Cases reported "Pre-Eclampsia"

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1/17. Hepatic infarction in preeclampsia as part of the hellp syndrome: CT appearance.

    We describe the computed tomographic (CT) findings of hepatic infarctions in two preeclamptic pregnant women. These infarcts were part of the hellp syndrome (hemolysis, elevated liver function tests, and low platelets count). In both cases, CT disclosed features characteristic of multiple nonenhancing, low-attenuation, peripheral lesions with vessels coursing through and a mottled appearance. The recognition of such CT findings in liver disease associated with preeclampsia can establish the correct diagnosis.
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2/17. retinal detachment in postpartum preeclampsia and eclampsia: report of two cases.

    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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3/17. Anticholinergics induce eclamptic seizures.

    Severe preeclampsia is a pathophysiological disorder specific to pregnancy and characterized by vasoconstriction and hypercoagulability. Eclampsia (convulsion associated with preeclampsia) and hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia (hellp syndrome) are serious complications in patients with severe preeclampsia. They are thought to be characterized by generalized vasoconstriction and reduction in blood flow to various organs that may be explained by increased sensitivity of the vascular smooth muscles and increased vasopressors. Liver involvement in eclampsia and preeclampsia is referred to as hellp syndrome, and epigastric and right upper quadrant pain is often a symptom of severe preeclampsia and may be indicative of imminent convulsions. In addition, marked dilatation of the stomach and the colon is often demonstrated in these patients. These phenomena result from the hyperactivity of the sympathetic nervous system but are not caused by the hyperactivity of the parasympathetic nervous system. The authors experienced two cases of eclamptic seizures after the administration of an anticholinergic (scopolamine butylbromide) in patients with severe preeclampsia complicated by hellp syndrome. Anticholinergics, blocking agents of the parasympathetic nervous system, can enhance the hyperactivity of the sympathetic nervous system; therefore, vasospasms of the vessels may be easily aggravated, and eclamptic seizures may be induced in patients with severe preeclampsia, especially in those complicated by hellp syndrome. The administration of anticholinergics should be avoided in patients with severe preeclampsia, especially when there is epigastralgia.
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4/17. Impaired dynamic cerebral autoregulation in eclampsia.

    Eclampsia is frequently associated with brain edema, cerebral infarction or hemorrhage. Its underlying cerebrovascular pathophysiology is still poorly understood. We examined cerebral autoregulation by a non-invasive multimodal assessment in a 28-year-old primaparous woman with postpartal eclampsia. Transcranial Doppler sonography showed considerably increased cerebral blood flow velocity (CBFV) of all basal cerebral vessels. magnetic resonance imaging demonstrated multifocal vasogenic brain edema. Using transfer function analysis, a severely decreased phase shift between respiratory-induced 0.1-Hz oscillations of arterial blood pressure and CBFV was observed, indicating substantial disturbance of dynamic cerebral autoregulation (DCA). In contrast, CO(2)-vasomotor reactivity of the right middle cerebral artery was only slightly reduced. We therefore assume that the cerebral arteriolar dysfunction in eclampsia leads primarily to an impairment of the autoregulatory mechanism that is followed by different degrees of arteriolar vasodilation. Because of its probably high sensitivity to hemodynamic disturbances, assessment of DCA might be of great value in early pre-eclampsia for risk prediction of cerebral arteriopathy and eclampsia.
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5/17. Severe preeclampsia presenting as third nerve palsy.

    Preeclampsia is a common complication of pregnancy and often manifests in severe cases with neurological symptoms. We present the first documented case of preeclampsia associated with third nerve palsy. A 19-year-old primigravida presented at 31 2/7 weeks' gestation with preeclampsia. In addition to classic preeclampsia symptoms, the patient had atypical visual disturbances. Exhaustive neurological and ophthalmological examinations revealed a third nerve palsy with no etiology other than preeclampsia. Deteriorating renal function necessitated preterm delivery. She ultimately underwent a cesarean section. Two months postpartum, the patient has shown complete spontaneous resolution of third nerve palsy. In this case of severe preeclampsia manifested by third nerve palsy, we hypothesize that the mechanism is attributed to vasospasm of the vessels supplying the oculomotor nerve.
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6/17. A case of reversible postpartum cytotoxic edema in preeclampsia.

