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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of preeclampsia-eclampsia leading to acute edematous pancreatitis is reported, probably related to microvascular abnormalities and splanchnic ischemia. Recovery was uneventful.
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PMID:Acute pancreatitis and preeclampsia-eclampsia: a case report. 907 33

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

The etiology of preeclampsia is unknown. At present, 4 hypotheses are the subject of extensive investigation, as follows: (1) Placental ischemia-Increased trophoblast deportation, as a consequence of ischemia, may inflict endothelial cell dysfunction. (2) Very low-density lipoprotein versus toxicity-preventing activity-In compensation for increased energy demand during pregnancy, nonesterified fatty acids are mobilized. In women with low albumin concentrations, transporting extra nonesterified fatty acids from adipose tissues to the liver is likely to reduce albumin's antitoxic activity to a point at which very-low density lipoprotein toxicity is expressed. (3) Immune maladaptation-Interaction between decidual leukocytes and invading cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophoblast cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines, proteolytic enzymes, and free radical species. (4) Genetic imprinting-Development of preeclampsia-eclampsia may be based on a single recessive gene or a dominant gene with incomplete penetrance. Penetrance may be dependent on fetal genotype. The possibility of genetic imprinting should be considered in future genetic investigations of preeclampsia.
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PMID:Etiology and pathogenesis of preeclampsia: current concepts. 1052 45

High blood pressure during pregnancy (BP > or = 140/90 mmHg) is sometimes already noted before conception, with usually a good prognosis (although it could predispose to preeclampsia). alpha-methyldopa is the best treatment when needed (agents blocking the renin angiotensin system are not recommended). Preeclampsia, a form of hypertension noted after 20 weeks of gestation with proteinuria is a more serious condition (BP > or = 140/90 mmHg or increase in BP from the 1st trimester > or = 25/15 mmHg). It is generated by placental ischemia and creates maternal endothelial lesions which in turn decrease the blood flow to placenta leading to maternal and fetal syndromes. Hospitalisation is mandatory. No measure other than delivery is known to attenuate or reverse its progression. Treating hypertension during pregnancy (when blood pressure > or = 170/110 mmHg) aims at preventing maternal risk (stroke or eclampsia) but has few effect on foetal lesions. Prevention of this syndrome, which represents the first secondary cause of hypertension, is until now disappointing.
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PMID:[Hypertension at pregnancy]. 1039 40

Hypoxia associated with perinatal events can result in brain damage in the neonate. In labor and eclampsia, hypoxia can be intermittent, which may result in more severe damage than sustained hypoxia. The pathogenesis of brain injury in sustained ischemia involves free radical production; therefore, we investigated whether higher levels of free radicals contribute to the greater injury induced by repetitive ischemia. Brains were obtained from fetuses of near-term, pregnant rabbits subjected to repetitive ischemia-reperfusion (RIR), sustained uterine ischemia-reperfusion (IR), or a control protocol. Compared with controls, fetal brains from RIR or IR groups had more brain edema. Brains from RIR fetuses exhibited higher levels of lipid peroxidation, 3-nitrotyrosine, and nitrogen oxides, and lower total antioxidant capacity and cortical cellular viability than those of IR or control fetuses. Maternal administration of antioxidants following RIR and fetal bradycardia resulted in lower levels of fetal cortical and hippocampal cell death. Coadministration of Trolox and ascorbic acid resulted in less brain edema and liquefaction, and fewer hippocampal ischemic nuclei as compared with the saline control. Higher free radical production may be responsible for the greater fetal brain injury following repetitive hypoxia-reoxygenation. Maternal antioxidant treatment resulted in transplacental passage of antioxidants and amelioration of brain injury, and may be a viable clinical option following diagnosis of fetal distress.
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PMID:Increased injury following intermittent fetal hypoxia-reoxygenation is associated with increased free radical production in fetal rabbit brain. 1049 39

The pathogenesis of cortical blindness as a rare complication in severe preeclampsia is still unclear. The case of a women with postpartum blindness is reported in which CT and MRI initially showed cortical and subcortical edema in the parieto-occipital lobes. At this time cerebral angiography and transcranial color-coded sonography (TCCS) revealed widespread cerebral vasospasm. Mean blood flow velocities in the middle and posterior cerebral artery and carotid syphon initially reached 380 cm/s and normalized within 2 weeks. While the patient's vision improved rapidly, follow-up MRI disclosed ischemic lesions and petechial hemorrhage in the occipital cortex. This case provides rare documentation that transient blindness in patients with preeclampsia may result from parieto-occipital ischemia due to cerebral vasospasm. In such patients TCCS may be useful to detect vasospasm associated with preeclampsia/eclampsia.
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PMID:[Transient cortical blindness in EPH gestosis caused by cerebral vasospasm]. 1055 88

