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Acute Spinal Cord Dysfunction

GENERAL PRINCIPLES

• Spinal cord dysfunction is demonstrated by a level below which motor, sensory, and autonomic functions are interrupted.

• Traumatic spinal cord injury (TSCI) may be obvious from history or examination but should also be considered in unconscious, confused, or inebriated patients with trauma or found down.

• Spinal cord concussion refers to posttraumatic spinal cord symptoms and signs that resolve rapidly (hours to days).

Etiology

See Table 27-9.

TABLE 27-9

CAUSES OF ACUTE SPINAL CORD DYSFUNCTION

Structural

• Tumor (primary or metastatic)

• Herniated disk

• Epidural abscess or hematoma

• Osteomyelitis

• Trauma ± fracture of bony elements

• Atlantoaxial instability (e.g., rheumatoid arthritis)

• Fibrocartilaginous

IschemiaZinfarction (particularly after aortic surgery)

• Aortic dissection or surgery

• Embolic (cardiogenic, gaseous embolus)

• Prolonged hypotension with underlying vascular disease

• Intravascular lymphoma

Toxic

• Nitrous oxide (typically in the setting of vitamin B12 deficiency)

• Heroin

Vascular malformations (e.g., AVM)

InflammatoryZinfectious (transverse myelitis)

• Multiple sclerosis

• Neuromyelitis optica (classically longitudinally extensive, gt;three spinal segments)

• Anti-myelin oligodendrocyte protein disease

• Acute disseminated encephalomyelitis

• Parainfectious processes (e.g., after Mycoplasma pneumoniae)

• Sarcoidosis

• Paraneoplastic (amphiphysin and CRMP-5)

• Systemic lupus erythematosus

• Sjogren syndrome

• Beheet disease

• Viruses (e.g., enterovirus, HSV, HIV, VZV, CMV, WNV)

• Fungal (extremely rare)

• Lyme disease

• TB

• Syphilis

AVM, arteriovenous malformation; CMV, cytomegalovirus; CRMP-5, collapsin response mediator protein 5; HSV, herpes simplex virus; VZV, varicella-zoster virus; WNV, West Nile virus.

DIAGNOSIS

Clinical Presentation

• Spinal cord compression often presents with back pain at the level of compression, progressive walking difficulties, sensory impairment, urinary retention with overflow incontinence, and diminished rectal tone. Rapid deterioration may occur.

• Spinal shock with hypotonia and areflexia may be present soon after a traumatic event.

• Transverse myelitis or myelopathy can present with symptoms and signs similar to cord compression.

• Acute presentations suggest traumatic or vascular insults, whereas a subacute course suggests an enlarging mass lesion or infectious process. AutoimmuneZinflammatory disorders can present in both ways.

• Radicular signs (lancinating pain, paresthesias, and numbness in the dermatomal distribution of a nerve root, with weakness and decreased tone and reflexes in muscles supplied by the root) suggest concurrent inflammation or compression of the corresponding nerve root. Tenderness to spinal percussion over the lesion may be present.

• Spinal cord syndromes

ξ Complete cord syndrome: Bilateral flaccid paralysis (quadriplegia or paraplegia) and loss of all sensation (anesthesia) below a dermatomal level, initially with areflexia and sphincter dysfunction (urinary retention/loss of rectal tone). With time, patients develop spasticity and hyperreflexia caudal to the lesion with possible lower motor neuron signs (areflexia and flaccid paralysis) at the level of the lesion and extensor plantar responses (Babinski signs).

ξ Brown-Sequard syndrome: Unilateral cord lesion resulting in contralateral pain and temperature loss, with ipsilateral weakness and proprioceptive loss.

ξ Anterior cord syndrome often results from anterior spinal artery lesions and produces bilateral pain and temperature loss and weakness below the site of the lesion with preserved proprioception and vibratory sensation.

ξ Cauda equina syndrome from compression of the lower lumbar and sacral roots produces sensory loss in a saddle distribution, asymmetric flaccid leg weakness, decreased reflexes, and urinary/bowel incontinence due to an areflexic bladder and loss of rectal tone.

