Reversal of coma with an injection of glue

Abstract

In June, 2006, a 68-year-old man was transferred to our hospital in a coma. He had a 2-day history of new-onset generalised headache followed by a decrease in his level of consciousness. He was on warfarin for atrial fi brillation. There was no history of trauma. On examination, the Glasgow coma scale score was 7 (E1 M4 V2) and there were bilateral Babinski signs. CT showed bilateral acute-on-chronic subdural haematomas (fi gure A). Laboratory test results showed a prolonged prothrombin time of 27·3 s (normal 10·6–14·0) and an INR of 2·4 (normal 0·8–1·3). We administered fresh frozen plasma. On further questioning, the patient’s wife revealed that his headache had been exquisitely positional, occurring only when he was upright and resolving completely within 1–2 min when he lay down. MRI confi rmed the clinical suspicion of spontaneous intracranial hypotension: it showed sagging of the brain, enhancement of the pachymeninges, and subdural fl uid collections (fi gure B). The patient was placed in the Trendelenburg position at a 45° angle, following which his level of consciousness improved rapidly (Glasgow coma scale score 14 [E4 M6 V4]). CT myelography showed an opening pressure of 3 cm water (normal 6·5–19·5) and a thoracic meningeal diverticulum associated with a cerebrospinal fl uid (CSF) leak. The patient received a lumbar epidural blood patch of 50 mL autologous blood. The patient then regained full consciousness for about 48 h, after which he deteriorated with a widely fl uctuating level of consciousness, his Glasgow coma scale scores varying between 6 and 14 depending on his position. 2 mL fi brin glue (Tisseel, Baxter BioScience, Westlake Village, CA, USA) was administered percutaneously through an 18 gauge needle at the site of the CSF leak. The next day, the patient was able to walk; he had a normal sensorium and no headache. An MRI scan showed that the brain was sagging less and the subdural haematomas were smaller; the pachymeninges were no longer enhanced. When last seen at follow-up in January, 2007, the patient was well. Spontaneous intracranial hypotension is caused by a spontaneous spinal CSF leak and is an important cause of new headaches in young and middle-aged adults. Mechanical factors combine with an underlying connective-tissue disorder to produce the CSF leak. Spontaneous intracranial hypotension is not rare, but it is frequently misdiagnosed. A positional headache is the prototypical symptom but other headache patterns occur as well. Various associated clinical manifestations have been reported, including coma: which, in this case, was caused by severe sagging of the brain leading to diencephalic deformation. Subdural haematomas are found in about 20% of cases. The typical MRI fi ndings are subdural fl uid collections, enhancement of the pachymeninges, engorgement of venous structures, pituitary hyperaemia, and sagging of the brain (mnemonic, SEEPS). Treatments should be directed at the CSF leak. They include—in order of invasiveness— bed rest, epidural blood patching, percutaneous injection of fi brin glue, and surgical repair. Although subdural haematomas can appear quite ominous, with a signifi cant mass eff ect, their primary treatment is rarely indicated. Indeed, evacuation of subdural haematomas in the setting of spontaneous intracranial hypotension is associated with a high risk of worsening or recurrence of the subdural haematomas if the CSF leak is left untreated. Careful history-taking is therefore required when patients present with new-onset headaches and coma. In this case, the subdural haematomas could easily have been attributed solely to the warfarin use, even in the absence of any trauma; the coma could have been attributed (incorrectly) to the subdural haematomas: but the positional feature of the headaches suggested the diagnosis of spontaneous intracranial hypotension.