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

Diabetic ketoacidosis may be associated with a wide variety of complications, some of which are uncommon and not widely appreciated. A case of severe ketoacidosis with multiple complications including septicaemia, pneumomediastinum, gastro-intestinal haemorrhage, magnesium depletion and multiple mononeuropathy is reported in a 17-year old girl who made a successful recovery. The patient had not taken insulin for almost 4 days, had no preceding illness and was admitted in a near moribund state with hypothermia (34.2 degrees C), hypotension (80/50) and an arterial pH less than 6.8. There was a leukocytosis 41,200, the blood culture grew haemolytic streptococci and chest radiology showed pneumomediastinum. I.v. therapy was continued for some days and the patient developed clinical features of magnesium depletion. During the recovery period she developed multiple mononeuropathy. A brief review of these complications is given.
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PMID:Multiple complications in severe diabetic ketoacidosis. A short review of the literature. 82 Dec 84

Diabetes mellitus is accompanied by a variety of alterations in metabolic, cardiovascular, and neuronal function. This paper provides a comprehensive review of the ways in which these pathophysiological aspects of diabetes may impair thermoregulatory function. The influence of diabetic neuropathy and vasculopathy on the control of peripheral blood flow is reviewed and the additional effects of changing levels of blood glucose and insulin are discussed. Both hypoglycaemia and diabetic ketoacidosis are associated with hypothermia, but the reasons for this in ketoacidosis are not clear. Impairment of heat conservation may contribute to and could be a consequence of autonomic neuropathy. The final section of the paper describes a study of our own in which metabolic stability was maintained by infusing insulin intravenously before and during the determination of the thermoregulatory responses to acute cold stress. Under these conditions, there was impairment of reflex vasoconstriction in the limbs of diabetics with neuropathy. This failure to reduce heat loss resulted in half the diabetics with neuropathy shivering in response to moderate cooling, which in some subjects was accompanied by a fall in core temperature. Diabetics without neuropathy and nondiabetics neither shivered nor dropped core temperature.
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PMID:Diabetes mellitus and thermoregulation. 330 96

Serial serum amylase and blood glucose levels were measured in 68 hypothermic (rectal temperature 35 degrees C or less) patients, including 15 who had hypothermic myxoedema (serum protein bound iodine 3.5 mug/100 ml or less). Raised amylase levels were found in 34 patients and probably reflected a mild acute pancreatitis. The high amylase levels correlated with low arterial PO(2) levels and significantly with high arterial PCO(2) levels and the base deficit but not with the severity or duration of the hypothermia. The acute pancreatitis does not explain why hypothermic patients with myxoedema have a poorer prognosis than those who are euthyroid. The pancreatitis occasionally contributed to the development, sometimes delayed, of diabetic ketoacidosis, blood glucose levels of over 120 mg/100 ml being found in 20 patients. There was a significant correlation between the raised serum amylase levels and the hyperglycaemia. Hypoglycaemia, sometimes profound, was found in 12 patients.
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PMID:Acute pancreatitis and diabetic ketoacidosis in accidental hypothermia and hypothermic myxoedema. 412 1

A 41-year-old woman with severe juvenile diabetes mellitus suffered from profound hypothermia after loss of thermoregulation in diabetic ketoacidosis. She was found unconscious, without measurable blood pressure; the electrocardiogram (ECG) showed bradycardia of 30 min and the rectal temperature was 23.7 degrees C. The patient received mechanical ventilation, fluid therapy, warmed gastric lavage, and, unfortunately, inotropic medication. She was transferred to a department of cardiac surgery in order to continue the therapy with cardiopulmonary bypass (CPB). On arrival, the patient had a rectal temperature of 27.3 degrees C, the ECG showed an absolute arrhythmia with a frequency of 70/min, and the blood pressure was 63/43 mmHg. We decided to use a rapidly available but not highly invasive venovenous hemofiltration technique for slowly rewarming the patient. Vascular access was achieved by percutaneous femoral vein cannulation with a Shaldon catheter. The hemofiltration system (Gambro AK-10, Gambro AB, Sweden) was instituted with a blood flow rate of 200 ml/min. The hemofiltration monitor controls the pumps for filtering and substituting fluid volumes and allows the infusion solutions to be heated up to 40 degrees C. Sinus rhythm resumed without antiarrhythmic medications at a temperature of 29.5 degrees C, and within 8 h the patient was rewarmed to 35.5 degrees C. After treatment of the adult respiratory distress syndrome caused by pneumonia, she was discharged from the intensive care unit to complete treatment with no evidence of any permanent organ damage. We conclude that hemofiltration may be the method of choice for rewarming deeply hypothermic patients when their circulation is preserved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic coma with deep hypothermia. Successful resuscitation with hemofiltration]. 784 Apr 4

