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

Hypothermia is a common intraoperative and immediate postoperative complication. Hypothermia causes morbidity from shivering, hypotension, cyanosis, and respiratory diseases. In severe cases, bradycardia, premature ventricular contractions, and even ventricular fibrillation may occur. The various causes of excessive heat loss, both intraoperatively and during the postanesthesia period, the methods of prevention, and the rewarming measures are important factors in administering patient care. Predisposing factors are large exposed body surface areas, open body cavities, prolonged exposure to low operating room temperature, rapid infusion of cold blood and intravenous (IV) fluids, cold irrigating solutions, ventilation with cold gases in long surgical procedures, age over 60 years, premedication that relaxes muscle tone, and the subcutaneous vasodilatation that occurs during anesthesia. Attempted prevention measures include active warming blankets, increased ambient temperatures, warmed IV and irrigating solutions, and metallized plastic sheeting. Restoration of normal body temperature is achieved by radiant heaters, heated mattresses, and heated humidifiers. Astute assessment, quick response, and correct interventions by the nurse can often minimize risk of postanesthesia hypothermia. These principles are illustrated in a case study of a PACU patient in a large teaching trauma hospital.
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PMID:Help! This postanesthesia care unit patient is hypothermic. 235 57

Although the conditions that cause hypoglycemia in adults may also be present in infants and children, there are many entities unique to the pediatric age group. This reflects the delicate balance that exists in the newborn and young child between glucose production and utilization. During fasting in infants and children, hepatic glucose production is normally two to three times that of adults when expressed on the basis of weight. In the newborn and young infants, hypoglycemia usually presents with irritability, feeding difficulties, lethargy, cyanosis, tachypnea, and/or hypothermia rather than the typical adrenergic or neuroglucopenic symptoms seen in the adult. The hypoglycemia may be due to abnormalities in hormone secretion, substrate interconversion, or mobilization of metabolic fuels. The hypoglycemia associated with hyperinsulinemia may be transient neonatal, sustained, or drug-induced. Inborn errors of metabolism caused by enzymatic defects are responsible for hypoglycemia associated with abnormalities of production and utilization of metabolic fuels. These can involve carbohydrate, protein, and fat metabolism. In addition, there may be acquired or transient defects in carbohydrate metabolism secondary to other diseases or ingestion of certain substances. Finally ketotic hypoglycemia appears to be due to abnormalities in substrate availability. A variety of tests are useful for establishing the etiologic basis of the hypoglycemia, and the appropriate treatment depends upon the underlying cause.
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PMID:Hypoglycemia in infants and children. 264 28

Tumor necrosis factor (TNF) is a macrophage product under active study as an anticancer drug. However, this agent can be very toxic and has been implicated in the pathogenesis of endotoxic shock. After intravenous injection of human recombinant TNF (4 micrograms/g), growing rats showed an unusual constellation of physiological responses, and all died within 2-4 hr. In 1 hr, TNF caused a sharp fall (2.5 degrees C) in body temperature and a large increase in plasma prostaglandin E2 levels. Blood glucose initially increased, but then a profound hypoglycemia developed by 2 hr. The TNF-treated animals also showed diarrhea, cyanosis, and a severe metabolic acidosis. A single injection of the cyclooxygenase inhibitors indomethacin or ibuprofen before the TNF treatment completely prevented the rapid killing and reduced eventual lethality by 70%. These agents blocked prostaglandin E2 production and prevented the hypothermia, changes in blood glucose, acidosis, and other symptoms. Since similar physiological changes have been reported after endotoxin injection, our data support the suggestion that TNF production is a critical factor in the development of septic shock. These findings also indicate that increased production of prostaglandins or thromboxanes is important in endotoxic shock and argue that cyclooxygenase inhibitors should be useful in its therapy. Indomethacin did not block the cytotoxic effects of TNF in vitro on several transformed cell lines (HeLa, Me 180, or L929). Therefore, combined use of TNF with a cyclooxygenase inhibitor may allow safer administration of high doses of this polypeptide to cancer patients.
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PMID:The toxic effects of tumor necrosis factor in vivo and their prevention by cyclooxygenase inhibitors. 310 90

