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)

Cold-reactive proteins, such as cold agglutinins, cryoglobulins, and cryofibrinogens, are reversibly precipitates, or gel, upon exposure to cold temperatures. Cryoglobulins are usually not of importance, but under special conditions, such as surgical hypothermia, hyperviscosity and damage in microcirculation may occur in patients with high plasma concentration of cryoglobulins. Several groups have reported their efforts to reduce further the risks of surgical hypothermia in patients with cold agglutinins, but rarely in patients with cryoglobulins. A 57-year-old woman with thoracic aneurysm, requiring replacement of the ascending aorta and the aortic arch, had mixed cryoglobulinemia (cryocrit 29%) associated with rheumatoid arthritis. Steroids therapy and preoperative plasmapheresis were performed, and cryocrit levels were decreased until 0% before operation. Systemic hypothermia (25 degrees C), hemodilution techniques during cardiopulmonary bypass, and cold crystalloid cardioplegia were successfully employed, and no clinical evidence of microcirculation damage was posed after operation.
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PMID:[A successful case of thoracic aortic aneurysm with mixed cryoglobulinemia]. 150 3

Complex hepatic surgery often requires occlusion of the portal triad in order to decrease parenchymal bleeding. This study was undertaken to evaluate the effects of topical hypothermia and intravenous steroids on liver ischemia by measuring adenosine triphosphate (ATP) levels within the hepatic parenchyma. Forty New Zealand white rabbits were divided into four experimental and four control groups. All experimental animals underwent laparotomy and ligation of the porta hepatis. Serial liver biopsy specimens were obtained at predetermined time intervals. Group I received no further intervention. Group II were topically cooled until intrahepatic temperature reached 30 degrees C. Group III received preligation intravenous methylprednisolone (30 mg/kg). Group IV received both steroids and topical hypothermia. The corresponding control groups underwent laparotomy and isolation of the porta without ligation. Adenosine triphosphate was extracted from the liver parenchyma and quantified by high-performance liquid chromatography (HPLC). The data were analyzed using a three-factor mixed analysis of variance (ANOVA). There was a statistically significant protective effect on ATP levels provided by topical hypothermia at 15 and 30 minutes of ischemia (p < 0.01), but not at 60 minutes (p > 0.05). Steroids were not found to have any protective effect on ATP levels at any time point. The combination of steroids and topical hypothermia provided significant preservation of hepatic parenchymal ATP levels, although less than that of hypothermia alone, at 15 and 30 minutes of ischemia (p < 0.01).
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PMID:The effects of topical hypothermia and steroids on ATP levels in an in vivo liver ischemia model. 793 3

Serum corticosteroid-binding globulin (CBG) levels were measured in children (mean age 4 years) during heart surgery. Considerable decrease in CBG level occurred between baseline examination (416 +/- 39 nM) and the day of surgery (314 +/- 30 nM). Relatively simple closed heart surgery did not influence CBG level with maximal cortisol level being 20 +/- 4 micrograms/dl. Open heart surgery under conditions of profound hypothermia (26 C, without extracorporeal circulation) caused dramatic lowering of CBG level, particularly striking after resuscitation (180 +/- 20 nM). At the same time cortisol level reached extremely high values (78 +/- 8 micrograms/dl). These data suggest that CBG is likely to play an important role in pituitary-adrenal response to surgery under severe conditions of hypothermia and cardiac arrest.
Steroids 1993 Nov
PMID:Serum corticosteroid-binding globulin levels in children undergoing heart surgery. 827 17

Serum corticosteroid-binding globulin (CBG) and cortisol levels as well as subsets of circulating immunocompetent cells (ICCs) were measured during cardiac surgery. Closed heart surgery (closed mitral commissurotomy) resulted in an elevation of cortisol levels (up to 32 +/- 5 micrograms/dL by the end of the surgery) with no changes in CBG and ICC levels observed. Open heart surgery (open reconstruction of the mitral valve) in surface-induced hypothermia (without extracorporeal bypass) caused a dramatic drop in CBG activity (from 250 +/- 17 microM before the beginning of anesthesia to 198 +/- 15 microM by the end of cooling (just before cardiac arrest) and 158 +/- 13 microM after 30 min of reperfusion), whereas cortisol levels were only slightly elevated by the end of cooling, and a significant increase (up to 17 +/- 2 micrograms/dL) was observed only at the end of the surgery (60 min of reperfusion and warming). Similar to CBG, a significant decline in circulating ICC contents occurred in response to cooling and circulatory arrest.
Steroids 1996 Jul
PMID:Corticosteroid and immune responses to cardiac surgery. 883 93

Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. medical management of increased intracranial pressure should include sedation and paralysis, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.
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PMID:Management of intracranial hypertension. 1723 51

Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors. At present, the following types of cerebral edema are differentiated: the vasogenic cerebral edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins; the cytotoxic cerebral edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier; the hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation; the osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephaly. Some authors also differentiate ischemic cerebral edema. At present, when various traumas and traumatic cerebral injuries are frequent causes of death in young people, treatment strategy for cerebral edema is of utmost importance. Monitoring of the patient's condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient--the head should be tilted at 30 degrees in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic-hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na(+)/K(+) ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely.
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PMID:[Cerebral edema and its treatment]. 1732 53

Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased intracranial pressure should include sedation, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.
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PMID:Management of intracranial hypertension. 1851 25