Spinal Cord Injury
Most spinal cord injuries are traumatic and may arise from partial or complete transection. The majority of injuries are due to fracture and dislocation of the vertebral column. The mechanism is usually either compression and flexion at the thoracic spine or extension at the cervical spine. Clinical manifesta-tions depend on the level of the injury. Injuries above C3–5 (diaphragmatic innervation) require patients to receive ventilatory support to stay alive. Transections above T1 result in quadriplegia, whereas those above L4 result in paraplegia. The most common sites of injury are C5–6 and T12–L1. Acute spinal cord tran-section produces loss of sensation, flaccid paralysis, and loss of spinal reflexes below the level of injury. These findings characterize a period of spinal shock that typically lasts 1–3 weeks.
Over the course of the next few weeks, spi-nal reflexes gradually return, together with muscle spasms and signs of sympathetic overactivity. Injury in the low thoracic or lumbar spine may result in cauda equina (conus medullaris) syndrome. The latter usually consists of incomplete injury to nerve roots rather than the spinal cord.
Overactivity of the sympathetic nervous system is common with transections at T5 or above, but is unusual with injuries below T10. Interruption of normal descending inhibitory impulses in the cord results in autonomic hyperreflexia. Cutaneous or visceral stimulation below the level of injury can induce intense autonomic reflexes: sympathetic dis-charge produces hypertension and vasoconstriction below the transection and a baroreceptor-mediated reflex bradycardia and vasodilation above the tran-section. Cardiac arrhythmias are common.
Emergent surgical management is undertaken whenever there is reversible compression of the spinal cord due to dislocation of a vertebral body or bony fragment. Operative treatment is also indi-cated for spinal instability to prevent further injury.
Anesthetic management depends on the age of the injury. In the early care of acute injuries, the empha-sis should be on preventing further spinal cord damage during patient movement, airway manipu-lation, and positioning. High-dose corticosteroid therapy (methylprednisolone) can be used for the first 24 hr following injury to improve neurologic outcome. Airway management of the patient with unstable cervical spine is discussed eariler. Patients with high transections often have impaired airway reflexes and are further predisposed to hypoxemia because of a decrease in functional residual capacity and atelectasis. Spinal shock can lead to hypotension and bradycardia prior to any anesthetic administration. Direct arterial pressure monitoring is helpful. An intravenous fluid bolus and the use of ketamine for anesthesia may help to prevent further decreases in blood pressure; vaso-pressors may also be required. Succinylcholine can be used safely in the first 24 hr, but should not be used thereafter because of the risk of hyperkalemia. The latter can occur within the first week following injury and is due to excessive release of potassium secondary to the proliferation of acetylcholine receptors outside of the neuromuscular synaptic cleft.
Anesthetic management of patients with nonacute transections is complicated by the possibility of autonomic hyperreflexia and the risk of hyperkalemia. Autonomic hyperreflexia should be expected in patients with lesions above T6 andcan be precipitated by surgical manipulations.
Regional anesthesia and deep general anesthesia are effective in preventing hyperreflexia. Many cli-nicians, however, are reluctant to administer spinal and epidural anesthesia in these patients because of the difficulties encountered in determining anes-thetic level, exaggerated hypotension, and technical problems resulting from deformities. Severe hyper-tension can result in pulmonary edema, myocardial ischemia, or cerebral hemorrhage and should be treated promptly. Direct arterial vasodilators should be readily available. Nondepolarizing muscle relax-ants may be used. Body temperature should be monitored carefully, particularly in patients with transections above T1, because chronic vasodilation and loss of normal reflex cutaneous vasoconstriction predispose to hypothermia.
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