elevated to promote dependent blood pooling and to lower the risk of intracerebral bleed, then 

the noxious triggering agent should be identified and 

eliminated (adequate bladder drainage can be ensured 

by catheterizing the bladder, flushing or replacing a 

possibly clogged indwelling catheter, or untwisting a 

condom catheter, and bowel impaction can be removed 

by digital evacuation; lidocaine jelly may be used as 

a rectal anesthetic to avoid further aggravating the 

condition). Other triggers of AD may include peptic 

ulcer, cholecystitis, appendicitis, bowel obstruction, 

rectal fissure, ureteral stone, UTI, ingrown toenail, 

fracture, or labor and delivery. If hypertension persists, 

nitroglycerine paste or oral hydralazine (10 mg) can 

be administered. Other antihypertensive medications 

are also used, including phenoxybenzamine, prazosin, 

mecamylamine, and clonidine.75 Patients are encouraged to carry an AD treatment card to facilitate prompt 

and appropriate treatment by health professionals less 

familiar with complications of SCI.

Orthostatic Hypotension

An early and occasionally chronic problem that is less 

threatening but nonetheless disabling is symptomatic 

OH. With OH, patients complain of dizziness, lightheadedness, and fainting when in an upright position. OH is 

most severe in patients with higher lesions (typically cervical and high thoracic SCI), complete injuries, and after 

prolonged periods of bed rest. Several factors contribute 

to OH, including impaired sympathetically-mediated 

vasoconstriction and consequent blood pooling in the 

lower limbs and splanchnic bed, decreased sympathetic 

drive to the heart, and relative volume depletion. Tetraplegic patients who typically run blood pressures of 

90/60 mm Hg are at highest risk for developing OH. 

These patients often become orthostatic when first sitting in the morning. To minimize these episodes, patients can be fitted with an abdominal binder, lower limb 

compression stockings, and elastic wraps. Liberal salt 

and fluid intake and elevating leg rests may also help 

avert orthostasis. Patients may also require midodrine 

or ephedrine sulfate administered 30 minutes before 

sitting. In patients with acute SCI, OH improves with 

repeated sitting trials; individuals with tetraplegia are 

known to have high renin and aldosterone levels, which 

presumably compensate for orthostasis. Late worsening of OH could suggest development of posttraumatic 

syringomyelia or a silent myocardial infarction.

Cardiovascular disease 

Cardiovascular disease has emerged as a leading 

cause of mortality in individuals with chronic SCI.76

Risk factors include hyperlipidemia, obesity, diabetes, 

sedentary lifestyle, and reduced physical function. 

As individuals with SCI live longer, cardiovascular 

disease has become a major source of morbidity and 

mortality, and is likely related to increased incidence of 

obesity, diabetes, and lowered high-density lipoprotein 

levels after SCI.77,78 Another cardiac complication for 

the cervical-cord injured is silent myocardial infarction. 

Cardiac ischemia and infarction in this population 

may be painless because the cardiac afferents course 

along cardiac-sympathetic nerves and enter the spinal 

cord at the T-1 to T-4 levels. In such cases, the clinical 

manifestations of myocardial infarct may be subtle and 

nonspecific, such as hypotension, dyspnea on exertion, 

orthopnea, or increased pedal edema.

Gastrointestinal Complications

SCI disrupts central nervous system coordination 

and direct nerve supply to the gastrointestinal tract. 

Consequences are addressed by region below.

Oral Cavity

The prevalence of periodontal disease and caries 

increases rapidly with age after SCI. A few of the major 

causes include failure of patients to control plaque, diet, 

deficits in saliva production, smoking, and problems 

with tooth occlusion.79 Plaque removal is affected by 

upper extremity function, habit, and caregiver commitment for those who require assistance. Saliva production 

is often reduced by anticholinergic medications, such as 
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Spinal Cord Injury Rehabilitation

those used to treat depression or detrusor overactivity. 

In addition, smoking deactivates salivary leukocytes, 

further promoting plaque formation and caries. Removing plaque once or twice per day with a fluoride 

toothpaste and integrating dental care into personal or 

attendant responsibilities reduces risk for tooth loss.

Esophagus

Dysphagia and esophagitis are the most common 

problems with the esophagus after SCI. The esophagus 

can be damaged by traumatic injury or surgery; perforation can cause mediastinitis, and local manipulation 

to place spine stabilization hardware can damage nerve 

supply, reducing sensation and peristalsis. Further iatrogenic contributions to swallowing problems include 

forced supine position, tong traction, and halo-vest 

immobilization. Dysphagia after acute cervical SCI occurs in up to 20% of cases, and half of the patients are 

asymptomatic. Predictors include age, tracheostomy, 

and anterior approach for cervical spinal surgery.80

Early specific diagnosis can be accomplished with bedside examination by a speech pathologist. Fiberoptic 

endoscopic examination and videofloroscopic study 

of swallowing provide further objective evidence of 

swallowing capabilities. Elevating the trunk to 30° 

or more for drinking and eating reduces aspiration 

risk. Interdisciplinary treatment of severe dysphagia 

can reduce up to 90% of symptoms and can prevent 

pnemonia.63 Reflux esophagitis is common after SCI 

because of abdominal distention, recumbent position, 

and altered peristaltic patterns. Low-amplitude esophageal contraction, a motility disorder commonly found 

in neurologically intact patients with gastroesophageal 

reflux disease, is highly prevalent among people with 

SCI.81,82 Patients should be queried for symptoms of 

heartburn or sour eructation. Mild symptoms should 

be managed with antacids, and persistent symptoms 

should be treated with acid-suppressing medication.

Stomach 

For the first few weeks following SCI, there is a risk 

for incomplete gastric emptying and vomiting, particularly in patients with lesions above the T-1 level. Slow 

gastric emptying can persist into chronic SCI.83 Acute 

treatment with intravenous metoclopramide (5–10 mg 

per dose) or bethanechol (25 mg 30 min before meals) is 

effective.84 Without prophylaxis, stress gastritis or peptic 

ulcers occur in 5% to 20% of acute SCI patients85,86; risk 

increases with age and in lesions above the T-5 level. 

Parasympathetic stimulation of acid secretion is unopposed because of reduced sympathetic tone, increasing 

the acidity of gastric juice. Additional sources of gastric 

lining irritation are corticosteroids (which decrease mucosal resistance), gastric distention, hypotension, and 

sepsis. Mechanical ventilation and anticoagulation with 

heparin are also independent risk factors for gastrointestinal bleeding. All these risks can be reduced with 

preventive use of H2 blockers, proton pump inhibitors, 

and stool fecal occult blood surveillance for gastrointestinal bleeding. Continuous suction via a nasogastric 

tube prevents gastric overdistension, and periodically 

monitoring gastric secretions for occult blood reduces 

risk and can detect gastric bleeding early. If prophylaxis 

is inadequate, upper gastrointestinal endoscopy or angiography (if the cervical spine is unstable) will locate 

gastrointestinal bleeding and facilitate treatment. 

