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

To study the cerebral protective effects of hypothermia in arterial hypoxia, anesthetized (70% N2O), mechanically ventilated rats were cooled to a body temperature of 27 C. Hypoxia was induced by decreasing the oxygen content in the inspired gas mixture either to 6-7 per cent or to 2.5-3 per cent. This reduced mean PaO2 to about 25 and 11-12 torr, respectively. At PaO2 torr, there was no change in cerebral blood flow (CBF), cerebrla oxygen consumption (CMRO2), or labile tissue metabolites. The absence of signs of cerebral hypoxia could be attributed to an effect of temperature and pH on the hemoglobin-oxygen dissociation curve. Thus, at 27 C with a PaO2 of 25 torr the total oxygen content (TO2) of arterial blood remained greater than 15 ml (100 ml)-1, about three times the value obtained at this PO2 in normothermic rats. At PaO2 11-12 torr, arterial TO2 was reduced to about 5 ml (100 ml) (-1). The hypoxia induced no change in CMRO2, a threefold increase in CBF, a moderate lactacidosis in the tissue, and a small decrease in phosphocreatine content, but no change in ATP, ADP, or AMP. These changes are less marked than those occurring at the same arterial TO2 in normothermic rats. It is concluded that hypothermia exerts a pronounced protective effect on the brain in hypoxic hypoxia, and that two mechanisms are involved. First, since hypothermia shifts the oxyhemoglobin-dissociation curve towards the left, and prevents or minimizes a rightward shift due to acidosis, it maintains a high TO2 in arterial blood at a given PaO2. Second, by reducing CMRO2, and thereby presumably also cellular energy requirements, hypothermia exerts a protective effect at the cellular level.
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PMID:Protective effect of hypothermia in cerebral oxygen deficiency caused by arterial hypoxia. 0 Sep 30

During 1969-77, 20 episodes of severe hypothermia occurred in 19 diabetic patients in Nottingham. Thirteen were associated with ketotic hyperosmolar coma, two with lactic acidosis, and one with hypoglycaemia, while in four there was no loss of diabetic control. Ketoacidosis accounted for 11.8% of all admissions for severe accidental hypothermia and was a commoner cause than hypothyroidism (8%). Patients with ketoacidosis were younger and developed hypothermia as often during the summer as during the winter. The metabolic disturbance was characteristic, with severe acidosis (mean pH 7.04), a high blood glucose concentration (mean 56.6 mmol/l; 1020 mg/100 ml), and high plasma osmolality (mean 379.7 mmol (mosmol)/kg). Eight of the 13 episodes proved fatal. Hypothermia may aggravate ketoacidosis and complicate treatment and should be sought in all patients with severe diabetic coma.
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PMID:Hypothermia: a complication of diabetic ketoacidosis. 10 2

Sixteen cases of lactic acidosis are reported: 7 phenformin treated diabetes, 5 cardiovascular diseases (2 myocardial infractions, 2 pulmonary embolisms, 1 heart failure). In 2 patients no etiology was found. Concomittant renal failure or liver diseases were found in respectively 9 and 4 cases. Patients presented the usual criteria of lactic acidosis: clinical, polypnea, severe hypotension (9/16), peripheral symptoms of shock (12/16), hypothermia (9/16), abdominal pain (9/16): biologically, acidosis (pH = 6,99 +/- 0,01, HCO3- = 5,9 +/- 1,5 mmol), hyperlactatemia (14,1 +/- 3,6 mmol/l) with hig lactate/pyruvate ratio (105 +/- 73), and anion gap (24,3 +/- 4,2 mmol/l). Sodium bicarbonate infusion was performed in all cases (2,5 to 42 mmol/kg). Few cases required volhemic expansion or furosemid induced diuresis. One patient was treated with extrarenal dialysis. 13 patients were alkalinised with less than 185% of estimated deficit measured from alkalin reserve: 12 died. 3 patients received 185% more than this deficit, associated with furosemid (1,8 to 12,5 mg/kg): only one patient died ten days after by casual disease, with lactatemia of 3,2 mmol/l. In spite of the small number of patients, these findings suggest that an early and massive alkalinisation, with large doses of furosemid, can improve the severe lactic acidosis prognosis.
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PMID:[Lactic acidosis and intensive care. 16 cases (author's transl)]. 23 77

