Autonomic Changes in Spinal Cord Transection

The most drastic of all alterations in the ANS that an anesthesiologist may encounter is complete spinal cord transection (see Chapter 53 ). Spinal cord transection affects motor and sensory function, and it also may result in profound changes in autonomic activity that can alter anesthetic care. As is obvious from the anatomy of the sympathetic and parasympathetic outflow, spinal cord injuries or transection can cause various degrees of autonomic dysfunction, depending on the site, extent, and timing of the lesion. Many autonomic reflexes are inhibited by supraspinal feedback that is lost after spinal cord transection. In paraplegic patients, small stimuli can evoke exaggerated sympathetic discharges.

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In patients with cervical spinal cord transection, sympathetic and parasympathetic outflows are detached from central control mechanisms. In addition to expected motor and sensory changes, there are profound abnormalities altering the cardiovascular, thermoregulatory, gastrointestinal, and urinary systems. The autonomic consequences of transection are not always apparent because the distal portion of the spinal cord may retain some function, resulting in unanticipated autonomic abnormalities.

There are fundamental differences between the acute and chronic effects of spinal cord transection. Initially, a transient state of decreased excitability occurs. This phenomenon, known as spinal shock, usually occurs immediately after the lesion and may last days to weeks. In these patients, the periphery is generally atonic, and the peripheral blood vessels are dilated. Investigators have suggested that methylprednisolone may be of some use in treating this phase of spinal shock.^[491] In patients with high thoracic lesions who have sustained recent injury, the basal supine blood pressure is usually low and accompanied by plasma catecholamine levels that are approximately 35% of normal.^[492] Patients with recent low spinal injuries may exhibit compensatory tachycardia from intact parts of the ANS.

Patients with high spinal lesions may fail to respond to hypovolemia with an increased heart rate and may exhibit bradycardia. The only intact efferent component of baroreflex pathways in quadriplegic patients is the vagus. Bradycardia occurs with changes in position and with Valsalva maneuvers or increased intrathoracic pressure.^[493]

One aspect of care that is frequently overlooked is the effect of tracheal suctioning on patients with high spinal transection. Given that many of these patients depend on artificial respiration because of their respiratory muscle paralysis, unopposed vagal stimuli may contribute to profound bradycardia. This vagal response is particularly accentuated during hypoxemia.

Because the sympathetic nervous system may be dysfunctional in these patients, the renin-angiotensin-aldosterone system compensates for the maintenance of blood pressure. Patients who have spinal cord transection may be exquisitely sensitive to ACEIs, even with modest changes in intravascular volume or posture. The release of renin may be independent of sympathetic stimulation and may be caused by renal baroreceptor stimulation that accompanies the decline in renal perfusion pressure.

Although pressure stimuli above the lesion do not usually change blood pressure, the phenomenon of autonomic dysreflexia can occur with stimulation below the lesion. Bladder or bowel distention can elicit the so-called mass reflex. This autonomic reflex includes a dramatic rise in blood pressure, a marked reduction in flow to the periphery, and flushing and sweating in areas above the lesion. The patient's heart rate may decline as a reflex. Surprisingly, evidence from microneurography studies indicates that there is only a modest rise in sympathetic nerve activity during activation of the mass reflex,^[494] and plasma levels increase only modestly. Speculation has arisen that the exaggerated blood pressure response may be caused by supersensitivity of adrenoreceptors. As anticipated, there is an increase in sensitivity to exogenously administered pressors in quadriplegic patients.^[492] Blood pressure in quadriplegic patients may increase 5- to 10-fold in response to the exogenous administration of angiotensin and to catecholamines. Impairment of descending inhibitory reflex pathways that are activated during hypertension may contribute to the supersensitivity. This hypothesis is supported by the finding that sensitivity is rarely increased when the lesion is below T5. There is apparently a normal level of adrenoreceptors in these patients, even those with long-standing quadriplegia.

The management of autonomic dysreflexia is of clinical importance. Although the anesthesiologist may be tempted to opt for minimal anesthesia in a patient without sensory or motor function, significant visceral reflexes can be evoked. The anesthesiologist may use spinal anesthesia, general anesthesia, or a vasodilator such as nitroprusside or nitroglycerin to attenuate this reflex even if pain is not appreciated. There has been some enthusiasm for using clonidine prophylactically to diminish this response.

An additional problem arising from the autonomic denervation of spinal cord transection is thermogenesis. In these patients, hypothermia may result from cutaneous vasodilation and the inability to shiver. Similarly, hyperthermia can occur because the normal sweating mechanism is impaired. It is therefore important to monitor temperature assiduously in these patients during the course of anesthesia.