    We report on a 32-year-old woman who developed reversible cortical blindness and right-sided weakness after cesarean section at 36 weeks of gestation, due to preeclampsia. An initial brain MRI demonstrated high signal intensity lesions in the bilateral occipito-parietal and left frontal lobes on T2-weighted and diffusion-weighted imaging. All of the lesions showed low signal intensity on apparent diffusion coefficient (ADC) map, which were compatible with cytotoxic edema, and MR angiography (MRA) showed diffuse vasospasm of the intracranial vessels. A follow-up brain MRI showed that most of the lesions disappeared and the vasospasm also resolved. This case suggests that the cytotoxic edema in preeclampsia may evolve differently from the pattern in cerebral infarction and explains the relatively benign course of the neurological signs in preeclampsia.
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7/17. Preeclampsia-associated reduction of cathepsin d activity in the umbilical cord.

    BACKGROUND: Preeclampsia is accompanied by an increase of collagen contents in the umbilical cord (UC) arteries and in Wharton's jelly. cathepsin d is one of the enzymes which participates in collagen degradation and activates precursor forms of collagenolytic metalloproteinases. It was decided to evaluate the activity of cathepsin d within umbilical cord arteries, veins and Wharton's jelly and its alterations in preeclampsia. MATERIALS AND methods: umbilical cord components were separated and submitted to homogenisation/extraction with 0.05 M Tris-HCl 0.2% Triton X-100, pH 7.5. Proteolytic activities of the extracts were studied with a use of cathepsin d-specific substrate. Western immunoblot technique was employed to detect this enzyme. RESULTS: It was found that human umbilical cord tissues contain both active and inactive forms of cathepsin d. Preeclampsia is associated with a distinct increase in the amount of this enzyme in the umbilical cord, whereas its activity deeply decreased. Activation with trypsin augments cathepsin d activity in preeclamptic umbilical cord to the values observed in control arteries or even exceeds the control values (veins, Wharton's jelly). CONCLUSIONS: Preeclampsia is associated with a reduction in the activity of cathepsin d in human umbilical cord. The low activity of cathepsin d may reduce collagen degradation and enhance its accumulation in the umbilical cord, especially in the arteries. Similar changes in other foetal blood vessels may result in an increase of vascular resistance and hypertension, which may persist after birth.
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8/17. Postpartum cerebellar infarction and haemolysis, elevated liver enzymes, low platelet (HELLP) syndrome.

    pregnancy is considered to be a hypercoagulable state per se with an increased risk for cerebrovascular events, however cerebellar infarction has been rarely described in pregnant women. A nulliparous pre-eclamptic woman at 25 weeks' gestation was submitted to an echocardiographic exam that showed an impaired cardiac structure and function. After 2 h, the patient underwent caesarean section for diagnosis of haemolysis, elevated liver enzymes, low platelet (HELLP) syndrome. Afterwards her platelet count raised, and eight days later she developed nystagmus, ataxia, dysmetria and motor deficit in the right limbs and sensory impairment in the right side of the face and in the left limbs. Cerebral magnetic resonance imaging (MRI) demonstrated a right cerebellar and median posterior bulbar infarction. Colour-coded sonography of cerebral vessels showed an occlusion of the right vertebral artery. Coagulation pattern analysis evidenced double heterozygosis of the methylenetetrahydrofolate reductase (MTHFR) gene and single mutation of the prothrombin gene. This case report gives evidence of the importance of considering the different risk factors involved in stroke occurrence during pregnancy.
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9/17. Endomyocardial ultrastructural findings in preeclampsia.

    Ultrastructural findings in endomyocardial biopsy specimens obtained during cardiac catheterization in a patient with severe preeclampsia are described. Intramyocardial vessels revealed prominent swelling of the endothelial cell cytoplasm. In addition, cardiac myocyte mitochondria showed swelling and clearing within the matrix. Endomyocardial ultrastructural injury occurs in severe preeclampsia.
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10/17. Increased plasma levels of the novel vasoconstrictor peptide endothelin in severe pre-eclampsia.

    plasma endothelin levels were studied in 29 pregnancies. Levels were found to be increased in 9 pregnancies complicated by pregnancy-induced hypertensive disease and/or pre-eclampsia as compared to levels in 14 normotensive pregnancies with gestational age varying between 24-40 weeks with normal Doppler flow velocity waveforms of the uterine arcuate arteries, and 6 normotensive pregnancies with abnormal Doppler flow velocity waveforms at 24 weeks' gestation. Two patients with severe pre-eclampsia showed a rise in plasma endothelin levels, suggesting a correlation between plasma endothelin levels and the disease process. Endothelin is produced by endothelial cells of blood vessels; it is the most potent vasoconstrictor known to date. For this reason it has been suggested that endothelin might be important in the control of systemic blood pressure and local blood flow, both disturbed in pre-eclampsia. The conclusion of this study is that the venous plasma level of endothelin would seem to be a marker for severe disease, however, without any predictive value.
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