Hypoplasia of the lungs is the cause of the high mortality of newborns with diaphragmatic hernia. Survival depends mainly on the development of the contralateral lung. Eighty percent of diaphragmatic hernias are postolateral hernias of the left side. The most serious postoperative complication is a relapse into fetal circulation with increased pulmonary vascular resistance and right-to-left shunting (Fig. 2). The clinical signs of diaphragmatic hernia are cyanosis and tachypnea. Intermittent suction via a nasogastric tube and early intubation without mask ventilation should be performed. The inspiratory pressure should not exceed 25 cm H2O to minimize the risk of pneumothorax. Survival of the baby is unlikely if the initial blood gas analysis shows pH less than 7.10, pO2 less than 50 mmHg, and pCO2 greater than 65 mmHg. Hypothermia should be strictly avoided because it leads to increased oxygen consumption. Intraoperative monitoring should include a precordial stethoscope, ECG, blood pressure, and rectal temperature. Anesthesia is maintained with fentanyl 0.02-0.03 mg/kg body wt. and pancuronium 0.08-0.1 mg/kg. One dose of atropine (0.02 mg/kg) is administered before fentanyl. Intraoperative ventilation is performed by hand or by use of a Siemens Servo ventilator. Thirty newborns were anesthetized for repair of a congenital diaphragmatic hernia with no intraoperative complication and an overall mortality of 27%.
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PMID:[Anesthesia for congenital diaphragmatic hernia]. 363 96

Prenatal starvation causes pulmonary hypoplasia in newborn guinea pigs, and is associated with postnatal cyanosis, hypothermia, and respiratory failure. To determine the effects of such starvation on ventilation, neonates from litters either fed ad libitum throughout gestation (control) or given 50% rations in the last trimester of pregnancy (starved) were studied at 29 degrees C by plethysmography in 21, 11, and 5% O2. After 15 min (steady-state) in 11% and then 5% O2, 13 of 14 controls (mean = 95 g) sustained increases in weight-specific minute ventilation of 46 and 75% compared to values in air (p less than 0.01), due to increases in respiratory frequency. Seven of 11 starved neonates (mean = 76 g) also sustained increases in respiratory frequency and weight-specific minute ventilation in 11 and 5% O2 similar in magnitude to those of the normal controls, although at higher weight-specific tidal volumes. One abnormal control (85 g) and four starved neonates (mean = 70 g) hyperventilated in air, did not respond to 11% O2, and then hypoventilated in 5% O2 due to a reduced weight-specific tidal volume. Neonates with normal ventilatory patterns did not alter weight-specific minute ventilation in 100% O2 and did not show a biphasic response in acute (1-5 min) exposures to moderate hypoxia, as noted for newborn of other species. Thus, hypoxia identified those starved neonates in which pulmonary immaturity or other starvation-induced pathologies necessitated a maximal ventilatory effect in air. The sustainable hyperventilation among normal guinea pigs during hypoxia emphasizes the precocial development in this species at birth, which may be compromised by intrauterine starvation.
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PMID:Prenatal starvation retards development of the ventilatory response to hypoxia in newborn guinea pigs. 377 4

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

Experimental studies to this point have not identified a selective neonatal pulmonary vasodilator. They have indicated that the neonatal pulmonary circulation is a complex, active vascular bed that has a number of endogenous vasodilatory mechanisms which oppose vasoconstriction under normal circumstances. It seems likely that a better understanding of how those mechanisms become deranged in various disease states will be required before we can substantially improve our drug therapy in pulmonary hypertensive infants. The data we have outlined above indicate that firm recommendations for drugs and their doses cannot be made. Nonetheless, several principles of therapy can be outlined. Because of the marginal benefits, which have resulted from current drug therapy [9, 24, 34, 79, 84, 100, 107], it seems clear that, at the moment, the most prudent initial course in neonates with pulmonary vasospasm should be nonpharmacologic: restoration of normal blood gases, use of high concentrations of inspired oxygen with hyperventilation to pH 7.6 if cyanosis persists [22, 79], avoidance of agitation and hypothermia [22], and correction of any metabolic derangements [92]. Decreased cardiac output should be identified and treated with blood volume expanders and/or cardiotonic agents as necessary. Finally, if physiologic efforts to lower pulmonary vascular resistance fail, drug therapy sometimes is helpful in effecting salvage. Treated infants should be carefully monitored, not only for signs of improved oxygenation, but also for changes in right-to-left ductal shunting and cardiac output. If a given agent does not produce beneficial effects at a range of doses by 60 min, it is unlikely that prolonged therapy will result in late improvement. In such circumstances, a change in drug therapy is probably indicated. Finally, it would seem wise to use multiple agents with extreme cautions, being careful to pair a direct vasodilator (e.g., nitroprusside, tolazoline, or prostacyclin) with a cardiotonic agent (e.g., isoproterenol or dopamine), or simultaneously administered volume expanders as the individual clinical situation dictates. Further animal experimentation will undoubtedly identify new and promising agents and provide an increasing understanding of the cellular physiology of the newborn pulmonary circulation. However, only careful clinical and experimental studies into the cause(s) of the vasoconstriction in newborns will allow the development of a truly rational approach to specific therapy in the human species.
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PMID:Neonatal 'pulmonary vasodilator' drugs. Current status. 642 57

