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

Hepatic encephalopathy is a major complication of portal-systemic shunts with an incidence ranging up to 52%. A small fraction of these patients are refractory to medical therapy. Shunt ligation and colonic procedures are the main surgical approaches. The goal of the latter is to diminish the colonic absorption of nitrogenous substances which are involved in the pathophysiology of hepatic encephalopathy. Six patients, whose average age was 55.7 +/- 2.6 years, were operated for severe postshunt encephalopathy requiring 4.3 +/- 0.9 admissions for a total duration of 76 +/- 26 days over 1-11 years. One patient had undergone a splenoral shunt and 5 had a portacaval shunt. One ligation of the shunt and 5 colon exclusions were performed. The average postoperative hospital stay was 21.5 +/- 3.9 days. The mean follow-up was 47 +/- 20 months. The patient with the shunt ligation remains free of encephalopathy 94 months after the procedure and has not bled from his esophageal varices. Among the 5 colon exclusion patients, there were 1 death and 3 complications. Three patients were completely relieved of their hepatic encephalopathy. One of those 3 died of a subarachnoid hemorrhage 28 months after the surgery. The fourth still needs medication to control a persistent, although improved, encephalopathy that required 2 further hospitalizations. Colon exclusion is a useful intervention in very selected cases. It has a lower operative mortality than total colectomy and the advantage over shunt ligation of not reestablishing hypertension in the portal system.
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PMID:Surgical treatment of severe postshunt hepatic encephalopathy. 199 94

Forty-one patients suffering subarachnoid hemorrhage (SAH) of unknown etiology were re-investigated at an average of 91 months after the bleed to determine functional capacity. Nineteen patients were performing at their previous level of work, five were employed part-time, and four could not work due to the SAH. Five patients showed a moderate disability in activities of daily living but were not dependent on help, one patient was severely disabled, and two had died. There was one rebleed. Early prognosis of an unfavorable outcome was possible on the basis of three clinical variables on admission: a history of hypertension, a Hunt and Hess grade of greater than II, and the presence of focal neurological deficits. In addition, the presence of an organic mental syndrome at discharge was identified as a predictive factor for reduced functional capacity later on. Other clinical variables in the acute stage, including sex, age, history of headache, interval between SAH and admission, impaired consciousness, and cognitive deficits, were not related to a limited functional level. Residual neurological deficits and the Glasgow Outcome Scale score on discharge were also not predictive of restrictions in global functions evaluated by means of the Karnofsky Performance Scale status at follow-up review.
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PMID:Subarachnoid hemorrhage of unknown etiology: early prognostic factors for long-term functional capacity. 200 74

A consecutive series of 145 patients with acute aneurysmal subarachnoid hemorrhage (SAH) were operated on within 7 days of SAH and were prospectively evaluated over a 4-year period to determine if the timing of aneurysm surgery influenced the development of delayed cerebral ischemia. All patients were managed with a standardized policy of urgent surgical clipping and treatment with aggressive prophylactic postoperative volume expansion. Patients with delayed ischemic symptoms were additionally treated with induced hypertension. Forty-nine patients underwent surgery on Day 0 or 1 (Group 1) post-SAH, 60 patients on Day 2 or 3 (Group 2), and 36 patients on Days 4 through 7 (Group 3). Postoperative delayed cerebral ischemia developed in 16% of (Group 1) patients, in 22% of Group 2 patients, and in 28% of Group 3 patients. Cerebral infarction resulting from delayed cerebral ischemia developed in only 4% of Group 1 patients, 10% of Group 2 patients, and 11% of Group 3 patients. A bad clinical outcome as a result of delayed cerebral ischemia occurred in one Group 1 patient (2%), two Group 2 patients (3%), and one Group 3 patient (3%). Preoperative grade was not significantly correlated with the incidence or severity of delayed cerebral ischemia at any time interval except that patients in modified Hunt and Hess Grade I or II who underwent surgery on Day 0 or 1 after SAH had no strokes or bad outcomes from delayed cerebral ischemia. This study demonstrates that there is no rationale for delaying aneurysm surgery based on the time interval between SAH and patient evaluation.
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PMID:Relationship between the timing of aneurysm surgery and the development of delayed cerebral ischemia. 204 19

Cerebral vasospasm occurs, following subarachnoid haemorrhage, in the majority of patients and is accompanied by cerebral ischaemia in 30%. The objectives of this article are to review (1) the effects of subarachnoid haemorrhage and vasospasm on cerebral blood flow (CBF); (2) the effects of induced hypotension and hypocapnia on CBF in these patients; (3) current therapy for cerebral ischaemia from vasospasm. The medical literature was searched using Index Medicus; for the period 1983-90 this search was done on a computer with the CD-ROM version of Index Medicus, Silver Platter. Papers were selected on the basis of validity and applicability to clinical practice; animal studies are included when human data is lacking. Cerebral vasospasm may decrease cerebral blood flow, disturb autoregulation and place the patient at risk for delayed cerebral ischaemia. Intraoperative induced hypotension and hypocapnia can decrease CBF further, although effects of either on outcome have not been evaluated. Calcium antagonists are effective for both the prevention and the treatment of delayed cerebral ischaemia. Of the mechanical treatments, systemic-arterial hypertension has the firmest scientific foundation, although this is frequently combined with haemodilution and blood volume expansion. There is a need for randomized clinical trials to assess the efficacy of these latter treatments.
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PMID:Haemodynamic considerations in the management of patients with subarachnoid haemorrhage. 206 13

