• R Nau, P Scheidt, B D Gonska, and H W Prange.
• Neurologische Universitätsklinik, Göttingen.
• Dtsch. Med. Wochenschr. 1992 Apr 24;117(17):658-62.

AbstractA 32-year-old man (weight 132 kg, height 190 cm) suddenly became unconscious and cyanosed with an unrecordable pulse and ventricular flutter on ECG. After resuscitation, the blood pressure was 200/100 mm Hg; the patient moved his arms and legs at times, but he did not regain consciousness. Focal neurological signs and meningism were not demonstrable. Subsequent ECGs showed a raised ST segment, followed later by terminal T wave inversion; marked pulmonary oedema was present clinically and radiologically. The creatine kinase activity was 344 U/l. As lateral myocardial infarction was suspected, the patient received heparin (1000-1700 IU/h) and nitroglycerin intravenously. Because the CK-MB isoenzyme failed to rise significantly and there was no reduction of R wave on the ECG, a CT scan of the brain was performed: this showed brain oedema as well as severe subarachnoid haemorrhage in the basal subarachnoid space, the posterior horn of the lateral ventricles and over the cerebral hemispheres. Despite implantation of an epidural pressure gauge, hyperventilation and administration of dexamethasone, osmotic diuretics and thiopental, the patient died 14 days after collapsing. At autopsy the heart showed no signs of myocardial infarction. The cause of the subarachnoid haemorrhage was a ruptured aneurysm of the anterior communicating artery.

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