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At least 415 records · Page 23Linked to original sources
PubMed1999

Uterine rupture associated with the use of misoprostol in the gravid patient with a previous cesarean section.

OBJECTIVE: Our purpose is to report our experience with uterine rupture in patients undergoing a trial of labor after previous cesarean delivery in which labor was induced with misoprostol. The literature on the use of misoprostol in the setting of previous cesarean section is reviewed. STUDY DESIGN: This report was based on case reports, a computerized search of medical records, and literature review. RESULTS: Uterine rupture occurred in 5 of 89 patients with previous cesarean delivery who had labor induced with misoprostol. The uterine rupture rate for patients attempting vaginal birth after cesarean section was significantly higher in those who received misoprostol, 5.6%, than in those who did not, 0.2% (1/423, P =.0001). Review of the literature reveals insufficient data to support the use of misoprostol in the patient with a previous cesarean delivery. CONCLUSION: Misoprostol may increase the risk of uterine rupture in the patient with a scarred uterus. Carefully controlled studies of the risks and benefits of misoprostol are necessary before its widespread use in this setting.

Adult↗
PubMed1999

Intravenous infusion of magnesium sulfate and regional redistribution of fetal blood flow during maternal hemorrhage in late-gestation gravid ewes.

OBJECTIVES: Even though magnesium sulfate is commonly prescribed for women with preeclampsia as prophylaxis against seizure and for women with preterm labor as a tocolytic agent there is limited information about its effects on the fetus. It is of particular concern that women with preeclampsia or in premature labor are at high risk for abruptio placentae with consequent compromise of fetal oxygenation. Magnesium sulfate is a vasodilator and thus may exert cardiovascular effects on the fetus. The goal of this study was to evaluate the effects of magnesium sulfate on fetal organ blood flow, especially regional cerebral blood flow, during the stressful condition of maternal hemorrhage. STUDY DESIGN: Studies were performed with 11 long-term instrumented pregnant ewes and their fetuses at 121 to 128 days' gestation (term, 147 days' gestation). Animals were randomly allocated to either the experimental (n = 5) or the control (n = 6) group. After a 60-minute baseline period, experimental fetuses received intravenous magnesium sulfate diluted in 0.9% sodium chloride (0.3 g loading dose, then 0.3 g/h at a rate of 3 mL/h) and control fetuses were infused with an equivalent volume of intravenous 0.9% sodium chloride. After 60 minutes of this infusion-only period, the infusions were continued and ewes were intermittently bled 4 times at a rate of 5 mL/kg for 10 minutes with 5 minutes between hemorrhages. The total blood lost at the end of the hemorrhage-plus-infusion hour was 20 mL/kg. The infusions were continued and the sheep were observed for 1 hour after this period (posthemorrhage period). At the end of baseline, infusion-only, and hemorrhage-plus-infusion periods, fetal and maternal blood pressures and blood gas values were measured and fetal organ blood flows were determined through a fluorescent microsphere technique. Repeated-measures analysis of variance and Wilcoxon tests were used to determine the significance of changes in hemodynamic, blood gas, and organ blood flow parameters between different time points within each group. Comparisons between groups were made with rank sum tests (Mann-Whitney tests). RESULTS: There were no significant differences between groups or within groups for baseline and infusion-only measurements in any measured hemodynamic or hematologic factor. Mean maternal blood pressure decreased significantly (P <.05) after hemorrhage, with similar median decrements in both control and experimental groups of 41 mm Hg (interquartile range, 24-57 mm Hg) and 41 mm Hg (interquartile range, 12-43 mm Hg), respectively. There were no significant differences between groups in fetal blood gas values or hemodynamic parameters. Fetal arterial PO(2) decreased significantly after hemorrhage plus infusion, with similar mean (+/-SEM) decreases in control and experimental groups of 5.9 +/- 1.4 mm Hg and 4.5 +/- 1.5 mm Hg, respectively. Fetal pH also decreased significantly in both groups. After hemorrhage plus infusion there were significant increases in fetal regional cerebral and myocardial blood flows in both groups. Adrenal blood flow increased significantly from baseline (214%, 183%-294%) in the control group after hemorrhage plus infusion but not in the experimental group. No other difference in organ blood flow between control and experimental groups was observed. Significant regional variations in cerebral blood flow were not observed in either group at any time. CONCLUSIONS: In these initially healthy, late-gestation fetal lambs magnesium sulfate exposure did not impair cardiac output redistribution, nor did it cause fetal death in response to maternal hemorrhage.

Animals↗
PubMed2003

Location of the appendix in the gravid patient: a re-evaluation of the established concept.

OBJECTIVES: To determine the anatomical location of the appendix, as it may change during pregnancy. METHODS: In this prospective study conducted from October 1995 to March 1999, 291 women of reproductive age were evaluated for appendix location. They were divided into three groups: group A, 165 women between 37 and 40 weeks of pregnancy who underwent elective cesarean delivery; group B, 26 women between 19 and 39 weeks of gestation with acute appendicitis who underwent appendectomy; and group C (the control group), 100 non-pregnant women with acute appendicitis who underwent appendectomy. Appendix location was considered normal within 2 cm of the McBurney point; otherwise, it was considered to be a position change. RESULTS: In group A, 2 (15%) of 165 women and in group B, 6 (23%) of 26 women had a change in the position of the appendix. In the control group, 17% had change in position. There were no significant differences between group A and B compared with group C. In group B, no relation between height of fundus and point of tenderness was seen. CONCLUSION: Our study did not show that pregnancy changes the location of the appendix.