Several risk factors for unfavorable outcome from subarachnoid hemorrhage (SAH) have been identified. The prevalence of such risk factors varies among ethnic groups and among men and women. The influence of ethnic background and gender as factors in the outcome after SAH has not been adequately studied and is the focus of the present investigation. Outcome in 145 consecutive patients was dichotomized as good and moderately disabled vs severely disabled, vegetative, and dead. A multiple logistic regression model was used to examine the factors of gender, ethnic group (white and non-white), age, admission neurological grade, pre-existing hypertension, and intravenous drug abuse. Our data reveal that hypertensive, white males, with a history of intravenous drug abuse, have a high risk of unfavorable outcome following SAH. These observations are important for the design and interpretation of future studies relating to SAH.
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PMID:Epidemiological characteristics of subarachnoid hemorrhage in an urban population. 206 44

It is suggested that endothelin-1 (ET-1), a potent vasoconstrictor peptide, is involved in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). We examined the effects of intracisternal administration of big ET-1 on the cerebral arteries in the absence or presence of pretreatment with phosphoramidon, an inhibitor of ET converting enzyme, in anesthetized dogs. After intracisternal administration of big ET-1 (10 micrograms/dog), the caliber of the basilar artery on the angiogram was decreased to about 59% of the control. This was accompanied by a marked increase in immunoreactive ET in the cerebrospinal fluid. Systemic arterial pressure was markedly elevated following big ET-1 injection. All changes induced by big ET-1 were effectively prevented with phosphoramidon. These data suggest that intracisternally administered big ET-1 is converted to ET-1 and that the generated ET-1 produces cerebral vasospasm and hypertension. A phosphoramidon-sensitive metalloproteinase appears to contribute to this conversion.
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PMID:Phosphoramidon inhibits the conversion of intracisternally administered big endothelin-1 to endothelin-1. 206 64

We present a 33-year-old female who had a ruptured aneurysm at the trifurcation of the right middle cerebral artery accompanied by coarctation of the aorta. The aneurysm was successfully clipped 15 hours after the attack of subarachnoid hemorrhage and approximately 3 months later the coarctation was surgically treated. Many authors reported that the incidence of cerebral aneurysm was higher in the patients with coarctation than the general population. Our review of the literatures, however, revealed that the incidence of cerebral aneurysm was the same in the population with or without coarctation. The incidence of rupture was higher when the aneurysms was accompanied by coarctation. The average age of the patients at the aneurysmal rupture was younger in the patients with coarctation than the patients without coarctation. These findings suggested that the growth and rupture of aneurysm in the patient with coarctation are related to the hypertension and atherosclerosis. Treatment of the patients with intracranial ruptured aneurysm accompanied by coarctation should begin with the clipping of the aneurysm, and then the coarctation surgically repaired. If the aneurysm is unruptured coarctation should be repaired first, and then the aneurysm clipped.
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PMID:[Ruptured cerebral aneurysm associated with coarctation of the aorta]. 207 50

The therapeutic effectiveness of calcium channel antagonists (CCA) in hypertension and angina are well established. More recently, CCAs have also been demonstrated to ameliorate neurologic dysfunction that often accompanies ischemia associated with subarachnoid hemorrhage and stroke. We have hypothesized that retinal degeneration associated with ischemia may also result from the accumulation of calcium intracellularly, so-called "Ca++ overload". To test this hypothesis, a rat model of acute retinal ischemia, produced by direct occlusion of posterior ciliary and central retinal arteries, was developed. The extent of retinal dysfunction induced by ischemia was evaluated by electroretinograms (ERGs). Occlusion of the retinal arteries resulted in the disappearance of both a- and b-waves during the occlusion period (30 minutes) in vehicle-treated rats. Total retinal ischemia did not produce any significant change in magnitude of ERG a-wave amplitude during three-hours of reperfusion. However, ERG b-waves amplitudes were significantly reduced by more than 60%. In rats, pretreatment with nifedipine (0.33 to 3.3 mg/kg, i.p.) 30 minutes prior to the occlusion of the retinal vessels produced a significant dose-dependent increase in the recovery of b-wave amplitude when compared to vehicle-treated rats. These data support the idea that "Ca++ overload", resulting from the deregulation of intracellular Ca++ homeostasis, is a primary factor involved in ischemic retinal degeneration and that CCAs can protect the retina from ischemic damage.
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PMID:Effect of the calcium antagonist, nifedipine, on ischemic retinal dysfunction. 209 13

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

The premise of this article is that morphologic changes observed in cerebral arteries after subarachnoid hemorrhage play an important role in the pathogenesis of associated ischemic deficits observed in this disorder. Secondly, the arteriopathic response of cerebral arteries to subarachnoid blood is similar in many respects to that observed in systemic vessels under various pathologic conditions, and common pathogenic mechanisms may exist. The data supporting these premises may be summarized as follows: 1. Morphologic changes in human and animal cerebral arteries after subarachnoid hemorrhage are temporally associated with angiographic and clinically significant vasospasm. 2. Profound morphologic changes in cerebral arteries after subarachnoid hemorrhage do not contribute to structural narrowing of the lumen through increases in vessel wall mass. Nevertheless, structural changes may act in concert with contractile mechanisms to alter normal physiologic responses and maintain a narrowed lumen. 3. The agent responsible for arterial narrowing and morphologic changes in cerebral arteries after subarachnoid hemorrhage is contained in the erythrocyte component of whole blood and is most likely hemoglobin. 4. The volume and duration of exposure of subarachnoid blood to the artery appears to be significant in the development of the angiopathic response. 5. Ultrastructural abnormalities in systemic vessels associated with hypertension, atherogenesis, and endothelial damage are similar in many respects to those seen after subarachnoid hemorrhage.
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PMID:Morphologic changes in cerebral arteries after subarachnoid hemorrhage. 213 52


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