The purpose of this study was to determine if the ketone body beta-hydroxybutyrate (beta-HBA) is a useful positive marker for sudden deaths in chronic alcoholics, thought to be due to hypoglycemia. Beta-HBA can be reliably measured in postmortem samples of vitreous humour and urine. In fatalities where there is a history of chronic alcoholism and routine investigations, including autopsy and routine toxicology, yield only a fatty liver as positive findings, a raised level of beta-HBA can be used as an indicator for alcoholic ketosis. Alcoholic ketosis is often associated with antemortem hypoglycemia. Caution should be observed in attributing the significance of ketosis exclusively to alcohol in those conditions where it would otherwise be expected (i.e. diabetic ketoacidosis and chronic starvation). A measurement of this marker of alcoholic ketosis may also help in the investigation of cases where hypothermia or alcohol withdrawal fits are suspected.
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PMID:The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. 830 32

We report a rare case of hypothermia with acute renal failure in a patient suffering from diabetic nephropathy. A 71-year-old male who had been receiving insulin therapy for the treatment of diabetes mellitus complicated with advanced diabetic nephropathy since 1998 was malnourished with an extremely decreased muscle mass. Without any prolonged exposure to excessively low external temperatures or hypothyroidism, pituitary insufficiency, adrenal insufficiency, sepsis, hypoglycemia, and diabetic ketoacidosis, acute hypothermia appeared together with an aggravation of diabetic nephropathy. His skin temperature fell to below measurable levels and his rectal temperature fell to 30.0 degrees C. His consciousness was drowsy and the hypothermia was not accompanied by shivering. Skeletal muscle is known to play an important role as a center of heat production and shivering thermogenesis in skeletal muscle mainly operates on acute cold stress. Therefore, in this case, hypothermia may have occurred because the shivering thermogenesis could not fully act on the acute cold stress due to the dramatically reduced muscle mass. We should always keep in mind that older, malnourished diabetic patients can easily suffer from impairments of the thermoregulatory system.
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PMID:Hypothermia with acute renal failure in a patient suffering from diabetic nephropathy and malnutrition. 1080 30

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

We describe a case of bacteremic, leukopenic pneumococcal pneumonia with respiratory failure, accompanied by diabetic ketoacidosis and hypothermia. Pulmonary leukostasis may play a role in the pathogenesis of the acute respiratory distress syndrome (ARDS) in pneumococcal pneumonia. The patient recovered with mechanical ventilation, intravenous antibiotics, pulse-steroid therapy, and continuous hemodiafiltration (CHDF). In particular, administration of steroid and the use of CHDF may improve the status of pulmonary leukostasis in leukopenic pneumococcal infection.
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PMID:Bacteremic and leukopenic pneumococcal pneumonia: successful treatment with antibiotics, pulse steroid, and continuous hemodiafiltration. 1237 89

Hypothermia usually occurs because a patient has been exposed to a cold environment; however, a number of nonenvironmental conditions may produce hypothermia. This report relates the clinical course of a patient whose hypothermia was due to severe diabetic ketoacidosis. In addition, we review the causes of hypothermia and Osborn waves beyond exposure to cold temperature. Hypothermia due to diabetic ketoacidosis is an uncommon complication of a common disease that carries with it clinically significant consequences. Accordingly, we believe that all clinicians should be aware of this potential complication of diabetic ketoacidosis and should be able to recognize the importance of the electrocardiogram in such patients.
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PMID:Osborn waves in the electrocardiogram, hypothermia not due to exposure, and death due to diabetic ketoacidosis. 1467 8

Rhabdomyolysis, a term used to describe the rapid breakdown of striated muscle, is characterized by rupture and necrosis of muscle fibers. This process results in the release of cell breakdown products into the bloodstream and extracellular space. Although direct muscle injury remains the most common cause of muscle injury, additional causes include hereditary enzyme disorders, drugs, toxins, endocrinopathies, malignant hyperthermia, neuroleptic malignant syndrome, heatstroke, hypothermia, electrolyte alterations, diabetic ketoacidosis and non-ketotic hyperosmolar coma, severe hypo- or hyperthyroidism and bacterial or viral infections. The classic triad of symptoms includes muscle pain, weakness and dark urine, although more than 50% of the patients do not complain of muscle pain or weakness. Additional systemic symptoms include fever, general malaise, tachycardia, nausea and vomiting. The laboratory diagnosis is based essentially on the measurement of creatine kinase in serum or plasma. Plasma and urine myoglobin measurement might be useful in the early stages of the syndrome and for identifying a subset of patients with minor skeletal muscle injury. Patient monitoring is pivotal (the mortality rate is as high as 8%), and should be focused on preventing the detrimental consequences, that often include renal disease and coagulopathy. In the pre-hospital setting, forced hydration with 1.5-2 L of sterile saline solution should be started immediately, followed by 1.5-2 L/h. Following hospital admission, continuous hydration should be ensured, alternating the saline solution with a 5% glucose solution. In the presence of myoglobinuria, urine should be alkalinized by use of sodium bicarbonate solution. Clin Chem Lab Med 2010;48:749-56.
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PMID:Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. 2044 60


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