Published works on intelligence quotient (IQ) and development following the use of profound hypothermia and circulatory arrest (TCA) to repair congenital heart defects in infants and young children suggest that little or no psychomotor impairment results. IQ scores derived from cognitive, memory, perceptual, quantitative, and verbal tests (McCarthy scale of the children's abilities, mean score 100, SD 16) were measured in 31 patients 5 years following operations performed with TCA between 1972 and 1976. These patients were compared with three control groups: (1) 19 patients with similar defects but operated upon using moderate hypothermia and continuous cardiopulmonary bypass (CPB); (2) 16 children who were the siblings of the TCA patients; and (3) 14 children who were the siblings of the CPB patients. The hypothermic temperatures reached were closely clustered around 15 degrees C in the TCA group and 28 degrees C in the CPB group. TCA time ranged from 22 to 71 minutes. Statistical analysis, which included, t test, chi square test of association, and Wilcoxon test, showed that the only baseline characteristic which differed between the two patient groups in respect to age at operation, age at testing, and preoperative physiological variables (level of cyanosis, weight, oxygen saturation, and hemoglobin concentration) was weight (p = 0.03). The mean score of the TCA group (91 +/- 4.0, SE) was significantly lower (p = 0.002) than that of their siblings (106 +/- 4.1, SE). The score for the CPB patients (102 +/- 5.2, SE) was not demonstrably different from that of their siblings (96 +/- 5.9, SE). The sibling and patient (TCA) IQ differences were associated with duration of arrest in verbal (p = 0.06), quantitative (p = 0.07), and general cognitive (p = 0.003) scores. A decrease of 0.53 point per minute of arrest time was estimated for the entire group of 31 patients; that is, in the 19 patients with siblings, for each minute increase in circulatory arrest time, the patients dropped 0.69 IQ point below their siblings. These results and analysis of other published data do not support the generally accepted view that TCA can be used entirely without penalty. We question the accepted "safe" limit of circulatory arrest of 60 minutes.
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PMID:Duration of circulatory arrest does influence the psychological development of children after cardiac operation in early life. 664 88

Two siblings, a boy and a girl, with agenesis of the corpus callosum, apneic spells, attacks of apnea, cyanosis and spontaneous hypothermia, are reported about. Both children died after a few months of life. Postmortem examination revealed a severe spongiosis of the white matter in addition to the agenesis of the corpus callosum and septum pellucidum, in both cases.
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PMID:Familial agenesis of the corpus callosum with hypothermia and apneic spells. 673 18

Forty-eight pediatric open heart surgical procedures were performed with bloodless techniques regardless of surgical complexity or presence of cyanosis at the Children's Hospital of Buffalo. Priming solution for cardiopulmonary bypass was reduced to avoid excessive hemodilution, and careful surgical techniques were used to minimize blood loss. Hypothermia compensated for decreased oxygen-carrying capacity and made it possible to reduce bypass flow safely. Tissue perfusion and oxygenation on bypass appeared comparable to or better than those in a control group that underwent open heart surgery with milder degrees of hemodilution. All patients tolerated bypass uneventfully without transfusion. Platelet counts were higher and blood loss less marked than those in the control group. Prevention of excessive dilution by priming solution seemed most important for preservation of platelets and subsequent hemostasis. Four of the smaller infants with complex cyanotic defects needed postoperative transfusion, while 44 patients did not receive transfusion at all during their hospital stay. Total blood product requirement was reduced from 11.5 to 0.35 units per patient. Intracardiac surgery without transfusion is possible in most pediatric patients without evidence of increased risk.
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PMID:Total bloodless open heart surgery in the pediatric age group. 674 68


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