Type of admission is associated with outcome of spontaneous subarachnoid hemorrhage.

BACKGROUND: Admitting facility may significantly affect outcome for spontaneous subarachnoid hemorrhage patients. We assessed outcomes of patients admitted directly to a comprehensive stroke center with those initially admitted to a general hospital and subsequently transferred. The comprehensive stroke center included a neurocritical care ICU, cerebrovascular neurosurgeons and endovascular specialists. METHODS: We identified 107 consecutive spontaneous subarachnoid hemorrhage cases. Of these cases, 31 (29%) patients were admitted directly and 76 (71%) were transferred from general hospitals. Univariate and multivariate analyses evaluated differences in mortality, complications, discharge disposition, and in-hospital length of stay. RESULTS: Differences in baseline parameters (age, gender, admission Glasgow Coma Scale, Fisher grade, admission Hunt and Hess grade) were not statistically significant between direct-admit and transfer patients at our institution. Transferred patients developed vasospasm more frequently (58% vs. 32%; P < 0.05) and had a longer delay time to surgery (3.9-days vs. 2.4-days: P < 0.05). Multivariate analysis showed that the likelihood of vasospasm was significantly higher for transfer patients (OR 3.46, CI: 1.2-10.3, P = 0.03). In addition, longer in-hospital stays and higher odds of non-routine discharge were observed in transferred patients (P < 0.01). No differences in outcome could be identified for surgical vs. endovascular treatment rates between direct-admit and transfer patients. An association, but no causative link, can be made between the effect of transfer and the outcomes of SAH patients due to the retrospective nature of our study. CONCLUSIONS: Spontaneous subarachnoid hemorrhage patients admitted directly to our comprehensive stroke center showed less complications compared to those transferred from general hospitals. This improvement was independent of time to treatment. Additional research in multiple centers using prospective analysis should be conducted to confirm that preferential direct transport to a comprehensive stroke center would likely yield considerable improvements in public health.

Anterior spinal artery syndrome in a patient with vasospasm secondary to a ruptured cervical dural arteriovenous fistula.

BACKGROUND: Spinal dural arteriovenous fistulas (DAVF) in the cervical spine are known to cause subarachnoid hemorrhage. Vasospasm after rupture of a DAVF, however, has not previously been reported. CASE PRESENTATION: A 48-year-old woman who presented with the sudden onset of altered mental status. Imaging demonstrated extensive subarachnoid hemorrhage and spinal DAVF at C1 to C2. The patient underwent a suboccipital craniotomy for DAVF ligation. On post-operative day three, she began having acute weakness in all her extremities with proprioception and vibration preserved, whereas pain and temperature sensation was lost. An angiogram demonstrated bilateral vertebral artery vasospasm with no filling of the anterior spinal artery. Bilateral angioplasty of the vertebral arteries was performed successfully and post-angioplasty, the right vertebral artery was filling the anterior spinal artery. The patient clinically improved. She subsequently required treatment with n-butyl cyanoacrylic acid (nBCA) embolization and gamma knife radiosurgery to achieve obliteration of the lesion. CONCLUSIONS: For patients with subarachnoid hemorrhage of unknown origin, differential diagnosis should include DAVF. This patient also presented with vasospasm in the context of ruptured DAVF, a complication previously unreported in the literature. This finding suggests that close monitoring for vasospasm after rupture of DAVF is warranted.

Distribution of delayed ischemic neurological deficits after aneurysmal subarachnoid hemorrhage and implications for regional neuromonitoring.

OBJECTIVES: Many neuromonitoring devices provide data applicable to a limited region of the brain. Risk of DIND is common after aSAH and may occur near or remote from the ruptured aneurysm. The aim of this study is to determine the distribution of DIND after aneurysms rupture as it relates to the potential value of regional monitoring in detection of vasospasm. PATIENTS AND METHODS: The study enrolled aSAH patients presenting to a tertiary referral center over a three year period who received treatment for an identified ruptured aneurysm and survived >10 days with subsequent DIND. Only those patients receiving routine neuroimaging were included. To account for the anticipated effect on infarct distribution, patients were divided into groups of midline and non-midline aneurysms and assessed for vasospasm and stroke with respect to vascular distribution. Comparisons of clinical characteristics were made to determine factors predisposing to remote infarction. RESULTS: Twenty-nine patients met criteria with 15 patients harboring non-midline aneurysms. The rarity of isolated remote DIND prohibited adequate assessment of predictive clinical characteristics. For non-midline aneurysms, DIND occurred ipsilateral to the ruptured aneurysm in 93% and within the same vascular territory in 86% of patients. Midline anterior circulation aneurysms frequently resulted in ACA infarction. A neuromonitoring device with 100% sensitivity for ischemia placed in the MCA territory ipsilateral to a non-midline ruptured aneurysm would identify 71% of DIND. CONCLUSION: Vasospasm related infarction occurs most commonly ipsilateral to or in the same distribution of the ruptured aneurysm. Less anatomical correlation is seen with midline aneurysms. Rupture of posterior circulation aneurysms infrequently results in supratentorial infarction. Decisions regarding placement of regional monitors for the purpose of vasospasm detection should consider this distribution of ischemic risk.

