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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old female with a 30-year history of untreated essential hypertension was noted to have a blood pressure of 290/175 mmHg during evaluation for elective gynecological surgery. At the time of hospitalization she complained chiefly of chronic frontal headaches. Physical examination revealed grade two hypertensive retinopathy, and laboratory studies showed left ventricular hypertrophy. Over the next 12 days the patient's blood pressure was successfully lowered to 178/106 mmHg. During revision of her therapy her mean blood pressure rose to 244/144 mm Hg (88% of the admission level) over 36 hours and she developed hypertensive encephalopathy with papilledema, headaches and projectile vomiting. Concomitant resolution of neurological symptoms and control of blood pressure occurred over the next nine days. The course of this patient suggests that autoregulation of cerebral blood flow may be acutely reversed and that the occurrence of hypertensive encephalopathy depends not only on the magnitude and duration of the blood pressure elevation but, more important, on the rate at which that blood pressure is attained.
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PMID:Iatrogenically induced hypertensive encephalopathy. 45 3

The clinical and pathologic findings in 20 patients with hypertensive encephalopathy were reviewed. The dominant central nervous system (CNS) symptoms were altered state of consciousness and severe headache. Nausea, vomiting, and visual disturbances were less common. Seizures and focal signs were infrequent. The changes seen were invariably accompanied both by the characteristic ophthalmoscopic alterations of malignant hypertension and by uremia. The neuropathologic changes consisted of severe vascular alterations (fibrinoid necrosis of arterioles, thrombosis of arterioles and capillaries), and of parenchymal lesions (microinfarcts, petechial hemorrhages) secondary to the vascular lesions. The vascular changes were not confined to the brain but were diffuse, affecting the eyes, kidneys, and other organs. In the CNS the brainstem was most severely affected. Cerebral edema was not observed, even in those patients who had increased cerebrospinal fluid pressure and papilledema.
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PMID:Hypertensive encephalopathy: a clinicopathologic study of 20 cases. 56 64

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

2 cases reports are described of patients with renal artery stenosis who presented with hypertensive encephalopathy, normal blood pressures having been recorded within the previous 6 months while taking oral contraceptives (OCs). A 27-year-old woman, admitted to the hospital following 2 grand mal fits, had suffered from increasing headaches, nausea, and vomiting over the previous month. Her blood pressure had been elevated at 160/110 mmHg 1 week prior to admission but had been normal over previous 11 years while taking OCs (various formulations of combined estrogen and progestogen) which she had stopped taking 2 months previously. She was a nonsmoker. Her blood pressure was controlled with atenolol, nifedipine, and bendrofluazide, and her conscious level returned to normal with no further fits. An intravenous urogram revealed a small left kidney with a delayed nephrogram, and subsequent arteriography showed bilateral medial fibromuscular dysplasia with a narrow stenosis of the left renal artery. Attempted balloon angioplasty was unsuccessful due to arterial spasm. 4 months after presentation she became pregnant. Blood pressure was controlled with methyl dopa during pregnancy which progressed uneventfully to full term. In the 2nd case, a 19-year old girl became confused and suffered a grand mal convulsion. She had complained of headaches over the previous 3 days. Her blood pressure had been normal over the previous 6 months while taking Logynon (phased formulation of ethinylestradiol and levonorgestrel). She was a nonsmoker. On admission to the hospital, she suffered further generalized convulsions. Despite control of her convulsions with intravenous chlormethiazole, her blood pressure rose to 220/140 mmHg, and this was controlled with intravenous hydralazine and propranolol. The following day she was conscious and was changed to oral therapy. A renogram and DMSA scan showed normal sized kidneys, but there was evidence of decreased blood flow to the left kidney with an increased transit time. Renal arteriography showed a stenosis of the left renal artery, typical of intimal fibromuscular dysplasia, which was dilated by balloon angioplasty. Anti-hypertensive medication was withdrawn postoperatively, and her blood pressure has remained well controlled. In both of the cases the onset of hypertension was rapid with encephalopathy being the presenting feature. Hypertensive encephalopathy is well recognized as a presenting feature of renal transplant artery stenosis but not in cases of native renal artery stenosis. 1 of the patients had stopped using OCs 2 months before presentation, suggesting that although there may have been an association between OC use and the development of fibromuscular dysplasia, it could not be implicated in the mode of presentation.
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PMID:Encephalopathy in renovascular hypertension associated with the use of oral contraceptives. 311 27

