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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a study of heat-stable alkaline phosphatase (HSAP65degreesC) concentrations in the serum of pregnant women with hypertension (42 cases), mild preeclampsia (40 cases) and severe pre-eclampsia (22 cases). The results are seen in relationship to the occurrence of intrauterine fetal death, growth retardation, intrauterine and neonatal asphyxia as well as the respiratory distress syndrome (RDS) in the newborn. The importance of a precise clinical classification of the patients is stressed. Pathological HSAP values are those which lie either over or under the normal range for HSAP activity. In addition "zig-zag" curves with values within the normal range are characterized as abnormal. Thus, serial estimations give the most reliable results. Serial estimations of HSAP are especially valuable in severe pre-eclampsia. Abnormal HSAP values in the 28th-38th week of pregnancy are a serious prognostic sign. False abnormal HSAP results were found in all 3 patient groups. One possible false normal HSAP curve also occurred.
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PMID:Serum alkaline phosphatase in pregnancy. II. Serial HSAP65degreesC estimations in pregnancy complicated with hypertension and pre-eclampsia. 93 83

Three hundred and forty-six nulliparous women with pregnancy-induced hypertension prior to term were monitored in a high-risk pregnancy unit while awaiting fetal maturity. Management included ambulation as desired, regular hospital diet without salf restriction, blood pressure measured 4 times daily, weight and urine protein determined 3 times each week, creatinine clearance determined weekly, and serial sonography to monitor fetal growth. Sedation and antihypertensive agents were not prescribed. Delivery was delayed until term unless hypertension persisted or recurred following an initial salutary response. Factors other than hypertension that contributed to the decision to effect delivery were 1) rapid weight gain, 2) decreasing creatinine clearance, 3) appearance of significant proteinuria, 4) suspected fetal growth retardation, and 5) the development of severe headache or scotomata. With this method of management the perinatal mortality rate was 9/1000. Only 5 infants developed the respiratory distress syndrome and all survived. There were 26 women who left the unit against medical advice. Severe hypertension subsequently developed in 7 of these women and 4 of their fetuses were stillborn. The perinatal mortality rate among this group of patients was 154/1000. It is concluded that the nulliparous patient with pregnancy-induced hypertension prior to term can be safely managed by hospitalization and close observation as a viable alternative to prompt delivery.
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PMID:Management of pregnancy-induced hypertension in the nullipara. 94 68

Twenty-eight anemic control dogs were subjected to isolated cerebral hypoxemic (PO2,35+/-5 mm Hg) perfusion for 2 hours. All were found to have functional pulmonary impairment. Two hours later, twenty were sacrificed and found to have the bilateral anatomic complex of the respiratory distress syndrome (RDS). All those not sacrificed expired within 20 hours with progressive respiratory distress and at autopsy had the bilateral anatomic complex. Twenty-three beagles with chronic denervation (autotransplantation) of the left lung also were subjected to the 2 hour isolated cerebral arterial hypoxemic perfusion. Minimal pulmonary functional impairment was measurable in all. Ten of sixteen were long-term survivors. The six that succumbed did not appear to suffer respiratory deaths. These six, as well as seven sacrificed 2 hours after perfusion, had the anatomic complex of RDS in the normally innervated right lungs. However, the denervated left lungs were anatomically normal. These findings are offered as additional evidence that RDS has a centrineurogenic etiology. We postulate the following sequence: "shock" causes cerebral (probably hypothalamic) cellular oxygen deprivation and dysfunction; there is autonomically mediated, increased resistance of the pulmonary venules ("postcapillary sphincters"); this leads to capillary hypertension, congestion, hemorrhage, edema, surfactant inactivation, and atelectasis. Pulmonary denervation blocks this sequence and protects the lung.
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PMID:The centrineurogenic etiology of the respiratory distress syndrome: induction by isolated cerebral hypoxemia and prevention by unilateral pulmonary denervation. 96 13

A group of 412 infants with birthweights between 501 and 2,500 gm and gestational ages of 36 weeks or less were studied for the influence of both prolonged ruputre of amniotic membranes and maternal hypertension on the incidence of idiopathic respiratory distress syndrome (IRDS). The occurrence of these complications was associated with a significant decrease in the incidence of IRDS only in infants with birthweights between 1,501 and 2,500 gm (37.4% in the no complications group versus 12.8% in the complications group; P less than .01) or gestational ages of 33 to 36 weeks (35.2% in the no complications group versus 13.1% in the complications group; P less than .01). In infants with birthweights of 1,500 gm or less or gestational ages of 32 weeks or less, the specific antecedent complications of pregnancy did not alter the incidence of IRDS. Rupture of the membranes for more than 72 hours had no greater effect on the incidence of IRDS than those lasting 24 to 72 hours.
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PMID:Respiratory distress syndrome of the newborn and complications of pregnancy. 98 Jun