Duodenum

Superior mesenteric artery syndrome is attributed 

to intermittent functional obstruction of the third 

segment of the duodenum between the superior mesenteric artery and the aorta. The syndrome is more 

common in patients with tetraplegia.87 The diagnosis 

can be confirmed with a barium upper gastrointestinal 

series. Findings include dilatation of the proximal duodenum and a “cut off” of the transverse duodenum, 

blocking barium flow. Sitting the patient up reduces 

the superior mesenteric forces on the duodenum and 

facilitates gravity flow in the gut. 

Pancreas

Sympathetic–parasympathetic imbalance may result 

in hyperstimulation of the sphincter of Oddi, leading to 

stasis of secretions and pancreatic damage.88 Pancreatitis may appear as early as 3 days after injury, but its 

presence may be masked because of a patient’s loss of 

sensory, motor, and reflex functions.89 A pancreatitis diagnosis is supported by increases in amylase and lipase 

over three times the upper limit of normal. 

Gallbladder

Imbalances in parasympathetic and sympathetic 

nervous system innervation and modulation of gallbladder activity after SCI may reduce contractility 

and lead to cholestasis. The gallbladder receives sympathetic innervation from the T-7 through T-10 levels. 

The development of cholelithiasis during acute SCI has 

been related to acute trauma, decreased gut motility, 

reduction in food intake, intravenous hyperalimentation, parenteral nutrition, rapid weight loss, and mobilization of peripheral fat stores.90,91 Gallstones are most 

prevalent in individuals with SCI and can affect 20% to 

30% of chronic populations.92 In spite of sensory defi-
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Care of the Combat Amputee

cits, patients with SCI usually present with symptoms 

that allow for acute diagnosis and cholecystectomy.93

The rate of complication following cholecystectomy is 

not significantly greater in individuals with SCI than in 

the neurologically intact population94; therefore, gallstones detected by ultrasound or other imaging should 

be documented and considered when patients present 

with nausea and right upper quadrant pain. 

Ileum

Abdominal distention is common during the first 

few days to weeks after SCI. This is often attributed to 

nonmechanical intestinal obstruction or paralytic adynamic ileus. Loss of gastrointestinal motility is noted in 

63% of SCI patients for several days, and occasionally 

for weeks, after acute SCI.89 Several risk factors for loss 

of gastrointestinal mobility are common in people with 

SCI, including major trauma, surgery, anesthesia, and 

severe medical illness.95 Evaluation requires a careful check for the presence of bowel sounds and focal 

tenderness (if sensation is present). An abdominal radiograph can gauge severity by revealing nonspecific 

gas patterns or dilated loops of intestine and air fluid 

levels, as seen in obstruction or severe ileus. Upright 

sitting and lateral decubitus position films screen for 

air, which indicates perforation, under the diaphragm 

or the abdominal wall. Management includes reviewing amylase levels, electrolytes, and complete blood 

counts. Hyponatremia and hypochloremia should be 

treated with intravenous electrolyte therapy. The intestines can be decompressed by placing a nasogastric 

tube and running it to suction. Symptoms typically 

improve in days. If not, intravenous metoclopramide is 

helpful in resolving prolonged gastroparesis or ileus.96

Colon

Neurogenic bowel is a term that relates colon dysfunction (constipation, incontinence, and discoordination of defecation) to a lack of nervous system control. 

There are two basic patterns of dysfunction. Upper 

motor neuron bowel results from a spinal cord lesion 

above the conus medullaris and typically manifests 

as fecal distention of the colon, overactive segmental 

peristalsis, hypoactive propulsive peristalsis, and a 

hyperactive holding reflex with spastic external anal 

sphincter constriction (requiring mechanical or chemical stimulus to trigger reflex defecation). Lower motor 

neuron bowel results from a lesion that affects the 

parasympathetic and somatic pudendal cell bodies or 

axons at the conus, cauda equina, or inferior splanchnic 

nerve and the pudendal nerve. Lower motor neuron 

bowel results in low descending colon wall tone and 

flaccid pelvic floor and anal sphincter. No spinal cord 

mediated reflex peristalsis occurs. Slow stool propulsion is coordinated by the myenteric plexus alone, and 

incontinence is common with movement. The denervated colon produces a drier, rounder stool because the 

prolonged transit time results in increased absorption 

of moisture from the stool.97

Obstipation, Fecal Impaction, Pseudoobstruction, 

Megacolon

Decreased colonic motility, increased colonic 

compliance, and anal sphincter spasticity in those 

with chronic SCI may result in obstipation and fecal 

impaction.98 Key elements of a bowel management program include the following: (a) adequate fluid intake 

(1,500–2,000 mL/day); (b) high fiber diet (40–60 gm/

day); (c) bulk cathartics, such as psyllium hydrophilic 

mucilloid; (d) regular mealtimes; and (e) timed bowel 

programs, with evacuations scheduled for every day 

or every other day, using rectal suppositories (glycerin 

or bisacodyl) and digital stimulation. Evacuation intervals of more than 3 days increase the risk of impaction and incontinence. The goal of a good program is 

continence, with focus on techniques that minimize 

mechanical damage and irritation to the colon and 

promote long-term health.99 

Patients reporting poor results with a bowel care 

program may manifest nausea, vomiting, abdominal 

distension, early satiety, and shortness of breath from 

compromised diaphragm descent. Reviewing the elements of the bowel program and ensuring that patients 

are not on medications that slow gut motility (eg, 

anticholinergics, narcotics, tricyclics, clonidine, etc) 

are the first steps to remediation. In addition, patients 

may require periodic hyperosmotic laxatives (milk 

of magnesia, lactulose, sorbitol). If these are unsuccessful, saline or phosphosoda enema or whole gut 

irrigation can be tried. Because enemas tend to stretch 

the bowel, causing a loss of muscle tone and perhaps 

AD, they should be used judiciously. In severe cases, 

nasogastric decompression, with or without a rectal 

tube, may be required. Rarely, colonoscopy or surgical 

decompression must be considered if cecal diameter 

is greater than 12 cm. For those with recurrent bowel 

obstruction or markedly prolonged bowel programs, 

refractory to conservative measures, colostomy may 

be a desirable solution.100 

Acute abdomen

Acute abdomen is often diagnosed late, with a 

resulting high morbidity and mortality in patients 

with SCI. Patients with injury at level T-10 or rostral 
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Spinal Cord Injury Rehabilitation

and resultant impaired sensation do not perceive 

abdominal pain or report poorly localized pain at a 

later stage of acute abdomen.101,102 The physician caring for the SCI patient must maintain a high index of 

suspicion for acute abdomen and be alert to its minimal 

manifestations in SCI patients, which may be limited 

to tachycardia, increased spasticity, and AD.

Endocrinologic Complications

SCI can directly and indirectly contribute to endocrine and metabolic disorders. One neurologic 

mechanism for determining endocrine function is 

via sympathetics that innervate the pancreas, adrenal 

medulla, and juxtaglomerular apparatus of the kidney 

and originate from the spinal cord at the T-5 through 

T-12 levels.103 Sympathetic activity inhibits insulin 

secretion, while parasympathetic activity stimulates 

insulin secretion. Reduced sympathetic activity, as occurs with SCI, elevates plasma renin, which can lead to 

production of angiotensin II, a potent vasoconstrictor. 

