Abstract
A 48-year-old woman was admitted to our emergency center for deterioration of consciousness. On arrival, her level of consciousness was 3 by the Japan Coma Scale and 10 by the Glasgow Coma Scale. Her blood pressure was 144/100 mmHg, and her pulse was regular at 136 beats/min. She was intubated under general anesthesia to lower the systolic blood pressure to 90-100 mmHg. Laboratory analysis showed elevated blood glucose (329 mg/dl), lactic dehydrogenase (311 U/l), creatinine kinase (CK, 410 U/l), and white blood cell count (19600/μl), and a reduced serum potassium (3.1 mmol/l). A computed tomographic scan showed a diffuse thick subarachnoid hemorrhage (SAH), and a chest X-ray revealed cardiomegaly and pulmonary edema. Electrocardiography on admission demonstrated sinus tachycardia and ST segment elevation in leads I, II, aVL, and V3 to V6, and a slightly prolonged QTc interval of 0.45 second. Echocardiography showed that wall motion of the left ventricular apex was significantly reduced, indicating specific “takotsubo” cardiomyopathy. Her cardiac function appeared to be well tolerant for direct surgery. Digital subtraction angiography was performed and disclosed an aneurysm at the P1 segment of the left posterior cerebral artery.
Surgical intervention was undertaken by the left pterional approach. While a subarachnoid clot in the prepontine cistern was being evacuated to expose the aneurysm via an opticocarotid triangle, her blood pressure suddenly dropped to 20 mmHg, her heart rate declined to 20 beats/min, and carotid pulsation disappeared. The surgery was discontinued and cardiac resuscitation was conducted by intravenous injection of 1 mg epinephrine and cardiac massage by chest compression. Twenty-five minutes later her cardiac function stabilized, and the aneurysm was successfully clipped. The postoperative course was uneventful, and the electrocardiogram showed inversion of T waves and gradual improvement of echocardiographic abnormalities.
An excessive catecholamine secretion related to hypothalamic damage is presumed to be the cause of cardiac dysfunction in the acute phase of SAH. Although evacuation of prepontine clot is a routine surgical maneuver, subtle compression or traction of the perforators from the P1 segment that feeds the hypothalamus might further injure the already affected hypothalamus to result in sudden cardiac arrest. In treatment of patients with SAH associated with cardiac dysfunction, preparation of an intra-aortic balloon pumping would be beneficial.
