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

Cerebral arterial aneurysms are common in the general population and their rupture is a catastrophic event. Considerable uncertainty remains concerning the conditions that predispose individuals to aneurysm formation or rupture. The role of systemic hypertension in aneurysm formation and rupture has been especially controversial. Demographic variables have rarely been addressed because of the small sample sizes in previous studies. The authors describe the demographics and prevalence of hypertension in 20,767 Medicare patients with an unruptured aneurysm and compared these to a random sample of the hospitalized Medicare population. The prevalence of hypertension in patients with unruptured aneurysms was 43.2% compared with 34.4% in the random sample. Patients who survived their initial hospitalization were separated into two groups: those with an unruptured cerebral aneurysm as the primary diagnosis and those with an unruptured cerebral aneurysm as a secondary diagnosis. Follow-up data for 18,119 patients were examined to determine the risk of subarachnoid hemorrhage (SAH) associated with age, gender, race, hypertension, insulin-dependent diabetes mellitus, and surgical treatment. For patients with an unruptured cerebral aneurysm as the primary diagnosis, hypertension was found to be a significant risk factor for future SAH (risk ratio: 1.46, 95% confidence interval (CI): 1.01-2.11), whereas surgical treatment (risk ratio: 0.29, 95% CI: 0.09-0.97) had a significant protective effect. Advancing age had a small but significant protective effect in both groups. Elderly patients identified with unruptured aneurysms are more likely to have coexisting hypertension than the general hospitalized population. In elderly patients hospitalized with an unruptured cerebral aneurysm as their primary diagnosis, hypertension is a risk factor for subsequent SAH, whereas surgical treatment is a protective factor against SAH.
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PMID:Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients: hypertension and other risk factors. 747 48

Only 53%-58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. PATHOPHYSIOLOGY. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6-12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. CALCIUM ANTAGONISTS. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. HYPERVOLAEMIC HAEMODILUTION. Volume expansion and haemodilution to a hematocrit of 30%-33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10-12 mm Hg and 15-18 mm Hg, respectively. But there is no evidence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. INDUCED ARTERIAL HYPERTENSION. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. CONCLUSION. Treatment of cerebral vasospasm following a SAB aims to avoid any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
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PMID:[Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Therapeutic value of treatment with calcium antagonists, hypervolemic hemodilution and induced arterial hypertension]. 778 50

Two cases of cerebral aneurysm rupture with repeat subarachnoidal haemorrhage are reported in patients with pneumococcal infection confirmed bacteriologically. It is concluded that in pathogenesis of the aneurysmal rupture in pneumococcal infection a significant role is played not only by pneumococcal tropism to the meninges, but also by affection of the endothelium and cerebral vascular membranes, hemostasis defects, arterial hypertension as manifestations of a general adaptation syndrome.
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PMID:[Aneurysms of the cerebral vessels and pneumococcal infection]. 804 1

Over a seven-year period, 130 patients with delayed ischaemia after cerebral aneurysm haemorrhage were treated with intravenous nimodipine. The delay from the last haemorrhage to the appearance of ischaemic symptoms was one to 18 days, and vasospasm was confirmed in most cases. Nimodipine treatment was started within three days of delayed ischaemic deficit (DID) onset, at a low dose increased quickly to 30-45 ug/kg/hr, and reduced gradually over the last day or two of the course. The duration of treatment was one to 27 days. Side effects were minor, and serious complications few. Hypotension occurred in 35 cases. During treatment, there were highly significant improvements in both clinical grade and Glasgow Coma Score. The final outcome was 98 good (Glasgow Outcome Score 1), 18 permanent deficits (eight GOS 2, ten GOS 3), and 14 dead. Ischaemia was directly involved in only half the deaths. These results are much better than the natural history (about 1/3 dead and 1/3 disabled), and a considerable improvement over fluid and hypertensive treatment (17% dead, 29% deficits), calculated from a literature review. Nimodipine is also safer than induced hypertension, especially pre-operatively.
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PMID:Treatment of symptomatic vasospasm with nimodipine. 821 89

