Chronic complications of spinal cord injury and

disease
Authors:
Gary M Abrams, MD
Marc Wakasa, MD
Section Editors:
Michael J Aminoff, MD, DSc
Maria J Silveira, MD, MA, MPH
Deputy Editor:
Janet L Wilterdink, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jan 2019. | This topic last updated: Dec 06, 2018.

INTRODUCTION Spinal cord injury (SCI) is a common event; in the United States, the
incidence of traumatic SCI is approximately 54 per million persons per year, with approximately
280,000 living survivors of traumatic SCI in 2017 [1]. The prevalence of nontraumatic SCI is
unknown, but it is estimated that it is three to four times greater than traumatic SCI [2]. SCI
produces a wide variety of changes in systemic physiology that can lead to a number of
complications, which rival the neurologic deficits in their impact on function and quality of life.

Medical complications after SCI are both common and severe. In the Model Spinal Cord Injury
Systems Database, rehospitalizations occurred in 55 percent of patients in the first year after
SCI and continued at a stable rate of approximately 37 percent per year over the next 20 years
[3]. Genitourinary and respiratory complications and pressure ulcers were the most common
reasons for hospitalization. Increased patient age and severity of the spinal cord lesion also
impacted on the risk of complications requiring hospitalization.

This topic reviews the management of common complications of chronic SCI, whether due to
trauma or other conditions. Acute manifestations and complications of SCI are presented
separately. (See "Acute traumatic spinal cord injury" and "Disorders affecting the spinal cord".)

LIFE EXPECTANCY Life expectancy is reduced among survivors of SCI. Mortality rates
are highest in the first year. For patients surviving at least one year after traumatic SCI, life
expectancy is approximately 90 percent of normal [4-6]. Higher neurologic level and severity of
injury and older age at the time of SCI negatively impact survival.

The most common causes of death after traumatic SCI are diseases of the respiratory system
followed by cardiovascular events [4,5]. In earlier decades (prior to 1972), urinary
complications were the leading cause of death. The risk of suicide is also increased among
patients with SCI [6]. (See 'Psychiatric complications' below.)

CARDIOVASCULAR COMPLICATIONS
Autonomic dysreflexia — SCI above T6 may be complicated by a phenomenon known as
autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to
demands on heart rate and vascular tone [7,8]. Uninhibited or exaggerated sympathetic
responses to noxious stimuli below the level of the injury lead to diffuse vasoconstriction and
hypertension. A compensatory parasympathetic response produces bradycardia and
vasodilation above the level of the lesion, but this is not sufficient to reduce elevated blood
pressure. SCI lesions lower than T6 do not produce this complication, because intact
splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.

The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of
patients with SCI lesions above T6 [7,8]. Autonomic dysreflexia is unusual within the first
month of SCI but usually appears within the first year [9,10].

Typical stimuli include bladder distention, bowel impaction, pressure sores, bone fracture, or
occult visceral disturbances [7,8]. Sexual activity can be a trigger. Autonomic dysreflexia can
also complicate medical procedures, as well as labor and delivery. (See "Neurologic disorders
complicating pregnancy", section on 'Spinal cord injury'.)

Common clinical manifestations are headache, diaphoresis, and increased blood pressure [9].
Flushing, piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur.
Bradycardia is common; however, some patients have tachycardia instead. The severity of
attacks ranges from asymptomatic hypertension to hypertensive crisis complicated by profound
bradycardia and cardiac arrest or intracranial hemorrhage and seizures. The severity of the
SCI influences both the frequency and severity of attacks.

Management of acute attacks includes [7,9]:

●Measuring and monitoring blood pressure.

●Immediately sitting the patient upright to orthostatically lower blood pressure.
●Removal of tight-fitting garments.
●Searching for and correcting noxious inciting stimuli. Bladder distension and fecal
impaction are the most common precipitants. Bladder catheterization and evaluation for
urinary tract infection (UTI) should be undertaken; indwelling catheters should be checked
for obstruction, and a rectal examination should be performed.
●Prompt reduction of blood pressure with a rapid-onset/short-duration agent, depending
on the severity of attack and response to above measures. Medications often used in this
setting include nitrates (1 inch, 2 percent nitropaste), nifedipine (10 mg oral or sublingual),
intravenous hydralazine (10 mg), and intravenous labetalol (10 mg). Nitrates should be
avoided in patients who may be using sildenafil for erectile dysfunction.

Recognition and avoidance of inciting stimuli are important in preventing

attacks. Nifedipine, prazosin, and terazosin have been reported to prevent an attack when
administered prophylactically; botulinum toxin used to treat bladder dysfunction in SCI may
also be effective in reducing attacks [7,8,11-13].

Coronary artery disease — With improved long-term survival, coronary artery disease (CAD)
has become an increasingly important complication in SCI [5]. CAD risk factors, such as
adverse lipid profile (low levels of high-density lipoproteins, elevated low-density lipoprotein
cholesterol) and abnormal glucose metabolism (impaired glucose tolerance, insulin resistance,
and diabetes) are more prevalent in chronic SCI patients than the able-bodied population [14].
Factors that contribute to the development of these disorders include decreased muscle mass,
increased fat, and inactivity [15]. Studies suggest that the prevalence of CAD is 3 to 10 times
higher in SCI patients compared with the general population [14]. In addition, a nationwide
cohort study in Taiwan found that SCI was associated with an increased risk of stroke (hazard
ratio [HR] = 2.9) [16].

CAD mortality also appears to be higher among SCI patients [5]. One contributing factor may
be that SCI lesions above the T5 level may lead to atypical presentations for cardiac ischemia;
manifestations may include autonomic dysreflexia or changes in spasticity rather than typical
chest pain.
Risk factor management and treatment for CAD are similar to that of able-bodied individuals.
(See "Overview of established risk factors for cardiovascular disease".)

Exercise options for SCI patients include hand-crank ergometry, hand cycling, swimming, and
functional electrical stimulation of muscles [17]. Body weight-supported treadmill training has
been reported to improve glucose regulation in incomplete SCI [18]. However, diminished
sympathetic responses, reduced cardiac output, impaired ventilation, and decreased muscle
mass lead to reduced exercise capacity in chronic SCI [14]. Physiologic responses to exercise,
including increased heart rate, increased cardiac contractility, and vasoregulation, are also
impaired with higher-level SCI.

Others — The autonomic nervous system dysfunction that results from SCI disrupts normal
cardiovascular homeostasis. With SCI above the T6 level, baseline blood pressure is usually
reduced, and baseline heart rate may be as low as 50 to 60 beats per minute [14,19]. This is
generally not a clinical problem but may contribute to hemodynamic instability and exercise
intolerance.

