Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this work is to summarize the experience in treatment of patients with acute destructive pancreatitis and to carry out comparative analysis of the results of "open" and "closed" types of the treatment for this disease. 233 patients of the study group underwent surgery which demanded parietal deperitonization and mobilization of the pancreas from the retroperitoneal space, drainage of all parts of retropancreatic bat and drainage of biliary tracts, total continuous retroperitoneal neuro-vegetative blockade, local hypothermia and omentobursostomy with further regular elective pancreosequesf8p4omies and sanation of the cavity of the omental bursae with local sorbtion--dehydration therapy. The number of the days of inhospital stay in the study group made up 43.5 +/- 3.3, and in the control group--64.2 +/- 4.1 (p < 0.05). The level of postoperative complications in the study group made up 36.6%, in control group--85.1%, lethality being 18.2 and 50.0%, respectively. In the study group long-term unfavourable follow-up results were obtained only in 2.9% of patients, whereas in control group--in 31.6%.
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PMID:[Surgical treatment of acute necrotizing pancreatitis]. 1062 83

Heat-shock proteins (HSPs) function in the cellular response to injury. Increased expression of these proteins was first described in response to hyperthermia, although their production may be prompted by a variety of metabolic insults. HSPs protect cellular proteins from degradation. The self-limited pancreatitis induced by hyperstimulation with supramaximal doses of cerulein is accompanied by increased HSP expression. It may be that HSPs serve a protective function in pancreatitis. We hypothesized that hyperthermia-induced production of HSP-70 would improve survival in a lethal murine model of necrotizing pancreatitis. Necrotizing pancreatitis was induced in two groups of 30 female Swiss Webster mice by feeding them a choline-deficient diet supplemented with 0.5 g% ethionine (CDE) for 72 hours. Immediately before initiation of the CDE diet, the core body temperatures of the mice in the experimental group were elevated to 42 degrees C for 12.5 minutes. Twenty mice from each group were killed after 24 hours. Pancreata were harvested, and pancreatic proteins were extracted from half of the pancreata. HSP-70 was assessed according to a standard Western blotting protocol. The remaining pancreata were used to make histologic comparisons. Serum interleukin 6 and tumor necrosis factor-alpha were determined by enzyme-linked immunosorbent assay (ELISA). Survival was determined by observation of the remaining mice. HSP-70 was expressed in pancreatic protein from all mice exposed to hypothermia but in none of the mice subjected to the CDE diet alone. Mortality was significantly reduced in mice pretreated with hyperthermia compared with control mice (p < 0.05). Survival in the hyperthermia group was 80%, whereas in the control group it was 30%. Hyperthermia resulted in expression of pancreatic HSP-70 in mice. Hyperthermia also reduced mortality in this lethal murine model of necrotizing pancreatitis. It is plausible that a causal relationship exists between HSP-70 production and improved survival in this model.
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PMID:Hyperthermia induces heat-shock protein expression, reduces pancreatic injury, and improves survival in necrotizing pancreatitis. 1097 4

The most important risk factors and findings of acute accidental hypothermia and concomitant local frostbites are reviewed. Both external and internal risk factors are usually present when exposure to cold is leading to death. The external factors are alcohol and psychic drugs, too light a clothing for the circumstances and wetness. Important internal factors are leanness, physical exhaustion and traumas in young persons and illnesses and degeneration of physiological heat conserving and production responses at old age. The signs caused by cold on the body are variable. In immersion hypothermia cases there are almost no changes, since the death occurs rapidly, most frequently from drowning. On the victims of dry frost first degree congelations, showing up as purple oedematic skin areas or spots, can be observed on the face and extremities. Stress ulcerations or haemorrhages in the stomach mucosa develop in ca. 70% of dry hypothermia cases. In long lasting exposures to cool temperature haemorrhagic pancreatitis, lung oedema and myxomatous skin oedema have been the characteristic signs. Frostbites developing concomitantly with fatal hypothermia show only oedema and hyperaemia, but no blisters or inflammation in the skin, which are the most conspicious vital reactions of frostbites after thawing.
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PMID:Some aspects on death in the cold and concomitant frostbites. 1099 30

