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

The Sudden Infant Death Syndrome (SIDS) is the most frequent cause of death in infants aged between one month and one year, yet its cause remains unknown. The present hypothesis is that most infants who die of SIDS have an abnormality of the catecholaminergic system, possible genetically determined, which results in a decreased thermogenic response to cold, owing to a deficiency in noradrenaline (NA), which eventually results in severe hypothermia. A series of complex, but interrelated reactions of the infant to the hypothermia and its consequences leads to death. The final mechanism of regulatory failure involves a deterioration of cardiorespiratory function resulting from hypoxia, metabolic acidosis and hypoglycemia. The etiology of "near miss" for SIDS is also unknown. It is postulated that these infants have a similar but milder deficiency which may be due, in part, to genetic factors. Determinations of central and peripheral catecholamines in "near miss" and normal infants will be performed to test this hypothesis.
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PMID:Sudden infant death syndrome: a testable hypothesis and mechanism. 53 16

The effects of social class, season, low temperature and sudden falls in temperature are investigated in 286 cases of Sudden Infant Death Syndrome in Cardiff in the years 1955--1974. The association with low temperature was striking: unsuspected hypothermia may be an important feature of these deaths. Sudden infant death incidence was associated with influenza A but not influenza B epidemics.
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PMID:Sudden infant death syndrome in Cardiff, association with epidemic influenza and with temperature - 1955-1974. 74 71

The sudden infant death syndrome (SIDS) remains a leading cause of death during the first year. The common epidemiological and pathological data which characterize SIDS include the curve for age at death (with 3 months as modal age), the stigmata of early maternal intrauterine injury, the seasonal predominance in winter, and the absence of an adequate cause of death at autopsy. Some data characterize risk factor subgroups: for example low socioeconomic level, environmental pollution, stress, and mistakes in baby care. Symptoms before death may be lacking, they may be common and non-specific, or rarely they may be acute, corresponding to "apparent life-threatening events" (ALTE). SIDS may be a magnesium-dependent disease of the transition from chemical to physical thermoregulation. This theory originates from a synthesis of our present knowledge of SIDS, maternal magnesium status, and thermoregulation in the baby. It is consistent with all the epidemiological and pathological prerequisites characterizing SIDS. It eliminates the hiatus between relatively minor thermal stress and induced lethal thermal stroke. Logical scepticism about the role of an implausible lethal superacute magnesium deficiency is no longer justified with regard to well established chronic marginal magnesium deficiency. Further experimental and clinical research will be interesting, i.e. ex vivo studies on brown adipose tissue (BAT) and magnesium deficiency under various conditions of thermal exposure. But even now the theory leads to three therapeutic consequences: (1) the need to define the importance of magnesium deficiency in diagnosis and treatment of ALTE; (2) an assessment of the use of new techniques of rewarming (i.e. extracorporeal circulation) in hypothermia cases to distinguish cot death from "apparent death"; (3) investigation of the prevention of SIDS with magnesium through a blinded and randomized multicentre prospective cooperative study of magnesium supplementation in pregnant and lactating women, followed not only in the mother, fetus, and neonate at birth, but also through the first year of life.
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PMID:Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a magnesium-dependent disease of the transition from chemical to physical thermoregulation? 179 50

When the body temperature of a small neonate falls below 35 degrees C, lassitude can be noted; severe derangements of cardiovascular, renal, hepatic, immunological, and hematological systems may also occur depending in part on the duration and severity of hypothermia. Diagnosis requires a low-reading thermometer, lacking which the diagnosis can be suspected, but most often is missed. Fatal cases of diagnosed cold injury commonly have terminal pneumonia or sepsis. Prevention involves identification and home visits to high-risk infants; intensive care of those with the diagnosis at Soroka Hospital Medical Center has reduced the case-fatality rate from 30% in 1971 to 3% in 1988-1989. During the same period in our region, the proportion of neonatal deaths occurring in winter months of December, January, and February has dropped from 55 to 27%. The expected proportion is 25%. We hypothesize that excess neonatal mortality during winter months, especially due to pneumonia and sepsis or sudden infant death syndrome (SIDS) is an indicator of missed cold injury syndrome. A preliminary evaluation was made form U.S. data by state, provided by the National Center for Health Statistics, which records no fatalities from cold injury during 1986. Contrasted with this are 26 cold injury deaths in Israel for 1977-1980. In the U.S., though, excess winter neonatal deaths in 1986 from SIDS, pneumonia, and sepsis are reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preventability of neonatal cold injury and its contribution to neonatal mortality. 195 41

