Autonomic dysreflexia a less common medical emergency

Dr. Ileana Bucur, Dr. Manuel Bucur, dr. cristina Florentina Plesa , Dr. Gilda Mologhianu, Lecturer, PhD Key words: autonomic dysreflexia, spinal cord injury, sympathetic reflex SUMMARY Autonomic dysreflexia is an acute syndrome occurring in patients with vertebral and spinal cord injuries above T7 level. It is characterized by an excessive sympathetic reaction and by paroxysmal hypertension which may be life threatening and requires emergency medical treatment. In most cases it is triggered by a nociceptive stimulus produced by bladder or rectal distention. Autonomic dysreflexia is a complication that may occur in spinal cordinjured patients with spinal lesions above T7 and at the same time a less common medical emergency. From a pathogenic perspective, it is triggered by a nociceptive stimulus (pain or irritation) following the loss of supraspinal inhibition as a result of a lesion of the ascending pathways. In the absence of modulatory control by the brain, the stimulus triggers an exaggerated autonomic sympathetic response (originating in the thoracolumbar nodes), reflex vasoconstriction caudally to the lesion and piloerection. Arterial blood pressure significantly increases by more than 20 mmHg as to the standard values (20-40 mm Hg). This can cause throbbing headaches and even hemorrhagic strokes as the arterial blood pressure may go above 180 mm Hg especially as vertebral and spinal cord-injured patients are hypotensive and bradycardic. Other complications that may occur are retinal hemorrhage, ischemic stroke, convulsions, and myocardial infarction. Reflex bradycardia (as a result of the stimulation of the aortic arch and carotid sinus baroreceptors) and vagal reflex also occur. Compensatory dilatation, skin redness on the face and neck, and profuse sweating may also occur cranially to the lesion. The patient may experience nausea, nasal stuffiness, anxiety, and arrhythmia. In case of lesions located cranially to T1, mydriasis may occur as a result of sympathetic hyperactivity (from the

center in the C8-T1 lateral horns through the efferent cervical sympathetic nerve). In the lesions located below this segment, myosis may appear as a result of the compensatory parasympathetic hyperactivity. Autonomic dysreflexia is a complication that may occur after the spinal shock disappears and as soon as the spinal reflexes return (2-6 months) and at any time during the patients lifetime. It was discovered and described by Anthony Bowlby in 1890. Its main cause is vertebral and spinal injuries, nowadays in most cases injuries resulting from road accidents. As it is a life threatening condition, it is essential that health care providers and particularly rehabilitation physicians, but also family members early recognize the symptoms so as to ensure that the patient receives prompt therapy. The stimulus originates below the spinal lesion and can include bladder or rectal overdistenstion, constipation, instrumental examination (cystoscopy, rectoscopy, etc.) or any other afferent somatic impulse originating below the lesion (urolithiasis, urinary sepsis, decubitus ulcer, burns, deep venous thrombosis, fracture, dislocation, sprain, menstrual cramps, sexual activity, gastroduodenal ulcer, appendicitis, cholelithiasis, hemorrhoids, etc.). The treatment consists in the immediate recognition of autonomic dysreflexia and removal of the triggering factors (nociceptive stimuli) urgent emptying of the bladder or rectum, and administration of antihypertensives if the systolic arterial pressure exceeds 150 mm Hg. Immediate catheterization of the bladder usually results in the quick lowering of the arterial blood pressure. The arterial blood pressure shall be monitored during the entire episode (2-5 minutes), and the clinical manifestations shall be monitored two hours after the cessation of the episode. The patient shall be asked to calm down and to sit in a comfortable position. Elastic pantyhoses, tight clothing or restrictive clothing shall be removed. Any instrumental or catheterization procedure shall be suspended at least until all symptoms disappear. The most frequent cause of autonomic dysreflexion is the distention of the bladder, requiring immediate catheterization. If the patient has a permanent urinary catheter, drainage should be checked. Compression or manual tapping of the hypogastric region shall be avoided.

Another frequent cause of autonomic dysreflexia is rectal distention. An anesthetic ointment shall be used to empty the rectum. Defecation will occur in maximum 5 minutes. If required a mild digital stimulation may be used. Rectal emptying must occur at least every three days. Pharmacological treatment must be administered whenever blood pressure does not go below 150 mm Hg, after the triggering factor is removed. Sublingual Nifedipine 10 mg or sublingual Nitroglycerin 0.5 mg (persons having received Sildenafil in the past 24 hours shall not be administered nitrates), or oral Clonidine 0.1-0.2 mg may be administered. These dosages may be administered after 20-30 minutes. Nifedipine should be chewed and swallowed for a complete absorption. Hydralazine, Diazoxide and endovenous administration of sodium nitroprusside for the quick lowering of arterial blood pressure may also be used. Patients with hypertensive emergencies shall receive treatment in specialized units (cardiology, neurology). It has been proven that oral Nifedipine (20 mg) administered 30 minutes before cystoscopy reduces the severity of the syndrome and that the acute hemodynamic effect may be addressed by using a ganglionic blocker administered parenterally or alpha-blockers (2). For preventative purposes, patients suffering from frequent episodes of autonomic dysreflexia and having high blood pressure values may be administered oral Prazosin 1 mg as chronic treatment.