Orthostatic hypotension due to peripheral vasodilatation is more common in the first several
months of SCI and tends to dissipate with the development of muscle tone in the lower
extremities [9]. However, it may also occur in chronic SCI, especially with excessive bed rest
and diminished fluid intake. Gradual position changes, compression stockings, and abdominal
binders decrease venous pooling and may improve orthostatic tolerance. Occasionally,
increased salt intake, alpha adrenergic agonists (midodrine), or mineralocorticoid agents
(fludrocortisone) may be required. (See "Treatment of orthostatic and postprandial
hypotension".)

Acute cervical SCI is associated with a risk of cardiac arrhythmia due to excess vagal tone, as
well as hypoxia, hypotension, and fluid and electrolyte imbalances. Arrhythmias are much less
frequent in chronic SCI. However, patients with complete cervical SCI appear to have an
ongoing risk of cardiopulmonary arrest [20,21].

PULMONARY COMPLICATIONS Cervical and high thoracic SCI affect respiratory

muscles. The severity of ventilatory failure and requirement for assisted ventilation depend on
the level and severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea
and exercise intolerance. Respiratory muscle training is effective for increasing respiratory
muscle strength and function for people with cervical SCI [22]. (See "Respiratory physiologic
changes following spinal cord injury" and "Respiratory complications in the adult patient with
chronic spinal cord injury", section on 'Respiratory insufficiency'.)

Because of impaired cough and difficulty mobilizing lung secretions, patients after SCI are also
at increased risk for pneumonia. Although the incidence of pneumonia is highest in the first
year following SCI, these patients remain at increased risk over their lifetime [23]. Older
patients are at higher risk than younger patients. Efforts to prevent pneumonia include chest
physiotherapy and vaccination. (See "Respiratory complications in the adult patient with
chronic spinal cord injury", section on 'Pulmonary infection'.)

Deep venous thrombosis and pulmonary embolism remain common early complications of SCI
despite advances in awareness and treatment. Prophylactic use of low molecular weight
heparin is the treatment of choice for most patients with SCI. While there are no good clinical
trial data to guide duration of treatment, we suggest that it should be continued in paralyzed
patients for at least three months after SCI, after which the risk appears to approximate that of
the general population [24]. Specific regimens are discussed separately. (See "Prevention of
venous thromboembolic disease in adult nonorthopedic surgical patients".)
URINARY COMPLICATIONS SCI produces bladder dysfunction, often referred to as the
neurogenic bladder. Other complications can result from this, including infections,
vesicoureteral reflux, renal failure, and renal calculi.

Urologic evaluation with regular follow-up is recommended for all patients after SCI; even
ambulatory patients with SCI may have bladder dysfunction that can lead to complications [25].
Complications such as vesicoureteral reflux, renal failure, and nephrolithiasis may not produce
symptoms and, if untreated, can have serious consequences. The frequency and specific
testing involved (serum creatinine, cystoscopy, urodynamic studies, renal ultrasound) are not
well defined but depend in part on the nature of the patient's urologic problems and other risk
factors [26,27].

Bladder dysfunction — SCI disrupts the two major functions of the bladder, storage and
emptying of urine. Bladder control is a complex activity requiring the coordinated function of the
cerebral cortex, pontine and sacral micturition centers, and peripheral nervous system [28]
(see "Anatomy and localization of spinal cord disorders", section on 'Autonomic fibers'). In SCI,
the sensation for bladder fullness as well as motor control of bladder and sphincter function are
impaired. Depending on the acuity, level, and completeness of the spinal cord lesion, a number
of problems can result:
●Bladder or detrusor hyperactivity produces reflexive bladder emptying. Patients may be
troubled by bladder spasms as well as urgency and frequency, often with incontinence.
Over time, this can lead to decreased capacity of the bladder.
●Sphincter hyperactivity can impair complete emptying of the bladder.
●Detrusor sphincter dyssynergia, a combination of detrusor and sphincter hyperactivity,
can lead to bladder contractions against a closed sphincter, leading to elevated bladder
pressures and vesicoureteral reflux.
●Bladder flaccidity is produced in lower motor neuron injuries affecting the cauda equina
or conus medullaris as well as with acute upper motor neuron injuries (spinal shock). This
leads to chronic urinary retention with overflow incontinence and incomplete emptying.

Most patients with incomplete SCI and all patients with complete SCI, regardless of the level of
the lesion, require assistance with bladder function [23]. Although there are no clinical trials
that guide the long-term management of bladder dysfunction in SCI, accumulated clinical
experience has led to some management strategies [29,30]. The efficacy of these approaches
may be manifest by the declining incidence of urinary tract-related morbidity and mortality in
SCI patients [5,23].

The goal of an SCI bladder program is to preserve renal function while eliminating urine at
regular and socially acceptable times, avoiding high bladder pressures, retention, incontinence,
and infection. This should begin as early as possible after SCI, with removal of the indwelling
Foley catheter.

Clean technique intermittent catheterization (CIC) has a lower infection rate compared with the
use of indwelling catheters [23]; there are insufficient data to recommend a catheter type or
clean versus aseptic technique [31]. CIC is performed at regular intervals, usually every four
hours. A bladder volume of less than 500 cm3 of urine is targeted in order to avoid bladder
distention, excessive intravesicular pressure, and reflux, as well as to reduce the incidence of
infections. The timing of CIC and the amount of fluid intake is adjusted to reach this goal. A
fluid intake restriction of two liters a day is common for patients with SCI. If present, a
sensation of fullness and attempt at voluntary voiding is encouraged prior to CIC, since some
incompletely injured persons will regain normal voiding function.

Intermittent urinary incontinence is expected. Condom catheters (for men) and adult diapers
are important short-term interventions. After ruling out an infection and adjusting the frequency
of CIC and fluid intake, medications are considered. Urodynamic studies should be considered
to assess physiology and guide pharmacologic intervention [26]:

●Anticholinergic medications (eg, oxybutynin, tolterodine) decrease bladder tone,

suppress bladder contractions, and may reduce urinary frequency and incontinence.
Tricyclic antidepressants such as imipramine have the added side effect of increasing
urethral resistance tone.
●Alpha adrenergic medications (ephedrine and phenylpropanolamine) can increase
bladder storage in patients with pathologic relaxation of the sphincter.
●Cholinergic medications (bethanechol) may help complete bladder emptying in those
with hypotonic bladders.
●Alpha-blockers (eg, prazosin, terazosin) help sphincter relaxation, lowering bladder
pressures during contraction. These can be prescribed for treatment of detrusor sphincter
dyssynergia but may aggravate hypotension.

Most patients are managed with a combination of CIC and oral anticholinergic medications
[32].

