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Uterine deaths

Inappropriate use of oxytocin can lead to uterine rupture, anaphylactoid and other allergic reactions, and possibly maternal death. Prolonged stimulation of uterine contractions can result in the following fetal adverse reactions persistent uteroplacental insufficiency, sinus bradycardia, premature ventricular contractions, other arrhythmias, and fetal death. Prolonged use of oxytocin can lead to water intoxication secondary to the antidiuretic hormone-like effects of oxytocin. Maternal and fetal cardiovascular parameters should be monitored during oxytocin administration. [Pg.718]

The uterine contents should be examined for numbers of embryonic or fetal deaths and viable fetuses. The degree of resorption should be described in order to estimate the relative time of death of the conceptus (4). [Pg.48]

When oxytocin is used judiciously, serious toxicity is rare. The toxicity that does occur is due either to excessive stimulation of uterine contractions or to inadvertent activation of vasopressin receptors. Excessive stimulation of uterine contractions before delivery can cause fetal distress, placental abruption, or uterine rupture. These complications can be detected early by means of standard fetal monitoring equipment. High concentrations of oxytocin with activation of vasopressin receptors can cause excessive fluid retention, or water intoxication, leading to hyponatremia, heart failure, seizures, and death. Bolus injections of oxytocin can cause hypotension. To avoid hypotension, oxytocin is administered intravenously as dilute solutions at a controlled rate. [Pg.844]

Atosiban Blocks oxytocin receptors Decreased uterine contractions Tocolysis for preterm labor IV infusion Toxicity Concern about rates of infant death... [Pg.847]

Thavarasah AS, Achanna KS. Uterine rupture with the use of Cervagem (prostaglandin El) for induction of labour on account of intrauterine death. Singapore Med J 1988 29(4) 351-2. [Pg.112]

A 30-year-old woman developed uterine atony and bleeding after induced abortion because of fetal death at 17 weeks of gestation (4). Sulprostone was given intravenously at a rate of 500 micrograms/hour. When additional sulprostone was injected into the uterine cervix, the patient sustained a myocardial infarction, with ventricular fibrillation and cardiocirculatory arrest, most probably due to coronary artery spasm. She was resuscitated and recovered completely. [Pg.133]

Per 100,000, age-adjusted to the 1970 US standard population. tUterus cancer death rates are for uterine cervix and uterine corpus combined. [Pg.231]

When oxytocin is used properly, serious toxicity is rare. Among the reported adverse reactions are maternal deaths due to hypertensive episodes, uterine rupture, water intoxication, and fetal deaths. Afibrinogenemia has also been reported. [Pg.876]

Although estrogen replacement therapy at menopause can prevent bone loss and cardiovascular disease, there is evidence that estrogens are associated with an increased risk of breast cancer as well as endometrial cancer(Gambrell, 1994), which thus seriously limits the use of estrogen replacement therapy. The ideal compound for women s health should be one able to decrease the risk of the most important causes of morbidity and mortality in women, namely breast cancer, uterine cancer, osteoporosis, bone fractures, and cardiovascular disease. Heart disease is, in fact, the leading cause of death in postmenopausal women (Lerner and Kannel, 1986). This ideal compound should also have an excellent safety profile to ensure compliance over 20 to 40 years of a woman s life. [Pg.295]

This test146 deals primarily with gross chromosomal damage. The dominant-lethal test is widely used and is usually performed on exposed males. Nongenetic maternal effects make it much more difficult to study induction of dominant lethality in females. Exposed male rats or mice are mated at weekly (or shorter) intervals to cover the span of spermatogenesis of interest. Females usually are killed for uterine examination around day 14, and the numbers of total implantations and fetal or embryonic deaths are recorded. The corpora lutea are also counted sometimes. The proportions can be analyzed statistically to see whether dominant lethality has been induced, and appropriate formulas are used in calculating the percentage of dominant lethality.107 146... [Pg.132]

The relative proportions of each 24-hour day that are devoted to wake, REM sleep, and non-REM sleep change dramatically over our lifetime. Exactly how and when these states develop in early uterine existence is not known (dotted lines), but data from premature infants suggests that REM sleep is almost all of life at 26 weeks of gestation age. After 26 weeks, waking increases progressively and inexorably until death. [Pg.69]

The next target is the gestation process itself. As outlined above, a number of alkaloids are mutagenic and lead to malformation of the offspring or directly to the death of the embryo (Table V). The last step would be the premature abortion of the embryo. This dramatic activity has been reported for a number of allelochemicals, such as mono- and sesquiterpenes and alkaloids. Some alkaloids achieve this by the induction of uterine contraction, such as the ergot and lupine alkaloids (312). [Pg.60]


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See also in sourсe #XX -- [ Pg.169 ]




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