Spinal cord injury

Acute spinal cord injury (SCI) is common with an estimated 8,000 to 10,000 new cases in the United States each year. The mean age of presentation is 31 years and the majority of patients are male. SCI is associated with significant long-term disability and mortality.

Etiology

Spinal cord injury has traditionally been classified as traumatic and nontraumatic. Traumatic spinal cord injury is usually due to motor vehicle collisions (MVCs) (MVAs) (20% to 25%), motorcycle collisions (MCCs) (25% to 30%), or falls (20% to 25%).

The most common locations for traumatic spinal cord injury are the cervical spine (50% to 55%), followed by the thoracolumbar region (15% to 20%), thoracic spine (10% to 15%), and the lumbosacral region (10%).

Nontraumatic causes of spinal cord injury are numerous. Such conditions include: various bacterial (including spinal epidural abscesses), viral, fungal, or parasitic infections; neoplastic lesions (usually extramedullary primary or metastatic tumors); vascular events (infarctions or hemorrhages from vascular malformations); demyelinating lesions such as multiple sclerosis; toxins; autoimmune disorders; and nutritional abnormalities such as vitamin B12 deficiency.

Clinical Presentation

Neurologic damage and the ensuing clinical manifestations will depend on the extent and level of the spinal cord injury. Physical examination usually reveals muscle weakness and a sensory level below the level of the lesion in complete lesions.

In those patients with incomplete spinal cord injury there is some preservation of motor and sensory functions below the level of compromise.

Initially patients with spinal cord injury will present with atonia and arreflexia below the level of the lesion (spinal shock) and within a few days or weeks will experience spasticity and hyperreflexia.

Venous Thromboembolism in spinal cord injury

Patients with spinal cord injury who do not receive prophylactic treatment have the highest incidence of deep venous thrombosis (DVT) and pulmonary embolism (PE) among all patients.

A symptomatic DVT has been found in 60% to 100% of spinal cord injury patients and PE represents the third leading cause of death.

Additional risk factors for DVT in spinal cord injury patients include age, concomitant lower limb fracture, and delayed initiation of prophylactic treatment.

It has been shown that spinal cord injury patients are at greatest risk of DVT and PE during the acute care phase.

However, the risk is still present during the rehabilitation period. The incidence of new DVT may be as high as 30% between 2 to 6 weeks following spinal cord injury.

Thromboprophylaxis after spinal cord injury

Six randomized studies (albeit small) have shown that the use of low-dose unfractionated heparin (LDUH) alone or sequential compression devices alone are not sufficient as thromboprophylaxis.

However, adjusted-dose unfractionated heparin and low-molecular-weight heparin (LMWH) have been found to be more efficacious. This finding has also been reported in SCI patients undergoing rehabilitation (uncontrolled studies).

There is also evidence that oral anticoagulants such as warfarin are also effective thromboprophylactic treatments when initiated shortly after SCI.

It is important to note that thromboprophylaxis should be initiated once practitioners feel secure about having achieved effective hemostasis after SCI.

Routine insertion of inferior vena cava filters (IVCFs) in SCI patients is still controversial. There is strong evidence that when appropriate thromboprophylaxis is given IVCFs are not necessary.

Even though IVCFs may theoretically reduce the incidence of PE, they are associated with complications and higher costs.

Patients who have been shown to benefit from IVCF insertion include those with concomitant long bone fractures, DVT formation despite thromboprophylaxis, and those with contraindications to anticoagulation.

The current recommendations for thromboprophylaxis after SCI include the following:

  • Thromboprophylaxis for all patients with acute spinal cord injury.
  • Single prophylaxis modalities (i.e., low-dose unfractionated heparin, graduated compression stockings, or sequential compression devices alone) should be avoided.
  • Thromboprophylaxis with LMWH is the preferred treatment once primary hemostasis from the injury is obtained. Alternatives to LMWH include the combined use of sequential compression devices and either low-dose unfractionated heparin or LMWH.
  • When anticoagulation is contraindicated early in spinal cord injury, sequential compression devices and/or graduated compression stockings should be used with consideration of an IVCF.
  • During the rehabilitation phase, spinal cord injury patients should be treated with LMWH or converted to oral warfarin (international normalized ratio range 2.0 to 3.0).
  • The insertion of IVCFs as primary prophylaxis is not recommended.

Suggested Readings

Geerts WH, Pineo GF, Heit JA, et al. Prevention of thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004

Maxwell RA, Chavarria-Aguilar M, Cockerham WT, et al. Routine prophylactic vena cava filtration is not indicated after acute spinal cord injury. J Trauma. 2002

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