For patients unable to perform CIC and without available caregivers, a chronic indwelling
catheter may be necessary. This is associated with an increased risk of urinary tract infection
(UTI) compared with CIC [33]. The indwelling catheter is changed every month to minimize
infections. Oxybutynin chloride (5 mg twice a day) can decrease catheter-induced bladder
spasms. With indwelling catheters, there is an increased risk of prostatitis, epididymitis, and
urethral stricture. Suprapubic tube placement can help minimize the risks of infection and
stricture. A cystoscopy every two years is recommended to monitor for the increased incidence
of bladder cancer and stone development [26].

Studies of detrusor injections of botulinum toxin A in patients with detrusor hyperactivity

suggest that this treatment is safe and effective in controlling symptoms and improving quality
of life [32,34-37]. However, the optimal dose has not been determined, and long-term efficacy
is unknown [38]. There have been no comparative studies with anticholinergic agents [39]. The
use of botulinum toxin for the treatment of non-neurogenic lower urinary tract dysfunction is
discussed separately. (See "Use of botulinum toxin for treatment of non-neurogenic lower
urinary tract conditions".)

Studies of implanted sacral nerve modulators show promise as a treatment for urinary
incontinence following SCI [40,41].

For patients with unsatisfactory response to medical and catheter management, other
treatments, bladder augmentation, urinary diversion, sphincterotomy, urethral stent, and
electrical implantation devices can be considered in selected cases, although there is limited
evidence of their comparative efficacy [2,26,38].

Urinary tract infection — UTIs are common in SCI, with an incidence of 2.5 episodes per
patient per year [42]. The urinary tract is the most frequent source of septicemia in SCI patients
and has a high mortality rate (15 percent) [42,43]. UTI is more common in women than men.
Low-frequency and high-volume catheterization increase the risk of UTI, as do indwelling
catheters and assisted (as opposed to self) intermittent catheterization [33,44,45].

Symptomatic UTI, as manifest by fever, autonomic dysreflexia, increased spasticity, foul-

smelling urine, incontinence, frequency, or dysuria, warrants prompt antibiotic treatment to
avoid septicemia and other complications. (See "Acute simple cystitis in women" and "Acute
simple cystitis in men" and "Acute complicated urinary tract infection (including pyelonephritis)
in adults".)
Asymptomatic UTIs are not generally treated; nor is there a role for routine use of prophylactic
antibiotics to prevent UTI in SCI patients, despite the fact that asymptomatic bacteriuria is
common after SCI and is associated with a higher risk of symptomatic UTI [44]. A meta-
analysis of published literature found that antibiotic prophylaxis in patients with SCI reduced
asymptomatic bacteriuria but not symptomatic infections, and was associated with a twofold
increase in the risk of drug-resistant bacteria [46]. However, some individuals with recurrent
UTI may benefit from prophylactic antibiotic treatment, depending on the frequency and clinical
severity of the infections. In particular, the combination of frequent UTI and vesicoureteral
reflux is associated with a high risk of renal failure. (See "Recurrent simple cystitis in women".)

Other methods of reducing the incidence of UTI are under investigation and include
colonization of the urinary tract with inert bacterial strains [47]. Cranberry juice is believed to
reduce bacterial adherence to the uroepithelium and thereby prevent UTI [48]. However, its
efficacy is unproven, and the associated fluid and caloric intake may be problematic in
individuals with SCI. In two small clinical trials, a cranberry supplement was found ineffective in
reducing bacteriuria, pyuria, or UTI in patients with SCI [49,50].

Urinary calculi — Calculi in the kidney, ureter, or bladder are increased after SCI, especially
in patients who have recurrent UTIs, indwelling catheters, and immobilization hypercalciuria
[23] (see 'Bone metabolism' below). Because of altered bladder sensation, there may not be
pain to alert the clinician to ureteral obstruction. Other clinical symptoms such as increased
limb spasticity and episodes of autonomic dysreflexia should suggest this as a possible
diagnosis. (See 'Autonomic dysreflexia' above.)

The diagnosis and treatment of urinary calculi are discussed separately. (See "Diagnosis and
acute management of suspected nephrolithiasis in adults" and "Options in the management of
renal and ureteral stones in adults".)

Vesicoureteral reflux — Impaired function of the vesicoureteral insertion may result from high
bladder pressures and recurrent UTI. The estimated incidence of this complication in SCI
patients is as high as 25 percent [51,52]. Because persistent reflux is associated with a higher
risk of pyelonephritis and renal dysfunction, it represents a treatment imperative. If reflux
persists despite the use of anticholinergic drugs and increased frequency of catheterization,
placement of an indwelling catheter or a surgical procedure may be necessary. The use
of oxybutynin may reduce phasic increases in bladder pressure caused by bladder spasms
with an indwelling catheter [53].

Renal insufficiency — The cumulative incidence of renal insufficiency increases with time

since SCI and is as high as 25 percent at 20 years [23,54,55]. Indwelling urethral catheters,
vesicoureteral reflux, and advanced age are associated with the development of renal failure.

SEXUAL DYSFUNCTION Consequences of SCI on sexual function include decreased

libido, impotence, and infertility [56].

●Male impotence occurs in 75 percent of patients with SCI [26]. Patients with complete as
opposed to incomplete injuries have the greatest incidence and severity of this
complication. There are a variety of treatment options for erectile dysfunction, including
medications, assistive devices, and surgically implanted prostheses. Sildenafil, vardenafil,
and tadalafil have documented efficacy in SCI, but are contraindicated (as are other
phosphodiesterase-5 inhibitors) if there is comorbid coronary artery disease (CAD) [57-
62]. (See "Treatment of male sexual dysfunction".)
●The prevalence of male infertility in SCI is high as a consequence of erectile dysfunction,
ejaculatory dysfunction, and/or poor sperm quality [27,56]. In general, male reproduction
 after SCI requires artificial insemination. (See "Approach to the male with
infertility" and "Treatments for male infertility".)
●Sexual responses in women may also be impaired after SCI, but ovulation and fertility
are generally unaffected [26,56]. The lower pregnancy rates among women with SCI as
compared with the general population are felt to reflect personal choice. Pregnancy in
women with SCI is generally categorized as high risk because of a high rate of
complications including infections and autonomic dysreflexia. This is discussed
separately. (See "Neurologic disorders complicating pregnancy", section on 'Spinal cord
injury'.)

GASTROINTESTINAL COMPLICATIONS Bowel dysfunction is common and disabling

after SCI and significantly affects functional and quality-of-life outcomes [63-65]. A
multidimensional program is frequently necessary to obtain the best results [66].

Two patterns of bowel dysfunction may occur [67]. With injuries above the conus medullaris,
neural connections between the spinal cord and bowel are maintained, resulting in
hyperreflexic pelvic muscle contraction and inability to voluntarily relax the external anal
sphincter. This causes constipation and fecal retention. A lower motor neuron or areflexic
bowel occurs with injuries below the conus medullaris, leading to slower transit, decreased
sphincter tone, and constipation with frequent incontinence.