A surgical procedure to expose the arterial bifurcation at the base of the rat brain was developed without sacrificing the animal. Using this technique, visualization of flow in and around the induced cerebral aneurysm was achieved by detecting and following fluorescent particles in the blood stream. Cerebral aneurysms were produced by ligating one common carotid artery, inducing experimental hypertension and feeding them with beta-aminopropionitrile. Flow studies of the arterial bifurcation with an early aneurysmal formation showed that there were spiral flows proximal and distal to the bifurcation. This was the first direct visualization of the actual flow in and around cerebral aneurysms in a vital state. This technology can add further information on the development, growth and rupture of cerebral aneurysms.
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PMID:In vivo flow visualization of induced saccular cerebral aneurysms in rats. 837 16

The objective of this review is to review the anaesthetic implications of vasoactive compounds particularly with regard to the cerebral circulation and their clinical importance for the practicing anaesthetist. Material was selected on the basis of validity and application to clinical practice and animal studies were selected only if human studies were lacking. Hypotensive drugs have been used to induce hypotension and in the treatment of intraoperative hypertension during cerebral aneurysm surgery. After subarachnoid haemorrhage, cerebral blood flow is reduced and cerebral vasoreactivity is disturbed which may lead to brain ischaemia. Also, cerebral arterial vasospasm decreases cerebral blood flow, and may lead to delayed ischaemic brain damage which is a major problem after subarachnoid haemorrhage. Recently, the use of induced hypotension has decreased although it is still useful in patients with intraoperative aneurysm rupture, giant cerebral aneurysm, fragile aneurysms and multiple cerebral aneurysms. In this review, a variety of vasodilating agents, prostaglandin E1, sodium nitroprusside, nitroglycerin, trimetaphan, adenosine, calcium antagonists, and inhalational anaesthetics, are discussed for their clinical usefulness. Sodium nitroprusside, nitroglycerin and isoflurane are the drugs of choice for induced hypotension. Prostaglandin E1, nicardipine and nitroglycerin have the advantage that they do not alter carbon dioxide reactivity. Local cerebral blood flow is increased with nitroglycerin, decreased with trimetaphan and unchanged with prostaglandin E1. Intraoperative hypertension is a dangerous complication occurring during cerebral aneurysm surgery, but its treatment in association with subarachnoid haemorrhage is complicated in cases of cerebral arterial vasospasm because fluctuations in cerebral blood flow may be exacerbated. Hypertension should be treated immediately to reduce the risk of rebleeding and intraoperative aneurysmal rupture and the choice of drugs is discussed. Although the use of induced hypotension has declined, the control of arterial blood pressure with vasoactive drugs to reduce the risk of intraoperative cerebral aneurysm rupture is a useful technique. Intraoperative hypertension should be treated immediately but the cerebral vascular effects of each vasodilator should be understood before their use as hypotensive agents.
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PMID:Vasodilators during cerebral aneurysm surgery. 840 62

Forty-two patients underwent cerebral aneurysm clipping at our institution in 1991, 35 with a ruptured aneurysm and 7 with an unruptured aneurysm. Preoperatively, 22 patients with a ruptured aneurysm were graded I or II according to the World Federation of Neurosurgical Societies and 21 underwent an operation on the first day. All underwent a standard cerebral protective general anesthesia, combining propofol with fentanyl, arterial normotension (mild hypertension with volume loading and/or dopamine during temporary clipping and once the aneurysm was secured), normocarbia or slight hypocarbia, brain relaxation with lumbar drainage, mannitol and propofol, and electroencephalogram burst suppression when temporary clipping (> or = 2 min) was required. Propofol doses for induction were 1.8 +/- 0.1 mg/kg (mean +/- standard error); for maintenance, doses were 86 +/- 3.5 micrograms/kg per min; and for burst suppression doses were 500 micrograms/kg per min. After clipping, the propofol dose rate was reduced to allow early recovery and neurological examination in the operating room. In 21 patients, temporary clipping was required for a mean duration of 8.8 +/- 1.3 minutes (range, 2-29); none of these patients deteriorated as compared with their preoperative neurological state. Twenty-four of the 42 patients (57%) had a Glasgow Coma Outcome Scale (GOS) score of 1, 7 patients had a GOS score of 2, 8 had a score of 3, and 3 had a score of 5. Thirty-two patients were extubated in the operating room with a mean GOS Score of 13.2 +/- 0.5, and 10 were extubated later in the intensive care unit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total intravenous anesthesia with propofol for burst suppression in cerebral aneurysm surgery: preliminary report of 42 patients. 843 62