End-stage renal disease remains the primary indication for the use of peritoneal dialysis. The therapy, however, has been used for the treatment of various other clinical conditions. Evidence has accumulated to support the use of peritoneal dialysis to maintain euvolemia, to improve functional status, and to reduce hospitalizations in patients with intractable chronic congestive heart failure. The use of peritoneal dialysis as a modality for core rewarming in patients with severe hypothermia has been established; in selected circumstances, it is probably the therapy of choice. The field of oncology has borrowed heavily from the technique of peritoneal dialysis for administering intraperitoneal chemotherapy; even though the therapy remains largely experimental today, it has great future potential. While efficacious in the treatment of acute, diuretic-resistant volume overload in patients with congestive heart failure and in patients with severe, disabling psoriasis, the introduction of alternative methods of management have rendered the use of peritoneal dialysis obsolete. Finally, the role of peritoneal lavage in the management of patients with pancreatitis remains controversial and is no longer routinely used.
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PMID:Peritoneal dialysis in adult patients without end-stage renal disease. 1104 64

Peritoneal dialysis is a technique that has been used to treat acute renal failure in humans since 1923. Peritoneal dialysis is used in people to manage acute and chronic renal failure, as well as to remove dialyzable toxins (ethylene glycol, barbiturates, and ethanol), reduce severe metabolic disturbances, and for the treatment of peritonitis, pancreatitis, uroabdomen, hypothermia, and fluid overload. In veterinary medicine, acute renal failure is the prevailing indication for dialysis. This report will discuss the pathophysiology of peritoneal dialysis, indications, and contraindications. Catheter selection and placement will be reviewed. Types of dialysate solution will be discussed and the protocol established for instituting peritoneal dialysis. The report will conclude with a discussion of potential complications and methods to minimize them.
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PMID:Peritoneal dialysis in emergency and critical care medicine. 1110 14

It is well recognized that acetaminophen overdose can cause severe hepatic injury. However, extra-hepatic manifestations may also develop following inappropriate use or ingestion of large amounts of acetaminophen. We present a 44-y-o female who manifested coma, metabolic acidosis, shock, hypothermia, hyperglycemia, rhabdomyolysis, hepatotoxicity, and renal insufficiency after suicidal ingestion of an unknown amount of acetaminophen. Although her consciousness and hemodynamic status gradually improved after treatment with N-acetylcysteine and other supportive measures, she was found to have pancytopenia, pancreatitis and hepatorenal failure during the hospitalization and eventually died 18 d post-admission. Review of relevant literature reports and the clinical findings in our patient suggests that direct toxic effects mediated by acetaminophen or its metabolites were most likely responsible for most of the observed clinical features.
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PMID:Pancytopenia, hyperglycemia, shock, coma, rhabdomyolysis, and pancreatitis associated with acetaminophen poisoning. 1175 93

A number of investigators have demonstrated that the preinduction of heat-shock protein (HSP) expression (particularly HSP60 and HSP72) by hyper- or hypothermia may have a protective effect against cerulein-induced acute pancreatitis. The aim of the present study was to induce HSPs in the pancreas and lungs by thermal (hot-water immersion, HWI) and nonthermal methods (injection of sodium arsenite intraperitoneally) and to investigate the potential effects of HSP preinduction on cholecystokinin-octapeptide (CCK) induced acute pancreatitis and pancreatitis-associated lung injury in rats. The dose-response and time-effect curves observed following HWI and sodium arsenite treatments were evaluated. Animals were injected with 3 x 75 microg/kg CCK subcutaneously at intervals of 2 hr at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were killed by exsanguination through the abdominal aorta 2 or 6 hr after the last CCK injection. HWI and the injection of sodium arsenite significantly elevated the expression of HSP72 in the pancreas and lungs, whereas they did not influence the levels of HSP60. Overall, HWI pretreatment had a protective effect against CCK-induced pancreatitis and pancreatitis-associated lung injury. In contrast, the nonthermal preinduction of HSP72 by sodium arsenite did not result in any beneficial effects on the measured parameters of the disease. The findings suggest that the preinduction of HSP72 is not sufficient to protect against CCK-induced acute pancreatitis and pancreatitis-associated lung injury or that the beneficial effect of hyperthermia may not be exclusively related to HSP72 expression.
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PMID:Induction of HSP72 by sodium arsenite fails to protect against cholecystokinin-octapeptide-induced acute pancreatitis in rats. 1214 22

