SPINAL CORD INJURY

Spinal Cord Injury
Urinary Tract Infection
A urinary tract infection should be suspected when a spinal-cord-injured patient presents with fever, discomfort over the kidney or bladder, worsening spasticity, development of urinary incontinence, autonomic dysreflexia, cloudy or foul-smelling urine, a change in energy level, or a feeling of apprehension.

Unless there are confounding factors, the urinalysis shows pyuria and significant bacteriuria. In a patient with the above-mentioned symptoms and signs and pyuria, empiric treatment for urinary tract infection should be initiated. Absence of pyuria makes the diagnosis less likely but does not completely exclude it. Conversely, pyuria in an asymptomatic patient with spinal cord injury does not warrant treatment. Pyuria without infection can occur from irritation of the bladder wall in patients with indwelling catheters and in those who use intermittent catheterization.

Significant bacteriuria for the spinal-cord-injured population is defined according to the method used for bladder emptying. For women who can spontaneously void, significant bacteriuria is defined as greater than 100,000 colony-forming units (CFUs) of bacteria per milliliter. For men who spontaneously void or use condom catheters, greater than 10,000 CFUs/mL is considered significant. For both women and men who use intermittent catheterization, greater than 100 CFUs/mL indicates significant bacteriuria. For patients with indwelling urethral or suprapubic catheters, any detectable level of bacteriuria is significant.

Urinary tract infections in the spinal-cord-injured population are considered complicated urinary tract infections.6 Antibiotics with broader-spectrum coverage should be used, since such organisms as Proteus, Klebsiella, Pseudomonas, Serratia, Providencia, enterococci, and Staphylococcus are more common. Because of the higher risk of upper-tract infection, 7 to 14 days of treatment should be considered.

Asymptomatic bacteriuria is very common in patients with a neurogenic bladder and requires periodic or indwelling catheterization. Asymptomatic bacteriuria should not be routinely treated.

Acute Abdomen
Classic signs of the acute abdomen are often missing in patients with spinal cord injury. The diagnosis of perforated peptic ulcer, intestinal obstruction, appendicitis, peritonitis, cholecystitis, and renal abscess is often delayed because the classic findings of abdominal muscle rigidity, rebound, abdominal tenderness, fever, and leukocytosis may not be present. In patients with spinal cord injury, other signs and symptoms suggestive of an acute abdomen are autonomic dysreflexia, referred scapular tip pain, abdominal distention, change in muscle spasticity, nausea and vomiting, and a sense of apprehension.
 
A high index of suspicion, along with laboratory and imaging tests, is necessary to avoid missing the diagnosis. One confounding factor is that urinary tract infections may present with similar signs and symptoms. Thus the finding of pyuria or bacteriuria alone should not be used to exclude the diagnosis of an acute abdomen. While abdominal radiographs are also useful in the diagnosis of intestinal obstruction, many patients with spinal cord injury have chronic dysmotility problems and have baseline increased bowel gas and air-fluid levels that may mimic a mechanical obstruction. Ultrasound, radiologic studies using radiocontrast media, and computed tomography (CT) imaging studies are often required for correct diagnosis in such patients.

Syringomyelia
Posttraumatic syringomyelia may present months to years after a spinal cord injury. This process produces a cystic cavitation of the central cord that may extend over several levels. Ascending sensory level (i.e., a decrease or loss of sensation above the preexisting sensory level) and pain are the most common presenting symptoms. Motor weakness, a change in spasticity, and a change in deep-tendon reflexes may also be seen. Magnetic resonance imaging is the imaging study of choice for making the diagnosis of syringomyelia. Surgery is indicated in progressive neurologic deterioration.

Immobilization Hypercalcemia
Risk factors for immobilization hypercalcemia include age less than 21 years, complete neurologic injuries, cervical injuries, prolonged immobilization, and dehydration. Presenting symptoms include anorexia, nausea, headache, malaise, and depression in mild cases. In more severe cases, patients may have persistent nausea and vomiting, gastric dilatation, fecal impaction, and abdominal pain. Microscopic calcium deposition in the kidney may impair its ability to concentrate urine, leading to polyuria and polydipsia. Patients may also develop cardiac dysrhythmias and seizures.

The pathophysiology of immobilization hypercalcemia is thought to be due to the combination of increased bone resorption and the inability of the kidneys to excrete the excess calcium. Compared to other age groups, adolescents are at higher risk due to a higher-than-normal bone turnover rate and more total bone mineral. Immobilization causes a decrease in osteoblastic activity in the weight-bearing bones and an increased rate of bone resorption. Together, these factors lead to a higher-than-normal serum calcium level during prolonged periods of immobilization. In most cases, the kidneys can usually excrete the calcium, but in some patients this ability breaks down.

Treating immobilization hypercalcemia starts with hydration and diuresis with NS solution 2 to 3 L/d with the addition of furosemide. Calcitonin in doses of 1 to 4 IU/kg SC every 12 h can also effectively reduce the serum calcium level.

Heterotopic Ossification
Heterotopic ossification (HO) is the formation of bone in the soft tissues. The mechanisms of the formation of heterotopic bone are not precisely known. In spinal-cord-injured patients, it is more common among those with spasticity. Symptoms may present as early as 1 month after injury. Pain is prominent in other patients with HO but is often absent in spinal-cord-injured patients. For spinal-cord-injured patients, the most common symptom of HO is a decreased range of motion. Other findings are a change in spasticity, fever, erythema, joint effusion, and swelling. The differential diagnosis includes DVT, infection, and tumor. Sometimes HO and DVT are seen together.

The incidence of HO in spinal-cord-injured patients has been reported to be 16 to 53 percent. The most common sites are the hip, knee, femur, and shoulder. Plain radiograph findings are often negative in the early stages of HO. The gold standard for diagnosis is the three-phase bone scan. Serum alkaline phosphatase (ALP) levels have been used as a screening test for HO, since developing bone produces ALP. However, this is a nonspecific test indicating increased bone metabolic activity, which may occur in fractures or tumors.

Treatment for HO is usually disodium etidronate 20 mg/kg per d for 2 weeks followed by 10 mg/kg per day for 10 weeks, along with gentle physical therapy. Referral to a physiatrist (a physician specializing in the care of patients with disabilities) or other spinal-cord-injury specialist is recommended to institute and monitor treatment.

Leg Pain
If a patient with spinal cord injury or a brain injury presents with a swollen and painful leg, the differential diagnosis includes trauma (e.g., contusion, sprain, or fracture), spasticity, DVT, heterotopic ossification, and reflex sympathetic dystrophy. For those individuals who have impaired sensation, language, or cognition that might hinder the history and physical examination, a high index of suspicion and liberal use of ancillary studies are critical. Plain radiographs are usually adequate for evaluating trauma. For those who have suffered from a recent spinal cord injury (within 8 weeks), the risk of deep vein thrombosis is substantial, most likely from venous stasis. Signs and symptoms include swelling, pain, and warmth. Noninvasive venous studies (duplex Doppler) are usually adequate for evaluating DVT.

Another likely cause of leg pain is spasticity. This condition is often chronic in nature, but certain noxious stimuli may acutely worsen the symptoms. Such causes include infections (UTI, upper respiratory infections, pneumonia, gastroenteritis, etc.), trauma, and stress. Initial treatment is to identify and eliminate these causes. Baclofen is the first line for medicinal treatment and should be started at a dose of 5 mg PO tid, and titrated upward according to symptoms. If the patient does not respond to baclofen, tizanidine, diazepam, and dantrolene may be tried. Once the patient is stabilized, a referral to a physiatrist or other specialist in the care of patients with spinal cord injury should be arranged.