Because few studies have evaluated the management of this problem, recommendations are
based on clinical experience and expert opinion [67,68]. With a goal of predictable and timely
bowel evacuation that avoids fecal incontinence and impaction, a consistent, structured
regimen is integrated into the patient's lifestyle as early as possible after SCI, using their
preinjury bowel pattern as a guide [9,56]. A typical routine may begin at a regular time point
each day (eg, 30 minutes after a meal) with insertion of a chemical stimulant rectal suppository.
After several minutes, digital stimulation with slow, gentle rotation of the finger for 15 to 60
seconds is repeated every 5 to 10 minutes, until stool evacuation is complete. Abdominal
massage, deep breathing, Valsalva maneuver, and forward-leaning position may assist
evacuation [66].

Oral bowel medications (stool softener, docusate sodium; bowel

stimulants, senna and bisacodyl; bulking agents, psyllium) are often used during the initial
phase of establishing a regular bowel pattern, and are then slowly eliminated [67]. Chronic use
of stimulant laxatives is associated with a number of side effects. (See "Management of
chronic constipation in adults", section on 'Other laxatives'.)

A regular diet is an important feature of the bowel program and should include adequate fiber
intake (30 g) and relatively lower amounts of dairy products and fat content [9,67]. Targets for
fluid intake are often dictated by the patient's bladder status, but if possible, should be high
enough to produce 2 to 3 liters of urinary output each day.

Despite these measures, complications of bowel dysfunction occur in some patients:

●If constipation or impaction develops, a trial of enemas, laxatives, or bulk-forming

agents may be considered [67]. Abdominal radiographs should be considered to screen
for evidence of obstruction. Diseases not related to the SCI, particularly colorectal cancer,
should be excluded. Prokinetic medications (eg, cisapride, metoclopramide) are reserved
for persistent, severe constipation that is unresponsive to modifications of the bowel
program [66]. Some patients with severe bowel dysfunction require a colostomy.
Uncontrolled observational studies suggest that regular transanal irrigation can reduce
constipation and fecal incontinence and improve quality of life in some patients with
 chronic bowel dysfunction following SCI [69-71]. Sacral and other electrical stimulation
techniques may be useful for some patients [72].
Details regarding the treatment of constipation and fecal incontinence are discussed
separately. (See "Management of chronic constipation in adults" and "Fecal incontinence
in adults: Management".)
●Hemorrhoids can be increased by the interventions (suppositories, enemas, digital
stimulation) commonly used in bowel programs for SCI. Treatment includes stool
softeners, minimizing trauma, topical anti-inflammatory creams, and suppositories.
Hemorrhoids causing persistent bleeding, pain, or autonomic dysreflexia warrant surgical
consultation. (See "Home and office treatment of symptomatic hemorrhoids".)
●Serious abdominal complications (cholecystitis, upper gastrointestinal bleeding,
pancreatitis, or appendicitis) account for 10 percent of deaths following SCI, with the most
significant risks during the first few months after injury [19,73]. There is an increased
prevalence of gallstones in patients with chronic SCI, perhaps in relationship to
denervation [74]. Sensory deficits resulting from SCI contribute to a delay in diagnosis
and increased mortality associated with these complications. Vague or nonspecific
symptoms such as nausea, anorexia, or autonomic dysreflexia should raise concern for
occult abdominal processes [19].
●The superior mesenteric artery syndrome is an unusual complication of SCI, usually
in patients with cervical cord injuries [75,76]. Weight loss leads to loss of the mesenteric
fat pad and compression of the duodenum by the superior mesenteric artery, leading to
symptoms of small bowel obstruction. (See "Superior mesenteric artery syndrome".)

BONE METABOLISM
Osteoporosis — After SCI, osteoporosis affects bones below the level of the injury and
increases the risk of lower-extremity fractures. In one series of 41 men, after a median of 15
years after SCI, 61 percent had osteoporosis and 34 percent had had a fracture [77].

The pathogenesis of osteoporosis is unknown; neural factors as well as disuse are believed to
play a role [78]. Biomarkers of bone resorption are increased, beginning as early as the first
week after injury, while markers of bone formation are normal or only minimally elevated
[78,79]. Some studies suggest that approximately two years after SCI, a new steady state level
between bone resorption and formation is reestablished [78]. Older age, higher spinal level of
injury, lesser degrees of spasticity, and longer chronicity of the injury have been inconsistently
associated with higher degrees of observed bone loss [23,78-82]. Rates of osteoporosis
among men and premenopausal women with SCI are similar; too few postmenopausal women
with SCI have been included in studies to know whether this population is at additional risk
[27].

Occasionally, symptomatic hypercalcemia and hypercalciuria complicate early resorption of

bone mass within the first few months of SCI [9]. Manifestations can include nausea, vomiting,
anorexia, lethargy, and polyuria. There is an increased risk of nephrolithiasis [79]. Treatment is
graded to severity of symptoms. Intravenous pamidronate has been used for acute
immobilization hypercalcemia after SCI [83,84]. (See "Clinical manifestations of
hypercalcemia" and "Treatment of hypercalcemia".)

Over time, patients with SCI develop a specific pattern of bone abnormalities, with marked loss
of bone density in the proximal tibia and femur, and relatively less bone loss in the spine
[80,85]. The impact of weight-bearing on the spine during sitting and wheelchair use may
contribute to this discrepancy [79]. Patients with quadriparesis may also experience bone loss
in the distal forearm [82].
In small observational and open-label, randomized studies, treatment with bisphosphonates
such as tiludronate, etidronate, pamidronate, and alendronate has been shown to attenuate
bone loss in patients with SCI [86-89]. In one small, double-blind, randomized trial (31
patients), alendronate (70 mg weekly) was also shown to prevent bone loss at the hip when
administered within 10 days of acute SCI [90]. Functional electrical stimulation has shown
minimal and largely unsustained benefits in improving bone density [79,91-93].

Heterotopic ossification — Heterotopic ossification refers to the deposition of bone within the

soft tissue around peripheral joints. This occurs in up to half of SCI patients, beginning at a
mean of 12 weeks after injury [94]. Although heterotopic ossification is common after SCI, only
10 to 20 percent of patients have clinical symptoms, with decreased range of motion and
inflammatory symptoms in the affected joints. The large joints below the level of injury are
typically affected, most commonly the hip. The pathogenesis of this phenomenon is
incompletely understood, but it is believed to originate from osteoprogenitor stem cells lying
dormant within the affected soft tissues. With the proper stimulus (as with hip surgery, SCI, and
stroke), these stem cells may differentiate into osteoblasts that form osteoid and eventually
bone. Heterotopic ossification in the setting of total hip arthroplasty is discussed separately. In
one case-control study of SCI patients, heterotopic ossification was more common in patients
with complete spinal cord lesions, more rostral injuries, and also in those with associated
thoracic trauma [95]. (See "Complications of total hip arthroplasty", section on 'Heterotopic
ossification'.)

