1/49. Early rebleeding from intracranial dural arteriovenous fistulas: report of 20 cases and review of the literature.OBJECT: In this study the authors sought to estimate the frequency, seriousness, and delay of rebleeding in a homogeneous series of 20 patients whom they treated between May 1987 and May 1997 for arteriovenous fistulas (AVFs) that were revealed by intracranial hemorrhage (ICH). The natural history of intracranial dural AVFs remains obscure. In many studies attempts have been made to evaluate the risk of spontaneous hemorrhage, especially as a function of the pattern of venous drainage: a higher occurrence of bleeding was reported in AVFs with retrograde cortical venous drainage, with an overall estimated rate of 1.8% per year in the largest series in the literature. However, very few studies have been designed to establish the risk of rebleeding, an omission that the authors seek to remedy. methods: Presenting symptoms in the 20 patients (17 men and three women, mean age 54 years) were acute headache in 12 patients (60%), acute neurological deficit in eight (40%), loss of consciousness in five (25%), and generalized seizures in one (5%). Results of the clinical examination were normal in five patients and demonstrated a neurological deficit in 12 and coma in three. Computerized tomography scanning revealed intracranial bleeding in all cases (15 intraparenchymal hematomas, three subarachnoid hemorrhages, and two subdural hematomas). A diagnosis of AVF was made with the aid of angiographic studies in 19 patients, whereas it was a perioperative discovery in the remaining patient. There were 12 Type III and eight Type IV AVFs according to the revised classification of Djindjian and Merland, which meant that all AVFs in this study had retrograde cortical venous drainage. The mean duration between the first hemorrhage and treatment was 20 days. Seven patients (35%) presented with acute worsening during this delay due to radiologically proven early rebleeding. Treatment consisted of surgery alone in 10 patients, combined embolization and surgery in eight, embolization only in one, and stereotactic radiosurgery in one. Three patients died, one worsened, and in 16 (80%) neurological status improved, with 15 of 16 AVFs totally occluded on repeated angiographic studies (median follow up 10 months). CONCLUSIONS: The authors found that AVFs with retrograde cortical venous drainage present a high risk of early rebleeding (35% within 2 weeks after the first hemorrhage), with graver consequences than the first hemorrhage. They therefore advocate complete and early treatment in all cases of AVF with cortical venous drainage revealed by an ICH.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/49. Fatal subarachnoid hemorrhage after endoscopic third ventriculostomy. Case report.In recent years, endoscopic third ventriculostomy has become a well-established procedure for the treatment of various forms of noncommunicating hydrocephalus. Endoscopic third ventriculostomy is considered to be an easy and safe procedure. Complications have rarely been reported in the literature. The authors present a case in which the patient suffered a fatal subarachnoid hemorrhage (SAH) after endoscopic third ventriculostomy. This 63-year-old man presented with confusion and drowsiness and was admitted in to the hospital in poor general condition. Computerized tomography scanning revealed an obstructive hydrocephalus caused by a tumor located in the cerebellopontine angle. An endoscopic third ventriculostomy was performed with the aid of a Fogarty balloon catheter. Some hours postoperatively, the patient became comatose. Computerized tomography scanning revealed a severe perimesencephalic-peripontine SAH and progressive hydrocephalus. Despite emergency external ventricular drainage, the patient died a few hours later. Although endoscopic third ventriculostomy is considered to be a simple and safe procedure, one should be aware that severe and sometimes fatal complications may occur. To avoid vascular injury, perforation of the floor of the third ventricle should be performed in the midline, halfway between the infundibular recess and the mammillary bodies, just behind the dorsum sellae.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/49. False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling.The authors present two comatose patients with brain swelling from anoxic encephalopathy. Nonenhanced computed tomography (CT) images showed increased density on the falx, on the tentorium, and in the basal cisterns, all of which falsely suggested subarachnoid hemorrhage. autopsy in both patients failed to show subarachnoid hemorrhage. In rare circumstances, anoxic encephalopathy can mimic subarachnoid hemorrhage on nonenhanced CT.