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

The effect of mild to moderate hypothermia (32/27 degrees C) was analyzed on the cell volume of C6 glioma cells and primary cultured astrocytes at normal pH, during lactacidosis (pH6.2) and during exposure to glutamate or arachidonic acid in vitro. The cells were suspended in an incubation chamber under continuous control of pH, pO2 and temperature. Cell swelling was quantified by an advanced Coulter-system. Following a control period at 37 degrees C, the ambient temperature was decreased to 27 and 32 degrees C for 30 min. Hypothermia alone led to an immediate and significant cell volume increase of 107.3 +/- 0.4% (mean +/- SEM) of control after 30 min at 32 degrees C. Yet, hypothermia (27 degrees C) afforded partial protection against the acidosis-induced cell swelling at pH 6.2, attaining 120.4 +/- 0.9% in the normothermic control group after 60 min, while only 111.3 +/- 0.9% at 27 degrees C. Hypothermia, however, was not associated with a reduction of the glutamate- or arachidonic acid-induced cell swelling. The results demonstrate that mild hypothermia per se induces glial cell swelling, but simultaneously inhibits cell swelling from acidosis, while not from glutamate- or arachidonic acid.
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PMID:Glial cell swelling--effect of hypothermia. 1049 43

We present the case of a patient with profound alcohol-related lactic acidosis (lactate = 16.1 mmol/L; pH = 6.67) associated with a multitude of metabolic derangements who made a remarkable recovery following aggressive management. The patient was in extremis upon arrival in the emergency department (ED), and resuscitation was begun immediately. While in the ED, the problem list generated included: acute alcohol intoxication, severe lactic acidosis, dehydration, hypothermia, hypoglycemia, acute renal insufficiency, and hepatic failure. Resuscitation continued in the intensive care unit with remarkable improvement and satisfactory outcome. In this patient, the severe lactic acidosis and associated abnormalities were all attributed to acute and chronic effects of ethanol. A brief summary of the proposed mechanism by which these metabolic derangements developed and an outline of her management follows.
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PMID:Survival from profound alcohol-related lactic acidosis. 1815 81

This study was done to determine the effects of hypothermia on brain cell membrane function and energy metabolism after transient hypoxia-ischemia (HI) in the newborn piglet. Cerebral HI was induced by temporarily complete occlusion of bilateral common carotid arteries with surgical clips and simultaneous breathing with 8% oxygen for 30 min, followed by release of carotid occlusion and normoxic ventilation for 4 hr. Rectal temperature was maintained between 38.0 and 39.0 degrees C in normothermic groups, and between 34.0 and 35.0 degrees C in hypothermic groups for 4 hr after HI. During HI, heart rate, glucose and lactate level in the blood and cerebrospinal fluid increased, and base excess, pH and blood pressure decreased significantly in both normothermic and hypothermic groups. After HI, these abnormalities returned to normal in normothermic group, but lactic acidosis persisted in hypothermic group. Decreased cerebral Na+,K+- ATPase activity and increased lipid peroxidation products, indicative of HI- induced brain injury, were more profound in hypothermic group than in normothermic group. Brain ATP and phosphocreatine levels were not different between normothermic and hypothermic groups. In summary, hypothermia applied immediately after HI for 4 hr did not improve the recovery of brain cell membrane function and energy metabolism in the newborn piglet.
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PMID:Effect of hypothermia on brain cell membrane function and energy metabolism after transient global hypoxia-ischemia in the newborn piglet. 1141 Jun 96

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

Survival after extreme arterial acidosis is uncommon. A case of metformin induced lactic acidosis is described where the presenting pH was 6.38 exacerbated by hypothermia (29 degrees C). Increased anion gap acidosis, its varied aetiology, potential reversibility, and the role of hypothermia are discussed. Early liaison with a medical toxicology unit is recommended when this rare condition is suspected.
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PMID:Recovery from pH 6.38: lactic acidosis complicated by hypothermia. 1190 73