A seventy-two-year-old man with hypertensive cerebral hemorrhage acutely developed severe headache, nausea, vomiting, agitation, and disorientation with abrupt rise in blood pressure on the sixth day after the onset. At that time, there were no remarkable changes in focal neurologic deficits, and repeated brain CT scans revealed a small hematoma located in the right basal ganglia without further enlargement or herniation. Blood chemistry and arterial gas analysis were within the normal ranges except for a slight rise in blood urea nitrogen. Similar episodes occurred three times within two days, and each time the cerebral symptoms disappeared in accordance with lowering of blood pressure by antihypertensive therapy. Complication of hypertensive encephalopathy was strongly suggested. The authors discuss the pathophysiology of this encephalopathy in relation to cerebral hemorrhage.
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PMID:Transient encephalopathy related to rapidly and markedly elevated blood pressure in acute stage of hypertensive cerebral hemorrhage--relationship to hypertensive encephalopathy--a case report. 317 64

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

Computed tomographic (CT) scans were evaluated in 11 patients with acute hypertensive encephalopathy. Hypertensive encephalopathy is characterized by an acute, severe rise in blood pressure associated with headache, nausea, vomiting, altered mental status, and focal neurologic deficits, and rapid improvement after control of blood pressure. The systolic blood pressure range is 200-280 mm Hg; diastolic is 130-170 mm Hg. The most common CT finding was white-matter edema, diffuse or focal, affecting the supratentorial compartment in all cases and the infratentorial compartment in eight. These changes resolved after the blood pressure was lowered in all six patients studied by follow-up CT. Permanent areas of infarction were demonstrated in three patients. These abnormalities are correlated with the neuropathologic findings in hypertensive encephalopathy.
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PMID:Computed tomographic changes of hypertensive encephalopathy. 392 95

A 36-year-old male presented with headache, vomiting, and gait disturbance. Examination found marked anemia, renal failure, markedly choked disks, and hypertensive encephalopathy. Magnetic resonance imaging demonstrated diffuse swelling of the brainstem and cerebellum, and obstructive hydrocephalus. Treatment with steroid, glycerol, and antihypertensive drugs resulted in a slow decrease in the brain swelling and cerebral edema. However, hydrocephalus and intracranial hypertension persisted, requiring a shunt operation. Hypertensive encephalopathy is usually improved by the treatment of hypertension, but shunt operation may be required to treat exacerbated intracranial pressure associated with obstructive hydrocephalus.
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PMID:Malignant hypertension associated with obstructive hydrocephalus--case report. 909 27

A 45-year-old man presented with severe hypertension, headache, cortical blindness, and a depressed level of consciousness. A second patient, a 33-year-old woman, was admitted with pre-eclampsia. She developed lethargy, headache, bilateral extensor plantar responses, and seizures. The third patient, a 62-year-old man, presented with acute renal failure due to necrotising vasculitis and glomerulonephritis. Five days after treatment with immunosuppressive drugs had been initiated, he developed headache, confusion, seizures, and cortical blindness. Hypertensive encephalopathy is characterised by headache, vomiting, disturbances in cognition and level of consciousness, visual abnormalities, and seizures. Imaging studies often demonstrate oedema of the white matter in the posterior parietal and occipital areas of the brain. This so-called reversible posterior leucoencephalopathy syndrome is well known in patients with severe hypertension, but it is also associated with immunosuppressive drug use and renal failure. It can be recognised by its fairly characteristic clinical features (different combinations of headache, vomiting, changes in cognition and level of consciousness, seizures, muscle weakness, and visual symptoms) and by its specific imaging findings. Treatment consists of reducing the blood pressure and reducing or discontinuing the use of immunosuppressive drugs. If the treatment is started promptly, symptoms and imaging abnormalities are usually reversible.
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PMID:[Hypertensive encephalopathy: does not only occur at high blood pressure]. 1205 26

The posterior reversible leukoencephalopathy syndrome (PRES) is a recently proposed cliniconeuroradiologic entity. The most common causes of PRES are hypertensive encephalopathy, eclampsia, cyclosporin A neurotoxicity and the uremic encephalopathies. Most patients are markedly hypertensive at presentation, although some have only mildly elevated or even normal blood pressure. Symptoms may include headache, nausea, vomiting, altered mental status, seizures,stupor, and visual disturbances. On CT and MR studies, edema has been reported in a relatively symmetrical pattern, typically in the subcortical white matter and occasionally in the cortex of the occipital and parietal lobes. These often striking imaging findings usually are resolved on follow-up studies obtained after appropriate therapy. Diffusion-weighted images would not show hyperintense signal because of the presence of interstitial rather than cytotoxic edema. We report a case of PRES due to hypertensive encephalopathy studied by CT and MRI.
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PMID:[Reversible posterior encephalopathy syndrome: case report]. 1224 91


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