Deep venous thrombosis, cellulitis, infection, hematoma, and tumor should be considered as
alternative diagnoses for localized pain in SCI patients. Because calcification may not appear
for weeks after clinical presentation, plain radiographs are of limited use in the early diagnosis.
An elevated serum alkaline phosphatase level can help differentiate early heterotopic
ossification from other conditions, but is not a specific finding [96]. The triple phase bone scan
is the most reliable test for diagnosis.

Early administration of nonsteroidal anti-inflammatory drugs (NSAIDs; indomethacin 75 mg

daily for three weeks or rofecoxib 25 mg daily for four weeks) after SCI appears to reduce the
incidence of heterotopic calcification according to a 2010 systematic review that included two
randomized trials [97-99]. Further research is required to identify which patients will benefit
from this intervention. Warfarin and pulse low-intensity electromagnetic field therapy may also
be useful in the prevention of heterotopic ossification, but a clinical role for these modalities for
this indication is not yet established.

The initial treatments of heterotopic ossification are passive range-of-motion exercise, with the
goal of maintaining joint mobility, and NSAIDS. Bisphosphonates may also be useful [97].
According to uncontrolled case series, etidronate (given intravenous for three days, followed by
six months of oral therapy) reduced swelling and retarded or halted progression of heterotopic
ossification, particularly if it was administered early, when bone scans were positive, but
radiographs remained normal [97,100-102]. Radiotherapy also appeared to limit progression in
one case series of 52 patients with heterotopic ossification after SCI [97,103]. For refractory
cases, surgery is a treatment option to allow functional range of movement; however, the
majority of patients experience recurrence after surgery [104]. A small retrospective study
found that intravenous pamidronate (a bisphosphonate) prevented recurrent heterotopic
ossification in patients undergoing excision surgery [94]. Reports of early resection in
combination with drug and radiation treatment also appear promising [105,106].

MUSCULOSKELETAL COMPLICATIONS After SCI, muscle contractures can result

from reorganization of the collagen tissue matrix that occurs when the muscle lies in the
shortened position for an extended period of time. Both immobility and spasticity contribute to
this occurrence [107]. Preventive management is extremely important and should begin
immediately after an SCI and continue for long-term care:

●Positioning. While in bed, the patient should be positioned, using pillows to minimize
flexion at the hip and knee, and adduction and internal rotation at the shoulder.
Wheelchair positioning should maintain normal lumbar lordosis. Frequent repositioning
prevents skin breakdown as well as contractures; these complications often coexist [107].
●Range-of-motion exercise. Paretic extremity joints should be exercised 5 to 20 minutes
daily. The intensity of exercises needed to prevent deformity varies among individuals,
but the goal is maintenance of full range. Any limitation warrants investigation for
heterotopic ossification, fracture, hematoma, infection, or thrombosis.
●Splinting. Upper-extremity flexion contractures and ankle plantar-flexion contractures can
be prevented with resting night splints or bivalve (removable) casting. The fitting and
timing of splints must be adjusted based on skin and pain tolerance.

The goal of these interventions is to induce prolonged muscle stretching of vulnerable muscles;
however, their efficacy in preventing contractures has not been documented [108]. Established
contractures may require surgical treatment.

Certain contractures can facilitate function. Patients with SCI at C6 level may gain improved
functional hand tenodesis with finger flexion contractures that enhance prehension with wrist
extension. A slight elbow flexion contracture can improve the mechanical advantage of a
weakened biceps muscle.

Repetitive over-use injuries in the upper extremities are common in SCI patients, related to
transfers and wheelchair use. Rotator cuff and other tendon injuries, carpal tunnel syndrome,
bursitis, and osteoarthritis are common sequelae [109-111]. The shoulders are most often
affected (75 percent), followed by wrists, hands, and elbows (53, 43, and 35 percent,
respectively). Specific exercise programs to minimize injuries and preserve joint function can
be helpful, as can the use of power wheelchairs and ergonomic assessments [112].
(See "Overview of joint protection".)

PRESSURE ULCERS Pressure ulcers result from tissue damage due to unrelieved
pressure that typically occurs over bony prominences. Shear, friction, poor nutrition, and
changes in skin physiology below the level of the lesion also contribute to the development of
pressure ulcers [23]. Prevalence rates for pressure ulcers in chronic SCI are difficult to obtain,
but have been estimated at approximately 30 percent at 20 years following SCI [23,113]. Both
the level and severity of SCI impact significantly on the risk of developing a pressure ulcer.

Multiple pressure ulcers occur in more than one-third of patients [21]. The most common
locations of pressure ulcers in the SCI patient are [23]:

●Ischium – 31 percent
●Trochanter – 26 percent
●Sacrum – 18 percent
●Heel – 5 percent
●Malleolus – 4 percent
●Feet – 2 percent

Preventive strategies include:

●Examining skin over areas most vulnerable to ulcer formation daily

●Application
of emollients daily to reduce friction over areas at risk
●Teaching patients with upper body strength to do "pressure releases" throughout the day
 ●Avoiding immobility and excess moisture in susceptible regions
●Use of pressure-relieving wheelchairs, cushions, and other devices
●Maintenance of adequate nutritional intake and weight

Comprehensive treatment includes assessment of health status and status of the ulcer. An
ulcer treatment plan consists of cleansing, debridement, nutritional support, and management
of tissue loads. The prevention and treatment of pressure ulcers are discussed in detail
separately. (See "Prevention of pressure-induced skin and soft tissue injury" and "Clinical
staging and management of pressure-induced skin and soft tissue injury".)

SPASTICITY Spasticity is a velocity-dependent increase in muscle tone. On examination, it

is elicited by a quick passive movement of the limb [114]. Spasticity is believed to result from
disruption of descending inhibitory modulation of the alpha motor neurons, producing
hyperexcitability, which is manifest as increased muscle tone and spasms [115,116].

Negative effects of spasticity include pain, decreased mobility, contractures, and muscle
spasms, all of which can interfere with sleep and activities of daily living [117]. At the same
time, spasticity has some positive aspects: Increased tone can facilitate some functional
activities, including standing and transfers. Increased muscle tone may also promote venous
return, minimizing deep venous thrombosis and orthostatic hypotension.

Abolishing spasticity is difficult and not necessarily desirable [116]. Treatment should be
directed at minimizing spasticity as it relates to functional impairment and should follow a
graded approach, starting with the least invasive approach. Nonpharmacologic treatments
include physical therapy. Regular stretching and use of braces can help maintain range of
movement and prevent contractures, but have not been clearly shown to have a benefit on
important clinical outcomes [116,117]. (See 'Musculoskeletal complications' above.)

