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

This report describes the case of an 88-year-old non-diabetic female who presented to the emergency department following a presumed hypoglycaemic collapse due to self-neglect. Subsequent rewarming and resuscitation demonstrated a number of the significant consequences of severe hypothermia, including apparent secondary impairment of glycaemic autoregulation. The phenomenon of reversible inhibition of insulin secretion due to severe hypothermia has been documented previously in the field of cardiac surgery. The hyperglycaemia was not treated with any antihyperglycaemic agent, and her recovery was uneventful. Subsequent blood sugar level monitoring was normal. If insulin is administered to the hypothermic patient, intensive monitoring of blood glucose is essential due to the increase in endogenous insulin secretion on rewarming.
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PMID:Failure of normal glycaemic regulation in a patient with severe hypothermia. 1621 6

The new CPR guidelines are based on a scientific consensus which was reached by 281 international experts. Chest compressions (100/min, 4-5 cm deep) should be performed in a ratio of 30:2 with ventilation (tidal volume 500 ml, Ti 1 s, FIO2 if possible 1.0). After a single defibrillation attempt (initially biphasic 150-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min. Endotracheal intubation is the gold standard; other airway devices may be employed as well depending on individual skills. Drug administration routes for adults and children: first choice IV, second choice intraosseous, third choice endobronchial [epinephrine dose 2-3x (adults) or 10x (pediatric patients) higher than IV]. Vasopressors: 1 mg epinephrine every 3-5 min IV. After the third unsuccessful defibrillation attempt amiodarone IV (300 mg); repetition (150 mg) possible. Sodium bicarbonate (1 ml/kg 8.4%) only in excessive hyperkalemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider atropine (3 mg) and aminophylline (5 mg/kg). Thrombolysis during spontaneous circulation only in myocardial infarction or massive pulmonary embolism; during CPR only during massive pulmonary embolism. Cardiopulmonary bypass only after cardiac surgery, hypothermia or intoxication. Pediatrics: best improvement in outcome by preventing cardiocirculatory collapse. Alternate chest thumps and chest compression (infants), or abdominal compressions (>1-year-old) in foreign body airway obstruction. Initially five breaths, followed by chest compressions (100/min; approximately 1/3 of chest diameter): ventilation ratio 15:2. Treatment of potentially reversible causes (4 "Hs", "HITS": hypoxia, hypovolemia, hypo- and hyperkaliemia, hypothermia, cardiac tamponade, intoxication, thrombo-embolism, tension pneumothorax). Epinephrine 10 microg/kg IV or intraosseously, or 100 microg (endobronchially) every 3-5 min. Defibrillation (4 J/kg; monophasic oder biphasic) followed by 2 min CPR, then ECG and pulse check. Newborns: inflate the lungs with bag-valve mask ventilation. If heart rate<60/min chest compressions:ventilation ratio 3:1 (120 chest compressions/min). Postresuscitation phase: initiate mild hypothermia [32-34 degrees C for 12-24 h; slow rewarming (<0.5 degrees C/h)]. Prediction of CPR outcome is not possible at the scene; determining neurological outcome within 72 h after cardiac arrest with evoked potentials, biochemical tests and physical examination. Even during low suspicion for an acute coronary syndrome, record a prehospital 12-lead ECG. In parallel to pain therapy, aspirin (160-325 mg PO or IV) and in addition clopidogrel (300 mg PO). As antithrombin, heparin (60 IU/kg, max. 4000 IU) or enoxaparine. In ST-segment elevation myocardial infarction, define reperfusion strategy depending on duration of symptoms until PCI (prevent delay>90 min until PCI). Stroke is an emergency and needs to be treated in a stroke unit. A CT scan is the most important evaluation, MRT may replace a CT scan. After hemorrhage exclusion, thrombolysis within 3 h of symptom onset (0.9 mg/kg rt-PA IV; max 90 mg within 60 min, 10% of the entire dosage as initial bolus, no aspirin, no heparin within the first 24 h). In severe hemorrhagic shock, definite control of bleeding is the most important goal. For successful CPR of trauma patients, a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation, and excessive ventilation pressure may impair outcome in severe hemorrhagic shock. Despite bad prognosis, CPR in trauma patients may be successful in select cases. Any CPR training is better than nothing; simplification of contents and processes remains important.
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PMID:[The new 2005 resuscitation guidelines of the European Resuscitation Council: comments and supplements]. 1691 4