Adolescent↗
PubMed1987

Renal disease in gravid animal models.

Micropuncture studies in the rat have indicated that in the short term, the superimposition of pregnancy on an experimentally induced, advanced, autologous phase glomerulonephritis (GN) does not lead to any worsening of the functional or morphological changes characteristic of this disease. Indeed, pregnant rats with GN exhibit a tendency toward higher GFR and plasma flow rate than do virgin rats with this disease. In chronic studies to investigate the long-term effects on kidney function of pregnancy, normal rats undergoing five closely spaced pregnancies and lactations exhibit glomerular hemodynamics, 24-hour protein excretions, and morphology similar to those of age-matched virgins. When repetitive pregnancies are superimposed on rats with the long-term hyperfiltration stimuli of uninephrectomy plus high dietary protein feeding, no worsening of the proteinuria occurs in comparison to virgin rats subjected to the same degree of renal ablation plus high protein. Although filtration and plasma flow rates are lower in these repetitively pregnant rats as compared with virgin rats, amino acid infusion revealed substantial renal reserve in the repetitively pregnant rats. These studies show that gestational hyperfiltration does not, in and of itself, provide an adverse stimulus to the maternal kidney.

Animals↗
PubMed1994

Glomerular filtration and volume regulation in gravid animal models.

The gestational increase in glomerular filtration rate that occurs in the normal rat is exclusively the result of an increase in renal plasma flow and there is no sustained increase in glomerular capillary blood pressure during a normal pregnancy. The factor or factors that initiate the gestational renal vasodilatation (and plasma volume expansion) are maternal, not fetoplacental in origin. The precise nature of the initiating factors has not yet been defined, although it is unlikely that the gestational plasma volume expansion can be the sole cause of the increased glomerular filtration rate seen in pregnancy. A number of vasoactive hormones are activated in pregnancy but as yet no clear candidate has emerged as 'the renal vasodilator'. Preliminary evidence suggests that nitric oxide may play an important role in gestational vasodilatation. The normal kidney in pregnancy exhibits substantial renal reserve to amino acid infusion and unimpaired autoregulatory ability despite being already vasodilated by the gestational stimulus. There are marked and sometimes contradictory changes in the various volume sensing and control systems in pregnancy. In general, the sensors perceiving and controlling intravascular volume are reset during a normal pregnancy to enable to mother to accommodate the increased plasma volume without provoking a natriuretic response. Whether the expanded plasma volume of pregnancy is perceived as normal or underfilled is not clear at this time and may vary according to the volume regulatory system. Repetitive pregnancies do not have any cumulative, long-term deleterious effects on renal function, when the underlying function is normal, when it has been compromised by removal of renal mass or during chronic systemic hypertension in the spontaneously hypertensive rat. In the short term, pregnancy does not worsen kidney function when underlying glomerular damage is due to immune stimuli, ablation of renal mass or gentamicin, or in the spontaneously hypertensive rat. Therefore, the chronic renal vasodilatation of pregnancy does not appear to be a damaging entity, unlike other states of low preglomerular arteriolar resistance, studied in the male rat. When pregnancy is superimposed on Adriamycin nephrosis or chronic blockade of nitric oxide, hypertension occurs and renal function declines. In both situations endothelial damage/dysfunction occurs, as is also seen in pre-eclampsia. Further study of the effects of pregnancy in animal models of endothelial dysfunction will prove rewarding.

Animals↗
PubMed1994

Renal tubular function in the gravid rat.

Pregnancy in the rat is accompanied by enhanced reabsorption of salt and water throughout most, if not all, of the gestational period. Many mechanisms have been suggested but definitive answers are still awaited. The major area of controversy centres around the detection of changes at term. There is general agreement that, at least in mid-gestation, the increase in reabsorption can be attributed to increases in the proximal tubules, the loop of Henle and the collecting duct. The contribution of the proximal tubule to the increased reabsorption at term is still uncertain. Enhanced salt and water reabsorption is demonstrated in distal nephron segments irrespective of the stage of gestation. Micropuncture and microperfusion experiments have identified increased reabsorption of water, sodium and chloride in the loop of Henle, but it appears that there is net addition of glucose, urea and potassium to the tubular fluid in this segment which, at least for potassium and glucose, offsets to some extent increased reabsorption by the proximal tubule. Altered renal handling of other solutes (uric acid, calcium and magnesium) also occurs throughout pregnancy but the mechanisms responsible and nephron sites involved remain to be investigated. Attempts to attribute altered reabsorption to direct renal effects of changes in maternal hormones are inconclusive. Prolactin mimics some of the pregnancy-associated increases in reabsorption following chronic administration to male and non-pregnant female rats. These effects might be due to a direct renal action of the hormone or even to the volume expansion following its dipsogenic action.

Absorption↗