1/181. 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 = blood pressure, pressure (Clic here for more details about this article) |
2/181. 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 = 0.19501095904831keywords = pressure (Clic here for more details about this article) |
3/181. 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 = 0.19501095904831keywords = pressure (Clic here for more details about this article) |
4/181. 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 = 1.3900219180966keywords = blood pressure, pressure (Clic here for more details about this article) |
5/181. Cervical subarachnoid hematoma of unknown origin: case report.OBJECTIVE AND IMPORTANCE: Spontaneous spinal subarachnoid hematoma is rare, having been reported in the English literature in only seven other cases. We describe the first case of spontaneous subarachnoid hematoma located in the cervical spinal cord of a 43-year-old man. The pathologic examination showed no apparent source of bleeding, but there was evidence of cervical spondylotic myelopathy. CLINICAL PRESENTATION: The patient presented with a 10-day history of severe neck pain, followed by the onset of quadriparesis that was more evident on the left side, urinary retention, and sensory loss below C5. His medical history included hypertension. magnetic resonance imaging showed a massive hemorrhage in the cervical spinal canal. INTERVENTION: A C4-C5 subarachnoid hematoma was removed. The patient died due to respiratory distress and uncontrollable hypotension on day 6 after surgery. Surgical exploration, neuroradiologic examinations, and autopsy showed no evidence of vascular malformations, tumors, or other possible sources of bleeding. CONCLUSION: After excluding more common causes of spontaneous subarachnoid hematoma in this patient, we suggest that chronic spinal cord compression (spondylotic myelopathy) and arterial hypertension in this patient may have caused the pathogenesis of this rare clinical entity. Experimental data supporting this hypothesis are discussed.- - - - - - - - - - ranking = 0.38859789103895keywords = hypertension (Clic here for more details about this article) |
6/181. 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 = 0.77933182266439keywords = pressure, hypertension (Clic here for more details about this article) |
7/181. Autonomic instability and hypertension resulting in subarachnoid haemorrhage in the guillain-barre syndrome.We report the case of a 47-year-old woman with guillain-barre syndrome who developed autonomic instability and hypertension and subsequently developed a subarachnoid haemorrhage. This was manifested clinically by a seizure which began focally and became generalised. Computer tomography demonstrated a localised haemorrhage in the left central sulcus. Control of the hypertension was achieved with intravenous labetolol. Autonomic instability and hypertension are frequently reported in guillain-barre syndrome. Subarachnoid haemorrhage is an uncommon but serious complication.- - - - - - - - - - ranking = 1.3600926186363keywords = hypertension (Clic here for more details about this article) |
8/181. Spinal dural arteriovenous fistula with perimesencephalic subarachnoid haemorrhage.A case is reported of a 66 year old woman presenting with perimesencephalic subarachnoid haemorrhage (SAH) which was caused by a spinal dural arteriovenous fistula at the C1 level. The fistula drained into the venous system of the posterior cranial fossa through a perimedullary vein. The bleeding was thought to result from venous hypertension induced by the fistula. This case may support the hypothesis that perimesencephalic non-aneurysmal SAH can be ascribed to venous bleeding and that venous hypertension is the key to its pathology.- - - - - - - - - - ranking = 0.38859789103895keywords = hypertension (Clic here for more details about this article) |
9/181. pathology of a dissecting intracranial aneurysm.The pathological findings of six autopsy cases of dissecting intracranial aneurysm are studied. Clinically, all cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited rupture of the vertebral artery and subarachnoid hemorrhage. Two types of lesion were present. First, all cases showed the formation of a dilatated pseudoaneurysm with widespread disruption of the entire arterial wall, which was composed of thin adventitia. Second, a medial disruption of the arterial wall and subadventitial dissecting hemorrhage, which formed a false lumen and stenosis of the 'true' lumen of the artery, was also found. However, these lesions were found to be connected to the site of rupture. The autopsy cases within 1 day of onset of intracranial dissecting aneurysm showed the formation of fibrin thrombus, a marked degree of leukocyte infiltration and necrosis of the arterial wall at the site of the lesion. The cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration. No arteriosclerosis was found in any lesion studied. These data suggest that the disruption of the entire arterial wall might initially occur and cause medial disruption and subadventitial hemorrhage. Hypertension and arteriosclerosis might function as causal and protective factors in the pathogenesis of dissecting intracranial aneurysms, respectively.- - - - - - - - - - ranking = 0.19429894551947keywords = hypertension (Clic here for more details about this article) |
10/181. 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 = 0.39002191809661keywords = pressure (Clic here for more details about this article) |
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