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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spectrum of disorders associated with an elevated blood pressure (BP) encompasses chronic uncomplicated hypertension and the hypertensive crises, including hypertensive urgencies and emergencies. Although these syndromes vary widely in their presentations, clinical courses, and outcomes they share pathophysiologic mechanisms and, consequently, therapeutic responses to specifically targeted antihypertensive drug types. Nevertheless, hypertensive crises are often treated with drugs which, in that setting are either unsafe or are of unsubstantiated efficacy. The purpose of this review is to examine the pathophysiology of commonly encountered hypertensive crises, including stroke, hypertensive encephalopathy, aortic dissection, acute pulmonary edema, and preeclampsia-eclampsia and to provide a rational approach to their treatment based upon relevant pathophysiologic and pharmacologic principles. Measurement of plasma renin activity (PRA) level often provides insight regarding pathophysiology and predicts efficacy of antihypertensive treatments in the individual patient. However, in hypertensive crises, drug therapy is initiated before the PRA level is known. Nevertheless, the renin-angiotensin dependence (R-type) or volume dependence (V-type) of hypertension can often be deduced by the BP response to drugs that interrupt the renin system (R-drugs) or that decrease body volume (V-drugs). Based upon these considerations, a treatment algorithm is provided to guide drug selection in patients presenting with a hypertensive crisis.
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PMID:Management of hypertensive crises: the scientific basis for treatment decisions. 1172 16

Hypertension is the most common medical complication of pregnancy in South Africa and a major cause of maternal and perinatal morbidity and mortality worldwide. At King Edward VIII Hospital in Durban, 18% of all admissions to the obstetric unit have some degree of high blood pressure. Hypertension in its most severe form produces convulsions, proteinuria, and edema and may lead to fetal and maternal death. High-risk groups for preeclampsia are teenage mothers, primigravidas, and women with a history of elevated blood pressure, previous preeclampsia, molar pregnancies, multiple pregnancies, or hydrops fetalis. Methods used to prevent preeclampsia include a low-salt diet supplemented with calcium, magnesium, zinc, fish, and pharmacological manipulation. In developing countries, prevention and detection of preeclampsia is difficult since women seek antenatal care late in their pregnancies. In Durban, the average gestational age at first antenatal attendance is 28 weeks, and 80% of patients presenting with eclampsia have defaulted antenatal care. Treatment includes admission to hospital to establish the etiology of the hypertension and maternal renal function tests . Fetal condition is a sensitive index of hypertension and is judged by 1) clinical evidence of fetal growth, 2) weekly antepartum cardiotocography, and 3) ultrasonographic screening. Patients are managed according to three clinical groups: 1) those identified before 36 weeks, 2) those identified after 36 weeks, and 3) patients in hypertensive crisis. Dihydralazine is the drug of choice for imminent eclampsia. If the patients has a ripe cervix, delivery is induced with 6-8 hours. Steroid contraception use in the older hypertensive patient should be avoided because of possible development of atherosclerosis and stroke. Puerperal tubal ligations in the hypertensive patient ought to be avoided because of the risks of thromboembolic phenomena and pulmonary embolism. Methyldopa is the treatment of choice in cases of moderate to severe hypertension. Intravenous dihydralazine is relatively safe for the rapid reduction of high blood pressure.
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PMID:Coping with hypertension in pregnancy. 1234 38

This review details the evidence that the risk of stroke is increased in the peripartum and postpartum period rather than the entire 9 months of pregnancy. In women with prior stroke, available evidence suggests that the excess risk of a stroke recurrence in pregnancy is approximately 1% to 2%. Although certain conditions have a particularly strong association with stroke in pregnancy, such as eclampsia, or with the postpartum period, such as cerebral venous thrombosis, the clinical and therapeutic approach to women with stroke during pregnancy should be similar to the approach to stroke in young adults. Strategies for stroke prevention should take into account the competing risks to mother and fetus.
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PMID:Pregnancy and stroke. 1250 7

