Porth's Essentials of Pathophysiology, 4e
911
Disorders of Neuromuscular Function
C h a p t e r 3 6
Flushed skin above level of injury
Headache
Vasodilation and sweating above the level of injury
f
Baroreceptors
Acute rise in blood pressure
Spinal cord injury— T6 or above with loss of CNS control of sympathetic reflexes below level of injury
Pale, cool, moist skin below level of injury
Vasoconstriction below level of injury
Thoracic
Uncontrolled activation of local sympathetic reflexes below level of injury
Piloerection (goose bumps)
Lumbar
Visceral stimulus (e.g., overdistended bladder, visceral pain)
Sacral
Bladder
FIGURE 36-18. Mechanisms of autonomic dysreflexia.
Spinal cord
cause or stimulus. The person should be placed in an upright position, and all support hose or binders should be removed to promote venous pooling of blood and reduce venous return, thereby decreasing blood pressure. If the stimuli have been removed or the stimuli cannot be identified and the upright position is established but the blood pressure remains elevated, drugs that block auto- nomic function are administered. Prevention of the type of stimuli that trigger the dysreflexic event is advocated. Postural Hypotension. Postural, or orthostatic, hypo- tension usually occurs in persons with injuries at T4 to T6 and above and is related to the interruption of descending control of sympathetic outflow to blood ves- sels in the extremities and abdomen. 62 Pooling of blood, along with gravitational forces, impairs the return of venous blood to the heart, causing a decrease in cardiac
output along with a drop in arterial blood pressure when the person is placed in an upright position. The disorder is characterized by dizziness, pallor, excessive sweating above the level of the lesion, complaints of blurred vision, and possible fainting. Postural hypoten- sion usually is prevented by slow changes in position and measures to promote venous return. Disruption of Bladder, Bowel, and Sexual Function Among the most devastating consequences of SCI are the loss of bladder, bowel, and sexual function. 18,64 Loss of bladder function results from disruption of neural pathways between the bladder and the reflex voiding center at the S2 to S4 level (i.e., a LMN lesion) or between the reflex voiding center and higher brain
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