Aldosterone promotes sodium retention and potassium release. 

Acute complications

Within days after SCI, antidiuretic hormone secretion is reduced, resulting in diuresis that can continue 

for a few days. Adrenocorticotrophic hormone is normally secreted in a diurnal pattern that disappears 

soon after SCI, causing a drop in blood pressure. 

Clinicians should be prepared for hypothalamic and 

pituitary abnormalities following SCI, as well. Stress 

can contribute to impaired release of growth hormone, 

which can lead to weakness. At the time of injury, the 

stress response triggers release of corticotrophin, and 

resultant release of hormone from the hypothalamus. 

Adrenocorticotrophic hormone is released and stimulates cortisol production. The syndrome of inappropriate antidiuretic hormone can contribute to free-water 

retention and electrolyte dilution.

Hypercalcemia, though uncommon, occurs most 

often in the first months after injury in adolescent 

males with complete tetraplegia and spinal shock. 

In addition to gender and youth, risk factors include 

complete neurologic injury, high cervical injury, and 

prolonged immobilization. Symptoms and signs are 

subtle and include malaise, anorexia, nausea, vomiting, constipation, polydipsia, and polyuria. Left untreated, hypercalcemia can progress to lethargy and 

coma. Treatment includes intravenous saline with 

furosemide and remobilization. Additional measures 

may be needed to inhibit osteoclast-mediated bone 

resorption, such as administering bisphosphonates (eg, 

etidronate or pamidronate), calcitonin, mithramycin, 

glucocorticoids, and gallium nitrate.104

Osteoporosis

Fracture risk increases with injury duration in 

individuals with chronic SCI. In general, there is no 

demineralization in bones above the SCI level. The 

major contributors to mineral loss after SCI include 

the amount of paralyzed muscle, lower limb weightbearing status, presence of spasticity, age, sex, and 

the time elapsed since injury. Long bones lose more 

calcium than the axial skeleton, and trabecular bone 

is more affected than cortical bone. The efficacy of 

preventive treatments used in the general population 

has not been conclusively demonstrated in nonambulatory individuals with SCI.

Insulin-Dependent Diabetes Mellitus 

SCI can produce profound metabolic consequences 

that result in disorders of carbohydrate and lipid metabolism.77 Abnormal glucose tolerance and hyperinsulinemia are common following SCI. SCI complicates 

the management of diabetes mellitus in two ways. 

First, individuals with SCI are prone to increased insulin resistance because of decreased muscle mass and 

obesity that can result from limited mobility. Second, 

those with tetraplegia fail to exhibit adrenergic hypoglycemic symptoms (diaphoresis and tachycardia). For 

the latter, clinicians must develop an increased awareness of the neuroglycopenic symptoms (drowsiness or 

impaired mental status). 

Dermatologic Complications

Pressure Ulcers

Pressure ulcers remain a major cause of morbidity 

and mortality after SCI. Pressure ulcers in individuals with acute SCI commonly delay remobilization, 

full participation in rehabilitation, and discharge to 

the community. A clinical practice guideline on the 

prevention and treatment of pressure ulcers in people 

with SCI was published in 2000 to improve the quality 

and consistency of care.105

Pressure ulcers are common in the acute care 

phase, during rehabilitation, and when living in the 

community.106–109 Despite efforts to prevent pressure 

ulcers, there is little evidence that the overall incidence 

or prevalence of pressure ulcers in people with SCI 

is decreasing. In addition to medical complications, 

prolonged bed rest, and loss of function, the cost of 

treating pressure ulcers is high, estimated to be $3 
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Care of the Combat Amputee

to $5 billion per year in the United States.110,111 Braun 

and colleagues reported that the cost to heal a severe, 

full-thickness pressure ulcer is $70,000.112

A common misconception is that pressure ulcers 

must first involve the skin; however, most severe pressure ulcers develop in deep body wall tissues over bony 

prominences and on areas of the body that have little 

body fat. This includes areas over the ischial tuberosity, 

sacrum, greater trochanter, heel, scapula, vertebra, malleolus, and occiput. The pathophysiology of pressure 

ulcers has been related to sustained high loads without 

pressure relief. Deep, severe pressure ulcers typically 

start at the bone-muscle interface. Frictional and shear 

injuries can result in more superficial ulcers.

External forces that result in pressure ulcers include unrelieved direct perpendicular pressure, skin 

shearing, and friction. Risk factors that predispose an 

individual to developing pressure ulcers are prolonged 

sitting, severe spasticity, contractures, edema, anemia, 

poor nutrition, bruises and skin damage from falls or 

scrapes, worn or inadequate cushions, urinary or fecal 

incontinence, excessive sweating, and smoking.113,114

Some conditions that put acute SCI patients at risk of 

developing pressure ulcers are anesthetic skin, immobility from paralysis, hypotension, spine immobilization, poor nutrition and subsequent weight loss, febrile 

illness, urinary and fecal incontinence, flexor spasm, 

and altered mental status, such as coma, depression, 

or chronic alcohol use. From 20% to 40% of patients 

develop pressure ulcers during the first month after 

SCI.105,115 Education, awareness, and behavioral change 

can minimize the risk of developing pressure ulcers. 

Optimizing equipment, posture, and seating are also 

critical to prevention, as is avoiding trauma and injury 

during activities of daily living. 

Risk should be assessed comprehensively and systematically, and is high with acute SCI and a significant 

degree of paralysis. Risk can be decreased by avoiding prolonged immobilization, periodically relieving 

pressure, using pressure-reducing support surfaces, 

preventing moisture accumulation, and applying pillows and cushions to pad-contacting surfaces. Use of 

bed-positioning devices and periodic turns while in 

bed are also important preventive measures. Pressurereducing bed support surfaces can be used for at-risk 

individuals during acute hospitalization, rehabilitation, and in the instance of acute illness. 

Specialized wheelchair cushions and mattresses 

should be used for all people with SCI who are at 

high risk for skin breakdown. Interface pressures 

should be evaluated when using foam, gel, and air 

cushions in a wheelchair. Foam, static air, alternating 

air, gel, and water mattresses are common pressurereducing tools. In people with one or more pressure 

ulcers, pressure-reducing bed support surfaces are an 

important consideration for healing and preventing 

ulcers on other surfaces. 

Regardless of predisposing factors, pressure ulcers 

are caused by prolonged pressure or shear sufficient 

to cause underlying skin and muscle necrosis from 

ischemia. Yet the exact timing of pressure reliefs (ie, 

relieving pressure on a periodic basis while sitting 

in a wheelchair or lying in bed) is still the subject of 

debate. It is reasonable to turn patients in bed every 2 

hours during their acute stay and during rehabilitation. 

When sitting, body weight is distributed over a smaller 

surface, so it is recommended that pressure be relieved 

for at least 15 seconds every 15 minutes.

Pressure can be relieved while sitting in a wheelchair by cushions that distribute weight optimally. 

