1/131. Bedside-microdialysis for early detection of vasospasm after subarachnoid hemorrhage. Case report and review of the literature.Continuous monitoring of cerebral metabolism would be desirable for early detection of vasospasm in SAH patients. Bedside-microdialysis, a new technique for on-line monitoring of cerebral metabolism, may reflect changes seen in cerebral vasospasm diagnosed by transcranial Doppler sonography (TCD). This report represents the first case of combined TCD monitoring and on-line microdialysis from the brain extracellular fluid in a SAH patient. A 48-year-old woman suffered subarachnoid hemorrhage grade IV according to Hunt and Hess. Angiography revealed an aneurysm of the left carotid artery. The aneurysm was clipped 45 hours after bleeding. The microdialysis catheter was inserted after aneurysm clipping into the white matter of the left temporal lobe. Sampling of microdialysates started immediately, analyzing time for glucose, lactate, pyruvate and glutamate was four minutes. Postoperatively, the patient was doing well and microdialysis and TCD parameters remained within normal range. On the third postoperative day a shift to anaerob metabolism (decrease of glucose, increase of lactate and the lactate-pyruvate ratio up to pathological levels) and an increase in glutamate was observed suggesting insufficient cerebral perfusion. The patient progressively deteriorated clinically. Vasospasm was diagnosed by TCD monitoring 36 hours after onset of ischemic changes monitored by microdialysis. After elevation of mean arterial blood pressure, TCD values and metabolic parameters normalized. Interestingly, the pathological changes in on-line microdialysis preceded the typical increase in blood flow velocity by TCD and the clinical deterioration. Our case suggests, that bedside-microdialysis may be useful for early detection of vasospasm and continuous surveillance of treatment and may be a new guide to treat ischemic neurological deficits following SAH.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/131. Carotid ligation for carotid aneurysms.Thirty patients with subarachnoid haemorrhage due to rupture of a carotid aneurysm were treated by ligation of the common carotid artery. Two patients died as a result of the procedure, two patients developed persisting hemisphere deficit. Eight of the ten patients who developed cerebral ischemia after the operation were operated within ten days after the bleeding. At present out aim is to guide the patient safely through the first ten days after his haemorrhage and perform ligation at the end of the second week. After a follow up period of 1-8 years recurrent haemorrhage did not occur. Common carotid ligation, preferably with control of carotid artery end pressure, cerebral blood-flow and EEG is considered to be a valuable method to treat ruptured intracranial carotid aneurysm.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/131. anesthesia for ruptured cerebral aneurysm surgery associated with chronic renal failure.The management of patients with chronic renal failure (CRF) undergoing cerebral aneurysm surgery has been documented on only a few occasions. We report a 58-year-old man with CRF and subarachnoid hemorrhage (SAH) due to aneurysm rupture. We describe the patient's perioperative anesthetic management, discussing the current methods for maintaining an appropriate cerebral perfusion pressure and for preventing rehemorrhage from the aneurysm. We suggest that heparin-aided hemodialysis be avoided in these cases.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/131. Acute left ventricular dysfunction and subarachnoid hemorrhage.OBJECTIVE: Severe left ventricular (LV) dysfunction associated with acute subarachnoid hemorrhage (SAH) due to cerebral aneurysm rupture. SETTING: An adult 12-bed surgical intensive care unit of a university hospital. PATIENT: A female patient presenting with SAH (Hunt & Hess grade III) and severe left ventricular dysfunction. INTERVENTIONS: central venous pressure, arterial blood pressure, extravascular lung water catheter, transesophageal echocardiography, blood gas analysis, electrocardiograms, and chest x-ray for clinical management. MEASUREMENTS AND MAIN RESULTS: On admission to the district hospital, an electrocardiogram (ECG) revealed a sinus rhythm with transient ST elevations. A transesophageal echocardiography showed a left ventricular ejection fraction (LV-EF) of approximately 10%. Severe LV dysfunction required inotropic and vasopressor support to maintain mean arterial pressure above 60 mmHg, while the first measurement of an extravascular lung water catheter revealed a cardiac index of 2.0 L/min/m2 and moderate hypovolemia. Despite stepwise volume loading that increased intrathoracic blood volume--an indicator of cardiac preload--from 719 mL/m2 to 927 mL/m2, cardiac index remained poor. enoximone lead to a marked increase of cardiac index up to 3.9 L/min/m2 and LV-EF to about 30%, but had to be stopped due to thrombopenia. Surgical clipping of an intracranial aneurysm was postponed because of the impaired cardiac function and was performed on day 18 after admission. Interestingly, neurologic outcome was not as poor as might be expected from the literature. CONCLUSION: Severe left ventricular dysfunction may occur in acute SAH and may necessitate delay of aneurysm surgery.- - - - - - - - - - ranking = 3keywords = pressure (Clic here for more details about this article) |
