A 28-year-old man with a history of spinal cord injury comes to the emergency department due to headache, restlessness, and excessive sweating for the past several hours. A year ago, the patient was involved in a motor vehicle collision that caused a C6 spinal cord injury, leading to paraplegia and neurogenic bladder. He has no other medical concerns. Temperature is 36 C (96.8 F), blood pressure is 170/100 mm Hg, and pulse is 52/min. Physical examination shows facial flushing and excessive perspiration. The lungs are clear to auscultation and heart sounds are normal. The abdomen is soft with a mass palpable in the lower abdomen. A suprapubic catheter is present. Neurologic examination demonstrates absence of pain and temperature sensation below the nipples and paraplegic and spastic lower extremities, unchanged from previous examination. Further evaluation reveals occlusion of the urinary catheter and urinary retention. The urinary catheter is changed, which leads to rapid improvement in the patient's symptoms and hypertension. Which of the following best explains the observed findings in this patient?

Question

A 28-year-old man with a history of spinal cord injury comes to the emergency department due to headache, restlessness, and excessive sweating for the past several hours.  A year ago, the patient was involved in a motor vehicle collision that caused a C6 spinal cord injury, leading to paraplegia and neurogenic bladder.  He has no other medical concerns.  Temperature is 36 C (96.8 F), blood pressure is 170/100 mm Hg, and pulse is 52/min.  Physical examination shows facial flushing and excessive perspiration.  The lungs are clear to auscultation and heart sounds are normal.  The abdomen is soft with a mass palpable in the lower abdomen.  A suprapubic catheter is present.  Neurologic examination demonstrates absence of pain and temperature sensation below the nipples and paraplegic and spastic lower extremities, unchanged from previous examination.  Further evaluation reveals occlusion of the urinary catheter and urinary retention.  The urinary catheter is changed, which leads to rapid improvement in the patient's symptoms and hypertension.  Which of the following best explains the observed findings in this patient?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d5cc_5dc4_bc81_b982338cb7d4_MD0003_00 This patient with C6 paraplegia has severe hypertension, headache, diaphoresis, flushing, and bradycardia in the setting of urinary retention. This presentation suggests autonomic dysreflexia (AD), a potentially life-threatening complication of spinal cord injury (SCI). In an intact spinal cord, sympathetic activity can be modulated by higher-level autonomic neurons. When a noxious stimulus triggers a sympathetic response (eg, diffuse vasoconstriction, increased heart rate, sweating), a compensatory parasympathetic response (due to baroreceptor activation) follows and leads to modulating inhibitory signals sent down the cord. baroreceptor activation In patients with SCI, these modulating pathways are disrupted below the level of the lesion. A noxious stimulus below the lesion (eg, urinary retention, constipation, pressure ulcer) still triggers sympathetic activity, but the subsequent response is uncoordinated and potentially dangerous: Above the lesion: The compensatory parasympathetic response is intact and causes bradycardia and vasodilation (eg, facial flushing). Below the lesion: The disrupted parasympathetic modulation results in an unregulated sympathetic response. For lesions above T6, continued vasoconstriction involves both the splanchnic and the peripheral vasculatures, causing severe hypertension that overwhelms any parasympathetic compensation. Prolonged, severe hypertension may cause headache and, if untreated, intracranial hemorrhage. Management includes placing the patient in an upright position to encourage orthostatic blood pressure reduction, removing noxious stimuli (eg, urinary retention, tight-fitting clothes), and treating the hypertension (eg, nitrates). (Choice B) Carotid sinus hypersensitivity typically causes bradycardia, hypotension (rather than severe hypertension), light-headedness, or syncope following carotid massage; it would not cause headache and perspiration. (Choice C) Pheochromocytoma, a catecholamine-secreting tumor, can cause episodic hypertension, sweating, and headache. However, patients are typically tachycardic rather than bradycardic. (Choice D) Peripheral autonomic neuropathy (eg, from diabetes) can cause a wide spectrum of symptoms, including hyperhidrosis and impaired autonomic control; however, cardiovascular involvement typically causes tachycardia and orthostatic hypotension. (Choice E) Renovascular hypertension (from renal artery stenosis) can cause severe, refractory hypertension; however, the hypertension is not typically episodic and would not resolve with the removal of noxious stimuli. (Choice F) Spinal shock occurs immediately after (vs 1 year after) SCI; because of temporary loss of all spinal cord function, it typically causes distal flaccid paralysis and may cause hypotension and bradycardia from loss of sympathetic tone. Educational objective: Spinal cord injury above T6 can be complicated by autonomic dysreflexia, in which noxious stimuli below the injury level trigger an unregulated sympathetic response, leading to severe hypertension. A compensatory parasympathetic response above the lesion typically causes bradycardia. Management includes removing noxious stimuli and treating the hypertension. References: Autonomic dysreflexia after spinal cord injury: systemic pathophysiology and methods of management. (http://www.ncbi.nlm.nih.gov/pubmed/28506502) Vascular dysfunctions following spinal cord injury. (http://www.ncbi.nlm.nih.gov/pubmed/20945818)

A 28-Year-Old Man with a History of Spinal Cord Injury