In a prospective study, patients who had an ejection fraction of 40% or more and who were undergoing elective coronary artery operation were randomly divided into three groups that differed in the method of anaerobic substrate enhancement during cardiopulmonary bypass. Group 1, the controls (n = 157), received no additional glucose, insulin, and potassium solutions and experienced immediate spontaneous defibrillation (10%), transmural myocardial infarction (10.3%), malignant ventricular arrhythmias (26%), and severe atrial arrhythmias (20%). Group 2 (n = 120) received a bolus of hypertonic glucose, insulin, and potassium in the pump perfusate before aortic cross-clamping. In this group, the rate of spontaneous defibrillation was 41%, of transmural infarction, 8.3%, of malignant ventricular arrhythmias, 31%, and of severe atrial arrhythmias, 19%. Group 3 (n = 114) had the aortic root continuously infused with glucose, insulin, and potassium solution at 4 degrees C during aortic cross-clamping. This group was significantly improved; the rate of spontaneous defibrillation was 60%, there were no transmural myocardial infarctions and the incidence of severe atrial arrhythmias was 6% and that of malignant ventricular arrhythmias, 5%. It is proposed that the superior clinical results in Group 3 resulted from better myocardial preservation achieved by more efficient means of providing continuous anaerobic substrate, coronary washout, and elution of lactic acidosis, uniform global hypothermia, and direct supplemental myocardial potassium in addition to mere cardioplegic effects.
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PMID:Reduction of intraoperative myocardial infarction by means of exogenous anaerobic substrate enhancement: prospective randomized study. 31 65

Lactic acidosis is defined as a state of metabolic acidosis (arterial pH below 7.36) due to an increase in the blood concentration of lactate above 2 mEq/l. Lactic acidosis may occur under a variety of conditions; the biguanide-induced lactic acidosis is due to the toxic effects of biguanides (buformin, metformin, phenformin). The clinical picture is characterized by the occurrence of disturbances of consciousness, severe acidosis with Kussmaul's respiration, shock, hypothermia and in about 30% of all cases hypoglycemia. Apart from the general principles of intensive medical care, therapy should comprise correction of the acid-base-disturbances and elimination of the offending biguanide. The efficacy of hemodialysis in the treatment of biguanide-induced lactic acidosis is difficult to evaluate. By a more sensible use of biguanides, lactic acidosis secondary to drug administration should become a rare event.
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PMID:[Lactic acidosis--a possible complication in buformin-treated diabetics (author's transl)]. 71 13

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.
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PMID:Fatal self-administration of sodium azide. 114 58

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.
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PMID:[Acid-base disturbances in surgical operation]. 143 18

The rapid infusion system (RIS), which can deliver fluids/blood products rapidly at precise rates and normothermic conditions, was compared with conventional fluid administration (CFA) in a randomized study of 36 hypovolemic trauma patients. Admission stratification criteria of the groups were similar relative to age, Glasgow Coma Score (GCS), Injury Severity Score (ISS) and plasma lactate. Despite the lack of difference in blood loss between the 24-h survivors of the two groups, the CFA group required greater total fluids (23.6/20.21), red blood cells (5.5/4.61), fresh frozen plasma (FFP) (2.8/1.91), platelets (523/204 ml), and crystalloids (12.9/10.61). Lactate levels were lower in the RIS group at virtually all times from hours 1 to 24 (4.3/5.3 mM/l, t-value = 3.3, DF = 279, P = 0.001). Post-admission hypothermia was greater in the CFA group at all times during the first 24 h (35.2/36.4 degrees C, t-value = 5.6, DF = 250, P = 0.001). The mean partial thromboplastin time was significantly higher in the CFA group (47.3/35.1 s, t-value = 3.1, DF = 279, P = 0.002). The PTT and PT were related to the degree of lactic acidosis (P = 0.0001) and hypothermia (P = 0.001) but not to the amount of FFP given (P = 0.14). The hospital costs, days in the ICU, and days on the ventilator were greater for the CFA group, as was the incidence of pneumonia (0/11 vs. 6/17; P = 0.03). Hypovolemic trauma patients resuscitated with the RIS needed fewer fluid/blood products and had less coagulopathy; more rapid resolution of hypoperfusion acidosis; better temperature preservation; and fewer hospital complications than those resuscitated with conventional methods of fluid/blood product administration.
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PMID:The rapid infusion system: a superior method for the resuscitation of hypovolemic trauma patients. 165 23

When rats were administered methyl isocyanate (MIC) by inhalation or subcutaneous route it produced severe hyperglycemia, clinical lactic acidosis, highly elevated plasma urea, and reduced plasma cholinesterase activity with unaltered erythrocyte acetyl cholinesterase activity. Irrespective of the route of administration, MIC also caused severe hypothermia, which was not ameliorated by prior administration of atropine sulphate. Acute toxic effects of MIC are essentially similar by either route except for the intensity of the effects.
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PMID:Acute toxicity of methyl isocyanate in mammals. II. Induction of hyperglycemia, lactic acidosis, uraemia, and hypothermia in rats. 235 32


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