Cases reported "Cerebral Hemorrhage"

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1/198. Efficacy of induced hypotension in the surgical treatment of large cavernous sinus cavernomas.

    OBJECT: cavernous sinus cavernomas are rare lesions associated with high rates of intraoperative mortality and morbidity resulting from profuse bleeding. In this paper, the authors report their experience in treating five patients with histologically confirmed cavernous sinus cavernomas and describe the efficacy of induced hypotension in facilitating excision of the lesion. methods: All five patients were women ranging in age from 25 to 54 years, with an average age of 42 years. The mass was small in one and large (>3 cm in diameter) in four. In one patient with a large mass, cardiac arrest occurred after the craniotomy, and remarkable reduction in the size of the cavernoma was evident on postmortem examination. The other three large lesions were successfully removed piecemeal after induction of hypotension (60-80 mm Hg systolic pressure), which remarkably reduced the mass and the bleeding during surgery. In the remaining patient, who had a small lesion, the cavernoma was removed in one piece. CONCLUSIONS: cavernous sinus cavernoma can be thought of as a cluster of sinusoidal cavities, the size of which varies depending on the systemic blood pressure. During surgery, reduction of the mass and control of bleeding from the cavernoma can be achieved by inducing hypotension, which enables the safe excision of this lesion. This technique should be considered by surgeons resecting a cavernous sinus tumor, especially when cavernoma is suspected.
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2/198. Thalamic hemorrhage following carotid endarterectomy-induced labile blood pressure: controlling the liability with clonidine--a case report.

    Carotid endarterectomy can lead to alterations in baroreceptor sensitivity. Impairment of this sensitivity can in turn lead to volatility of blood pressure (baroreflex failure syndrome--BFS). Rapid elevations in blood pressure can cause hypertensive encephalopathy in a patient with BFS. A patient is presented with hypertensive intracerebral hemorrhage associated with BFS.
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3/198. methamphetamine-related stroke: four cases.

    Amphetamine use in certain parts of the united states has risen dramatically. methamphetamine, the most-common illicitly abused type of amphetamine, can be inhaled, injected intravenously, or smoked. It is a potent sympathomimetic that may lead to vascular events including myocardial infarction and stroke. Because of the demographics of drug use, these potentially devastating events usually occur in relatively young patients. The pathophysiology of stroke related to amphetamine use is multifactorial. Elevation in blood pressure, vasculitis, or other vascular toxicity are postulated as major mechanisms. Four cases of stroke associated with the use of methamphetamine, all occurring in patients ranging in age from 29-45 years, are described. methamphetamine use appears to be a risk factor for the development of stroke. The rise in methamphetamine use will undoubtedly result in increased Emergency Department admissions with clinical presentations very similar to those of cocaine intoxication.
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4/198. rupture of several parasagittal bridging veins without subdural bleeding.

    This case reports on a fatal craniocerebral trauma involving numerous ruptured cerebral bridging veins that did not bleed subdurally, despite approximately 15 hours of survival. A 15-year-old girl was severely injured as the passenger of a car that crashed sideways into a tree. She-suffered a cerebral trauma of the "diffuse injury" type and was unconscious after the accident. Her computed tomographic scan at admission showed massive brain edema, axial herniation, and marked hypodensity of the bilateral carotid flow area. Despite intensive care measures, the clinical course was characterized by central decompensation with therapy-resistant cardiocirculatory insufficiency. The autopsy revealed ruptures of numerous parasagittal bridging veins. The injured vessels were not thrombosed, and yet there was absolutely no subdural bleeding. This unusual combination of findings is assumed to be caused by an isolated collapse of cerebral circulation occurring shortly after the accident and primarily attributed to a rapid increase of intracranial pressure.
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5/198. Induced hypertension after head injury.

    The use of induced hypertension in head injury patients is controversial. We present the case of a 19-year-old man admitted with severe head trauma after a road accident and describe the beneficial effects that increasing arterial blood pressure had on the cerebral perfusion pressure, cerebral blood flow and jugular bulb oxygen saturation in this patient.
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6/198. Fatal cerebral reperfusion hemorrhage after carotid stenting.

    BACKGROUND: The hyperperfusion syndrome is a recognized complication of carotid endarterectomy. Reports of cerebral hyperperfusion injury following internal carotid artery (ICA) angioplasty are few, and this complication has never been reported following internal carotid stenting. CASE DESCRIPTION: A 68-year-old normotensive man was referred to our hospital for assessment 5 months after experiencing a left hemispheric ischemic stroke. angiography confirmed 95% stenosis of the left ICA. Left carotid percutaneous transluminal stenting was performed without any initial complications. color Doppler ultrasound of the ICA immediately after stenting revealed an elevated peak systolic velocity of 2.3 m/s, in the absence of significant vessel stenosis or spasm on angiography. Seven hours after the procedure, the patient suddenly deteriorated. CT of the brain revealed extensive intracerebral hemorrhage (ICH), and he subsequently died 18 days later. There was no history of headache or seizure activity, and his blood pressure was only mildly elevated at the time of the deterioration. This is the first report of ICH after internal carotid stenting. CONCLUSIONS: ICH may occur as a hyperperfusion phenomenon after internal carotid stenting, in the presence of mild to moderate arterial hypertension, without being heralded by any of the typical symptoms of the hyperperfusion syndrome. patients with increased velocities on color Doppler ultrasound of the ICA after angioplasty should be monitored closely for features of cerebral hyperperfusion injury. Further studies are warranted to determine whether more aggressive treatment of mild to moderate hypertension after carotid stenting would reduce the likelihood of this potentially fatal complication.
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7/198. electroconvulsive therapy and subdural hemorrhage.