ξ Conus medullaris syndrome has similar features to cauda equina syndrome with one important difference being the presence of mixed upper and lower motor neuron signs due to involvement of the caudal spinal cord.

ξ Central cord syndrome is often characterized by motor impairment in upper extremities more than lower extremities, bladder dysfunction, and variable degree of sensory loss at the site of the lesion. Trauma is a common cause.

Diagnostic Testing

IMAGING

• The presence and extent of spinal cord injuries should be confirmed with neuroimaging.

• Plain radiographs of the spine may reveal metastatic disease, osteomyelitis, discitis, fractures, or dislocation.

• Emergent MRI scan of the entire cord can confirm the exact level and extent of the lesion(s). CT myelography may be necessary in individuals unable to undergo MRI.

ξ CT of the spine is not sufficient to “rule out” spinal cord compression.

• CT of the spine with and without contrast can also be used to evaluate for epidural abscess, osteomyelitis, and/or discitis in patients unable to undergo MRI.

DIAGNOSTIC PROCEDURES

Inflammatory and infectious etiologies often require an LP with CSF analysis for pleocytosis, malignant cells, abnormal protein/glucose, oligoclonal bands, and IgG index; if indicated, tests for specific pathogens and cytology/flow cytometry can be considered. If possible, imaging should be performed prior to performing an LP to rule out abscess, tumor, or other structural contraindication to LP. Remember to always check an opening pressure when possible and save CSF for additional studies that may be deemed indicated once additional clinical data have been gathered.

TREATMENT

• Vital signs should be continuously monitored, and adequate oxygenation and perfusion should be ensured.

• Respiratory insufficiency from high cervical cord injuries requires immediate airway control and ventilatory assistance, without manipulation of the neck.

• Immobilization, especially of the neck, is essential to prevent further injury while the patient's condition is stabilized and radiographic and neurosurgical assessment of the injuries is performed.

• Autonomic dysfunction is common and can lead to fluctuating vital signs and BP. Bladder distension can cause sympathetic overactivity (headache, tachycardia, diaphoresis, and hypertension) as a result of autonomic dysreflexia.

ξ Management of autonomic dysreflexia should incorporate the help of a spinal cord rehabilitation specialist. These patients require strict attention to bowel and bladder functions (e.g., manual disimpaction, promotility agents, straight catheterization) as a means to prevent an autonomic crisis.

° Do not treat fluctuations in vital signs blindly because changes can occur precipitously with potential for iatrogenic inj ury. Alw ays look first for a cause and treat fluctuations in heart rate or BP with caution.

Medications

• Treatable infections require appropriate antimicrobial therapies (e.g., acyclovir for varicella-zoster myelitis).

• Dexamethasone, 10-20 mg IV bolus followed by 2-4 mg IV q6-8h, is often administered for compressive lesions, tumors, or spinal cord infarction, although benefit has not been proven for all etiologies.

• For TSCI, methylprednisolone, 30 mg/kg IV bolus, followed by an infusion of 5.4 mg/kg/h for 24 hours when initiated within 3 hours of injury, and infusion for 48 hours when initiated within 3-8 hours of injury, may improve neurologic recovery.

• Pharmacologic deep venous thrombosis prophylaxis is extremely important. LMWH is superior to

unfractionated heparin for prevention of venous thromboembolism and pulmonary embolism.

Surgical Management

Neurosurgical consultation should be obtained because in many cases, spinal cord compression can be decompressed and stabilized. Penetrating injury, foreign bodies, comminuted fractures, misalignment, and hematoma may require surgical treatment.

SPECIAL CONSIDERATIONS

Emergent radiation therapy combined with high-dose steroids is usually indicated for cord compression due to malignancy and generally requires a histologic diagnosis.

Monitoring/Follow-Up

Long-term supportive care is important for patients with spinal cord dysfunction. Pulmonary and urinary infections, skin breakdown, joint contractures, spasticity, and irregular bowel and bladder elimination are common long-term problems.

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Source: Ancha S., Auberle C., Cash D., Harsh M., Hickman J., Kounga C.. The Washington Manual of Medical Therapeutics, 37th edition, LWW, 2022. —1250p.. 1250
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