If spasticity worsens, then an explanation should be sought and treated if possible. Causes of
increased spasticity in such patients include infection, pain, and neurologic lesions such as
syringomyelia. (See 'Neurologic deterioration' below.)

Oral medications — Though often prescribed for spasticity, the evidence of efficacy for
commonly used oral medications is not substantial, side effects are often dose limiting, and the
relative benefit of these treatments has not been established [117,118]. With all medications,
slow dose escalation may mitigate adverse side effects, which include sedation, dry mouth,
dizziness, and weakness. Dosing guidelines and adverse effects of these medications are
summarized in the table (table 1).
●Baclofen, a gamma-aminobutyric acid B (GABA-B) agonist, is the most commonly used
oral medication for spasticity, despite the paucity of evidence-based support for its
efficacy [118-120]. Although adverse effects of sedation and weakness can be dose-
limiting, baclofen is safe for long-term use, without evidence of tolerance [116]. Baclofen
should not be stopped abruptly, because of potential withdrawal symptoms.
(See "Neuroleptic malignant syndrome", section on 'Other drug-related syndromes'.)
●Tizanidine, a centrally acting alpha-2 adrenergic agonist, was compared with placebo in
one of the largest studies of spasticity treatment in SCI patients [121]. Among the 78 of
124 randomized patients who completed the study, tizanidine produced a significant
reduction in spasticity, but had no effect on activities of daily living and other functional
assessments. Sedation was the most common limiting side effect [122].
●Diazepam, a GABA-A agonist, is the most commonly used benzodiazepine for spasticity,
often in conjunction with baclofen or tizanidine[115,123]. Sedation, confusion,
hypotension, and gastrointestinal symptoms can be dose-limiting. Diazepam
or clonazepam may be particularly useful in controlling nighttime spasms.
 Benzodiazepines should not be prescribed concurrently with opioids due to the added risk
of opioid overdose [124].
●Dantrolene sodium differs from other medications discussed in that it acts peripherally,
inhibiting calcium release from sarcoplasmic reticulum of the muscle [116]. More than the
other agents used, it produces weakness of both affected and unaffected muscles [120].
Its potential for hepatotoxicity requires liver function test monitoring every three to six
months [115].
●Less commonly used medications used for spasticity include clonidine, gabapentin,
cannabinoids, and cyproheptadine; these have less certain benefits (table 1) [115-
117,125-128].

Intrathecal baclofen — Baclofen is centrally acting, but crosses the blood-brain barrier

ineffectively, limiting its bioavailability when taken orally. Intrathecal baclofen allows for four
times the amount of baclofen to be delivered to the spinal cord with 1 percent of the oral dose
[19,116]. Treatment is administered by a surgically implanted, computer-programmed infusion
pump with a catheter extending into the intrathecal space. In general, patients undergo a trial
of intrathecal baclofen infusions prior to pump implantation. Although systemic side effects of
baclofen are generally avoided with this approach, complications of intrathecal baclofen
therapy can include spinal fluid leaks, hemorrhage, infection, catheter dislodgement, and pump
failure; however, pumps are generally well tolerated by most patients, especially those who are
vigilant and/or have vigilant caregivers.

Two double-blind crossover studies compared intrathecal baclofen infusion with saline placebo

in patients after SCI [129,130]. Patients treated with intrathecal baclofen had both reduced
spasticity and improved disability. This approach may also reduce pain associated with
spasticity [131].

Injection techniques — Chemodenervation provides a localized treatment of spasticity within

a muscle or muscle group. Although systemic side effects associated with medications are
avoided, the large number of muscles involved in SCI limit the use of this approach for these
patients. However, in some patients, targeted relief of spasticity in certain muscle groups can
improve ambulation and other specific functions. Agents include botulinum toxin, phenol, and
alcohol.

Botulinum toxin acts at the neuromuscular junction, preventing acetylcholine release.

Treatment effects are seen within a few days, peak at four to six weeks, and last a few months;
repeated injections are required to maintain efficacy [117]. Side effects include muscle
weakness and injection-site reactions, but in general this treatment is safe and effective [132].
One randomized study compared botulinum toxin injections with tizanidine for upper limb
spasticity following stroke or traumatic brain injury [122]. Botulinum toxin treatments were more
effective in reducing tone and were associated with fewer adverse effects than tizanidine.
Treatment of upper and lower limb spasticity is now a US Food and Drug Administration (FDA)
approved indication for botulinum toxin.

Phenol and ethanol nerve blocks essentially superimpose a lower motor neuron lesion on the
upper motor neuron deficit [115,116]. Weakness, injection site pain, phlebitis, permanent nerve
damage, and sensory dysesthesia can be problematic complications of this procedure.

Surgery — Surgical destructive procedures, rhizotomy, myelotomy, cordotomy, and

cordectomy are reserved for refractory cases [19]. Surgical muscle or tendon releases can be
used to treat established contractures.

PAIN SYNDROMES A significant number of patients develop a chronic pain syndrome

several months to years after SCI. Reported prevalences vary considerably. On average, two-
thirds of patients suffer chronic pain and approximately one-quarter to one-third of patients
have severe pain that significantly affects quality of life [120,133].

Neurogenic pain after SCI can be both spontaneous and stimulus evoked, is often poorly
localized, and is often described as burning, stabbing, or electrical in quality. Hyperesthesia is
a common component. These qualities can help distinguish neurogenic from musculoskeletal
pain (usually dull, aching, and well-localized) that can result from a number of complications
common to SCI patients. (See 'Musculoskeletal complications'above.)

Although neurogenic pain appears to be associated with neuronal hyperexcitability,

mechanisms are poorly understood. Two types of neurogenic pain syndromes are recognized:
at-level pain (ie, pain in segments at the level of SCI) and below-level pain. These are believed
to have different neuroanatomic and pathophysiologic bases, with injury to nerve roots and
dorsal gray matter causing at-level pain, and injury to spinothalamic tracts and/or thalamic
deafferentation responsible for below-level pain [134]. Development of at-level pain should
provoke an evaluation for post-traumatic syringomyelia, with which it is associated.
(See 'Syringomyelia' below.)