Well-fitted wheelchairs with solid (rather than sling) 

seats; high-quality foam, gel, or air cushions; and pressure releases are standard preventative equipment.116

The region over the ischial tuberosities is generally at 

greatest risk when an individual is seated, although 

postural abnormalities and incorrect seating can put 

excessive pressure on the sacrum or greater trochanters. 

Patients and caregivers must be taught to check 

the skin daily. If redness or skin breakdown is noted, 

patients must alter their positions and routines to 

keep the affected areas free of pressure until redness 

disappears or the skin heals. For pressure ulcers in 

regions that receive high pressure while seated, this 

usually requires strict bed rest. Patients should be 

made aware that burns can occur by dropping cigarette 

ash on anesthetic skin, using hot water bottles, placing 

hot plates or mugs on the thighs, sitting too close to 

fires or radiators, and bathing in water that is too hot 

(greater than 98°F or 36.5°C). To avoid skin breakdown, 

condom catheters or leg straps should not be applied 

too tightly, feet and nails should be cared for, and shoes 

should fit well or loosely and be checked for sharp 

objects before donning. To avoid scrotal breakdown, 

men must routinely reposition the scrotum forward 

after transferring to a wheelchair or sitting surface.

Following onset of a pressure ulcer, it is important 

to assess and describe the ulcer so appropriate treatment can be promptly initiated. Several parameters 

should be described, including anatomical location, 

general appearance, size (length, width, and depth 

of the wound area), stage, exudate, odor, necrosis, 

undermining, sinus tracts, healing, wound margins, 

surrounding tissue, and signs of infection. Staging 

ulcers is an important part of pressure ulcer assessment (Table 16-4).117

Superficial pressure ulcers may heal with conservative treatment; deeper wounds may require surgical 

intervention. Pressure ulcer treatment involves debrid-
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Spinal Cord Injury Rehabilitation

ing necrotic tissue, cleaning the wound bed at each 

dressing change, and applying appropriate dressings. 

Dressings that maintain a continuously moist ulcer 

bed and keep the surrounding intact skin dry are 

generally preferred. Other important considerations 

include controlling exudate and filling wounds that 

have tracks and undermining. Many comorbid conditions may interfere with wound healing. Cardiac, 

pulmonary, and metabolic (eg, diabetes mellitus) 

diseases should be stabilized. Nutritional status 

requires optimization, and tobacco cessation should 

be strongly encouraged. Wound infection and osteomyelitis will interfere with healing and should be 

treated. Other issues related to SCI that may interfere 

with pressure ulcer healing include incontinence, 

spasticity, HO, and UTI. 

Surgical intervention is made when an ulcer is too 

large to heal with conservative measures, a deep soft 

tissue or bone infection must be surgically debrided, 

there are nonhealing tracts, or a bony deformity must 

be corrected. Myocutaneous or fasciocutaneous flaps 

are the standard surgical treatment, preceded by inspection of bony prominences and debridement of osteomyelitis (Figure 16-5). A pedicle flap with the suture 

line away from the area of direct pressure releases skin 

and underlying muscle while preserving blood supply, repositioning it over the ulcer. The most common 

examples of pedicle flaps are gluteus maximus rotation 

flaps to cover sacral or ischial ulcers, hamstring V-Y 

advancement flaps to cover ischial ulcers, and tensor 

fascia lata, vastus lateralis, or rectus abdominus flaps to 

cover trochanteric ulcers. Skin grafts can be used over 

granulated tissue, but they are not very durable over 

weight-bearing areas. The possibility for future surgeries should be considered when tissue sites are chosen. 

Postoperative care requires rigorous attention to keep 

TABLE 16-4

NATIONAL PRESSURE ULCER ADVISORY PANEL PRESSURE ULCER STAGES

Suspected Deep Tissue Injury Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure or shear. The area may be preceded by tissue 

that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue.

Deep Tissue Injury Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure or shear.

Stage I Intact skin with nonblanchable redness of a localized area usually over a bony prominence. 

Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.

Stage II Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound 

bed, without slough. May also present as an intact or open/ruptured serum-filled blister.

Stage III Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are 

not exposed. Slough may be present but does not obscure the depth of tissue loss. May 

include undermining and tunneling.

Stage IV Full thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be 

present on some parts of the wound bed. Often include undermining and tunneling.

Unstageable Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough 

(yellow, tan, gray, green or brown) or eschar (tan, brown, or black) in the wound bed.

Adapted from: National Pressure Ulcer Advisory Panel. Updated Staging System Web site. Available at: http://www.npuap.org/pr2.htm. 

Accessed September 15, 2008.

Figure 16-5. With deeper ischial pressure ulcers, the ischial 

tuberosity commonly develops osteomyelitis. This pelvic 

radiograph shows an area of marked sclerosis, with a wide 

zone of transition and cortical irregularity involving the left 

ischial tuberosity (thin arrow). Areas of lucencies are seen in 

the adjacent soft tissue (arrowheads).
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Care of the Combat Amputee

pressure off the surgical site and allow healing. Following surgery, patients should remain on an air-fluidized 

bed for a period of 3 to 6 weeks. During this time, tension 

on flap incisions should be avoided. For patients with 

spasms, this may mean increased spasmolytic medication and positioning to minimize hip flexor spasms. 

After 3 to 6 weeks, if the flap is healing well, the patient 

progresses to a regular hospital bed and lower extremity range-of-motion exercises are allowed, with direct 

observation of the flap suture lines. Later, the patient is 

gradually remobilized in a fitted wheelchair. Using progressively longer flap-sitting times over several weeks 

has been successful following surgery. It is important to 

reinforce the need to perform regular pressure releases 

and twice-daily skin checks.

Pressure ulcers may result in complications such 

as cellulitis and osteomyelitis, which frequently 

originate through the direct spread of infection. The 

common presenting symptoms of cellulitis are swelling, redness, local warmth, and fever. The symptoms 

of osteomyelitis include fever, shaking chills, and purulent drainage. Laboratory findings in both include 

leukocytosis, elevated erythrocyte sedimentation rate, 

and positive blood cultures. A radiograph may show 

periosteal reaction or lytic lesions. Bone scans are of 

limited use because they are usually positive below a 

pressure ulcer, whether the underlying bone is infected 

or not. Magnetic resonance imaging (MRI) findings are 

somewhat more specific, but false positive tests are still 

possible. Definitive diagnosis of osteomyelitis is possible through bone biopsy and histologic confirmation, 

with more reliable results obtained through a needle 

biopsy or at the time of operative treatment of an ulcer. 

Cellulitis is treated with oral or parenteral antibiotics (usually taken for 10 to 14 days). Osteomyelitis 

is usually treated with 6 weeks or more of antibiotic 

administration and requires bone debridement. Other 

complications of pressure ulcers that require treatment 

include wound infection, AD, and malnutrition.

Musculoskeletal Disorders

Musculoskeletal disorders are common among 

individuals with SCI. Many types of musculoskeletal 

problems have been reported, including soft tissue and 

osseous injuries at the time of SCI; traumatic injuries 

after SCI; unique musculoskeletal disorders precipitated by SCI; and chronic upper limb disorders related 

to repetitive use, poor biomechanics, and aging. The 

impact of musculoskeletal problems on the overall 

function and well-being of a person with SCI cannot 

be overstated. Even relatively minor musculoskeletal 

pathologies can result in significant secondary disabilities and new limitations.

