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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In utero fetuses are evidently exposed to several factors that cause an interruption of the oxygen flow through the umbilical cord causing asphyxia leading to hypoxia and metabolic acidosis. These conditions are important causes of intra-partum and neonatal mortality. The main objective of this review is to provide current information regarding the pathophysiology of asphyxia in piglets around parturition; the physiological mechanisms invoked by affected piglets to compensate perinatal hypoxemia are discussed. This review also addresses some similarities and differences of asphyxia between piglets and other mammals, including human neonates. Metabolic acidosis and hypoxia are sequela to asphyxia and can cause profound health effects in postnatal performance because of an abnormal suckling, a reduced absorption of colostrum and inadequate passive transfer of neonatal immunity. Acidosis also cause hypothermia, increased mortality and reduced survival in neonates. One of the first deleterious effects of intrauterine hypoxia is the expulsion of meconium into the amniotic sac leading to meconium staining of the skin, and in severe cases, meconium aspiration into the lungs. Even though there have been technological changes and improvements in husbandry, piglet mortality due to asphyxia remains a major problem. One potential alternative to reduce neonatal mortality in pigs is the monitoring of fetal stress during birth and the implemention of strategies such as the Apgar score, that is often used in human pediatrics. It is also important to consider the physiological, behavioral and biochemical changes that take place during parturition which subsequently impact the vitality, maturity and development of neonatal pigs. Understanding the pathophysiology of fetal hypoxia should help practitioners and farmers implement more effective delivery techniques aimed at reducing neonatal mortality and improving postnatal performance.
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PMID:Perinatal asphyxia pathophysiology in pig and human: a review. 1625 94

Intrauterine or fetal growth restriction is best defined by using customised birth weight percentiles based upon the growth potential for an individual infant. Growth restriction in utero may be classified as asymmetric or symmetric depending upon the duration of the process. Asymmetric growth restriction is caused by placental insufficiency, maternal hypertensive conditions, long-standing maternal diabetes, smoking, living at altitude or multiple gestation. Symmetric growth restriction may be due to congenital infections, chromosomal or other abnormalities, fetal alcohol syndrome, low socioeconomic status or be constitutional. The underlying cause of growth restriction often predicts the potential adverse effects on the foetus and newborn and later effects in childhood and adulthood. With placental insufficiency, there may be chronic or acute on chronic fetal hypoxia with birth asphyxia and hypothermia, neonatal hypoglycaemia, polycythaemia and coagulopathy. Management is directed at prevention or early treatment of these conditions. In contrast, symmetrically growth-restricted infants should be examined carefully to look for congenital infections and malformations that may need specific interventions. Infants with constitutional short stature generally do not need any specific management. Feeding of growth-restricted infants is important to overcome deficiencies incurred in utero. Most infants show catch-up growth although about 10% do not. Those with excessive catch-up growth may be at greatest risk of developing insulin resistance in adulthood leading to diabetes, obesity and heart disease. The so-called fetal origins of disease may actually have a postnatal onset related more to excessive weight gain in infancy. There is still controversy over the indications for growth hormone treatment in growth-restricted infants who remain of short stature in early childhood. Intrauterine growth restriction is also associated with a five- to seven-fold increased risk of cerebral palsy probably due to chronic placental insufficiency.
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PMID:Neonatal management and long-term sequelae. 1963 99

Infective Endocarditis (IE) during pregnancy is a rare but grave condition. The diagnosis and management can be challenging, especially when the pregnant patient warrants a cardiac operation under cardiopulmonary bypass. The present article describes IE during pregnancy based on a series of published case reports in the literature. IE during pregnancy often causes embolic events and mycotic aneurysms. Two-thirds of IE in the pregnant patients requires timely or urgent cardiac surgery to alleviate patients' deterioration. At least a 3-week antibiotic therapy is mandatory before cardiac surgery aiming at improving the patients' conditions. During cardiac surgery, fetal heart rates may temporarily be slowed down but may gradually recover to normal after the operation. The fetal and maternal mortalities were 16.7% and 3.3%, respectively. The fetal deaths were apparently associated with a cardiac surgery during early pregnancy. Cardiopulmonary bypass, hypothermia and rewarming can adversely affect both the mother and the fetus by triggering placental deficits, fetal hypoxia and uterine contraction. Avoidance of cardiac operations before 24th gestation week and preferably deferred until after 28th gestation week have been a plausible argument as per the possible fetal deaths related to immaturity.
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PMID:Infective Endocarditis during pregnancy. 2570 59

An adverse outcome is still encountered in 45% of full-term neonates with perinatal asphyxia who are treated with moderate hypothermia. At present pharmacologic therapies are developed to be added to hypothermia. In the present article, these potential neuroprotective interventions are described based on the molecular pathways set in motion during fetal hypoxia and following reoxygenation and reperfusion after birth. These pathways include excessive production of excitotoxins with subsequent over-stimulation of NMDA receptors and calcium influx in neuronal cells, excessive production of reactive oxygen and nitrogen species, activation of inflammation leading to inappropriate apoptosis, and loss of neurotrophic factors. Possibilities for pharmacologic combination therapy, where each drug will be administered based on the optimal point of time in the cascade of destructive molecular reactions, may further reduce brain damage due to perinatal asphyxia.
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PMID:Drugs for neuroprotection after birth asphyxia: Pharmacologic adjuncts to hypothermia. 2679 92