Metformin belongs to a class of drugs known as the biguanides that are widely used in the treatment of type 2 diabetes mellitus. Its association with lactic acidosis is well established, although rare. Metformin-associated lactic acidosis is recognized as a potentially lethal condition that can occur in patients with contraindications to the drug, such as renal dysfunction, liver diseases, alcoholism, and cardiopulmonary diseases. In these cases, the plasma concentration of metformin is not necessarily abnormally high. We describe a 75-year-old diabetic woman with acute renal failure and life-threatening lactic acidosis due to metformin intoxication. Clinical manifestations included vomiting, diarrhea, hypothermia, hypotension and transitory blindness. Her initial renal function was recovered after hemodialysis and she was discharged 3 months after admission.
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PMID:Metformin-associated lactic acidosis and acute renal failure in a type 2 diabetic patient. 1460 17

Lactic acidosis is a recognised complication of the antihyperglycaemic biguanide agent metformin, especially in patients with renal failure. We report a case of severe lactic acidosis and hypothermia due to metformin treatment and renal impairment. The favourable outcome despite extremely unfavourable clinical signs and symptoms for survival after admission and initial treatment was unexpected. Specific aspects of the clinical course are addressed.
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PMID:Unexpected survival from severe metformin-associated lactic acidosis. 1470 12

A 15-year-old female with short intestine syndrome due to chronic intestinal pseudo-obstruction associated with kidney failure underwent a multivisceral (stomach-duodenum-jejunum-ileum-pancreas-liver) and kidney transplant. She had required parenteral nutrition for the last 5 years, with numerous complications such as sepsis from the central catheter, deep venous thrombosis, severe liver dysfunction, pancytopenia due to bone marrow failure, and severe malnutrition. Surgery lasted 15 hours and was free of complications other than hypothermia, which worsened after revascularization of the grafts. Replacement of 6 units of blood products and crystalloids was required. Biochemical and hemodynamic variables were stable, apart from the development of hypernatremia, hyperglycemia, and lactic acidosis. The anesthetic approach included preoperative assessment of problems related to chronic parenteral nutrition (liver dysfunction, coagulopathy, and restricted venous access), the prevention of hypothermia, correction of electrolyte imbalance and the acid-base status, treatment of reperfusion syndrome, and the replacement of fluids and blood products to maintain circulatory homeostasis and assure sufficient splanchnic perfusion.
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PMID:[Anesthesia for a pediatric multivisceral transplant]. 1507 2

Three important issues concerning homeostasis in the acute care of trauma patients that are related directly to the stress response are hyperglycemia, lactic acidosis, and hypothermia. Recently, there has been a resurgence of interest in investigating the effects of aggressive thermal and glucose concentration and volume resuscitation on outcomes in critically ill and trauma patients. Significant reason exists to question the "conventional wisdom" relating to current approaches to restoring homeostasis in this patient population.
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PMID:Trauma and aggressive homeostasis management. 1740 Jan 55

Cardiopulmonary bypass (CPB) is widely used to maintain systemic perfusion and oxygenation during open-heart surgery. Tissue hypoperfusion with resultant lactic acidosis during CPB, may occur during hypothermia, extreme haemodilution, low flow CPB, and excessive neurohormonal activation. There has been no documentation of the correlation between blood lactate level elevations in the perioperative period, and its relation to preoperative New York Heart Association (NYHA) classification and the use of ionotropic support during weaning from CPB, duration of postoperative ventilatory support and perioperative mortality. We studied the perioperative blood lactate levels in 82 patients undergoing valvular heart surgery. Arterial blood samples were collected at different stages of CPB. The observed mean baseline lactate levels were 1.9+/-0.8 mmol/L (normal range of 0.9 to 1.7 mmol/L). The mean circulating lactate levels at 15 min and 45 min after institution of CPB increased to 7.01+/-2.6 mmol/L and 9.92+/-3.5 mmol/L. A progressive decline in the mean lactate level, was seen during rewarming (at 35 degrees C), immediately off-bypass, 24 hours and 48 hours postoperatively with mean lactate levels being 7.01+/-3.2 mmol/L, 4.75+/-1.01 mmol/L, 3.06+/-1.1 mmol/L, and 2.10+/-1.05 mmol/L respectively. Comparison of mean lactate levels in NYHA class I, II, III, and IV patients showed that in the intraoperative period and immediately after CPB, the elevation in lactate levels were statistically significant (p< 0.001) in patients in NYHA Class IV. However the values, in all classes, were similar at 24 and 48 hours after CPB. Also, patients with lactate levels >4 mmol/ L required prolonged inotropic and ventilatory support.
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PMID:Blood lactate levels during cardiopulmonary bypass for valvular heart surgery. 1782 85


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