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

The use of high-dose corticosteroids in the treatment of severe sepsis and septic shock remains controversial. Our study was designed as a prospective, randomized, double-blind, placebo-controlled trial of high-dose methylprednisolone sodium succinate for severe sepsis and septic shock. Diagnosis was based on the clinical suspicion of infection plus the presence of fever or hypothermia (rectal temperature greater than 38.3 degrees C [101 degrees F] or less than 35.6 degrees C [96 degrees F]), tachypnea (greater than 20 breaths per minute), tachycardia (greater than 90 beats per minute), and the presence of one of the following indications of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels, or oliguria. Three hundred eighty-two patients were enrolled. Treatment--either methylprednisolone sodium succinate (30 mg per kilogram of body weight) or placebo--was given in four infusions, starting within two hours of diagnosis. No significant differences were found in the prevention of shock, the reversal of shock, or overall mortality. In the subgroup of patients with elevated serum creatinine levels (greater than 2 mg per deciliter) at enrollment, mortality at 14 days was significantly increased among those receiving methylprednisolone (46 of 78 [59 percent] vs. 17 of 58 [29 percent] among those receiving placebo; P less than 0.01). Among patients treated with methylprednisolone, significantly more deaths were related to secondary infection. We conclude that the use of high-dose corticosteroids provides no benefit in the treatment of severe sepsis and septic shock.
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PMID:A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. 330 74

From November 1, 1982 through December 31, 1985, there were 19 centers and 382 patients that evaluated the effect of methylprednisolone sodium succinate (MPSS) on the septic syndrome. Seventeen of these centers enrolled 304 patients in a prospective, randomized, double-blind, placebo-controlled study to determine if early treatment with MPSS would decrease the incidence of severity of the adult respiratory distress syndrome (ARDS) in patients at risk of ARDS from sepsis. To ensure early institution of the MPSS or placebo therapy (PLA), patients with the presumptive diagnosis of sepsis were identified. That diagnosis was based on the presence of fever or hypothermia (temperature greater than 38.3 degrees C or less than 35.5 degrees C, rectal), tachypnea (greater than 20 bpm), tachycardia (greater than 90 bpm) and the presence of one of the following indices of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels or oliguria. The treatment, either MPSS 30 mg/kg or PLA, was given in four 20-minute infusions six hours apart and was initiated within two hours of the presumptive diagnosis of sepsis. The development and reversal of the adult respiratory distress syndrome (ARDS) was followed and resulted in data on 304 of the 382 randomized patients. A trend toward increased incidence of ARDS was seen in the MPSS group 50/152 (32 percent) compared to the placebo group 38/152(25 percent) p = 0.10. Significantly fewer MPSS patients reversed their ARDS 15/50 (31 percent) compared to placebo 23/38 (61 percent) p = 0.005. The 14-day mortality in patients with ARDS treated with MPSS was 26/50 (52 percent) compared to placebo 8/22 (22 percent) p = 0.004. We conclude that early treatment of septic syndrome with MPSS does not prevent the development of ARDS. Additionally, MPSS treatment impedes the reversal of ARDS and increases the mortality rate in patients with ARDS.
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PMID:Early methylprednisolone treatment for septic syndrome and the adult respiratory distress syndrome. 331 78

A newborn female child with hypothermia, tachypnoea and poor Agpar scores was demonstrated to have absent septum pellucidum, partial agenesis of the corpus callosum and misshapen left lateral ventricle on ultrasound examination. Fundoscopic examination noted hypoplastic optic discs. Given the appropriate clinical setting and fundoscopic examination, cranial ultrasound can be the preliminary evaluation for septo-optic dysplasia and related anomalies in infants with open fontanelles.
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PMID:Ultrasound evaluation of septo-optic dysplasia in the new born. Report of a case. 354 Jul 12

Hypoplasia of the lungs is the cause of the high mortality of newborns with diaphragmatic hernia. Survival depends mainly on the development of the contralateral lung. Eighty percent of diaphragmatic hernias are postolateral hernias of the left side. The most serious postoperative complication is a relapse into fetal circulation with increased pulmonary vascular resistance and right-to-left shunting (Fig. 2). The clinical signs of diaphragmatic hernia are cyanosis and tachypnea. Intermittent suction via a nasogastric tube and early intubation without mask ventilation should be performed. The inspiratory pressure should not exceed 25 cm H2O to minimize the risk of pneumothorax. Survival of the baby is unlikely if the initial blood gas analysis shows pH less than 7.10, pO2 less than 50 mmHg, and pCO2 greater than 65 mmHg. Hypothermia should be strictly avoided because it leads to increased oxygen consumption. Intraoperative monitoring should include a precordial stethoscope, ECG, blood pressure, and rectal temperature. Anesthesia is maintained with fentanyl 0.02-0.03 mg/kg body wt. and pancuronium 0.08-0.1 mg/kg. One dose of atropine (0.02 mg/kg) is administered before fentanyl. Intraoperative ventilation is performed by hand or by use of a Siemens Servo ventilator. Thirty newborns were anesthetized for repair of a congenital diaphragmatic hernia with no intraoperative complication and an overall mortality of 27%.
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PMID:[Anesthesia for congenital diaphragmatic hernia]. 363 96