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/49. Superior sagittal sinus thrombosis induced by thyrotoxicosis. Case report.There is a wide variety of disorders associated with thrombosis of the superior sagittal sinus (SSS), including infectious disease. noninfectious conditions such as vasculitis and hypercoagulable states, and complications arising from pregnancy or use of oral contraceptive medications. Despite these well-defined associations, approximately 25% of the cases remain idiopathic. In this article the authors describe a patient who was found to have SSS thrombosis while experiencing a thyrotoxic phase of graves disease. The patient presented with intracerebral hemorrhage, subarachnoid hemorrhage, seizure, coma, a raised fibrinogen concentration, low protein c activity, and atrial fibrillations. Thrombolysis was successfully performed despite the coexistence of thrombosis and intracranial hemorrhage. patients with thyrotoxicosis and a diffuse goiter may be predisposed to the development of SSS thrombosis, as a result of hypercoagulation and stasis of local venous blood flow. In the present case, a patient in whom thrombosis coexisted with intracranial hemorrhage was successfully treated using thrombolytic therapy.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/49. Dissecting aneurysm of the vertebral artery causing subarachnoid hemorrhage after non-hemorrhagic infarction--case report.A 45-year-old male presented with lateral medullary infarction. cerebral angiography showed dissecting aneurysm as pearl and string sign in the right vertebral artery (VA). Conservative treatment was administered with antiplatelet agent. However, subarachnoid hemorrhage occurred 2 days after admission, inducing coma. Intraaneurysmal embolization and proximal occlusion of the right VA by intravascular surgery resulted in only mild neurological deficits. Conservative treatment including strict control of blood pressure is the first choice of treatment. Antiplatelet therapy and anticoagulant therapy should not be administered. patients must be followed up by serial angiography and surgery considered if signs of aneurysmal progression are seen.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/49. Severe subarachnoid hemorrhage with pulmonary edema successfully treated by intra-aneurysmal embolization using Guglielmi detachable coils--Two case reports.A 48-year-old male and a 39-year-old female presented with subarachnoid hemorrhage (SAH) due to ruptured anterior communicating artery aneurysms. Both patients were comatose on admission. Chest radiography disclosed pulmonary edema. They were conservatively treated under controlled ventilation, but cardiopulmonary dysfunction persisted over 2 days. The patients were then treated by intra-aneurysmal embolization with Guglielmi detachable coils (GDCs) 2 days after the onset. The postoperative courses were uneventful, and the patients showed full recovery from pulmonary edema and were discharged without neurological deficits. Neurogenic pulmonary edema is one of the serious complications of SAH, and is a leading cause of poor clinical outcome. The favorable outcomes of the present cases suggest that intra-aneurysmal embolization with GDCs is an excellent choice for the patients with severe aneurysmal SAH complicated with pulmonary edema, in whom conventional surgical treatment under general anesthesia is difficult to perform in the acute stage.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/49. Metastatic bronchogenic carcinoma with human chorionic gonadotropin production manifesting as cerebellar hemorrhage--case report.A 58-year-old male presented with a rare case of brain metastatic bronchogenic carcinoma with human chorionic gonadotropin (hCG) production causing cerebellar hemorrhage with symptoms of nausea, vomiting, and headache. Bronchogenic carcinoma manifesting as gynecomastia had been resected a few months previously. Neurological examination revealed left cerebellar ataxia. neuroimaging showed multiple cerebellar metastases with cerebellar hemorrhage adjacent to the tentorium. Angiography demonstrated tumor staining fed by the hemispheric branch of the left posterior inferior cerebellar artery. Suboccipital craniectomy was performed. The left cerebellar hematoma was evacuated and the tumor was partially removed to prevent massive intraoperative hemorrhage and avoid brain stem injury. Histological examination showed the resected tumor was large cell carcinoma. hCG was detected in the cerebrospinal fluid and was identified by immunohistochemical staining in tumor cells. The primary lesion of bronchogenic carcinoma showed choriocarcinomatous change because the tumor could produce hCG. The choriocarcinomatous cells with higher metastatic potential formed lesions in the brain, and finally intratumoral hemorrhage occurred producing the rapid development of symptoms.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/49. Subarachnoidal hemorrhage following carotid stenting with the distal-balloon protection.A 61-year-old man underwent carotid stenting with the distal-balloon protection system for symptomatic carotid artery stenosis. During the procedure, progressive elevation of the systolic blood pressure occurred, reaching a peak of 220 mm Hg immediately following deflation of the distal balloon. This was associated with severe headaches and progressive deterioration in the mental status to a coma. Head CT scan showed massive subarachnoidal hemorrhage contralateral to the stented side and a secondary intracerebral hemorrhage. Despite immediate successful blood pressure control, his condition deteriorated and he died 2 days later.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