Among the rarer causes of acute pancreatitis listed in surgical texts is hypothermia. To assess the evidence for cause and effect, we questioned selected consultants about their experience and examined the case-notes of patients admitted with hypothermia. The 31 consultants who returned our questionnaire (69% response rate; 317 consultant-years' experience) could recall only 5 cases of pancreatitis associated with hypothermia, in 2 of which other aetiological factors were judged primary. In case-notes for 100 months of emergency admissions at a single hospital we identified 310 patients with hypothermia and 1153 with acute pancreatitis; none had the dual diagnosis. Of the hypothermic patients, none had abdominal pain typical of acute pancreatitis. In 43 serum amylase was measured because the patient was unable to give a full history and in 2 of these the enzyme was slightly raised; both had experienced a cerebrovascular accident, which is a known cause of hyperamylasaemia. Considered alongside the weak evidence from previous studies, these findings offer negligible support for the idea that hypothermia is a clinically relevant risk factor for acute pancreatitis.
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PMID:Hypothermia and acute pancreatitis: myth or reality? 1272 32

Ethanol concentrations were measured in femoral venous blood in deaths attributed to acute alcohol poisoning (N = 693) or chronic alcoholism (N = 825), according to the forensic pathology report. Among acute alcohol poisonings were 529 men (76%) with mean age 53 years and 164 women (24%) with mean age 53 years. In the chronic alcoholism deaths were 705 men (85%) with mean age 55 years and 120 women (15%) with mean age 57 years. The blood-ethanol concentrations were not related to the person's age (r = -0.17 in acute poisonings and r = -0.09 in chronic alcoholism). The distribution of blood-ethanol concentrations in acute poisoning cases agreed with a normal or Gaussian curve with mean, median, standard deviation, coefficient of variation, and spread of 0.36 g/100 mL, 0.36 g/100 mL, 0.086 g/100 mL, 24% and 0.074 to 0.68 g/100 mL, respectively. The corresponding concentrations of ethanol in chronic alcoholism deaths were not normally distributed and showed a mode between 0.01 and 0.05 g/100 mL and mean, median, and spread of 0.172 g/100 mL, 0.150 g/100 mL, and 0.01 to 0.56 g/100 mL, respectively. The 5th and 95th percentiles for blood-ethanol concentration in acute poisoning deaths were 0.22 and 0.50 g/100 mL, respectively. However, these values are probably conservative estimates of the highest blood-ethanol concentrations before death owing to metabolism of ethanol until the time of death. In 98 chronic alcoholism deaths (12%) there was an elevated concentration of acetone in the blood (>0.01 g/100 mL), and 50 of these (6%) also had elevated isopropanol (>0.01 g/100 mL). This compares with 28 cases (4%) with elevated blood-acetone in the acute poisoning deaths and 22 (3%) with elevated blood-isopropanol. We offer various explanations for the differences in blood-ethanol and blood-acetone in acute poisoning and alcoholism deaths such as chronic tolerance, alcohol-related organ and tissue damage (cirrhosis, pancreatitis), positional asphyxia or suffocation by inhalation of vomit, exposure to cold coupled with alcohol-induced hypothermia, as well as various metabolic disturbances such as hypoglycemia and ketoacidosis.
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PMID:Comparison of blood-ethanol concentration in deaths attributed to acute alcohol poisoning and chronic alcoholism. 1287 10

After inconspicuous pregnancy and birth, a 16-year-old mother presented her male baby 5 days later with severe diarrhoea and vomiting. During the following weeks, the child temporarily showed hypotension, hypothermia and increased body temperature, bradyarrythmia with apnoea, continuing diarrhoea, sometimes vomiting and developed signs of pancreatic insufficiency. Due to increasing loss of weight and obviously severe dystrophia, parenteral nutrition had to be initiated. All clinical investigations revealed no underlying disease. Numerous biopsies, mainly from the gastrointestinal tract were taken, but no relevant pathological findings were disclosed. The baby was found lifeless by his mother, 4 months after birth. According to the death certificate, the physicians regarded the lethal outcome as a case of sudden infant death syndrome (SIDS). Histological and immunohistochemical investigations of organ samples revealed signs of myocarditis, pancreatitis and focal pneumonia. Molecularpathological techniques were used to detect enterovirus RNA from tissue samples from the myocardium, liver and pancreas. Enteroviral myocarditis with concomitant pancreatitis was determined as cause of death.
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PMID:Lethal enterovirus-induced myocarditis and pancreatitis in a 4-month-old boy. 1641 Jan 53


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