A single oral dose of levamisole hydrochloride given at the rate of 12 mg/kg was believed responsible for bradycardia, tachypnea, hypothermia, cerebrocortical depression, and diarrhea in a dog. Supportive treatment and symptomatic treatment for the bradycardia were required for 4 days. In addition to these previously reported abnormalities associated with levamisole toxicosis, cerebrocortical depression and multiple foci of irritation were characterized by electroencephalography.
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PMID:Levamisole toxicosis in a dog. 375 34

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83

1. The hypothermic effect on unanaesthetized cats of tetrodotoxin injected I.V. or into the lateral cerebral ventricle was examined.2. At an ambient temperature (T(a)) of 22 degrees C, tetrodotoxin given intraventricularly was over 400 times more potent in lowering body temperature (T(b)) than when given I.V. The magnitude of the hypothermia was dose-dependent for both routes. Decreases in T(b) as great as 6.8 degrees C were induced by infusions or multiple injections of tetrodotoxin into the ventricle.3. Tetrodotoxin also lowered T(b) at T(a) = 13, 30 or 35 degrees C. Tachypnoea, which lasted for longer durations and which became more intense the higher the T(a), accompanied development of hypothermia. Shivering was observed only during recovery from hypothermia at 13 degrees C.4. During the tetrodotoxin-induced hypothermia, animals were still able to regulate against environmental thermal stresses.5. EDTA disodium salt, leucocytic pyrogen and prostaglandin E(1) antagonized the hypothermic effect of tetrodotoxin when they were administered during recovery from tetrodotoxin.6. Activation of heat-loss mechanisms, and the absence of compensatory shivering during development of hypothermia after tetrodotoxin administration, plus lowering of T(b) by tetrodotoxin at T(a) above as well as below the thermoneutral temperature, indicate that lowering of the thermoregulatory set-point is the mechanism by which centrally or peripherally administered tetrodotoxin lowers T(b). Further evidence for set-point lowering after intraventricular administration of tetrodotoxin is provided by persistence of the ability to regulate against both heat and cold stresses during hypothermia. The possibility that the decrease in set-point could be due to the well known action of tetrodotoxin to block transient increases in membrane sodium ion conductance is discussed in terms of a recent hypothesis regarding ionic control of the thermoregulatory set-point.
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PMID:The hypothermic effect of tetrodotoxin in the unanaesthetized cat. 419 99

1. Injections of tetrodotoxin or saxitoxin (25 ng in 0.10 ml.) into a lateral cerebral ventricle caused deep body temperature of cats to fall approximately the same amount (2 degrees C) whether the animals were resting in the cold (4 degrees C) or were responding to escape heat.2. Continuous exposure to heat either prevented the hypothermic response or enhanced the level of tachypnoea required to lower body temperature. Tetrodotoxin also caused hypothermia when an animal was lever pressing to obtain heat in the cold environment.3. These results provide evidence that agents which alter the set-point for physiological thermoregulatory activity produce a complementary shift in the behavioural set-point as well.
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PMID:Complementary lowering of the behavioural and physiological thermoregulatory set-points by tetrodotoxin and saxitoxin in the cat. 483 4

Snake bite was diagnosed in 125 dogs and 115 cats over 10 years. Young sporting dogs and young cats were mainly affected. More dogs (48%) were seen in contact with tiger snakes than cats (7%). One hundred and four (84%) dogs and 89 (76%) cats were bitten in the warmer months of the year (October to March). As the incidence rose in September/October, dogs were bitten on days when the temperature was near 20 degrees C or over. The commonest presenting signs were dilated pupils and absences of pupillary light reflex. Dyspnoea, hypothermia, hindleg ataxia and glycosuria were common features in cats. Vomiting, tachypnoea, hyperthermia and complete flaccid paralysis were often seen in dogs. The overall recovery rate after administering antivenene was 90% for cats and 83% for dogs. Death from anaphylaxis as a result of giving antivenene occurred in 3 cats and one dog. Dogs treated soon after being bitten recovered more rapidly. There was no correlation between the bite-to-treatment period and the treatment-to-recovery period for cats.
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PMID:Clinical features therapy and epidemiology of tiger snake bite in dogs and cats. 649 4

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


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