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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the immediate and long-term results of surgical treatment for intracranial meningioma in patients aged 65 and over. Average patient age was 69 years. The most frequent localizations were the convexity (29.8%) and the sphenoid wing (20.1%). Preoperative risk factors included hypertension (16.1%), cardiopathies (16.1%), diabetes (12.9%) pneumopathies (12.9%) and peripheral vascular diseases (9.6%). All patients were assessed according to the Karnofsky Performance Status (KPS). Operative mortality was 18.5% (23 cases). At long term follow up (minimum 4 months, maximum 12 years, average 5 years) 31.5% of patients were cured, 32.3% had improved and 4% had worsened. The risk factors that mainly influenced results included poor preoperative clinical condition as expressed by low KPS, while the most frequent medical postoperative complications that increased the rate of operative mortality were brain edema, infections and lung embolism.
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PMID:Meningiomas in elderly patients. Clinico-therapeutic considerations. 847 51

In fulminant liver failure, brain edema may progress to intracranial hypertension. However, the rise in intracranial pressure is a late event in this sequence. We investigated the relationship between cerebral perfusion and development of intracranial hypertension in a well-characterized model of fulminant liver failure, the rat subjected to hepatic devascularization (n = 11). In addition, we examined the effects of hyperglycemia on the development of brain edema because high blood glucose level can exacerbate other forms of brain edema, as seen in stroke. Intracranial pressure was continuously monitored with a cisterna magna catheter; relative changes in blood flow were continuously assessed with a Doppler flow probe on the internal carotid artery. Cerebral perfusion decreased by 62%, with the greatest reduction before the onset of increased intracranial pressure. Intracranial pressure did not change until 2 hr before death, at which time it increased exponentially. Brain water in fulminant liver failure rats was significantly increased compared with that in controls. Hyperglycemia (200 to 220 mg/dl) had no effect on time elapsed until loss of corneal reflex, percentage of brain water, maximal intracranial pressure or pattern of change in cerebral perfusion compared with euglycemia (80 to 100 mg/dl). Sham-operated animals showed no changes in measured parameters. We conclude that a linear reduction in cerebral perfusion precedes the rise of intracranial pressure in this model, a decrease that may reflect changes in brain metabolic activity at the time that brain edema develops. Carotid blood flow monitoring may be a useful noninvasive tool for the detection of cerebral events in fulminant liver failure.
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PMID:Reduction of cerebral perfusion precedes rise of intracranial pressure in rats with ischemic fulminant liver failure. 851 62

The postoperative hyperperfusion syndrome describes an abrupt increase in blood flow with loss of autoregulation in surgically reperfused brain. Reports described a spectrum of findings, including severe headache, transient ischemia, seizures, and intracerebral hemorrhage. Hypertension is common after carotid artery surgery and often plays a role in the pathophysiology. We now report five patients with severe white matter edema after carotid surgery, a finding not previously included in the hyperperfusion syndrome. Five to 8 days after carotid surgery and after hospital discharge, each patient developed hypertension, headache, hemiparesis, seizures, and aphasia or neglect due to severe white matter edema ipsilateral to the carotid surgery. One patient had a small hemorrhage within the edematous area. Hypertension was severe in four patients and moderate in one. The carotid artery was patent by ultrasound or angiography in each patient after surgery. Transcranial Doppler showed increased velocities ipsilateral to surgery in two patients and bilaterally in one. Computed tomographic abnormalities and neurologic signs resolved within 3 weeks in four of the five patients treated with antihypertensives and anticonvulsants. The fifth patient died from herniation secondary to massive edema. Brain edema with focal neurologic signs should be included as a serious but potentially reversible component of the postoperative hyperperfusion syndrome.
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PMID:Brain edema after carotid surgery. 904 Jul 62