Patients with sickle cell disease appear to have a high incidence of cerebral aneurysm. These aneurysms are not associated with the usual risk factors of hypertension, renal disease, or connective tissue disease. We present two recent cases of patients with sickle cell disease and multiple cerebral aneurysms, review the literature on the association between sickle cell disease and cerebral aneurysms, and discuss a mechanism by which sickle cell disease may lead to the formation of cerebral aneurysms.
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PMID:Multiple cerebral aneurysms in patients with sickle cell disease. 846 34

Autosomal dominant polycystic kidney disease is one of the most commonly inherited diseases in the United States. It affects nearly 500,000 Americans and accounts for 5 to 10 percent of patients with end-stage renal disease. Diagnosis is usually made in middle age, when complications such as hypertension, pain and hematuria develop. Renal complications include hypertension, cyst infection and hemorrhage, hematuria and flank pain. Other manifestations and related conditions include polycystic liver disease, cerebral aneurysm, cardiac valve abnormalities and diverticulosis. The severity and course of the disease vary in individual patients. Management involves the control of hypertension and treatment of complications. Genetic counseling is important. Dialysis and renal transplantation often are successful treatments in patients who develop renal failure.
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PMID:Autosomal dominant polycystic kidney disease. 859 59

A case is presented of a de novo aneurysm of the distal posterior inferior cerebellar artery with intraventricular hemorrhage. A 67-year-old woman was admitted to our hospital with sudden onset of severe headache and loss of consciousness. Computed tomography (CT) scans showed subarachnoid hemorrhage. Angiography demonstrated three aneurysms: an aneurysm of the right vertebral-posterior inferior cerebellar artery, an aneurysm of the bifurcation of the basilar artery, and an aneurysm of the left middle cerebral artery. Considering the distribution of the hemorrhage on CT scans, we concluded that the cause of the hemorrhage was rupture of the vertebral-posterior inferior cerebellar aneurysm. The vertebral-posterior inferior cerebellar aneurysm and the middle cerebral aneurysm were successfully clipped, postoperative angiograms showing the complete clippings. At that time, however, there were no abnormal findings in the left posterior inferior cerebellar artery. Six years later, she was readmitted to our hospital because of sudden onset of headache, nausea, and vertigo. CT scans showed an intraventricular hemorrhage, especially in the fourth ventricle, although subarachnoid hemorrhage was not clearly found. Angiography revealed an aneurysm of the left distal posterior inferior cerebellar artery. She underwent clipping of the aneurysm verified by postoperative angiograms. However she had bacterial meningitis and died from pneumonia and disseminated intravascular coagulopathy. De novo aneurysms of the anterior circulation have often been reported. Carotid, ligation, smoking, the use of oral contraceptives, congenital anomalies and hypertension are major risk factors in the formation of aneurysms. A de novo aneurysm of the distal posterior inferior cerebellar artery is, however, extremely rare. In this case, the right posterior inferior cerebellar artery disappeared when the de novo aneurysm was found. So it is supposed that hemodynamic changes caused by the clipping of the right vertebral-posterior inferior cerebellar aneurysm and the left middle cerebral aneurysm had contributed to the formation of the de novo aneurysm of the left distal posterior inferior cerebellar artery. In the present study, we review the literature on the aneurysm at the distal posterior inferior cerebellar artery and on the de novo aneurysm of the vertebrobasilar artery, and discuss the radiological findings and features.
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PMID:[A case of de novo aneurysm of the distal posterior inferior cerebellar artery with intraventricular hemorrhage]. 869 75


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