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Encephalopathy hypertensive

Elevated blood pressure should remain untreated in the acute period (first 7 days) after ischemic stroke because of the risk of decreasing cerebral blood flow and worsening symptoms. The pressure should be lowered if it exceeds 220/120 mm Hg or there is evidence of aortic dissection, acute myocardial infarction, pulmonary edema, or hypertensive encephalopathy. If blood pressure is treated in the acute phase, short-acting parenteral agents (e.g., labetalol, nicardipine, nitroprusside) are preferred. [Pg.171]

The possibility of cerebrovascular action of PCP was raised by the development of focal seizures and hemiparesis in a 6-year-old boy who had ingested what was presumed to be PCP (18). Hypertensive encephalopathy with a blood pressure of260/160 occurred in an 18-year-old woman who used PCP (43). These clinical findings are compatible with in vitro studies indicating that cerebral artery spasms can be produced by PCP as well as by LSD and mescaline (4). Whether such cerebrovascular actions are pertinent to the mental effects of these drugs is questionable. [Pg.144]

Preeclampsia/eclampsia/nephritis (magnesium sulfate) - Prevention and control of convulsions of severe preeclampsia and eclampsia and for control of hypertension, encephalopathy, and convulsions associated with acute nephritis in children. [Pg.23]

Albumin (human) Epoetin alfa contains albumin, a derivative of human blood. Based on effective donor screening and product manufacturing processes, it carries an extremely remote risk for transmission of viral diseases. No cases of transmission of viral diseases or Creutzfeldt-Jakob disease have ever been identified for albumin. Anemia Not intended for CRF patients who require correction of severe anemia epoetin alfa may obviate the need for maintenance transfusions but is not a substitute for emergency transfusion. Not indicated for treatment of anemia in HIV-infected patients or cancer patients due to other factors such as iron or folate deficiencies, hemolysis, or Gl bleeding, which should be managed appropriately. Hypertension Up to 80% of patients with CRF have a history of hypertension. Do not treat patients with uncontrolled hypertension monitor blood pressure adequately before initiation of therapy. Hypertensive encephalopathy and seizures have occurred in patients with CRF treated with epoetin. [Pg.83]

Acute nephritis in chiidren To control hypertension, encephalopathy, and convulsions associated with acute nephritis in children. [Pg.1270]

Diazoxide is administered intravenously for the treatment of hypertensive emergencies, particularly malignant hypertension, hypertensive encephalopathy, and eclampsia. It is effective in 75 to 85% of the patients to whom it is administered and rarely reduces blood pressure below the normotensive range. [Pg.230]

Hypertensive encephalopathy, thrombosis, cerebrovascular accident. Ml, and seizures have occurred rarely. [Pg.439]

Hypertensive encephalopathy is a classic feature of malignanthypertension. Its clinical presentation consists of severe headache, mental confusion, and apprehension. Blurred vision, nausea and vomiting, and focal neurologic deficits are common. If untreated, the syndrome may progress over a period of 12-48 hours to convulsions, stupor, coma, and even death. [Pg.242]

Diazoxide [dye az OX ide] is a direct-acting arteriolar vasodilator. It has vascular effects like those of hydralazine. For patients with coronary insufficiency, diazoxide is administered intravenously with a p-blocker, which diminishes reflex activation of the heart. Diazoxide is useful in the treatment of hypertensive emergencies, hypertensive encephalopathy, and eclampsia. Excessive hypotension is the most serious toxicity. [Pg.202]

Grewal RP, Miller BL. Cocaine induced hypertensive encephalopathy. Acta Neurol (Napoli) 1991 13(3) 279-81. [Pg.530]

If the perfusion pressure rises above the autoregulatory range, where compensatory vasoconstriction and cerebral perfusion pressure are maximal, then hyperemia occurs followed by vasogenic edema, raised intracranial pressure and the clinical syndrome of hypertensive encephalopathy. [Pg.45]

Naylor AR, Evans J, Thompson MM et al. (2003). Seizures after carotid endarterectomy hyperperfusion, dysautoregulation or hypertensive encephalopathy European Journal of Vascular Endovascular Surgery 26 39-44... [Pg.301]

Intoxication with vitamin D causes weakness, nausea, loss of appetite, headache, abdominal pains, cramps, and diarrhea. More seriously, it also causes hypercalcemia, with plasma concentrations of calcium between 2.75 to 4.5 mmol per L, compared with the normal range of 2.2 to 2.5 mmol per L. At plasma concentrations of calcium above 3.75 mmol per L, vascular smooth muscle may contract abnormally, leading to hypertension and hypertensive encephalopathy. Hypercalciuria may also result in the precipitation of calcium phosphate in the renal tubules and hence the development of urinary calculi. Hypercalcemia can also result in calcinosis - the calcification of soft tissues, including kidneys, heart, lungs, and blood vessels. This is assumed to be the result of increased calcium uptake into tissues in response to excessive plasma concentrations of the vitamin and its metabolites. [Pg.105]