In a nationwide prospective survey on very preterm and very-low-birthweight infants in The Netherlands, the incidence of cot death in infants discharged alive was 15%. The postnatal age at death in these infants did not differ significantly from age at death in other cot death infants. Using a case-control design, possible risk factors associated with cot death were identified: lower maternal age at first pregnancy; maternal smoking during pregnancy; hypothermia of the infant immediately after birth; decreased number of white blood cells and thrombocytes in the infant on the first day of life. Intrauterine hypoxia is hypothesized as the entity common to these factors.
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PMID:Prenatal risk factors for cot death in very preterm and small for gestational age infants. 220 73

Recreational diving is a popular sport, although human ability to stay in and under water is severely limited physiologically. An understanding of these limitations enhances safety and enjoyment of sports diving. Breath-hold diving involves head-out water immersion, apnoea and submersion, exercise, cold stress, and pressure exposure. Each of these components, by itself, elicits prominent and specific physiological effects. Combination of these factors produces a unique and interesting physiological response generally known as diving reflex. Humans display weak diving responses, but exhibit no oxygen conservation function. Nevertheless, application of diving-induced physiological changes is now finding its way into clinical practice. Apnoea, face immersion, and head-out water immersion all show promise of clinical application. There are several spin-offs from diving research worth noting. Diuresis, enhancement of cardiac performance, and redistribution of blood flow, all produced by head-out water immersion, have been shown to be clinically useful, besides providing physiological data useful to space travel. Results from investigations on apnoea have been shown to be relevant to the following: treating some forms of cardiac arrhythmias; understanding drowning, sudden infant death syndrome and sleep apnoea; and confirming hyperventilation as the major cause of drowning. In comparison to marine mammals, humans are poor divers because of severe physiological constraints which limit their breath-hold time, diving depth, and ability to conserve body heat. Although under special circumstances humans can achieve unusually long breath-hold time and reach exceptional depth with a single breath, the sustainable working time and depth are only about 1 minute and 5 metres, respectively. Hypothermia inevitably results in divers working in the ocean. Without thermal protection, the intolerable limit of 35 degrees C is reached within 30 minutes in winter (10 degrees C) water and within 60 to 90 minutes in summer. Nevertheless, effective harvest work can be performed by humans in the ocean, and recreational benefits enhanced when these physiological limitations are respected. An unusual circulatory state exists during head-out water immersion in that there is a sustained increase of stroke volume. This results in 30% increase in cardiac output when the subject is resting in thermal neutral water, indicating a substantial overperfusion for the oxygen requirement. Furthermore, animal experiments showed that the elevated blood flow is preferentially channeled to the liver, fat, and the organs in the splanchnic region.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Applied physiology of diving. 327 55

Clostridium botulinum can colonize and produce botulinal toxin in the human infant intestine, which the toxin then permeates to cause generalized flaccid paralysis, and occasionally, sudden death. This study was undertaken to test the hypothesis that toxins produced by other intestinal clostridia, e.g., C. difficile, might also cause systemic illness and sometimes death in infants (J Pediatr 100:568, 1982). Because this hypothesis could not be evaluated clinically until the systemic manifestations of C. difficile toxins in primates were known, infant rhesus monkeys were given 6 to 11 micrograms/kg of the recently purified C. difficile toxins A or B, either intravenously or intraperitoneally. The animals showed no abnormalities for several hours, but then developed lethargy, hypotonia, hypothermia, and, shortly before death, sudden elevation of serum concentrations of potassium, magnesium, and phosphorus and of enzymes that derived mainly from skeletal muscle, heart and brain. Five of six animals died quietly 3.5 to 8.0 hours after onset of symptoms. Death appeared to result from cessation of breathing, after which the sinus tachycardia then deteriorated to a flat ECG. Necropsy findings were insufficient to explain the cause of death. It appears that in infant monkeys microgram amounts of C. difficile toxins A and B can produce a rapid quiet death, the cause of which is undetectable at necropsy, a situation pathologically reminiscent of crib death in human infants, although the possible clinical identity of these two conditions has yet to be established.
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PMID:Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: physiologic and pathologic basis. 669 Jun 74