Fractures

Fractures at the time of SCI are common and directly 

related to extrinsic factors (eg, force of injury) and 

intrinsic factors (eg, bone density). Fractures of vertebrae, limb girdles, and long bones are most common. 

A high index of suspicion and use of imaging studies 

are necessary to identify fractures below the neurologic 

level of injury. 

Fractures also commonly occur after SCI (Figure 

16-6). The incidence of long bone fractures in the lower 

limb has been estimated to be 4% to 7%.118 Fractures are 

related to osteoporosis that occurs within months after 

injury below the level of injury. The injury that results 

in fracture may be minor as bone mineral density decreases and less force is required to produce failure in 

the bone. The Model SCI System has reported fracture 

rates based on time following SCI, with cumulative 

Figure 16-6. Supracondylar fracture in osteoporotic bone in 

a male with long-standing paraplegia. The fracture occurred 

secondary to a fall from a gurney. 
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Spinal Cord Injury Rehabilitation

incidences of 14% at 5 years, 28% at 10 years, and 39% 

15 years after injury.119 

Managing fractures includes immobilizing the 

limb and preventing complications. AD may occur 

in individuals with SCI at level T-6 and above. Other 

potential complications include DVT, increased spasticity, and the development of pressure ulcers. Wellpadded, bivalved casts allow frequent inspection of 

skin. Delayed union, malunion, and nonunion are 

common problems after fracture in SCI. Functional 

consequences, such as difficulty transferring, must be 

anticipated and addressed.

Heterotopic Ossification

HO is the development of ectopic bone within periarticular soft tissues and is a well-described complication of SCI and traumatic brain injury. Although HO 

may develop around any joint or within muscle below 

the level of SCI, it develops most commonly about the 

hips (Figure 16-7). Onset is typically within the first 5 

weeks after SCI, although it may not become clinically 

apparent for an additional few weeks. The prevalence 

is thought to be approximately 20% to 30%, although 

only about half the cases are clinically significant. Between 3% and 8% develop complete ankylosis of the 

involved joint.120,121

Diagnosing hip and shoulder HO may be challenging because the periarticular structures are not as 

easy to examine as more superficial joints (eg, knee 

and elbow). HO may present with erythema, swelling, warmth, decreased range of motion, increased 

spasticity, pain, and fever. Bone scintigraphy and MRI 

are more sensitive diagnostic tests than plain film radiographs, which may not be helpful if the HO matrix 

is not yet calcified. Complications include decreased 

range of motion affecting transfers and seating, skin 

breakdown, increased spasticity, and DVT.

The mainstay of treatment for HO has been pharmacologic. Bisphosphonates, such as etidronate 

Figure 16-7. (a) Radiograph showing severe heterotopic ossification involving bilateral hips. (b) Computed tomography 

scan shows large mass of bone anterior to the left acetabulum. 

(c) Heterotopic ossification can indirectly cause pressure 

ulcers through restriction of joint range of motion, which 

results in pelvic obliquity when seated. In this patient with 

severely limited left hip flexion, a seating interface pressure 

transducer map placed between the patient and wheelchair 

cushion demonstrates increased pressure (yellow and red 

colors) posterior to the right greater trochanter.

a b

c
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Care of the Combat Amputee

disodium, and nonsteroidal antiinflammatories (eg, 

indomethacin) have been used to treat HO. Low-dose 

radiation, manipulation, and surgical excision are 

also reportedly useful for treating HO that does not 

respond to medications.122,123

Contractures 

Progressive shortening (contracture) of muscles, 

tendons, ligaments, and joint capsules results in stiffness, movement limitation, and deformity. Contractures limit self-care, transfers, bed positioning, standing, sitting, and walking. Finger flexion deformities 

compromise hand function and skin care. Ankle plantar flexion contractures may lead to pressure ulcers 

and limit footwear. Knee and hip flexion contractures 

increase the energy cost of standing and walking. Hip 

adductor contractures limit perineal care. Preventing 

contractures involves daily range-of-motion exercise, 

which may be complicated by spasticity. Early contracture may be reversed with stretching with or without 

heat treatments, such as ultrasound diathermy. Severe 

contractures may require surgical release.

Chronic Upper Limb Disorders

Upper limb pain and dysfunction are common following SCI. Using the upper limbs for weight-bearing 

purposes over decades creates biomechanical challenges for limbs that are designed primarily for prehension and mobility. Rotator cuff disease, tendonitis, 

epicondylitis, arthritis, and carpal tunnel syndrome 

are all common upper limb problems. Recommendations in Preservation of Upper Limb Function Following 

Spinal Cord Injury address biomechanical stressors, 

techniques, equipment, musculoskeletal health, and 

the environment.47 Most address well-established 

ergonomic associations between strenuous tasks and 

musculoskeletal disorders. Minimizing the force and 

frequency of tasks, such as wheelchair pushing, is 

achieved by optimizing equipment (eg, wheelchair 

weight and setup) and technique. Optimizing technique includes education and training in performing 

tasks (eg, transfer, wheelchair propulsion) and avoiding extreme limb postures. Equipment, technological, 

and environmental interventions are effective. For 

example, an elevated wheelchair seat, standing position, or lowered environment prevents repetitive 

overhead reaching. 

Neurological Disorders

A variety of secondary neurologic complications 

can develop following SCI, including spasticity, 

neuropathic pain, posttraumatic syringomyelia, and 

peripheral nerve entrapment.

Spasticity

Spasticity develops in individuals with upper 

motor neuron damage and spared reflex pathways, 

with hyperactive phasic stretch reflexes mediated 

by 1A afferents from the muscle spindle. The 1A afferents respond to rapid stretch, as in a tendon tap, or 

rapid passive movement of a joint. Clinically, spasticity manifests as hyperactive tendon reflexes, clonus, 

velocity-dependent hypertonus, and extensor spasms. 

The latter are commonly elicited by the passive stretch 

of hip flexors, for example, as the patient moves from 

sitting to supine-lying position or performs a pushup pressure release. Extensor spasms may interfere 

during transfers, although some patients use them to 

aid standing. Flexor spasms can interfere with prone 

or supine positioning in bed, bed mobility, transfers, 

and walking; they can also interfere with sleep and 

contribute to pressure ulcers. 

Spasticity and other hypertonus require treatment 

only if they interfere with function, cause discomfort 

or poor sleep, hinder caregivers’ tasks, or contribute 

to medical complications, as with pressure ulcer formation.124 Treatment benefits must always be weighed 

against the possible beneficial effects of spasticity, such 

as positioning extremities or aiding standing transfers 

and walking.