The medical work load seems to increase both with heat and humidity, and with cold and rainy conditions. Heat tolerance during exercise is variable and heat intolerance may contribute to collapse and increase medical encounters. Exposure to cold, wet conditions results in increasing incidence of hypothermia in exhausted marathon runners. Finish-line encounters and course dropouts increase as conditions cool and warm away from the most advantageous conditions in the 4.4-15 degrees C (40-59 degrees F) wet bulb globe temperature (WBGT) range. The risk of requiring medical attention and not finishing rises considerably when the WBGT is >15.5 degrees C (60 degrees F). Comparing the correlation coefficients of the Boston Marathon and Twin Cities Marathon data suggests that the risks of medical problems and not finishing are associated with the warmest temperature of the race and not the start temperature. The community consequences of races conducted in hot and humid conditions can be significant, particularly when the WBGT is >15.5 degrees C. The emergency medical systems can be overwhelmed with a surge of patients, some very ill, and the emergency call response times drop to unacceptable levels blocking access for the citizens of the community. With respect to marathon encounters, heat stress increases both the finish-line medical encounter rate and the on course drop-out rate, and seems to increase the incidence of hyponatraemia and heat stroke. Cold conditions increase the drop-out rate along the course and, if associated with wet conditions, also increase the encounter rate.
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PMID:Heat and cold: what does the environment do to marathon injury? 1746 19

Carnitine-acylcarnitine translocase (CACT) deficiency is a rare disorder that results in long-chain fatty acids being unavailable for mitochondrial beta-oxidation and ketogenesis. It can present in the neonatal period or infancy with a severe clinical form, typically with convulsions, hypothermia, encephalopathy, cardiomyopathy and liver dysfunction, or with a milder phenotype with episodes of hypoglycaemia and hyperammonaemia during intercurrent illness. Investigations show hypoketonaemia, intermittent dicarboxyluria and hypocarnitinaemia with grossly elevated acylcarnitines. Enzyme assay or DNA analysis confirms the diagnosis. The severe phenotype results in severe disability or death. The less severe phenotype can also cause significant disability secondary to hypoglycaemia and/or hyperammonaemia at presentation. We report the outcome of two siblings with CACT deficiency. The index patient presented at the age of 2 months during a respiratory illness with hypoglycaemia, hyperammonaemia and cardiorespiratory collapse. Acylcarnitine profiles showed decreased free carnitine but striking elevations of long-chain acylcarnitines. Urine organic acids showed dicarboxylic aciduria. Fatty acid oxidation studies showed reduced oleate and myristate oxidation. His acylcarnitine profile normalized after he was started on a medium-chain triglyceride (MCT) low-fat diet and carnitine supplementation. Low CACT activity on enzyme assay confirmed the diagnosis. He has resulting profound developmental delay and epilepsy. The sibling was prospectively treated with a low-fat MCT diet and carnitine supplementation. Acylcarnitine profile at birth also showed elevated long-chain acylcarnitines. Fatty acid oxidation studies confirmed the diagnosis. To date he has normal development and has not had any significant periods of hypoglycaemia or hyperammonaemia.
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PMID:Prospective treatment in carnitine-acylcarnitine translocase deficiency. 1750 64

A 77-year-old male, who had undergone the Bentall procedure 27 years ago, was admitted to our hospital for the repair of postoperative pseudoaneurysm. This was the 3rd repair, and the pseudoaneurysm was close to the sternum. Total extracorporeal circulation was established with femorofemoral cannulation and sternotomy was performed under deep hypothermia. During sternotomy, we encountered massive hemorrhage due to injury of the aortic graft. We coped effectively with the situation utilizing temporary circulatory arrest. Aortic graft reimplantation was performed under continuous retrograde cerebral perfusion. Collapse of the suture line of the left coronary orifice was recognized and was reconstructed. The patient was discharged uneventfully on the 26th postoperative day.
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PMID:[The third repair for pseudoaneurysm following Bentall procedure: report of a case]. 1787 17

Rewarming patients from accidental hypothermia are regularly complicated with cardiovascular instability ranging from minor depression of cardiac output to fatal circulatory collapse also termed "rewarming shock". Since altered Ca2+ handling may play a role in hypothermia-induced heart failure, we studied changes in Ca2+ homeostasis in in situ hearts following hypothermia and rewarming. A rat model designed for studies of the intact heart in a non-arrested state during hypothermia and rewarming was used. Rats were core cooled to 15 degrees C, maintained at 15 degrees C for 4h and thereafter rewarmed. As time-matched controls, one group of animals was kept at 37 degrees C for 5h. Total intracellular myocardial Ca2+ content ([Ca2+]i) was measured using 45Ca2+. Following rewarming we found a significant reduction of stroke volume and cardiac output compared to prehypothermic control values as well as to time-matched controls. Likewise, we found that hypothermia and rewarming resulted in a more than six-fold increase in [Ca2+]i to 3.01+/-0.43 micromol/g dry weight compared to 0.44+/-0.05 micromol/g dry weight in normothemia control. These findings indicate that hypothermia-induced alterations in the Ca2+-handling result in Ca2+ overload during hypothermia, which may contribute to myocardial failure during and after rewarming.
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PMID:Myocardial mechanical dysfunction and calcium overload following rewarming from experimental hypothermia in vivo. 1798 15