1. This paper reviews current knowledge regarding interactions between body temperature and the respiratory responses to hypoxia and/or hypercapnia, with special emphasis on how these interactions might predispose towards sudden infant death syndrome (SIDS). 2. Use has been made of an adult rat model in which body core temperature is fixed by means of an intra-abdominal heat exchanger. Initial studies indicated that hyperthermia (Tb approximately 41 degrees C) enhanced the ventilatory response to hypercapnia, whereas hypothermia (Tb approximately 35 degrees C) interacted with hypoxia to depress respiration. 3. Studies involving hypothalamic lesions in urethane-anaesthetized rats have implicated the posterior hypothalamic area in the hypoxia/hypothermia interaction. Further studies are directed towards examining the role played by more caudal areas, including the raphe nuclei. 4. It has been shown that not only does the hypoxia/hypothermia interaction depress breathing but it also reduces, or sometimes eliminates, the ventilatory response to hypercapnia, which under normal circumstances provides one of the most powerful excitatory inputs to the respiratory centres. This implies that an expected reversal of the respiratory depression by build up of CO2 levels may not occur, which in turn has important implications for SIDS. 5. The literature dealing with the effects of hyperthermia on hypoxic and hypercapnic responses is also reviewed. It is concluded that environmental heat stress may only become a significant problem when it accompanies a febrile infection, under which circumstances it may seriously compromise thermoregulatory ability and alter breathing responses to chemical stimuli.
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PMID:Influence of body temperature on responses to hypoxia and hypercapnia: implications for SIDS. 758 8

Blood acid-base changes were studied during acute hypothermia (4-6 h) induced by cold exposure in the unanesthetized rat. Stewart's quantitative analysis was applied as a complementary approach to determine the relative contributions of several non-respiratory components to the arterial acid-base response. Acute decrease in body temperature (TB) lowered PaCO2 (32.5 to 14.5 mmHg) and [HCO3-]a(24.20 mEq/L to 17.56 mEq/L), increased pHa (7.481 to 7.608) and diminished the [OH-]/[H+] ratio, but had no significant effect on [SID] or [Atot], although both total phosphorus [PT] and inorganic phosphate [Pi] increased. The acid-base changes found were intermediate between those predicted by alpha-stat and pH-stat hypotheses. Deviation from the regulative alpha-imidazole strategy was more apparent in the plasma than in the intraerythrocyte compartment. We conclude that blood pH changes observed were mainly caused by increased relative ventilation (lung ventilation per unit of CO2 removed) and by resulting changes in PCO2, with a minor metabolic component but without significant contribution from ionic shifts or changes in plasma protein concentration.
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PMID:Factors influencing acid-base status during acute severe hypothermia in unanesthetized rats. 762 15

It is strange that some aspects of infant care have been strongly promoted by modern medicine while others have been neglected. Thus prone sleeping which has been strongly promoted is now related to an increase in SIDS, whereas the promotion of breast feeding in developed countries has been less successful. Unfortunately there has not been sufficient physiological investigation of many infant care practices and some of the proposed mechanisms for SIDS and prone sleeping have not been substantiated. Thus further work is needed on hypercapnia, hypothermia and periodic breathing and respiratory control. Studying infants alone may leave out important physiological mechanisms such as the effect on body warmth when the infant is close to the mother. More investigation is needed of antenatal factors related to SIDS and it is critically important that physiological investigation should not look for single mechanisms but be concerned with the interaction of many physiological factors.
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PMID:Infant care practices and the investigation of physiological mechanisms. 782 Dec 61


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