autonomic responses to stimuli that are harmless in normal people. It occurs only after spinal shock has resolved. This syndrome is characterized by a severe, pounding headache with paroxysmal hypertension, profuse diaphoresis (most often of the forehead), nausea, nasal congestion, and bradycardia. It occurs among patients with cord lesions above T6 (the sympathetic visceral outflow level) after spinal shock has subsided. The sudden increase in blood pressure may cause a rupture of one or more cerebral blood vessels or lead to increased ICP. A number of stimuli may trigger this reflex: distended bladder (the most common cause); distention or contraction of the visceral organs, especially the bowel (from constipation, impaction); or stimulation of the skin (tactile, pain, thermal stimuli, pressure ulcer). Because this is an emergency situation, the objectives are to remove the triggering stimulus and to avoid the possibility of serious complications. The following measures are carried out: • The patient is placed immediately in a sitting position to lower blood pressure. • Rapid assessment is performed to identify and alleviate the cause. • The bladder is emptied immediately via a urinary catheter. If an indwelling catheter is not patent, it is irrigated or replaced with another catheter. • The rectum is examined for a fecal mass. If one is present, a topical anesthetic agent is inserted 10 to 15 minutes before the mass is removed, because visceral distention or contraction can cause autonomic dysreflexia. • The skin is examined for any areas of pressure, irritation, or broken skin. • Any other stimulus that could be the triggering event, such as an object next to the skin or a draft of cold air, must be removed. • If these measures do not relieve the hypertension and excruciating headache, a ganglionic blocking agent (hydralazine hydrochloride [Apresoline]) is prescribed and administered slowly by the IV route. • The medical record is labeled with a clearly visible note about the risk of autonomic dysreflexia. • The patient is instructed about prevention and management measures. • Any patient with a lesion above the T6 segment is informed that such an episode is possible and may occur even many years after the initial injury Monitoring and Managing Potential Complications Patients are at high risk for VTE after SCI. The patient must be assessed for symptoms of VTE including DVT and PE. Chest pain, shortness of breath, and changes in arterial blood gas values must be reported promptly to the primary provider. The circumferences of the thighs and calves are measured and recorded daily; further diagnostic studies are performed if a significant increase is noted. Patients remain at high risk for thrombophlebitis for several months after the initial injury. Patients with paraplegia or tetraplegia are at increased risk for the rest of their lives. Immobilization and the associated venous stasis, as well as varying degrees of autonomic disruption, contribute to the high risk and susceptibility for DVT. Anticoagulation is initiated once head injury and other systemic injuries have been ruled out and other risk factors assessed. The use of low-