Changes in fetal heart rate-uterine contraction patterns associated with eclampsia

Paul, Richard H.; Koh, Kee Seng; Bernstein, Steven G.

doi:10.1016/0002-9378(78)90361-7

Cited by 58 publications

(13 citation statements)

References 5 publications

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“…This apparent paradox is explained by the realization that endogenous norepinephrine released as part of the normal human hemodynamic response to any major physiologic insult has significant uterotonic effects; thus, the increased uterine activity commonly seen at or even just preceding the onset of discernible maternal or fetal physiologic response is a manifestation of evolving amniotic fluid embolism syndrome rather than being causative. 45 These observations confirm earlier statistical observations by Morgan based on the frequency of oxytocin use and the rarity of amniotic fluid embolism as well as conclusions of the American College of Obstetricians and Gynecologists that there is no causative link between uterine stimulation and amniotic fluid embolism. 32,46 In addition, many studies examining risk factors have a common weakness, namely a shotgun approach to risk factor identification.…”

Section: Risk Factorssupporting

confidence: 89%

Amniotic Fluid Embolism

Clark

2014

Obstetrics &Amp; Gynecology

160

129

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Amniotic fluid embolism remains one of the most devastating conditions in obstetric practice with an incidence of approximately 1 in 40,000 deliveries and a reported mortality rate ranging from 20% to 60%. The pathophysiology appears to involve an abnormal maternal response to fetal tissue exposure associated with breaches of the maternal-fetal physiologic barrier during parturition. This response and its subsequent injury appear to involve activation of proinflammatory mediators similar to that seen with the classic systemic inflammatory response syndrome. Progress in our understanding of this syndrome continues to be hampered by a lack of universally acknowledged diagnostic criteria, the clinical similarities of this condition to other types of acute critical maternal illness, and the presence of a broad spectrum of disease severity. Clinical series based on population or administrative databases that do not include individual chart review by individuals with expertise in critical care obstetrics are likely to both overestimate the incidence and underestimate the mortality of this condition by the inclusion of women who did not have amniotic fluid embolism. Data regarding the presence of risk factors for amniotic fluid embolism are inconsistent and contradictory; at present, no putative risk factor has been identified that would justify modification of standard obstetric practice to reduce the risk of this condition. Maternal treatment is primarily supportive, whereas prompt delivery of the mother who has sustained cardiopulmonary arrest is critical for improved newborn outcome.

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Section: Risk Factorssupporting

confidence: 89%

Amniotic Fluid Embolism

Clark

2014

Obstetrics &Amp; Gynecology

160

129

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“…Most of the clinical data are based on single case studies (e.g., Paul et al 1978;Teramo et al 1979;Yerby 1987) and on studies of the effects of anticonvulsant drugs (for reviews see Delgado-Escueta et al 1982;Adams et al 1990). In studies of the effects of anticonvulsant drugs, the vast majority of studies report CNS developmental and learning impairments associated with use of the anticonvulsant phenytoin during pregnancy, but no deleterious effects associated with maternal seizures.…”

Section: Seizuresmentioning

confidence: 99%

“…At the drug dose used in our previous studies (4 mg/kg per injection), cocaine occasionally elicits grand mal or generalized tonic clonic seizures (GTCSs). GTCSs could result in hypoxia-associated CNS defects independent of the effects of cocaine (Paul et al 1978;Teramo et al 1979). …”

Section: Introductionmentioning

confidence: 99%

Cocaine administration in pregnant rabbits alters cortical structure and function in their progeny in the absence of maternal seizures

et al. 1997

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Previous studies have reported that cocaine exposure in utero results in structural and functional alterations in the development of the anterior cingulate cortex (ACC). In the present study, the effects of maternal cocaine dosage and of cocaine-elicited maternal seizures on the progeny were studied. The incidence of maternal generalized tonic clonic seizures (GTCSs) elicited by cocaine was recorded. No GTCSs were elicited in pregnant rabbits by doses of 2 or 3 mg/kg of cocaine, but GTCSs were sometimes elicited by the highest dose (4 mg/kg per injection). We analyzed the offspring of cocaine-exposed and control animals using three assays of ACC development: (i) the structure of apical dendrites of pyramidal neurons, (ii) the distribution of a calcium binding protein (parvalbumin) in the dendrites of GABAergic neurons, and (iii) coupling of D 1 -like receptors and their G proteins. In all progeny of rabbits exposed to 3 or 4 mg/kg of cocaine during pregnancy, there was a significant change in the structure of apical dendrites, a significant increase in the number of dendrites of GABAergic neurons which were parvalbumin immunoreactive, and a significant reduction in D 1 /G protein coupling. In assays of apical dendrites, the effects on offspring of rabbits given 2 mg/kg cocaine were as pronounced as in offspring of rabbits given 3 or 4 mg/kg, but the effects on parvalbumin immunoreactivity and D 1 /G protein coupling were reduced at this low dose. Thus, previous findings of ACC developmental abnormalities in offspring of rabbits given a dose of 4 mg/kg were replicated, the effects were shown to be dose-related and to be independent of maternal seizures. A mechanism by which dysfunction of the D 1 receptor system could mediate cocaine-associated changes in all three parameters of ACC structure and function is discussed.

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“…The fetal deceleration was judged to be a result of uterine tetany associated with a surge in catecholamines and possible other inflammatory mediators in response to vigorous pleurodesis, reperfusion of collapsed and hypoxic pulmonary tissue, or both, rather than being associated with placental abruption. 4 Terbutaline at 0.25 mg was given with resolution of the uterine tetany and fetal deceleration. The fetal heart tones again returned to 130 bpm.…”

Section: Casementioning

confidence: 99%