Medical treatments are often unsatisfactory; antidepressant, antiseizure, and standard

analgesic medications are tried, often in combination:

●Antiseizure drugs are believed to improve neuropathic pain by suppressing abnormal

neuronal hyperexcitability. Two randomized studies of pregabalin (150 to 600 mg daily) in
patients with pain after SCI have reported improvements in blinded assessments of pain
scores, as well as in disturbed sleep, anxiety, and depression [135,136]. Other
randomized trials have studied lamotrigine, gabapentin, and valproate in SCI, with mixed
evidence of efficacy [137-140].
●Antidepressant medications are also used in a variety of central and peripheral
neuropathic pain syndromes. Randomized trials of trazodoneand amitriptyline in SCI have
not demonstrated efficacy [140-142].
●Medical marijuana has some efficacy on neuropathic pain [143].
●Botulinum toxin type A injected into the painful area was found to be effective in a small
randomized study of 40 patients with neuropathic pain after spinal cord injury [144].
●Opiates may provide relief in anecdotal reports, but side effects, tolerance, dependence,
and overdose are significant considerations [145]. Chronic opiates should be avoided
unless all other options (medical, manual, surgical, and interventional) have been
exhausted first. Opiates are especially to be avoided in patients with untreated sleep
apnea, mental illness, and polysubstance abuse, or who are taking benzodiazepines, due
to the risk of overdose [146]. Palliative care can be helpful in monitoring patients who are
receiving opiates.

It is reasonable to believe that non-oral routes of administration may provide better efficacy
with fewer side effects; however, evidence supporting these therapies is somewhat limited in
SCI. Therapies have included intrathecal administration of morphine, clonidine,
and baclofen [147,148].

Invasive treatments, including deep brain stimulation, motor cortex stimulation, cordotomy, and
dorsal root entry zone lesions have been tried, again without substantive evidence of success
[120,149,150]. In the absence of good therapies, it is not unreasonable to also consider
nontraditional treatments such as acupuncture, biofeedback, and cognitive behavioral therapy
despite the unavailability of evidence demonstrating efficacy [19,150].
Details regarding dosing regimens, side effects, and other aspects of chronic pain
management are discussed separately. (See "Overview of the treatment of chronic non-cancer
pain".)

NEUROLOGIC DETERIORATION
Syringomyelia — A delayed progressive intramedullary cystic degeneration complicates 3 to 4
percent of traumatic SCI as well as other acute myelopathies. The interval since SCI can vary
from several months to many years [151]. Postulated mechanisms include scarring with
obstruction of cerebrospinal fluid (CSF) flow and altered tissue compliance leading to
expansion of the central canal and compression of surrounding cord tissue [152]. Symptoms
are consistent with a progressive myelopathy and include worsening motor, sensory, bowel,
and bladder deficits and pain [151]. Arachnoiditis, cord compression and/or a narrowed spinal
canal, and bony deformity, especially kyphosis, seem to be risk factors for progressive
enlargement of the cyst and neurologic deterioration [153-156].

An asymptomatic syrinx is a common incidental finding on neuroimaging in SCI patients. This

entity usually has a benign prognosis, and likely represents a focal area of liquefaction
necrosis of cord tissue.

Treatment is aimed at reducing expansile intracystic pressure and improving CSF flow [151].
Surgical approaches include shunt placement, lysis of subarachnoid adhesions, cyst
fenestration, and dural augmentation. Extradural decompression is anecdotally reported to be
helpful when there is significant bone deformity and compression of the spinal canal with
restriction of spinal fluid circulation [157,158]. Unfortunately, long-term treatment benefits are
seen in less than half of patients, and shunt failure is common [158,159]. Pain may be more
responsive to intervention than are motor symptoms [160,161].

Progressive posttraumatic myelomalacic myelopathy — Progressive posttraumatic

myelomalacic myelopathy is a less frequent complication of SCI and is characterized
pathologically by microcysts, reactive gliosis, and meningeal thickening. Adhesions and cord
tethering appear to be causally related; surgical untethering and duraplasty with expansion of
the subarachnoid space can lead to clinical improvement [151,162].

PSYCHIATRIC COMPLICATIONS Psychosocial complications associated with SCI

include depression, suicide, drug addiction, and divorce [6,9].

Between 20 to 45 percent of patients are depressed after traumatic SCI [9,163]. This symptom
often emerges early on, within the first month after SCI, and is not closely tied to the severity of
injury. Patients with SCI have a four to five times higher rate of suicide compared with age-
matched population samples [6,164]. Suicide is a leading cause of death in traumatic SCI
patients younger than 55 years; 75 percent of suicides occur within the first five years of injury
[9]. Similar rates of depression and suicide are observed after transverse myelitis [165].

Because of its high prevalence and serious consequences, patients with SCI should be
regularly screened for symptoms of depression. High levels of pain and lack of social support
identify patients at high risk for depression and suicidality [163]. Screening instruments for
depression are discussed separately. (See "Screening for depression in adults", section on
'Screening instruments'.)

Depression and anxiety following SCI should be treated; it should not be assumed that
symptoms are a "normal" reaction to the circumstances and do not require treatment [9].
Recommended interventions include psychologic counseling, pharmacologic intervention, and
peer support groups. The serotonin-norepinephrine reuptake
inhibitor venlafaxine hydrochloride extended release was effective and well tolerated in
treatment of major depression in one study of patients with spinal cord injury [166]. The
diagnosis and management of depression is discussed in detail separately. (See "Unipolar
depression in adults: Assessment and diagnosis" and "Unipolar major depression in adults:
Choosing initial treatment".)

THERMOREGULATORY DYSFUNCTION Disrupted autonomic pathways following

SCI can lead to impaired vasomotor and sudomotor responses in regions of insensate skin,
reduced thermoregulatory effector response for a given core temperature, and loss of skeletal
muscle pump activity from paralyzed limbs [167]. Consequences can include hyperthermia
during exercise or high ambient heat and hypothermia in lower ambient heat. There can be a
blunted fever or a hypothermic response to infection. Others have noted episodes of
hyperthermia or hypothermia in the absence of infection or environmental temperature change
in SCI patients.

FUNCTIONAL DEFICITS The level and completeness of the SCI are the principal
determinants of the needs, goals, and expectations in functional abilities. Age, general health,
body habitus, concurrent injuries, spinal instrumentation, intelligence, and motivation also
influence recovery [168].

Functional recovery after an SCI begins in the acute care setting as soon as the patient is
medically stable with range-of-motion and resistive exercise, upright positioning, and transfer
work. In the inpatient rehabilitation setting, physical and occupational therapists experienced in
SCI rehabilitation develop individualized programs that emphasize strengthening, joint
protection, and compensatory strategies, combined with creative use of assistive devices and
equipment to maximize function. There are no studies that suggest one form of therapy is more
effective than another; despite evolving technological advances, the simplest traditional
approaches are often the best [169,170].

The general expectations for functional recovery based on motor level are outlined in the table
(table 2) [171]. These assume an uncomplicated, complete SCI followed by appropriate
rehabilitation interventions in a healthy, motivated individual.

