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

Thyroid storm is a rapid decompensation of severe hyperthyroidism which can best be described by the three criteria of hyperthermia, tachycardia and altered mental state with severe agitation. There has to be a precipitating factor such as infection, iodine contamination, surgery or even I-131 treatment. Severe hyperthyroidism not fulfilling the criteria of thyroid storm can also be an indication for emergency treatment, particularly in the elderly with heart disease. Suppressed serum TSH and elevated free T4 levels are essential to confirm the diagnosis. When rapidly available, radioiodine uptake of the thyroid can be useful. Therapy aims at rapidly reducing the active circulating hormone pool, hypermetabolic state, tachycardia, and finally hormone synthesis. Thyroid secretion can be blocked by ioipanoic acid or ipodate while hypermetabolic state can be reduced with beta-blockers or calcium channel-blockers. Treatment of hyperthyroidism in patients with iodine contamination is a real therapeutic challenge. Myxoedema coma, a complication of severe hypothyroidism, is defined by hypothermia (rectal temperature less than 36 degrees C), bradycardia, slow mentation, precipitating factor such as infection or drug overdose, and increased serum creatine phosphokinase levels. Diagnosis of severe hypothyroidism should be confirmed by serum measurements of TSH and free T4. Treatment consists of general supporting measures including rewarming, correction of serum electrolyte disturbances, and adequate alimentation. Thyroid hormone treatment should initially be aggressive using either 300-400 micrograms of T4 or 20-40 micrograms of T3 intravenously. Cortisone therapy may be added. Patients should be under close monitoring as arrhythmias and myocardial infarction are frequent complications of myxoedema coma and/or its treatment with thyroid hormones.
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PMID:Thyroid emergencies. 173 98

A case of hypopharyngeal lipoma is reported and the fundamental role of C.T. in the diagnosis of laryngo-pharyngeal neoplastic pathologies is emphasized. Laryngoscopy made it quite easy to detect the lesion, showing the smooth surface of a large tumor, although it proved difficult to explore the lower portion because of the narrowing of the larynx. Thermography showed a hypothermia area in the right neck region but did not offer any further information. Only C.T. made correct identification of the site and extension of the lesion possible. It was also possible to identify its fat composition, as suggested by the typical density pattern. The tumor presented a homogeneous hypodense structure and its limits were well defined throughout their entire extension. Furthermore, it was possible to rule out any macroscopic infiltration of the adjacent cartilaginous surfaces of the larynx. The latter feature was confirmed by the C.T. images obtained after intravenous administration of an iodine contrast medium and was consistent with the hypothesis of a benign lesion. Thus the lesion could be considered a lipoma; a highly uncommon non-epithelial tumor of the hypopharyngeal region but which occurs more frequently than liposarcoma. Nonetheless, such C.T. tissue characterization requires histological support so as to prevent distinguishing a well differentiated liposarcoma only after recurrence. The greatest likelihood for accurate diagnosis lies in complete utilization of the data derived from the entire diagnostic procedure. The direct laryngoscopy of the lesion is very important as it makes it possible to inspect the surface and first evaluate any anatomo-pathological alterations. Nonetheless, the most extensive information is provided by C.T.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lipoma of the hypopharynx: role of computerized tomography in the diagnosis protocol]. 239 26

The susceptibility of lung tissue to ischemia-reperfusion injury has made distant procurement of heart-lung allografts difficult. The effects of hypothermia, ventilation without perfusion, and various reperfusion solutions (PSS/Ficoll or whole blood) on the development of ischemia-reperfusion lung injury were investigated. Use of an ex vivo rat lung model in which the above variables were individually varied permitted a direct approach for these studies. Normothermic ischemia for 1 hour caused significant damage, documented by increased iodine 125 bovine serum albumin (125I-BSA) in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Hypothermic (4 degrees C) ischemia for 4 hours in lungs reperfused with salt solution and for as many as 12 hours in lungs reperfused with whole blood caused no significant increase in 125I-BSA in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Lungs ventilated without perfusion showed no increase in 125I-BSA leakage compared with controls. The ex vivo rat lung model is excellent for studying ischemia-reperfusion injury. It is reproducible, allows for variance of reperfusion solutions, and permits change in temperature and ventilation easily.
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PMID:Hypothermia or continuous ventilation decreases ischemia-reperfusion injury in an ex vivo rat lung model. 265 79

Treatment of palmoplantar hyperhidrosis was carried out with a conventional galvanic generator in 40 patients and with a newly developed iontophoresis apparatus, which is suited for home treatment, in 31 patients. The new apparatus is operated by a rechargeable energy source or by batteries and is disconnected from the electrical net during treatment. It conforms to most recent safety regulations as approved by Underwriter's Laboratory. Hyperhidrosis was completely controlled after 10-12 treatments as revealed by quantitative gravimetric measurements of sweat rates and semiquantitative estimation of starch iodine paper imprints. There was no apparent difference in efficacy between the two apparatuses. Not only hyperhidrosis was abolished, but associated symptoms, such as lividity of palms or soles, acral hypothermia and edema of fingers or toes, also subsided. Skin temperature on palms rose from 29.7 +/- 1.8 degrees C before treatment to 32.2 +/- 1.4 degrees C thereafter. Maintenance treatment was continued on an average for 14 months, in 4 patients for more than 3 years. No loss of efficacy was found during that period. Side effects were minimal and depended upon amperage used. Only slight discomfort during treatment and mild short-lasted skin irritation were observed. Long-term side effects did not occur.
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PMID:Long-term efficacy and side effects of tap water iontophoresis of palmoplantar hyperhidrosis--the usefulness of home therapy. 365 60