Stroke during pregnancy is a special category of stroke in young women. Although the absolute risk is small, there are diverse causes, including those inherent to the pregnant state, that may have a significant impact on maternal and fetal outcome. Severe pre-eclampsia and eclampsia are commonly associated with ischemic and hemorrhagic stroke, but must not be presumed the sole cause of stroke in pregnant women. Magnesium sulfate is the treatment of choice to prevent eclampsia. Randomized clinical trials in pregnant women are not available to provide guidance for the treatment of ischemic and hemorrhagic stroke in pregnant women. Various antithrombotic agents may be safely used during specific stages of pregnancy for treatment and prevention of ischemic stroke, with low-dose aspirin, unfractionated heparin, and low molecular weight heparin the preferred agents. Low molecular weight heparin may be safer than unfractionated heparin. Treatment of parenchymatous intracerebral hemorrhage and subarachnoid hemorrhage during pregnancy and the puerperium must be individualized. Aneurysms may be treated with neurosurgical clipping or endovascular coiling, depending on neurosurgical considerations. Cesarean or vaginal delivery may be used depending on the timing of delivery, adequacy of aneurysm occlusion, and risk to mother and fetus. Arteriovenous malformations are best treated in a multimodal fashion at a specialized treatment center.
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PMID:Cerebrovascular Disease in Pregnancy. 1289 2

The difficult types of preeclampsia and eclampsia are presented with the neurological symptoms. The break of cerebral autoregulation mechanism plays the most important role in pathogenesis of cerebral vasospasm. Nevertheless, eclampsia isn't just an ordinary hypertensive encephalopathy because other pathogenic mechanisms are involved in its appearance. The main neuropathologic changes are multifocal vasogenic edema, perivascular multiple microinfarctions and petechial hemorrhages. Neurological clinical manifestations are convulsions, headache, visual disturbances and rarely other discrete focal neurological symptoms. Eclampsia is a high-risk factor for onset of hemorrhagic or ischemic stroke. This is a reason why neurological diagnostic tests are sometimes needed. The method of choice for evaluation of complicated eclampsia is computerized brain topography that shows multiple areas of hypodensity in occipitoparietal regions. These changes are focal vasogenic cerebral edema. For differential diagnosis of eclampsia and stroke other diagnostic methods can be used--fundoscopic exam, magnetic resonance brain imaging, cerebral angiography and cerebrospinal fluid exam. The therapy of eclampsia considers using of magnesium sulfate, antihypertensive, anticonvulsive and antiedematous drugs.
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PMID:[Neurologic aspects of eclampsia]. 1460 66

A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage, such as aortic dissection, pulmonary edema, acute coronary syndromes, cerebral infarction or hemorrhage, hypertensive encephalopathy, acute renal failure and eclampsia. With the exception of stroke, blood pressure must be reduced quickly, usually by using intravenous antihypertensive agents. Blood pressure reduction should be gradual while maintaining organ perfusion, which may be easily compromised in elderly and chronically hypertensive patients. In the absence of new or worsening end-organ injury, the indication of immediate therapy should be carefully evaluated. If indicated, the use of an orally long-acting antihypertensive agent is preferred to avoid an acute and unpredictable fall in blood pressure. In particular, the use of short-acting nifedipine should be condemned.
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PMID:[Hypertensive crisis: when and how to treat?]. 1515 59

Pregnancy may increase the risk of stroke. However, few studies have compared strokes in women of reproductive age that occur in pregnancy or the puerperium (pregnancy-related stroke, PRS) with those unrelated to pregnancy. This study assesses risk factors and etiologies of stroke in these women based on relationship to pregnancy. From 1984 to 2002, all female patients 15 through 40 years of age with a first-ever stroke at National Taiwan University Hospital were included in this study. PRS was defined as patients who had stroke occurrence during pregnancy or within 6 weeks postpartum. Stroke was categorized as cerebral infarction (CI), cerebral hemorrhage (CH), or subarachnoid hemorrhage (SAH) and divided into subtype according to etiology. Risk factors and etiologies were compared for patients with PRS and stroke unrelated to pregnancy. We identified 49 patients with PRS, and 353 patients with stroke unrelated to pregnancy. There was no statistically significant difference in distribution of CI subtypes. Cerebral venous thrombosis (CVT) was more common in PRS than stroke unrelated to pregnancy (39% vs. 7%, P<0.001), and 73% of these cases occurred postpartum. Preeclampsia-eclampsia was an important cause of peripartum CH (37%), but not CI (4%). Among PRS cases, postpartum cerebral venous thrombosis and preeclampsia-eclampsia were the major causes of CI and CH, respectively.
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PMID:Stroke in women of reproductive age: comparison between stroke related and unrelated to pregnancy. 1517 9