Cerebral injury is seen in one of three patients with multiple traumas; thus efficient shock treatment is a most important measure against the development of secondary brain damage. Small-volume resuscitation in severe hemorrhagic shock by hypertonic/hyperoncotic saline/dextran has been shown to instantaneously normalize cardiac output and to raise systemic blood pressure. In this study, the fluid regimen was compared with hypertonic mannitol to investigate their therapeutic efficacy in intracranial hypertension. The experiments were performed in rabbits subjected to a focal lesion of the brain to induce acute, vasogenic brain edema. The resulting intracranial hypertension was enhanced in a standard manner by inflation of an epidural balloon until an intracranial pressure (ICP) of 17 mm Hg was obtained. Intravenous administration of either 7.2% saline/10% dextran-60 or of 20% mannitol rapidly decreased the elevated ICP. After the first injection, ICP lowering was maintained longer by the mannitol than by the hypertonic saline/dextran, whereas no differences in duration of ICP lowering were found when the infusions of these solutions were repeated. The systemic blood pressure increased after injection of the saline/dextran solution, but it tended to decrease after injection of the mannitol. Transient increases in plasma osmolality, colloid-osmotic pressure, and plasma-Na+ were more pronounced after administration of the saline/dextran solution than after the administration of the mannitol. No difference in the tissue water content between the traumatized and contralateral hemisphere was observed in the animals receiving mannitol; however, after saline/dextran infusion, the water content was somewhat increased in the exposed hemisphere but decreased in the nonexposed, contralateral hemisphere (decreased to a point even below the corresponding level of animals who received the mannitol). The increase of the cerebral water content of the traumatized hemisphere was associated with a respective increase of the cerebral Na+ content and a (nonsignificant) decrease of the K+ content. The present findings demonstrate that the hypertonic/hyperoncotic saline/dextran was as efficient as the mannitol in reducing ICP that had been increased by a cerebral lesion and a space-occupying mass; the underlying mechanisms responsible for the reduction might differ. Because of the powerful hemodynamic properties of the saline/dextran in circulatory shock, administration of the solution in patients with multiple traumas and head injury might be particularly advantageous for the prevention of secondary ischemic brain damage.
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PMID:Reduction of post-traumatic intracranial hypertension by hypertonic/hyperoncotic saline/dextran and hypertonic mannitol. 858 98

Operative interventions in subarachnoid hemorrhages caused by brain vessel aneurysm require meticulous dissection of the latter. Regardless of the preoperative preparation of hypertensives, hypertension is a factor predisposing to intraoperative blood pressure fluctuation which, in turn, is extremely unfavourable and interferes with the operation proper on the aneurysm. What is more, it augments the spasm of cerebral vessels and brain edema. Any increase in blood pressure may result in a rupture of the aneurysm. As shown by a parallel study on two groups of patients with hypertension, following intraoperative administration of calcium antagonists having a preventive effect on brain, the stabilization of blood pressure attained is persistent, with the spasm of cerebral vessels and brain edema lending themselves more readily to control. The application of controlled hypotension is more easily effected, and administration of ganglioblocking agents is unnecessary.
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PMID:[Controlled hypotension against a background of nimodipine during an operation on neurosurgical patients with hypertension]. 864 61

Traditional shunts were primarily designed to manage hydrocephalus by regulating intracranial pressure. However, in some circumstances, their performance characteristics can cause them to underdrain or overdrain CSF. Overdrainage has been linked with clinical complications such as valve-dependent shunt syndrome, cranial stenosis, slit-ventricle syndrome, and subdural hematomas, and it may contribute to ventricular catheter occlusion. In addition to complications associated with hypertension and ventriculomegaly, underdrainage has been linked with residual brain edema, and subcutaneous CSF effusion has been observed at the site of cranial perforation, mainly in pediatric patients. Newer designs attempt to reduce these complications, but fall short for various reasons. The author presents a new shunt design, which utilizes variable aperture technology (patent pending) that results in the physiologic regulation of CSF flow under both positive and negative pressure conditions. This new design offers encouragement for the management of hydrocephalus and the prevention of complications due to overdrainage.
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PMID:A new self-adjusting flow-regulating device for shunting of CSF. 893 23