The photomotogram (P.M.G.) of the Achilles tendon reflex was studied in 26 patients with hypothermia (rectal temperature 33.3 degrees C or less), 10 of whom also had myxoedema (serum protein bound iodine 2.8 mug/100 ml or less). No reflex could be elicited in eight (31%) of these patients, including three of those with myxoedema. Hypothermia increases both the contraction and the relaxation times of the reflex, the relaxation phase being particularly prolonged in those with myxoedema. In those patients from whom the reflex was elicited the ratio of the contraction time to the "half-relaxation time" in the P.M.G. was less than unity in six of the seven with myxoedema, and considerably greater than unity in eight of the 11 (73%) who were euthyroid. Thus, analysis of the Achilles tendon reflex P.M.G. correctly predicted the thyroid status in 14 of the 18 hypothermic patients in whom the Achilles tendon reflex was present (78%). The wider use of this rapid test of thyroid function would allow a more rational use of thyroid hormones in hypothermic patients and so lead to a better assessment of their value.
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PMID:Achilles tendon reflex in accidental hypothermia and hypothermic myxoedema. 412 92

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

Intraoperative hypothermia has become a common occurrence. Postoperative rewarming often is accompanied by shivering and results in increased metabolic and circulatory demands. We examined the metabolic, hemodynamic, and biochemical variables in 2 groups of hypothermic (greater than 35.8 degrees C) patients requiring mechanical ventilation after a major operation. One was observed during routine medical management whereas the other group received 40 mg of metocurine iodide and then observed during routine medical management. All patients were allowed to rewarm passively. O2 consumption (VO2, ml/min, STPD), CO2 production (VCO2, ml/min, STPD) and respiratory quotient (RQ) measurements were made every 15 min using a Beckman Metabolic Measurement Cart. Esophageal temperature, arterial blood pressure, heart rate (HR), rate pressure product, CVP, arterial blood gases, serum lactate concentration, and duration of shivering also were recorded. Suppression of the shivering by metocurine increased rewarming time significantly and decreased VCO2, VO2, HR, rate pressure product, mean arterial pressure (MAP), and the O2 cost of rewarming. Thus, the elimination of shivering during postoperative rewarming is associated with a decrease in caloric, metabolic demands and myocardial work (as assessed by the rate pressure product) while rewarming time is prolonged. In the postoperative, hypothermic, critically ill patient, suppression of the shivering response in selected patients may be indicated.
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PMID:Physiologic requirements during rewarming: suppression of the shivering response. 640 3

A 48-year-old woman with a known history of hypothyroidism was admitted to the intensive care unit with a diagnosis of thyroid storm secondary to acute thyroid hormone poisoning and the possible hyperfunction of a singular thyroid nodule. Her clinical manifestations included pyrexia, tachycardia, tachypnea, hypertension, RUQ abdominal pain, psychotic behavior, and pharyngitis. She was successfully treated with sodium iodide, PTU, propranolol, antibiotics, and a hypothermia mattress, with her serum T4 level returning to normal range prior to discharge. The patient was discharged 9 days after admission in good medical health with no medication. This article clearly shows that the functions of the endocrine system remain a frontier in today's medicine. With research, perhaps one day we might fully understand the intricate pathophysiology that results in thyroid storm. The potential problem format has been utilized in the development of the nursing care plan to assist the nurse with identifying and defining her patient's problems, as well as directing her assessment and nursing intervention. As more is learned about thyroid storm, nurses should update their knowledge so that they will be prepared to care for the patient with these difficult nursing problems.
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PMID:Thyroid storm--a nursing crisis. 655 51

The effects of pyridine-2 aldoxime methyl iodide (PAM), N-methyl-1,6-dihydro-pyridine-2-carbaldoxime hydrochloride (proPAM), and diisopropyl phosphorofluoridate (DFP) on performance of a conditioned avoidance response (CAR), body temperature, and in vivo acetylcholinesterase (AChE) activity in five brain regions in the rat were examined. Sublethal doses of DFP (1.5 to 2.5 mg/kg, IP) markedly degraded CAR performance. This effect was antagonized by 5 mg/kg, subcutaneously injected (SC) atropine. A 50 mg/kg, SC dose of PAM had no effect on the CAR, but an equal dose of proPAM caused a transient deterioration of performance. Given 10 min or 2 hr after DFP, 50 mg/kg proPAM initially exacerbated the behaviorally toxic effects of DFP. Neither PAM nor proPAM antagonized DFP-induced hypothermia. PAM did not reactivate DFP-inhibited brain AChE, and proPAM reactivated it by only 6 to 12% of control activity.
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PMID:Effects of PAM, proPAM, and DFP on behavior, thermoregulation, and brain AChE in rats. 717 95

The cellular and molecular mechanisms of hypoxic/ischemic neurodegeneration are sensitive to numerous factors that modulate the time course and degree of neuronal death. Among such factors is hypothermia, which can dramatically protect neurons from injury. To examine and control for temperature-dependent effects, we developed a technique that provides for a high-throughput, accurate, and reproducible determination of the time course and degree of neurotoxicity in cultured cortical neurons at precisely defined temperatures. We used a fluorescence multiwell plate scanner, modified by us to permit the control of temperature, to perform serial quantitative measurements of propidium iodide (PI) fluorescence in cortical neuronal cultures exposed to excitotoxic insults. In validating this approach, we show that these time course measurements correlate highly with manual counts of PI-stained cells in the same cultures (r = 0.958, p < 0.0001) and with lactate dehydrogenase release (r = 0.964, p < 0.0001). This method represents an efficient approach to mechanistic and quantitative studies of cell death as well as a high-throughput technique for screening new neuroprotective therapies in vitro.
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PMID:Determination of the time course and extent of neurotoxicity at defined temperatures in cultured neurons using a modified multiwell plate fluorescence scanner. 914 28


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