Fig. 8 Patient with hypertensive encephalopathy secondary to eclampsia with the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome, (a) A T2-weighted MRl showing the extensive cerebral edema in the posterior white matter regions with less involvement of the gray matter, (b) Diffusion-weighted images with only one small area of involvement. The lack of DWl changes is consistent with this being a vasogenic type of edema, and the patient had a good recovery without residual... Fig. 8 Patient with hypertensive encephalopathy secondary to eclampsia with the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome, (a) A T2-weighted MRl showing the extensive cerebral edema in the posterior white matter regions with less involvement of the gray matter, (b) Diffusion-weighted images with only one small area of involvement. The lack of DWl changes is consistent with this being a vasogenic type of edema, and the patient had a good recovery without residual...
There have been cases of hypertensive encephalopathy, cerebrovascular accidents, and death after abrupt discontinuation... [Pg.83]

Ciclosporin-induced vasculopathy, with endothelial injury and derangement of the blood-brain barrier, is the postulated mechanism of neurological damage. Transient cerebral perfusion abnormalities, demonstrable in SPECT scans of the brain, have been suggested as a reliable indicator of ciclosporin neurotoxicity (SEDA-20, 344). Clinical symptoms as well as CT and/or MRI scans were very similar to those observed in hypertensive encephalopathy, with predominant and reversible white-matter occipital lesions (23). There was complete neurological recovery in most patients after blood pressure was normalized, and deaths due to intracranial hemorrhage are reported only exceptionally. [Pg.745]

Acute hypertensive encephalopathy has occurred in a patient given methylergotamine (SEDA-3, 121). [Pg.1231]

Hypertensive encephalopathy can arise in connection with the sudden and extreme rises in blood pressure that occur in some patients given epoetin (52,68). [Pg.1244]

A 14-year-old child developed hypertensive encephalopathy, a known rare adverse effect of erythropoietin, after 2 months (69). [Pg.1244]

During an open, uncontrolled study in 22 patients with end-stage renal disease treated with epoetin omega there was one case of hypertensive encephalopathy (70). [Pg.1244]

It is not clear why certain patients develop hypertension and hypertensive encephalopathy and others do not, but transfusion-dependent anemic patients with a low hematocrit (<20%) are particularly susceptible, as are those with previous hypertension and seizures. Careful control of blood pressure at the start of epoetin treatment and the use of low doses are therefore advised in patients at high risk. [Pg.1245]

Taylor J, Pahl M, Rajpoot D. Erythropoietin-induced hypertensive encephalopathy in a child possible mechanisms. Dial Transplant 2002 31 170-88. [Pg.1250]

Rodrigo E, San MiUan JCR, Heras M, Pinera C, Fresnedo F, Sanz De Castro S, Martin De Francisco YM, Arias AL. Posterior leukoencephalopathy in erythropoietin induced hypertensive encephalopathy. Neurologica 1999 19 360-4. [Pg.1251]

In two cases prolonged intake of relatively small amounts of licorice resulted in hypertension, encephalopathy, and pseudohyperaldosteronism (37). Both patients were highly susceptible to the adverse effects of glycyrrhizinic acid because of 11-beta-hydroxysteroid dehydrogenase deficiency. [Pg.1314]

Russo S, Mastropasqua M, Mosetti MA, Persegani C, Paggi A. Low doses of liquorice can induce hypertension encephalopathy. Am J Nephrol 2000 20(2) 145-8. [Pg.1316]

Intestinal transplantation is combined with liver transplantation in 46% of cases, because of terminal liver failure (93). Of 78 patients who had received parenteral nutrition for more than 2 years n — 66) and/ or had short bowel syndrome and could not be weaned from parenteral nutrition (n = 12), 58 developed chronic cholestasis and 37 developed one or more severe liver complication (serum bilirubin concentration 60 pmol/l, factor V (proaccelerin) 50%, portal hypertension, encephalopathy, ascites, bleeding from the gastrointestinal tract, or histological findings consisting of extensive fibrosis and cirrhosis) after 6 (3-132) months and 17 (2-155) months respectively. Liver disease was responsible for deaths in 6.5% of the patients (22% of deaths). [Pg.2710]


See other pages where Encephalopathy hypertensive is mentioned: [Pg.45]    [Pg.45]    [Pg.46]    [Pg.586]    [Pg.924]    [Pg.94]    [Pg.32]    [Pg.286]    [Pg.46]    [Pg.114]    [Pg.253]    [Pg.300]    [Pg.105]    [Pg.491]    [Pg.364]    [Pg.762]    [Pg.857]    [Pg.978]   
See also in sourсe #XX -- [ Pg.46 ]




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Encephalopathies

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