Knowledge of the pathophysiology in accidental hypothermia is essential for clinical decision-making. The prognosis should be favourable provided the condition is recognized and treated accordingly. Progressive organ dysfunction is associated with a declining core temperature which is reversible on rewarming. Other reactions occur during rewarming of which rewarming collapse has received much attention. More detailed knowledge of rewarming collapse which has come out is examined in this paper.
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PMID:[Pathophysiology in accidental hypothermia. Hypothermia is not only a cold body]. 1803 55

Death due to hemorrhage from ruptured peripheral varicose veins is an uncommon event. A review of the files of Forensic Science SA (FSSA) in Adelaide, South Australia, was undertaken over a 10-year period from January 1996 to December 2005 for such cases. A total of 8 cases were found out of a total of 10,686, representing <0.01% of autopsy cases. The male to female ratio was 1:3, with an age range of 58-84 years (mean = 78 years). The victims were all located at their home addresses, where they had been alone at the time of their deaths. Scene investigations revealed considerable blood loss, with pooling around the victims' bodies, and also in other parts of the house, particularly the bathroom/toilet areas. Four ulcers were of an acute perforative type and 2 were of a chronic ulcerative type. In 2 cases, bleeding followed trauma. Toxicologic evaluation was performed in only 3 of the cases, revealing blood alcohol levels of 0.06% and 0.14% in 2 cases, respectively. A further victim had been prescribed anticoagulant drugs for an unrelated condition. Additional findings of significance were ischemic heart disease in 3 cases and deep venous thrombosis of the calf veins on the side of the fatal hemorrhage in another case (with no evidence of pulmonary thromboembolism). One victim had acute gastric erosions, suggesting that hypothermia following collapse played a role in the terminal event. Autopsy evaluation of such cases should include careful layer dissection of the area of hemorrhage to confirm the presence of the ruptured varix and to enable directed histologic sampling.
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PMID:The incidence and characteristic features of fatal hemorrhage due to ruptured varicose veins: a 10-year autopsy study. 1804 15

In a morning in January, a male in his early sixties was found dead in an outdoor parking area. The minimum temperature during the night before he was found dead was estimated to be 4.0 degrees C. Autopsy revealed the pinkness of hypostasis, slight abrasions and bruises on the face and the extremities, collapse of the lungs, and slight gastric submucosal hemorrhage. Histologic examination revealed compact arrangement of cardiac muscle fibers and cytoplasmic vacuolation in the adenohypophysis. Toxicologic examination demonstrated hyperacetonemia (51.2 microg/mL). Ubiquitin, one of the stress proteins that are induced by several stimuli, including severe cold, was detected in several organs. We concluded that the cause of his death was lethal hypothermia. In addition, hemorrhages were observed in the subfascial and/or intramuscular parts of the pectoralis minor, first intercostal, and iliopsoas muscles. Although it has been reported that iliopsoas muscle hemorrhage can result from hypothermia, there have been few reports concerning hypothermia-associated hemorrhages of the pectoralis minor and/or intercostal muscles. We presumed that intense shivering and/or effort ventilation during the course of lethal hypothermia might cause these muscle hemorrhages.
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PMID:A fatal case of hypothermia associated with hemorrhages of the pectoralis minor, intercostal, and iliopsoas muscles. 1804 25

Our intensive care unit has been treating comatose patients, following an out-of-hospital cardiac arrest, with therapeutic hypothermia since 2002. In all, 139 out-of-hospital cardiac arrest patients were admitted in the 4-year period 2002-5. Of these, 27% had a favourable outcome (discharged home or to rehabilitation). Forty-one per cent of patients presenting with ventricular fibrillation (VF) and 7% of non-VF patients had a favourable outcome. No patient with an estimated time from collapse to first attempt at cardiopulmonary resuscitation over 12 min survived to hospital discharge. Twenty-two per cent of patients over 70 years were discharged home, suggesting age was not a barrier to surviving out-of-hospital cardiac arrest. The introduction of a therapeutic hypothermia clinical pathway, at the end of 2003 improved the efficiency of cooling. The percentage of patients cooled to below 34 degrees C within 4 h increased from 15 to 51% and those cooled for more than 12 h increased from 30 to 83%.
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PMID:Therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest. 1869 3


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