5/131. subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma.In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an intensive care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.- - - - - - - - - - ranking = 3keywords = pressure (Clic here for more details about this article) |
6/131. nimodipine-induced acute hypoxemia: case report.OBJECTIVE AND IMPORTANCE: nimodipine is commonly used to improve neurological outcomes after subarachnoid hemorrhage. Although nimodipine reportedly has high specificity for the cerebral vasculature, adverse systemic effects such as hypotension have been described. This case report describes a patient with traumatic subarachnoid hemorrhage who experienced two episodes of previously undescribed, life-threatening hypoxemia that was directly related to nimodipine therapy. CLINICAL PRESENTATION: The patient experienced acute hypoxemia (partial pressures of oxygen of 32.9 and 58.7 mm Hg), on two separate occasions (3 d apart), that was temporally related to single doses of nimodipine therapy for traumatic subarachnoid hemorrhage. Other disease- and medication-related causes did not explain these episodes. INTERVENTION: After the inspired oxygen concentration was increased to 100% (both episodes) and the positive end expiratory pressure was increased to 7.5 mm Hg (first episode), the arterial oxygen saturation of the patient returned to baseline levels (>99%) within 40 minutes in each instance. nimodipine therapy was discontinued after each episode. CONCLUSION: It is hypothesized that, in the presence of concomitant adult respiratory distress syndrome, nimodipine increased ventilation/perfusion ratio mismatch, through its direct vasodilatory effects on the pulmonary artery, and possibly interfered with the reflex hypoxic pulmonary vasoconstriction necessary to maintain adequate oxygenation for this patient. Clinicians should carefully monitor the oxygenation status of patients when nimodipine therapy is initiated.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
7/131. Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage.OBJECT: The mechanism of reduction of cerebral circulation and metabolism in patients in the acute stage of aneurysmal subarachnoid hemorrhage (SAH) has not yet been fully clarified. The goal of this study was to elucidate this mechanism further. methods: The authors estimated cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), O2 extraction fraction (OEF), and cerebral blood volume (CBV) preoperatively in eight patients with aneurysmal SAH (one man and seven women, mean age 63.5 years) within 40 hours of onset by using positron emission tomography (PET). The patients' CBF, CMRO2, and CBF/CBV were significantly lower than those in normal control volunteers. However, OEF and CBV did not differ significantly from those in control volunteers. The significant decrease in CBF/CBV, which indicates reduced cerebral perfusion pressure, was believed to be caused by impaired cerebral circulation due to elevated intracranial pressure (ICP) after rupture of the aneurysm. In two of the eight patients, uncoupling between CBF and CMRO2 was shown, strongly suggesting the presence of cerebral ischemia. CONCLUSIONS: The initial reduction in CBF due to elevated ICP, followed by reduction in CMRO, at the time of aneurysm rupture may play a role in the disturbance of CBF and cerebral metabolism in the acute stage of aneurysmal SAH.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
8/131. Spinal leptomeningeal metastases of giant cell glioblastoma associated with subarachnoid haemorrhage: case report.A case of subarachnoid haemorrhage (SAH) due to spinal leptomeningeal metastases of a giant cell glioblastoma is described. A 51 year old male presented with a four week history of headache. Neurological examination was normal except for a slight left hemiparesis. Computed tomography (CT) revealed a large cyst with a mural nodule in the right temporal lobe. The tumour was removed followed by 60 Gy of radiation therapy. Thirty-two months later he developed headache and shoulder pain with symptoms of normal pressure hydrocephalus. Head CT showed ventriculomegaly and SAH. magnetic resonance imaging showed spinal leptomeningeal metastases at the C4-5, T12, and L2 levels, but no local recurrence or tumour dissemination in the brain. He died 34 months after surgery. autopsy revealed diffuse SAH over the whole brain and spinal cord, associated with spinal leptomeningeal metastases, but no cerebral aneurysms. Spinal radiotherapy and ventriculoperitoneal shunting could possibly have extended survival in this patient.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
9/131. 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 = pressure (Clic here for more details about this article) |
10/131. Neurovascular lessons from a pair of identical twins with cerebral aneurysms.A pair of hypertensive identical twins are reported, one of whom was non-compliant with her antihypertension medication, and after a subarachnoid haemorrhage was found to have multiple cerebral aneurysms. The other asymptomatic compliant twin was noted to have only a single small cerebral aneurysm. As both identical twins are likely to share the same cerebral vascular architecture it is suggested that good control of blood pressure contributed to the cerebral vascular integrity of the asymptomatic twin. This is the first report on the role of blood pressure in the formation of cerebral aneurysms and provides insights for an alternative approach to the controversial management of asymptomatic cerebral aneurysms.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
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