autonomic dysreflexia

**Definition:** A medical emergency of acute, uncontrolled hypertension (a rise of 20-40 mmHg or more over baseline SBP; baseline BP is often low in these patients) in patients with spinal cord injury (SCI) at or above T6. It is rare with lesions below T10 and typically appears after spinal shock resolves (weeks to months after injury).

**Pathophysiology:** 1. A noxious or visceral stimulus below the level of injury sends afferent signals up the spinal cord. 2. The signals cannot ascend past the lesion, so the brain does not modulate them. 3. This triggers an unopposed sympathetic reflex at the thoracolumbar (T6-L2) level. The splanchnic outflow (T5-T9 and below) drives splanchnic and peripheral vasoconstriction, causing severe hypertension. 4. Baroreceptors in the carotid sinus and aortic arch sense the hypertension. They signal through CN IX and X, and the brainstem responds with vagal (parasympathetic) outflow, causing **reflex bradycardia**. 5. Descending inhibitory signals from the brain cannot cross the lesion, so the vasoconstriction below it persists. 6. Above the lesion, compensatory vasodilation produces **flushing, sweating, nasal congestion, and pounding headache**. Below the lesion, there is pallor, cool skin, and piloerection.

**Triggers (most to least common):** - Bladder distension (blocked catheter, UTI, stones): the most common cause - Bowel: fecal impaction or constipation - Skin: pressure ulcers, ingrown toenails, tight clothing, burns - Others: menstruation, labor and delivery, pregnancy, fractures, sexual activity, and procedures

**Clinical presentation:** Severe throbbing headache, hypertension, bradycardia, flushing and diaphoresis above the lesion, nasal stuffiness, blurred vision, and anxiety. Pallor and cool skin appear below the lesion.

**Complications if untreated:** Hypertensive crisis leading to intracranial hemorrhage, seizures, retinal hemorrhage, MI, pulmonary edema, arrhythmias, and death.

**Management (stepwise):** 1. Sit the patient upright and lower the legs. This uses orthostasis to lower BP. 2. Loosen tight clothing, binders, and stockings. 3. Monitor BP every 2-5 minutes. 4. Find and remove the trigger. Check the bladder first (catheterize, or flush or replace a blocked catheter). Then check the bowel (use lidocaine jelly before a rectal exam or disimpaction), then the skin. 5. If SBP stays ≥150 mmHg despite these steps, give a fast-acting, short-duration antihypertensive. Options include nifedipine, nitrates (nitroglycerin paste or sublingual), and captopril. Avoid sildenafil-type drugs in patients who have used nitrates. 6. Monitor after resolution for recurrence.

**Boards pearls:** - The classic vignette is a patient with a cervical or high thoracic SCI and a headache, flushing, and hypertension with bradycardia. The most likely cause is a full bladder or a blocked Foley catheter. - Do NOT give beta-blockers as first-line treatment, because the patient already has bradycardia. - Pathophysiology differs from **spinal shock**, which is hypotension and flaccid paralysis in the acute phase. - It differs from **neurogenic shock**, which is hypotension and bradycardia from loss of sympathetic tone in acute high SCI. - Prevention: bowel and bladder programs, skin care, and patient and caregiver education. Patients often carry a wallet card.