The idea of using induced hypertension to treat the symptomatic ischaemia resulting from vasospasm after subarachnoidal hemorrhage, and the effect of this therapy on the blood-brain barrier, is checked in animal experiments. This therapy is combined with the application of nimodipine, which is recognised as the standard medication for prophylaxis of vasospasm. The effects of the induced hypertension combination with Nimodipine and in combination with another calcium antagonist, Flunarizine are compared. Seventy-four narcotised rats, one group with 22 animals treated with Nimodipine and 22 with placebo, and a second group 20 animals treated with Flunarizine and 10 with placebo, are evaluated. The blood pressure is raised to 150-180 mmHg by i.v. application of norfenephrine and measured continuously. The standard tracer, horseradish peroxidase, is applied as indicator for the blood-brain barrier function. 15 minutes later the experimental animals are exsanguinated by perfusion with saline, then perfused with Karnovsky's solution. After removal, the brains are stained for peroxidase to visualise extravasation of the horseradish peroxidase, and after evaluation of the results each brain is assigned to its experimental group. In the Nimodipine group, a significant accumulation (p < 0.001) of perivascular deposits of peroxidase reaction product were found, these were not found in the placebo group. The Flunarizine group does not differ from its placebo group in the number of extravasates, and thus, with respect to protein extravasation, appears better than the Nimodipine group. In electron micrographs of the extravasates one sees intact tight junctions and a neuroendothelial transport, and also vesicles, filled with horseradish peroxidase in the endothelium, the muscle cells, and the brain parenchyma, which arise from pinocytosis. The vesicles, which transport the high-molecular-weight protein, horseradish peroxidase, also transport other proteins and can, therefore, cause a brain edema. It follows from these morphological results that Nimodipine can disrupt the blood brain barrier function and can, therefore, also interfere with cerebral autoregulation, which depends on the resistance of vessels.
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PMID:Ultrastructural changes in the blood-brain barrier in rats after treatment with nimodipine and flunarizine. A comparison. 900 89

Aggressive treatment of patients with severe head injury increases the chance for survival and good functional outcome in most cases. To prevent irreversible cerebral lesions, the key point of treatment is the management of intracranial hypertension caused by intracranial hematomas, brain edema and impaired circulation of cerebrospinal fluid (CSF). Therapeutic standards are surgery of traumatic hematoma, osmotherapy and mild hyperventilation for brain edema, and CSF drainage. In highly elevated intracranial pressure (ICP) administration of barbiturates and forced hyperventilation can be considered.
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PMID:[Management of craniocerebral trauma in a neurosurgery center]. 903 46

With the wide acceptance of liver transplantation as a therapeutic alternative in fulminant hepatic failure (FHF), the successful management of patients with this syndrome has acquired a new urgency. Topping the list of medical problems is the development of brain swelling. Two decades after the recognition of its importance, brain edema and intracranial hypertension still constitute a major cause of death in these patients. In a more recent classification of FHF, brain edema was especially prominent in those subjects with "hyperacute failure," in whom a period of 7 days or less elapsed between the development of jaundice and encephalopathy. The goal of this review is to discuss two aspects of this clinical problem. On one hand, elucidation of its pathogenesis should lead to a more rational therapeutic approach; such an information would also be valuable to understand the relationship between hepatic encephalopathy and brain edema, a source of controversy. Studies of pathogenic mechanisms are difficult to perform in humans and animal models of FHF have proven valuable, as brain swelling can be detected with some regularity. On the other hand, an increasing array of techniques is now available in the intensive care setting to monitor patients with FHF. Of these, intracranial pressure monitoring has received the most critical attention. However, concerns with the risks of craniotomy and the need to acquire more dynamic information has led several groups to explore non-invasive methods that evaluate the consequences of intracranial hypertension. Their role, though potentially exciting, is still uncertain.
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PMID:Cerebral edema and intracranial pressure monitoring. 934 64

Intracranial hypertension is a serious consequence of the impaired intracranial volume homeostasis. It can be encountered in practically all fields of clinical praxis. The article reviews bibliographic data of the mechanisms of the intracranial hypertension development: Intracranial expansion, Brain edema, Hemodynamic brain edema, Liquor accumulation--hydrocephalus. A pathophysiological approach to the hypotheses of edema and brain swelling is stressed. Outlines of the modern diagnostics and therapy of the intracranial hypertension are presented.
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PMID:[Intracranial hypertension]. 965 Apr 17


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