Prolonged transcranial Doppler monitoring after aneurysmal subarachnoid hemorrhage fails to adequately predict ischemic risk.

BACKGROUND: Stroke is common after aneurysmal subarachnoid hemorrhage (aSAH). Transcranial Doppler ultrasound (TCD) monitoring is often employed to identify vasospasm and allow intervention to avoid infarction. The required duration of monitoring has not been established. We aim to determine if 10 days of TCD monitoring identifies all patients at risk for infarction. METHODS: A 3 year retrospective analysis of aSAH patients admitted to a neurovascular center was undertaken. Eligible patients were aged 18-85 years, presenting within 2 days of hemorrhage who had underwent TCD monitoring through post bleed day 10. Patients were assessed to determine if vasospasm onset occurred after 10 days with resulting stroke. Assessment of variables potentially impacting vasospasm onset and infarction were completed. RESULTS: 107 patients met criteria with 51 (48%) demonstrating vasospasm and 31 (29%) developing stroke. Of those suffering stroke, 22 (71%) demonstrated vasospasm while 9 (22%) did not. Two (2%) patients developed vasospasm only after day 10, neither experiencing stroke. Time to vasospasm onset (5.5 ± 2.5 days) was not impacted by common radiologic or clinical scales. Glasgow Coma Scale (GCS), Hunt and Hess Score (H&H), WFNS, ventriculostomy placement, intubation, and intraventricular hemorrhage were associated with likelihood of stroke (P < 0.05). The negative predictive value of TCD for identifying stroke risk was 84% while the sensitivity was 71%. CONCLUSIONS: TCD identification of vasospasm after day 10 is rare. Stroke is more likely to result from poor detection than from brevity of TCD monitoring. Improved or alternative monitoring is needed to effectively identify ischemia and prevent stroke.

Predictors of long-term shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage. Clinical article.

OBJECT: The purpose of this study was to identify predictors of shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage (SAH). METHODS: The authors evaluated the incidence of shunt-dependent hydrocephalus in a consecutive cohort of 580 patients with SAH who were admitted to the Neurological Intensive Care Unit of Columbia University Medical Center between July 1996 and September 2002. Patient demographics, 24-hour admission variables, initial CT scan characteristics, daily transcranial Doppler variables, and development of in-hospital complications were analyzed. Odds ratios and 95% CIs for candidate predictors were calculated using multivariate nominal logistic regression. RESULTS: Admission glucose of at least 126 mg/dl (adjusted OR 1.6; 95% CI 1.0-2.6), admission brain CT scan with a bicaudate index of at least 0.20 (adjusted OR 1.43; 95% CI 1.0-2.0), Fisher Grade 4 (adjusted OR 2.71; 95% CI 1.2-5.7), fourth ventricle hemorrhage (adjusted OR 1.78; 95% CI 1.1-2.7), and development of nosocomial meningitis (adjusted OR 2.2; 95% CI 1.4-3.7) were independently associated with shunt dependency. CONCLUSIONS: These data suggest that permanent CSF diversion after aneurysmal SAH may be independently predicted by hyperglycemia at admission, findings on the admission CT scan (Fisher Grade 4, fourth ventricle intraventricular hemorrhage, and bicaudate index ≥ 0.20), and development of nosocomial meningitis. Future research is needed to assess if tight glycemic control, reduction of fourth ventricle clot burden, and prevention of nosocomial meningitis may reduce the need for permanent CSF diversion after aneurysmal SAH.

In vivo effect of propranolol dose and timing on cerebral perfusion after traumatic brain injury.

BACKGROUND: In vivo models of traumatic brain injury (TBI) demonstrate increased cerebral perfusion, decreased cerebral hypoxia, reduced cerebral edema, and improved neurologic recovery with propranolol administration. The purpose of this study was to determine the effect of different propranolol doses and timing on cerebral perfusion in a murine TBI model. METHODS: Fifteen minutes after TBI, three groups of mice (four mice per group) were randomized to receive intravenous injections of placebo, 4 mg/kg propranolol, or 1 mg/kg propranolol. Two delayed treatment groups were randomized to receive placebo or 4 mg/kg propranolol 60 minutes after TBI. Cerebral perfusion was then imaged by micropositron emission tomography. RESULTS: With placebo injection 15 minutes after TBI, the standard uptake value (SUV) mean was 0.395 +/- 0.01; with 4 mg/kg propranolol, the SUV mean was 0.515 +/- 0.04; and with 1 mg/kg propranolol, the SUV mean was 0.46 +/- 0.01. Animals receiving 4 mg/kg propranolol demonstrated significant improvement (p < 0.01) in cerebral perfusion compared with placebo and compared with 1 mg/kg propranolol. With placebo injection at 60 minutes after TBI, the SUV mean was 0.26 +/- 0.03; and with 4 mg/kg propranolol, the SUV mean was 0.43 +/- 0.02. After 60 minutes, animals receiving 4 mg/kg propranolol demonstrated significant improvement (p < 0.01) in cerebral perfusion compared with placebo. CONCLUSION: In a murine model of TBI, higher doses of propranolol were preferable to lower doses and both early and late propranolol administration improved cerebral perfusion. Potential mechanisms and therapeutic potential require further research.