9/49. Proposed use of prophylactic decompressive craniectomy in poor-grade aneurysmal subarachnoid hemorrhage patients presenting with associated large sylvian hematomas.OBJECTIVE: As a group, patients who present in poor neurological grade after aneurysmal subarachnoid hemorrhage (SAH) often have poor outcomes. There may be subgroups of these patients, however, in which one pathological process predominates and for which the initiation of specific therapeutic interventions that target the predominant pathological process may result in improved outcome. We report the use of prophylactic decompressive craniectomy in patients presenting in poor neurological condition after SAH from middle cerebral artery aneurysms with associated large sylvian fissure hematomas. Craniectomy allowed significant parenchymal swelling in the posthemorrhagic period without increased intracranial pressure (ICP) or herniation syndrome. methods: Eight patients (mean age, 56.5 yr; age range, 42-66 yr) presented comatose with SAH (five Hunt and Hess Grade IV, three Hunt and Hess Grade V). Radiographic evaluations demonstrated middle cerebral artery aneurysm and associated large sylvian fissure hematoma (mean clot volume, 121 ml; range, 30-175 ml). patients were brought emergently to the operating room and treated with a modification of the pterional craniotomy and aneurysm clipping that included a planned craniectomy and duraplasty. A large, reverse question mark scalp flap was created, followed by bone removal with the following margins: anterior, frontal to the midpupillary line; posterior at least 2 cm behind the external auditory meatus; superior up to 2 cm lateral to the superior sagittal sinus; and inferior to the floor of the middle cranial fossa. Generous duraplasty was performed using either pericranium or suitable, commercially available dural substitutes. RESULTS: All of the eight patients tolerated the craniectomy without operative complications. Postoperatively, all patients experienced immediate decreases in ICP to levels at or below 20 mm Hg (presentation mean ICP, 31.6 mm Hg; postoperative mean ICP, 13.1 mm Hg). ICP control was sustained in seven of eight patients, with the one exception being due to a massive hemispheric infarction secondary to refractory vasospasm. Follow-up (> or = 1 yr, except for one patient who died during the hospital stay) demonstrated that the craniectomy patients had a remarkably high number of good or excellent outcomes. The outcomes in the hemicraniectomy group were five good or excellent, one fair, and two poor or dead. CONCLUSION: The data gathered in this study demonstrate that decompressive craniectomy can be performed safely as part of initial management for a subcategory of patients with SAH who present with large sylvian fissure hematomas. In addition, the performance of decompressive craniectomy in the patients described in this article seemed to be associated with rapid and sustained control of ICP. Although the number of patients in this study is small, the data lend support to the hypothesis that decompressive craniectomy may be associated with good or excellent outcome in a carefully selected subset of patients with SAH.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/49. life-threatening hyperkalaemia following therapeutic barbiturate coma.OBJECTIVE: To report the occurrence of life-threatening hyperkalaemia following treatment with therapeutic thiopentone coma. SETTING: The neurosurgical intensive care units of Royal North Shore Hospital and Liverpool Hospital, Sydney, australia. patients: Three patients treated with theraputic thiopentone coma. One patient with raised intracranial pressure secondary to a severe traumatic brain injury and two patients with refractory vasospasm secondary to subarachnoid haemorrhage. Two of the three patients developed hypokalaemia on starting thiopentone, which was resistant to potassium supplementation. All three patients developed severe hyperkalaemia during the recovery phase of coma. This was life-threatening in all three patients and fatal in one. CONCLUSIONS: Severe hypokalaemia refractory to potassium therapy may occur during therapeutic thiopentone coma. Severe rebound hyperkalaemia may occur after cessation of thiopentone infusion. Protocols for the management of patients with therapeutic barbiturate coma should recognise this potentially serious complication.- - - - - - - - - - ranking = 9keywords = coma (Clic here for more details about this article) |
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