    electroconvulsive therapy (ECT) was used to treat severe depressive illness in two patients, one of whom had undergone recent neurosurgery for subdural hemorrhage (SDH) and another with a concurrent SDH in the absence of raised intracranial pressure. Although the second patient died 1 month after the completion of ECT, in neither case did ECT extend the SDH or lead to other intracranial complications. It would seem that ECT can be performed safely in the presence of SDH without mass effect or after surgical drainage of SDH, although clinicians should proceed cautiously in close collaboration with neurosurgical colleagues, review neuroimaging scans at regular intervals during and after the course of ECT, and use the dose-titration method of treatment with unilateral electrode placement away from the site of the lesion or surgery to minimize adverse effects.
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8/198. Sevoflurane mask anesthesia for urgent tracheostomy in an uncooperative trauma patient with a difficult airway.

    PURPOSE: Proper care of the trauma patient often includes tracheal intubation to insure adequate ventilation and oxygenation, protect the airway from aspiration, and facilitate surgery. airway management can be particularly complex when there are facial bone fractures, head injury and cervical spine instability. CLINICAL FEATURES: A 29-yr-old intoxicated woman suffered a motor vehicle accident. Injuries consisted of multiple abrasions to her head, forehead, and face, right temporal lobe hemorrhage, and complex mandibular fractures with displacement. mouth opening was <10 mm. blood pressure was 106/71 mm Hg, pulse 109, respirations 18, temperature 37.3 degrees C, SpO2 100%. Chest and pelvic radiographs were normal and the there was increased anterior angulation of C4-C5 on the cervical spine film. Drug screen was positive for cocaine and alcohol. The initial plan was to perform awake tracheostomy with local anesthesia. However, the patient was uncooperative despite sedation and infiltration of local anesthesia. Sevoflurane, 1%, inspired in oxygen 100%, was administered via face mask. The concentration of sevoflurane was gradually increased to 4%, and loss of consciousness occurred within one minute. The patient breathed spontaneously and required gentle chin lift and jaw thrust. A cuffed tracheostomy tube was surgically inserted without complication. Blood gas showed pH 7.40, PCO2 35 mm Hg, PO2 396 mm Hg, hematocrit 33.6%. Diagnostic peritoneal lavage was negative. Pulmonary aspiration did not occur. Oxygenation and ventilation were maintained throughout the procedure. CONCLUSION: Continuous mask ventilation with sevoflurane is an appropriate technique when confronted with an uncooperative trauma patient with a difficult airway.
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9/198. Stress-related primary intracerebral hemorrhage: autopsy clues to underlying mechanism.

    BACKGROUND: research into the causes of small-vessel stroke has been hindered by technical constraints. Cases of intracerebral hemorrhage occurring in unusual clinical contexts suggest a causal role for sudden increases in blood pressure and/or cerebral blood flow. CASE DESCRIPTION: We describe a fatal primary thalamic/brain stem hemorrhage occurring in the context of sudden emotional upset. At autopsy, the brain harbored several perforating artery fibrinoid lesions adjacent to and remote from the hematoma as well as old lacunar infarcts and healed destructive small-vessel lesions. CONCLUSIONS: We postulate that the emotional upset caused a sudden rise in blood pressure/cerebral blood flow, mediating small-vessel fibrinoid necrosis and rupture. This or a related mechanism may underlie many small-vessel strokes.
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10/198. Posterior-fossa haemorrhage after supratentorial surgery--report of three cases and review of the literature.

    We present clinical details of three patients with posterior fossa haemorrhage after supratentorial surgery and discuss possible pathomechanisms of this rare complication. All patients were males of advanced age. Two patients presented with a history of hypertension. In all patients the occurrence of haemorrhage was associated with loss/removal of large amounts of cerebrospinal fluid (CSF) either intra-operatively (one patient undergoing aneurysm surgery) or postoperatively (all three patients: drainage of subdural hygromas or chronic subdural haematomas in two, external ventricular drainage in one patient). Treatment consisted in haematoma evacuation and/or external ventricular drainage. Two patients died, one patient recovered completely. Although haematomas distant from a craniotomy site are a well known entity, a review of the literature identified only 25 published cases of posterior fossa haemorrhage after supratentorial procedures in the CT era. Most often disturbances of coagulation, positioning of the patient and episodes of hypertension have been associated with this complication. Only one author described the occurrence of a haemorrhage after drainage of a supratentorial hygroma. We suggest that the loss of large amounts of CSF intra-operatively and post-operatively may lead to parenchymal shifts or a critical increase of transmural venous pressure with subsequent vascular disruption and haemorrhage.
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