Spontaneous spinal cerebrospinal fluid leak as a cause of coma after craniotomy for clipping of an unruptured intracranial aneurysm.

Spontaneous spinal CSF leaks are best known as a cause of orthostatic headache, but may also be the cause of coma. The authors encountered a unique case of a spontaneous spinal CSF leak causing coma 2 days after craniotomy for clipping of an unruptured aneurysm. This 44-year-old woman with autosomal dominant polycystic kidney disease underwent an uneventful craniotomy for an incidental anterior choroidal artery aneurysm. No intraoperative spinal CSF drainage was used. Two days after surgery the patient became comatose with a left oculomotor nerve palsy. Computed tomography scanning revealed a right extraceberal hematoma and loss of gray-white matter differentiation. The hematoma was evacuated and a diagnosis of hemodialysis disequilibrium syndrome was made. Continuous hemodialysis and hyperosmolar therapy were instituted without any improvement. The CT scans were then reinterpreted as showing sagging of the brain, and the patient was placed in the Trendelenburg position which resulted in prompt improvement in her level of consciousness. A CT myelogram demonstrated an upper thoracic CSF leak that eventually required surgical correction. The patient made a complete neurological recovery. Neurological deterioration after craniotomy may be caused by brain sagging caused by a spontaneous spinal CSF leak, similar to intracranial hypotension due to intraoperative lumbar CSF drainage.

Predictors and clinical implications of shivering during therapeutic normothermia.

BACKGROUND: Shivering during induced normothermia (IN) remains a therapeutic limitation. We investigated potential risk factors and clinical implications of shivering during IN. METHODS: Post hoc analysis was performed on 24 patients enrolled in a clinical trial of an automated surface cooling system to achieve IN. Hyponatremia was defined as serum levels <136 mmol/L and hypomagnesaemia as levels <1.5 mg/dL. Continuous heat energy transfer (kcal/h) was averaged hourly. Glasgow Coma Scale (GCS) scores were recorded every 2 h. Shivering status was documented hourly. Mixed effects modeling was used to determine clinical measures associated with shivering. Generalized estimating equation (GEE) models were used to compare baseline-adjusted repeated-measures GCS scores. RESULTS: About of 24 (39%) patients demonstrated shivering. Shivering was associated with men (67% vs. 21%, P = 0.03), hyponatremia (44% vs. 7%, P = 0.03), and hypomagnesaemia (56% vs. 7%, P = 0.02). The average kcal/h (158 +/- 645 kcal/h vs. 493 +/- 645 kcal/h, P = 0.03) was greater in shivering patients. Shivering was positively associated with increases in heart rate (P < 0.001), respiratory rate (P < 0.001), and kcal/h (P < 0.001). Non-shivering patients showed a greater increase from baseline GCS (GEE, P = 0.02) at 24 h. No differences in sedative doses or fever burden were noted between shiverers and non-shiverers. CONCLUSIONS: Men, hyponatremia, and hypomagnesaemia may predispose febrile patients treated with IN to shivering. Shivering dramatically increases the amount of heat transfer required to maintain normothermia, and may be associated with adverse effects on level of consciousness.

Treatment of massive cerebral infarction.

Stroke is the third leading cause of death in the United States, with a person dying every 3 minutes of a stroke. Massive ischemic stroke accounts for 10% to 20% of ischemic strokes, has traditionally been associated with a high mortality and morbidity, and requires a unique management strategy. Recent advances in management, fueled by an increased understanding of the pathophysiology, may help decrease mortality and improve outcomes. Rapid access to reperfusion therapies remains the most critical element of stroke care and the cornerstone of therapy. This article focuses on newer therapies, including osmotic therapy, hypothermia, maintained normothermia, strict glycemic control, induced hypertension, and hemicraniectomy, all of which show promise for reducing mortality and improving functional outcome. These interventions have become integrated into neurologic intensive care units around the world. They are complicated, require a high level of expertise, and carry a significant learning curve. In order for these new management techniques to be effective, an expedited, aggressive, meticulous, and potentially prolonged medical management approach is needed. To accomplish this there is a growing need for focused specialists in the areas of neurointensive care and stroke.