Once spasticity is determined to be more detrimental than beneficial and nociceptive sources such as UTI, 

renal stone, or fecal impaction have been ruled out, 

various treatments may be undertaken. The least invasive is daily passive stretching of hypertonic muscles, 

which reduces tone and spasms for several hours and 

maintains joint range of motion. Oral medications, 

such as baclofen, tizanidine, or diazepam most commonly, gabapentin or dantroline rarely, must often 

be administered. If these prove insufficient, invasive 

techniques should be considered. Focal spasticity can 

often be treated with percutaneous injection of botulinum toxin, phenol, or alcohol. Generalized and severe 

spasticity usually responds to continuous intrathecal 

baclofen delivered via a subcutaneous pump. Surgical options, such as tenotomy or rhizotomy, are rarely 

required for severe spasticity that fails to respond to 

other treatments. 

Pain 

About one third of individuals with chronic SCI 

experience severe pain, and up to 80% experience at 

least some pain on a regular basis. Pain is far more 
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Spinal Cord Injury Rehabilitation

common in the spinal cord injured than in the general 

population,125 and it frequently contributes to lower 

psychological functioning, interferes with daily activities, and hinders social integration. 

Pain usually originates centrally within the spinal 

cord. It presents with any combination of burning, 

tingling, or lancinating unaffected by neck movements 

or posture, and is thought to represent spontaneous 

discharge of neurons in the ascending pain pathways. 

Individuals with cauda equina injury experience a 

series of stabbing pains that radiate down one or both 

lower limbs every few seconds to minutes. These 

shock-like pains may be continuously present or appear intermittently. Another type of pain presents as a 

segmental hyperesthesia over one or two dermatomes 

at the level of injury. This hypersensitivity to light 

touch may only be a minor inconvenience and often 

does not require treatment. Central pain has been 

treated with a variety of agents, including nonnarcotic analgesics (acetaminophen, acetylsalicylic acid, 

ibuprofen); anticonvulsants (gabapentin, phenytoin, 

clonazepam); tricyclic antidepressants (amitriptyline, 

doxepin); and opioids. Chronic opioid use (eg, methadone and sustained-release morphine) should be administered only in a highly structured setting in which 

the patient’s compliance and psychological status can 

be carefully monitored. 

It is essential to distinguish central dysesthetic SCI 

pains from pain arising due to mechanical causes, 

such as persisting cord or nerve root impingement, an 

enlarging posttraumatic syrinx, or a number of common musculoskeletal conditions. These latter types of 

pain are generally aggravated by spinal movements or 

postural changes and may be clinically distinguishable 

from central pain. Treatment involves addressing the 

underlying cause of mechanical pain, if possible.

Posttraumatic Syringomyelia

Symptomatic posttraumatic syringomyelia is an uncommon but potentially severely disabling complication of SCI.126,127 The prevalence of clinically significant 

posttraumatic syringomyelia has been estimated at 

4.5% for tetraplegia and 1.7% for paraplegia. Posttraumatic syringomyelia results from a syrinx at the level of 

the cord injury (Figure 16-8). It can cause progressive 

spinal cord damage by extending rostrally or caudally 

from the injury site, and can extend the length of the 

spinal cord up to the brainstem. Syringomyelia may 

develop within months after SCI, but more typically 

develops over many years. 

The earliest symptoms of syringomyelia may be 

subtle. They include pain, often aggravated by postural 

change; altered spasticity; sweating; worsening OH; 

ascending loss of pain and temperature sensation; and 

ascending loss of segmental reflexes. Ascending weakness is a late manifestation, the appearance of which 

often indicates that the condition is advanced and 

may not be reversible. MRI is definitive for diagnosing posttraumatic syringomyelia, but up to 60% of all 

SCI patients have at least a small intramedullary cystic 

structure at their level of injury. Careful serial clinical 

examinations and MRI are useful for determining 

whether a syrinx is causing neurologic deterioration. 

Treatment may include minimizing Valsalva maneuvers and spine movements, surgical decompression 

with syringosubarachnoid, syringopleural or syringoperitoneal shunting of syrinx fluid, or duraplasty. 

For those with complete cord injury, cordectomy is an 

alternative.

Peripheral Nerve Entrapment

Upper limb peripheral nerve entrapment is highly 

prevalent in individuals with SCI because of the 

physical demands placed on the upper limbs during functional tasks.128 Predisposing factors include 

increased use of the upper extremities for transfers 

and wheelchair propulsion, resulting in an increased 

incidence of carpal tunnel syndrome; absent pain senFigure 16-8. Nine months following a motor vehicle accident with upper thoracic fractures and level T-3 complete 

paraplegia, this patient presented with an ascending sensory 

level and increasing left hand weakness. Magnetic resonance 

imaging demonstrated a posttraumatic syrinx extending 

from the C-1 level through the conus. 
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Care of the Combat Amputee

sation, particularly in posttraumatic syringomyelia, 

resulting in ulnar nerve entrapment; and proximal 

compression of motor neurons and motor axons in 

the presence of cervical spondylosis. Radial nerve 

entrapment, as in Saturday Night Palsy and thoracic 

outlet syndrome, also occurs with increased frequency. 

Preventive measures include use of wheelchair gloves, 

optimized wheelchair setup and propulsion technique, 

and avoidance of direct pressure to the ulnar groove. 

New sensory loss, weakness, or loss of function should 

prompt electrodiagnostic studies to rule out nerve 

entrapment. Wrist splints, elbow pads, and surgical 

decompression are common treatments.

Genitourinary Complications

Morbidity and mortality due to urosepsis and renal 

failure in individuals with SCI have decreased significantly since the 1940s because of improved management principles and techniques. Understanding how 

the level of the cord lesion relates to bladder function 

aids in anticipating possible urinary dysfunctions.129,130

Upper motor neuron/spastic bladder dysfunction is 

generally associated with fractures at the T-12 vertebral 

level and above (ie, cervical and thoracic fractures). 

For patients with these conditions, voluntary control 

from the brain is disrupted, but reflex activity recovers 

after spinal shock dissipates. SCI patients with upper 

motor neuron lesions rostral to and sparing the conus 

(S-2 through S-4 neurological levels, located at the L-1 

vertebral body) usually develop reflex bladder emptying after the resolution of spinal shock. Many of these 

patients also develop detrusor-sphincter dyssynergia, 

in which the reflex detrusor contraction occurs simultaneously with external urethral sphincter contraction.131–133 The result is high bladder pressures that may 

lead to detrusor muscle hypertrophy, vesicoureteral 

reflux, hydroureter, hydronephrosis, and renal failure. 

This process is often clinically silent and needs to be 

regularly monitored. Lower motor neuron/flaccid/

areflexic bladder dysfunction generally occurs when 

the bony injury is at level L-1 and below and affects the 

conus medullaris or cauda equina. Individuals do not 

regain reflex contraction; the bladder remains flaccid 

and overfills. Mixed dysfunctions may occur with injuries at the T-12 or L-1 vertebral levels, with a variable 

degree of upper and lower motor neuron dysfunction 

and less predictable effects on voiding. 

Goals for bladder management in individuals with 

SCI include urinary continence, complete bladder emptying, maintaining safe vesicular pressures during storage and voiding, and minimizing the need for physical 

assistance. Factors predisposing individuals with SCI 

to chronic renal failure include high-pressure voiding 

with reflux nephropathy, nephrolithiasis from ureasplitting bacteria, chronic pyelonephritis, and amyloidosis from chronic pressure ulcers and osteomyelitis. 