Migraine and TTH are primary headache disorders that occur commonly during pregnancy. Migraine sometimes occurs for the first time with pregnancy. The majority of migraineurs improve while pregnant; however, migraine often recurs post partum. Some disorders that produce, headache, such as stroke, cerebral venous thrombosis, eclampsia, and SAH, occur more frequently during pregnancy. Diagnostic testing serves to exclude organic causes of headache, to confirm the diagnosis, and to establish a baseline before treatment. If neurodiagnostic testing is indicated, the study that provides the most information with the least fetal risk is the study of choice. Drugs commonly are used during pregnancy despite insufficient knowledge about their effects on the growing fetus. Most drugs are not teratogenic. Adverse effects, such as spontaneous abortion, developmental defects, and various postnatal effects, depend on the dosage and route of administration and the timing of the exposure relative to the period of fetal development. Although medication use should be limited, it is not absolutely contraindicated in pregnancy. In migraine, the risk for status migrainosus may be greater than the potential risk of the medication used to treat the pregnant patient. Nonpharmacologic treatment is the ideal solution; however, analgesics, such as acetaminophen and narcotics, can be used ona limited basis. Preventive therapy is a last resort.
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PMID:Headaches in pregnancy. 1547 64

Subarachnoid hemorrhage from a ruptured aneurysm is a subset of stroke. The young age (median 55 years) and poor outcome (50% of patients die; 30% of survivors remain dependent) explain why in the population the loss of productive life years from aneurysmal subarachnoid hemorrhage (SAH) is as large as that from brain infarcts, the most common type of stroke. Ischemia plays an important role in the pathophysiological process after SAH. A period of global cerebral ischemia firstly occurs in the acute phase, immediately after rupture of the aneurysm, due to acute vasoconstriction and elevated intracranial pressure, which leads to a drop in perfusion pressure. This is quite distinct from the secondly, delayed cerebral ischemia (DCI), which is focal or multi-focal. DCI usually occurs between 4 and 10 days after the initial bleeding, has a gradual onset and is multi-focal, and is an important cause of death and dependency after SAH. The interval between the bleeding and the onset of ischemia provides an opportunity for preventive treatment. Magnesium is readily available, inexpensive and has a well-established clinical profile in obstetrical and cardiovascular practice. It is beneficial in the treatment of eclampsia, a disease with a pathophysiology comparable to DCI after subarachnoid hemorrhage. Neuroprotective mechanisms of magnesium include inhibition of the release of excitatory amino-acids and blockade of the NMDA-glutamate receptor. Magnesium is also a non-competitive antagonist of voltage dependent calcium channels, has cerebrovascular dilatory activity and is an important co-factor of cellular ATPases, including the Na/K-ATPase. Magnesium can reverse delayed cerebral vasospasm and reduces the extent of acute ischemic cerebral lesions after experimental subarachnoid hemorrhage in rats. In this article we discuss the neuroprotective potency of magnesium in SAH by describing the pathophysiology of ischaemia after SAH and the many ways magnesium may interfere with this.
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PMID:Potentials of magnesium treatment in subarachnoid haemorrhage. 1572 6

Eclampsia is a well-recognised major cause of maternal death and perinatal morbidity and mortality. The incidence of eclampsia, its presentation patterns, maternal and perinatal outcomes were investigated in a retrospective study conducted at the University of Benin Teaching Hospital, Nigeria over an 8-year period, 1995 - 2002. There were 103 cases of eclampsia of 7835 deliveries, giving an incidence of one in 76 (1.32%). The mean age of the women was 27.1 +/- 5.6 years. Eclampsia significantly (P < 0.001) occurred in nulliparous and unbooked mothers. Eighty-nine (86.4%) of the patients developed fits in the predelivery stage; 85 (83%) of the patients had at least one premonitory symptom including headache (82.4%) visual disturbance (10.6%) and epigastric pain (7%). There were nine stillbirths and 16 early neonatal deaths for a perinatal mortality rate of 214/1000. The major causes of perinatal mortality were prematurity and birth asphyxia. Eleven maternal deaths occurred with a maternal case fatality rate of 10.7% and a maternal mortality ratio from eclampsia of 140/100 000. The clinical causes of deaths were cardiopulmonary failure, acute renal failure, haemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome and cerebrovascular accident. Timely referral of high-risk patients coupled with availability of emergency obstetric and neonatal care services would reduce the incidence eclampsia associated mortality and morbidity in our facility.
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PMID:Maternal and fetal outcome in eclamptic patients in Benin City, Nigeria. 1576 83


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