Retinal detachment is an unusual complication of hypertensive disorder in pregnancy. It has been reported in 1% to 2% of patients with severe preeclampsia and in 10% of patients with eclampsia. Choroidal ischemia may be the cause of retinal detachment. We know that mild arteriolar spasm involving the bulbar conjunctival vessels has been observed in the normal pregnancy, but in pregnancy-induced hypertension the vasospasm may be severe and result in choroidal ischemia. Most patients with retinal detachment in pregnancy-induced hypertension have had full spontaneous resolution within a few weeks, and they did not have any sequelae. Medical treatment with antihypertensive drugs and steroids may be helpful. We report two rare cases of retinal detachment and persistent hypertension in association with postpartum eclampsia and post-cesarean section preeclampsia. These patients had normotension throughout pregnancy. Preeclampsia or eclampsia developed after delivery, and blurred vision, headache, and reduced vision accompanied serous retinal detachment. The serous retinal detachment disappeared within 3 weeks. Good outcomes were found in the follow-up examinations in both of these cases. For women who had been normotensive at the time of delivery and then complained in the postpartum period of blurred vision, headaches, nausea and vomiting, we should consider the possibility of retinal detachment and perform fundoscopy.
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PMID:Retinal detachment in postpartum preeclampsia and eclampsia: report of two cases. 1058 29

Blood pressure (BP) elevations may correspond to different clinical situations. Hypertensives emergencies are situations that require immediate reduction in BP because of acute or rapidly progressing target organ damage: accelerated malignant hypertension, hypertensive encephalopathy, acute myocardial infarction, acute aortic dissection, acute left ventricular failure, and eclampsia. Hypertensive urgencies are those with marked elevated BP in which it is desirable to reduce BP progressively within few hours, such as severe hypertension, progressive target organ damage, perioperative hypertension. Cerebrovascular accidents have to be individualized. In most patients in the immediate post-stroke period, BP should not be lowered. Caution is advised in lowering BP in these patients because excessive falls may precipitate cerebral ischemia. In situations without symptoms or progressive target organ it is necessary to exclude proximate causes of elevated BP such as pain and elevated BP alone rarely requires antihypertensive treatment. Among parenteral antihypertensive (AH) drugs labetalol, nicardipine, urapidil, and nitroprussiate are generally used, and the choice of AH drug depends on the clinical situation. It is not required to normalize BP immediately but to reduce mean BP no more than 25%, then toward 160/100 mmHg as recommended by JNC VI, in order to avoid an impairment of renal, cerebral or coronary ischemia. Oral long-acting dihydropyridines are often subsequently administrated, except in myocardial ischemia. Therapeutic attitudes vary considerably according to the clinical situation: abstention, immediate decrease or progressive decrease in BP have to be decided.
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PMID:[Acute blood pressure elevations]. 1119 Feb 94

Clinical trials for ischemic stroke have been characterized by a disappointing series of negative results, using a panoply of pharmacologic agents. This paper emphasizes five physiologic measures that can be taken to mitigate ischemic brain damage. These are (1) hypothermia, (2) insulin, (3) arterial hyperoxemia, (4) blood pressure control and (5) magnesium. Hypothermia is protective in both focal and global ischemia, even postischemically protecting against selective neuronal necrosis and infarction. The total equation for protection includes the (i) postischemic delay, (ii) depth, and (iii) duration of hypothermia. Insulin operates by lowering glucose levels to the normal range in focal ischemia. It is possible that very low glucose levels are detrimental in focal ischemia with paradoxical augmentation of the infarct size, and that spreading depression plays a role in this. Controlled arterial hyperoxemia seems effective experimentally in reducing infarct size, operating mechanistically by either a direct effect of oxygen, or vasoconstriction causing shunting of blood into the infarct, or both. Blood pressure is a critical determinant of infarct size, and raising blood pressure improves collateral blood flow and reduces stroke size. To be used clinically, however, hemorrhage must be ruled out. The most dramatic clinical effects of blood pressure are seen in aneurysm patients with vasospasm, where minor increases in blood pressure reverse temporary hemiparesis by reducing ischemia. Magnesium is likely the safest NMDA antagonist, with a long history of safe administration to pregnant women with eclampsia. There is potential interaction with insulin, in that magnesium causes hyperglycemia, which requires insulin to counteract it. Magnesium and insulin together have been shown effective in experimental brain ischemia. In the absence of safe and effective pharmacologic neuroprotection agents, clinical trials should be designed and launched to test these physiologic measures, singly and in combination, to reduce brain damage after ischemia.
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PMID:Non-pharmacologic (physiologic) neuroprotection in the treatment of brain ischemia. 1146 80

Hypertensive disorders of pregnancy are prototypical of maternal conditions associated with reduced uteroplacental blood flow. Hypertensive disorders in pregnancy include chronic hypertension, preeclampsia-eclampsia, superimposed preeclampsia, and gestational hypertension. Pathophysiology of these disorders include deficient uterine vascular modeling in the process of placentation and aberrations of vasomotor regulation. Aberrations of uterine renin-angiotensin system may play a proximate role in the pathogenesis of preeclampsia syndrome. Clinical manifestations are explained in this review based on resultant vasoconstriction and ischemia in systemic and regional circulations. Perinatal implications of hypertensive disorders both in terms of early neonatal outcome and long-term neurodevelopmental effects are described. Methods of antenatal assessment of the fetus and, briefly, principles of clinical management are described.
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PMID:Perinatal implications of maternal hypertension. 1146 57


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