Bladder Management Techniques

During the initial period of spinal shock, before 

reflex emptying develops, bladder drainage is managed with an indwelling Foley catheter until fluid 

intake can be regulated to less than 2 L per day. If 

they have adequate hand function to perform selfcatheterization, patients may be transitioned to intermittent catheterization every 4 to 6 hours to keep 

maximal bladder distension to less than 500 mL. Fluid 

intake must be limited to prevent the need for more 

frequent catheterizations. After several months, reflex 

detrusor contractions develop in patients with upper 

motor neuron/spastic bladder; this can be anticipated 

in those with preserved bulbocavernosus and anal 

reflexes. When spontaneous reflex bladder emptying 

develops, anticholinergics may be needed to prevent 

incontinence between catheterizations. In individuals 

whose hand function is inadequate to perform selfcatheterization, long-term use of an indwelling Foley 

catheter or suprapubic catheter may be considered. 

In males with SCI, the use of a condom catheter in 

conjunction with sphincterotomy or urethral stents 

may be a reasonable bladder management option. Postvoid residuals should be less than 100 mL to prevent 

bacterial colonization in the bladder from achieving a 

concentration that will cause symptoms. The less common lower motor neuron bladder (in which the S-2, 

S-3, S-4 reflex arc is interrupted) can be managed with 

intermittent catheterization. Although voiding into a 

condom catheter can sometimes be achieved with prolonged direct compression over the bladder (Crede’s 

maneuver), this can lead to vesicoureteral reflux and 

hydronephrosis and is therefore discouraged.134

Pharmacological treatment can be used to improve 

urinary continence. Anticholinergic drugs bind to 

muscarinic receptors in the bladder. Medications, 

including oxybutinin and tolterodine, are used to 

decrease detrusor contractility and increase bladder 

compliance. Side effects are dry mouth, decreased 

sweating, and constipation. Alpha antagonists (eg, 

prazosin, terazosin, doxazosin) can occasionally allow 

patients with incomplete injuries to initiate voiding. 

Side effects may include hypotension and dizziness. 

Injections with botulinum toxin have been used to 

control detrusor hyperactivity.135

Surgery is sometimes used to manage neurogenic 

bladder.136 Surgeries for hyperreflexic bladder include 

bladder augmentation with or without urinary diversion (ie, continent ileal conduit diversion and cath-
441

Spinal Cord Injury Rehabilitation

eterization via an abdominal stoma) or cystoplasty 

and detrusor myectomy. In instances of areflexic 

bladder, outlet resistance may be enhanced by artificial 

sphincters or bladder neck procedures. Additionally, 

periurethral injections and fascial slings have been 

used to achieve continence. Newer strategies are 

arising to manage hyperreflexic bladder.136 Electrode 

stimulation involves surgical posterior rhizotomy of 

the sacral nerve roots and electrode placement at the 

anterior nerve roots. Stimulation of the anterior roots 

causes contraction of the detrusor and voiding. 

Renal function should be regularly monitored and 

compromise detected and treated early. A yearly urologic examination is recommended for individuals 

with chronic SCI, although there is no consensus on the 

examination components.136 The exam often includes 

an evaluation of the upper (via ultrasound, renal scan, 

computed tomography [CT] scan, or intravenous 

pyelogram) and lower (via urodynamics, cystogram, 

or cystoscopy) tracts. 

Urinary Tract Infection

Bacteriuria (> 100,000 organisms per mL) is a nearly 

inevitable consequence of neurogenic bladder.137 Bacteriuria is not treated if it is asymptomatic. Symptoms 

of UTI prompting antibiotic treatment may include 

fever, shaking chills, leukocytosis, hematuria, pyuria, 

and unexplained increase in spasticity. Preventing UTI 

may involve ensuring adequate bladder drainage with 

a low postvoid residual, perineal hygiene, cleaning the 

drainage tube and bag, clean catheterization (washing 

hands and catheter with soap and water for those on 

intermittent catheterization), and eliminating urinary 

tract stones.138 The role of prophylactic antibiotics in 

preventing recurrent UTIs has not been clarified because of concerns about promoting multidrug-resistant 

organisms.137 High fevers and shaking chills suggest 

urosepsis, which requires broad antibiotic coverage 

(including antipseudomonal coverage), placement of 

an indwelling catheter to assure bladder drainage, and 

a renal ultrasound to rule out upper tract obstruction. If 

the patient fails to respond to antibiotics within 48 to 72 

hours or sustains septic shock, an abdominal CT scan 

should be performed to rule out perinephric abscess.

Bladder and Renal Calculi

Bladder stones may cause bladder spasms or urinary sediment and are often removed by transurethral 

cystolithectomy. Renal stones are most commonly 

infection-associated struvite stones caused by vesicoureteral reflux and urea-splitting organisms, such 

as Proteus mirabilis. Another risk factor for stone formation in recently injured patients is hypercalciuria 

in response to paralysis. If stones are large enough to 

obstruct the ureter, SCI patients must be closely monitored until treated because upper tract obstruction may 

be relatively silent in patients with impaired sensation 

until urosepsis develops. Upper tract stones may be 

removed by extracorporeal shock wave lithotripsy or 

percutaneous procedures.

Bladder Carcinoma

SCI patients with long-term indwelling catheters 

have an increased risk of bladder carcinoma.139 There 

is no consensus on appropriate screening, although 

some advocate for yearly cystoscopy and biopsy of the 

bladder for those who have had indwelling catheters 

for more than 10 years.

Sexual Function and Fertility

Individuals with SCI need to be reassured of their 

ability to express their sexuality, and they may need 

to be provided with information about techniques and 

devices they can use to assist them with that expression. Individuals should be encouraged to consider 

how increased physical dependency will play a role in 

their feelings of control or powerlessness and desirability. Sexual activities and barriers to sexual expression 

should be identified and addressed. 

Individuals with SCI should be provided with information on sexual function and made aware that sexual 

desires are psychological and hormonal, not affected 

by nerve damage. Pleasurable sexual experience may 

be realized by focusing on skin, lips, and other areas 

where sensation is intact. Information about manual 

stimulation, oral–genital sex, positioning, and effects 

of spasticity can be discussed. 

Despite absent sensation below the level of injury, 

many males, particularly those with neurologic lesions above the S-2 to S-4 levels or incomplete lower 

lesions, are sometimes able to achieve and maintain 

erections (the overall rate is 50% for all categories of 

injury). Oral medications (ie, phosphodiesterase type 5 

inhibitors), external appliances, intracavernosal injections (eg, prostaglandin E, papaverine), and implanted 

penile prostheses are additional options to maintain 

sexual function. Although many men with SCI are 

able to achieve erections, most are unable to ejaculate. 

Vibration-induced ejaculation or electroejaculation 

can yield sperm for artificial insemination in some 

individuals. AD is a small risk with these procedures 

in men with injuries at or above level T-6. Fertility in 

men diminishes to less than 5% with clinically complete injuries. Semen quality declines rapidly after SCI, 
442

Care of the Combat Amputee

possibly because of recurrent UTIs and increased testicle temperature. Nonetheless, artificial insemination 

with semen obtained by electroejaculation or more 

invasive techniques has resulted in pregnancies and 

healthy live births.