Certain common but seldom recognized clinical features of renovascular hypertension peculiar to infancy are emphasized in this communication from the observations made in a 9-month-old infant. Failure to thrive, extreme irritability, hypotonia, anorexia, vomiting, diarrhea, respiratory distress, and congestive heart failure are common clinical findings. Unless the physician is aware of this symptomatology or blood pressure is routinely obtained in all infants, the condition is likely to be missed. Renovascular hypertension is malignant and carries a high mortality but if diagnosed early may be cured by surgical intervention.
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PMID:Clinical features of renovascular hypertension in infancy: report of a 9-month-old infant. 115 42

A case of angioedema induced by antihypertensive therapy with lisinopril is presented. The patient was a 70 year old black woman, with a history of hypertension for 15 years. The patient presented with acute onset of swelling involving the oro-facial region and respiratory distress after ingestion of three doses of lisinopril over a three day period. A clinical diagnosis of drug induced angioedema was made based on clinical presentation. The patient was treated with diphenhydramine, 50 mg intravenously, and hydrocortisone 100 mg every eight hours with resolution of her symptoms over a 24 hour period. Angioedema should be recognized as a possible life threatening complication of therapy with lisinopril, and other angiotensin converting enzyme (ACE) inhibitors. This usually responds to therapy with antihistamines and steroids if recognized early.
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PMID:Angioedema complicating lisinopril therapy. 133 26

We report the pregnancy of a 35 year old diabetic woman with a positive Australia antigen, 3 years after a successful cadaver kidney transplant. Immunosuppressive therapy with prednisone, azathioprine and cyclosporine was maintained. Pregnancy was complicated by an acute rejection episode on week 13, mild hypertension and intrahepatic cholestasis on week 22. Cesarean section and tubal ligation were performed at 32 and a half weeks. A 2020 g female infant was delivered, with Apgar scores of 8 and 9 at 1 and 5 min, respectively. Mild respiratory distress, jaundice and hypocalcemia were noted. The Australia antigen was negative. No fetal anomalies were detected. The high risk of pregnancy in a class T diabetic patient is confirmed in this case.
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PMID:[Pregnancy in a class-T diabetic patient]. 134 82

Obstetric management of severe preeclampsia between 26 and 32 weeks' gestation presents a significant management dilemma. We examined the antenatal courses and perinatal outcomes of 67 such affected pregnancies and compared them with a group of 134 patients, matched for gestational age, who delivered after preterm rupture of membranes or preterm labor. Although the severe preeclamptic group had more patients with chronic hypertension and renal disease, 67% had no prior medical problems. The obstetric and other medical characteristics of both groups were similar. Neonatal outcomes in the severe preeclampsia group differed from those in the control group: they had lower mean birthweight, 5-minute Apgar score and umbilical arterial pH were lower, and their rates of respiratory distress syndrome and perinatal death were higher. Temporization for more than 72 hours was not possible in 60 of 67 preeclamptic pregnancies due to rapid deterioration of the mother (56 cases) or fetus (4 cases). The rate of poor neonatal outcomes in severe preeclampsia exceeded that expected with preterm delivery alone and may reflect preexisting fetal compromise, served better by early intervention and delivery.
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PMID:Severe preeclampsia in preterm pregnancy between 26 and 32 weeks' gestation. 141 33

The HELLP-syndrome is a severe complication in late pregnancy. The etiology is still largely unknown. It is defined as a separate disease but also as a severe course of EHP-gestosis. It is mainly characterised by increased liver enzymes, a low platelet count, increased haemolysis and hypertension. According to primary organ affection, neurological symptoms and acute respiratory distress syndrome, acute renal insufficiency and/or upper abdominal complaints may occur. The only causal therapy is immediate caesarean section. Postoperative intensive care must be guaranteed. As a gentle anaesthetic method neuroleptanalgesia is recommended. Based on 7 of our own case reports, pathophysiology and therapy are discussed.
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PMID:[The HELLP syndrome--a challenge to the obstetrician and the intensive care therapist]. 141 82

Extracorporeal membrane oxygenation (ECMO) is lifesaving for infants with severe respiratory distress but is complicated by severe intracranial hemorrhage in 10% to 30% of patients. Intracranial venous hypertension, as a result of ligation of the internal jugular vein (IJV), has been hypothesized as a contributing factor to cerebral edema and subsequent hemorrhage. Accessory cephalad IJV cannulation may serve as a means of additional venous drainage to the pump as well as protection against intracranial venous hypertension. Proximal and distal cannulation of the IJV were studied in a primate model. The parameters monitored included sagittal sinus, right and left ventricular pressures as well as venous pressure in the ECMO circuit. The cephalad venous cannula was clamped and unclamped at 30-minute intervals. There was no significant difference in sagittal sinus or intracranial pressures during periods of cephalad cannula clamping or unclamping. Venous return was augmented when the cephalad cannula was unclamped. Cephalad cannulation has no demonstrable protective effect on intracranial, subarachnoid or venous pressures but does improve venous return to the ECMO circuit. It is concluded that cephalad venous cannulation is not necessary in all cases and should be reserved for those patients requiring additional venous drainage to support pump flow.
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PMID:Proximal and distal cannulation of the internal jugular vein for ECMO in a primate. 143 26


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