ADVANCE CARE PLANNING Life expectancy is reduced following SCI. Thus, it is

recommended that patients' primary health care provider discusses goals for care, preferred
surrogate decision maker, and preferences for cardiopulmonary resuscitation (CPR) and life-
sustaining care. These should be readdressed periodically, especially after acute episodes of
illness and/or hospitalization. Patients' choices should be extensively documented in the
medical record, disseminated across patients' providers, and translated into orders. Patients
should be encouraged to complete advance directives and provider orders for life-sustaining
treatment (POLSTs) when possible. (See "Advance care planning and advance directives".)

PALLIATIVE CARE Because of the high emotional, physical, and social burden patients
with SCI and their families carry, providers are well advised to involve palliative care consult
services when SCI patients have physical symptoms, emotional distress, or social needs that
cannot be addressed through patients' existing sources of care. Through palliative care, SCI
patients can access an additional layer of support from clinicians who have expertise in
managing symptoms and distress, and social workers who can help patients and caregivers
arrange home-based services and navigate financial issues. Palliative care is typically provided
through consult services, in hospitals or at home; in large health systems, palliative care often
is available through outpatient clinics. (See "Benefits, services, and models of subspecialty
palliative care".)
HOSPICE Hospice can provide an additional layer of support for patients with SCI who wish
to avoid returning to the hospital for end-stage complications of SCI. Hospices have
multidisciplinary teams that can come to the patient's home or long-term care facility to assess
and address physical and emotional symptoms, assist with advance care planning, and help
caregivers. They also provide 24/7 telephone support for the patient and caregiver, medical
supplies (eg, oxygen, hospital beds), as well as medication delivery to the home. A patient with
SCI can qualify for hospice care when she/he has [172]:

●Increasing emergency department visits, hospitalizations, or physician visits related to a

complication of SCI.
●A complication of SCI that no longer responds to medical management (eg, recurrent
serious infection or stage 3-4 decubiti).
●A life-threatening complication of SCI and has decided that the existing treatment
options are not acceptable to him/her (eg, when patients develop end-stage renal disease
[ESRD] and refuse dialysis or hypoventilation and refuse ventilatory support).
●Progressive inanition (eg, >10 percent weight loss in the last six months, an albumin
<2.5 [despite feeding tube if the patient has one]).

When in doubt about the appropriateness of hospice for a patient, a hospice informational visit
in the patient's home can be arranged through the hospice of choice. In this "Hospice Pre-
Election Evaluation," a hospice representative will review the services available with the patient
and caregiver, and confirm the patient's eligibility for hospice.

INFORMATION FOR PATIENTS UpToDate offers two types of patient education

materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are
written in plain language, at the 5th to 6th grade reading level, and they answer the four or five
key questions a patient might have about a given condition. These articles are best for patients
who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics
patient education pieces are longer, more sophisticated, and more detailed. These articles are
written at the 10th to 12th grade reading level and are best for patients who want in-depth
information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Neurogenic bladder in adults (The

Basics)" and "Patient education: Paraplegia and quadriplegia (The Basics)")

SUMMARY AND RECOMMENDATIONS Medical complications after spinal cord injury

(SCI) are both common and severe, contributing to a high rehospitalization rate and decreased
life expectancy. (See 'Life expectancy' above.)

●Autonomic dysreflexia can complicate SCI above T6. This is an exaggerated

sympathetic response characterized by headache, diaphoresis, and increased blood
pressure that occurs with noxious stimuli such as pain from bladder distension,
constipation, or pressure sores. (See 'Autonomic dysreflexia' above.)
●Patients with SCI also have an increased incidence of coronary artery disease (CAD).
Hemodynamic instability and cardiac arrhythmias can be problematic in the acute and
subacute SCI and are less frequent problems in chronic SCI. (See 'Cardiovascular
complications' above.)
●The severity of ventilatory failure and requirement for assisted ventilation depends on the
level and severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea
 and exercise intolerance. (See "Respiratory physiologic changes following spinal cord
injury" and "Respiratory complications in the adult patient with chronic spinal cord injury",
section on 'Respiratory insufficiency'.)
●An increased risk of pneumonia is highest in the first year following SCI, but patients
remain at increased risk over their lifetime. (See "Respiratory complications in the adult
patient with chronic spinal cord injury", section on 'Pulmonary infection'.)
●Prophylactic use of low molecular weight heparin to prevent deep venous thrombosis
and pulmonary embolism should be continued for at least three months after SCI, after
which the risk appears to approximate that of the general population. (See "Prevention of
venous thromboembolic disease in adult nonorthopedic surgical patients".)
●SCI produces bladder dysfunction, often referred to as the neurogenic bladder. Other
complications can result from this, including infections, vesicoureteral reflux, renal failure,
and renal calculi. Clean intermittent catheterization, supplemented by medications as
needed, is the usual initial treatment. Some patients require a chronic indwelling catheter.
Botulinum toxin and sacral nerve modulators are alternative treatment options to
traditional pharmacotherapy. (See 'Urinary complications' above.)
●Sexual dysfunction after SCI can include decreased libido, impotence, and infertility.
Erectile dysfunction may respond to treatment with a phosphodiesterase-5 inhibitor.
(See 'Sexual dysfunction' above.)
●Bowel dysfunction after SCI usually requires treatment with a bowel evacuation protocol
and a multidimensional approach. A regular diet that includes adequate fiber is an
important part of management. (See 'Gastrointestinal complications' above.)
●Osteoporosis affects bones below the level of the SCI and increases the risk of fracture.
The role of bisphosphonates in this setting is under investigation. (See 'Bone
metabolism' above.)
●Positioning and mobilization can help ameliorate contractures and pressure ulcers after
SCI. (See 'Musculoskeletal complications' above and 'Pressure ulcers' above.)
●Spasticity is common after SCI and has positive as well as negative effects. Treatment is
empiric and is aimed at minimizing pain while maximizing function. Options include oral
medication, intrathecal baclofen, botulinum toxin, and nerve blocks. Refractory spasticity
may require surgery. (See 'Spasticity' above.)
●Neurogenic pain after SCI is often refractory but may respond to standard analgesic
therapy, antiseizure drug therapy, and/or antidepressant therapy. Chronic opioids should
be avoided. (See 'Pain syndromes' above.)
●Depression frequently complicates SCI; patients are at high risk for suicidality and
should be monitored. (See 'Psychiatric complications'above.)
●Functional neurologic deficits are determined by the level and completeness of the SCI
and are ameliorated by appropriate rehabilitation interventions. If patients experience
neurologic decline, neuroimaging is indicated to exclude syringomyelia, posttraumatic
myelomalacic myelopathy, or other neurologic pathology. (See 'Functional deficits' above
and 'Neurologic deterioration' above.)
Use of UpToDate is subject to the Subscription and License Agreement.

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