For females, loss of sensation and lack of vaginal 

lubrication are the primary sexual changes after SCI. 

Many women with SCI are able to achieve orgasm, 

although the perception of orgasm may be altered 

from preinjury experience.140 Use of a vibrator and 

lubricants can be helpful when engaging in sexual 

activity. Emptying the bladder by catheterization and 

decreasing fluid intake prior to intercourse can help 

reduce the chance of bladder incontinence.

Female fertility returns to preinjury level once 

the body has recovered from the initial trauma and 

menses return. Oral contraceptives and intrauterine 

devices carry extra risks for women with SCI, making 

foam and condoms better birth control choices. The 

physiology of labor is unaltered by SCI; however, 

impaired sensation may lead to undetected labor 

pains and presentation in later stages of labor, or, 

rarely, unsupervised birth. Prolonged or mechanically assisted labor (due to compromised ability to 

push), and AD in those with SCI above level T-7 are 

additional risks of pregnancy and childbirth in this 

population.

Because of the extraordinary physical and emotional demands on patients following SCI, sexual 

and marital counseling should be offered during 

rehabilitation. It is essential that the rehabilitation 

team respect individuals’ values and approach this 

topic with sensitivity. 

Psychological Issues

Assessment and support are the two major psychological services offered to individuals with SCI. 

Assessment is the evaluation of the individual’s 

potential to learn, think, and interact with the environment and others. Standardized tests that measure 

psychosocial function and intelligence are used for 

assessment. These tests provide a clear picture of an 

individual’s potential for rehabilitation and suggest 

appropriate guidelines for educational and vocational 

pursuits.

The other major psychological service to SCI patients, support, should extend to patients and family 

members. It should be grounded in knowledge of 

the patient’s history, disposition, values, limitations, and 

potential. In addition to psychologists, members of the rehabilitation team, particularly social workers, vocational 

counselors, and recreation therapists, also contribute to 

a patient’s psychosocial adjustment to SCI. 

Denial or inability to accept SCI is common and can 

interfere with rehabilitation, although expectations 

for recovery may be a source of motivation. Patients 

are counseled to focus on current rehabilitation issues 

without destroying hopes of recovery. Confronting 

a patient’s denial can destroy the physician–patient 

relationship. Eventually, many patients accept their 

conditions and approach their physicians for information on prognosis.

Associated Traumatic Brain Injury

A significant percentage of SCI patients incur traumatic brain injuries at the time of SCI or have a prior 

history of traumatic brain injury.141–143 Resulting agitation, impulsiveness, impaired judgment, and impaired 

new learning may all impact rehabilitation.

Premorbid Personality

Premorbid factors affect rehabilitation outcomes 

and should be considered during acute rehabilitation. 

Risk-taking behavior and drug and alcohol abuse are 

associated with some cases of SCI and affect adjustment to disability after SCI. More preinjury education 

is associated with greater likelihood of employment 

after SCI; among those with less than 12 years of education, only 38% returned to work after SCI, compared to 

93% of those with 16 or more years of education.43

Reactive Depression and Suicide

A depressed mood is common following SCI. When 

depression is extreme or prolonged, it can interfere 

with rehabilitation and precipitate suicide. Suicide 

rates are higher in individuals with SCI than in a 

matched general population.144 Risk factors for suicide 

include chronic pain and alcohol or drug abuse.

Marital Adjustment and Discord

Divorce is common after SCI. Factors that may contribute to divorce are altered family roles, dependence 

on a caregiver–spouse (with subsequent burnout), and 

impaired sexual function.

Health Maintenance

Periodic comprehensive evaluations of medical and functional status are recommended for 

individuals with SCI after initial rehabilitation. 

Although the optimal frequency for each type of 

assessment has not been determined, it is standard 

practice to perform comprehensive evaluations an-
443

Spinal Cord Injury Rehabilitation

nually. In addition to a general history and physical examination, the assessment should evaluate 

the neurologic system, skin, urogenital system and 

neurogenic bladder management, functional status, 

and equipment needs. The patients’ psychosocial 

and vocational adjustments should also be assessed.

ORGANIZATION OF A SPINAL CORD INJURY UNIT

Acute trauma facilities, including those used by 

the US military, usually lack comprehensive SCI 

units. Rather, they have orthopedists, neurosurgeons, 

physiatrists, physical and occupational therapists, psychologists, social workers, and skilled nurses who can 

decompress the spinal cord, establish spine stability, 

prevent acute medical complications, and begin the 

initial process of rehabilitation. As soon as patients 

are medically stable, they are transferred to specialized SCI rehabilitation facilities. The US military has 

a long-standing agreement with the US Department 

of Veterans Affairs to transfer patients to one of 23 

Veterans Affairs SCI centers. A comprehensive SCI 

facility employs physiatrists, urologists, orthopaedic 

surgeons, neurosurgeons, internists, plastic surgeons, 

rehabilitation nurses, physical and occupational 

therapists, psychologists, social workers, vocational 

counselors, orthotists, recreation therapists, respiratory 

therapists, and dietitians. Specialized facilities in an 

SCI unit include urodynamics with videofluoroscopy, 

advanced neuroimaging, a physical and occupational 

therapy gym, and a wheelchair-accessible pool. All 

patient care space must be wheelchair and gurney accessible. An independent living apartment, where SCI 

patients can live with spouse or attendant support, is 

particularly useful when the patient’s ability to return 

to the community is uncertain.

Compared to a medical, surgical, or general rehabilitation ward, a specialized SCI unit can anticipate and 

minimize complications and enhance functional outcomes, which results in shorter hospitalizations, fewer 

rehospitalizations, and less economic cost. Expertise, 

unique team relationships, and specialized equipment 

and facilities contribute to the efficiency of an SCI unit. 

Specialized SCI centers allow clinical and applied basic 

research to further improve SCI care.

SUMMARY

Prior to World War II, SCI was usually fatal. Now, 

most SCI patients survive, return home completely or 

partially independent, have only modestly reduced life 

expectancy, and achieve satisfactory quality of life. For 

most SCI patients, these favorable outcomes can be 

expected if the emergency, acute, and rehabilitative interventions during the first 6 months following injury 

are appropriate. SCI leads to multiorgan dysfunction, 

partially mediated by autonomic dysfunction, and loss 

of somatic sensation, making diagnosis challenging. 

Strength, sensation, blood pressure control, bladder 

and bowel emptying, and sexual function are often 

impaired in individuals with SCI. Life-threatening or 

disabling conditions that affect organ systems, such as 

pressure ulcers, DVT with pulmonary embolism, AD, 

OH, HO, posttraumatic syringomyelia, depression, 

and suicide, must be prevented or diagnosed and 

treated early. In addition, SCI patients must undergo 

extensive training in order to resume maximum function. Specialized training and adaptive equipment 

is required for mobility and independent self care. 

Guidance and instruction is required for psychological, 

social, financial, vocational, and avocational adjustment to disability.

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