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)

A 71-year-old male was admitted to our hospital for examination of mediastinal abnormal shadow, which was diagnosed aortic arch aneurysm. Once he was discharged and stayed at home for 2 weeks, and then re-admitted for surgery. On the 3rd day of 2nd admission, he suddenly fainted away in the ward and was in shock by hemorrhagic cardiac tamponade. He was transferred to operation room within an hour from onset of rupture. Emergent aortic arch replacement was performed under circulatory arrest with deep hypothermia and retrograde cerebral perfusion. His postoperative course was uneventful without any neurological deficits. Prompt diagnosis and surgery may contribute to improvement of surgical result in patients with ruptured aortic arch aneurysms.
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PMID:[Successful emergent replacement of ruptured aortic arch aneurysm in an inpatient waiting for surgery: report of a case]. 1285 65

A 39-year-old man presented with multiple intracranial cavernous malformations manifesting as intractable seizures persisting for more than 20 years. He underwent gamma knife radiosurgery (GKRS) for right frontal and left temporal cavernous malformations. He began to suffer from progressive left hemiparesis and inattention 2 years 5 months after the GKRS. Magnetic resonance imaging showed abnormal ring enhancement and extensive brain edema around the right frontal lesion. Conservative therapies such as external decompression, low-dose barbiturates, and mild hypothermia had no effect on his clinical status. Stereotactic biopsy of the ring-enhanced area demonstrated gliosis. Signs of cerebral herniation appeared, so we performed partial resection of the right frontal lobe. His symptoms recovered immediately. Subsequent hyperbaric oxygen (HBO) therapy significantly improved the extensive brain edema. Delayed radiation necrosis associated with potentially fatal brain edema may occur after GKRS for cavernous malformations. Internal decompression and subsequent HBO therapy were very effective for the treatment of these lesions.
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PMID:Delayed radiation necrosis with extensive brain edema after gamma knife radiosurgery for multiple cerebral cavernous malformations--case report. 1296 6

W. James Gardner, a skillful neurosurgeon and inventor, is best remembered for his cervical tongs and hydrodynamic theory of syringomyelia. A pioneer of modern neurosurgery, Gardner trained under Charles Frazier in Philadelphia, and in 1929 he moved to Ohio where he became chief of neurosurgery at the Cleveland Clinic, a position he was to hold for the next 33 years. A large surgical practice made it imperative for Gardner to develop surgical methods that were quick, effective, and advantageous for patient and surgeon. He was an early proponent of the sitting position for patients undergoing cranial surgery, which led to the development of a neurosurgical chair with a head fixation device. To reduce the risks of hypotension and air embolism when the patient is in the sitting position, Gardner invented the clinical G suit. He was the first to advocate and use induced arterial hypotension for intracranial surgery and the first neurosurgeon in the US to publish his experiences performing lumbar discography. He converted an operating table so that he could induce hypothermia during aneurysm surgery and then applied pneumatic cuffs to occlude the major arterial supply to the brain. His pioneering work has been documented in many other areas such as hemifacial spasm and trigeminal neuralgia, for which he performed the first vascular decompression, in cervical sympathectomy for treatment of various ailments, and in the use of intrathecally delivered steroid drugs for sciatica. During his career, he authored 256 publications and one book on the dysraphic states. Many of his contributions to the discipline of neurosurgery are now taken for granted.
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PMID:W. James Gardner: pioneer neurosurgeon and inventor. 1513 20

Olanzapine, an atypical antipsychotic, is often regarded as a safe choice for psychosis management. We hereby report an aged case that presented with conscious depression, bradycardia, hypotension, miosis and hypothermia. Olanzapine was thought to be the offending agent. His condition improved with supportive therapy.
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PMID:Severe cardiovascular side effects of olanzapine in an elderly patient: case report. 1515 90

During an open-heart procedure in a 69-year-old man, a damaged mitral valve was being examined when suddenly the venous return line from the oxygenator of the heart-lung machine became filled with gas. After the venous line had been flushed and cardiopulmonary bypass had been reinstated, the line again filled with gas, and the aortic line also had to be clamped to prevent a massive air embolism. The oxygenator was immediately exchanged, bypass was resumed after 7 to 8 minutes, and the surgical procedures were completed. The patient survived, and a year and a half later continues in good health. His survival was attributed to three factors: intraaortic balloon support, hypothermia to 28 degrees C, and the prompt exchange of oxygenators.
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PMID:Full recovery of a patient after oxygenator replacement during open-heart surgery. 1521 68

Hypothermia is an important preservation method for tissues and solid organs. The aim of the present study was to assess in rat cremaster muscle the effect of hypothermia, without or with pre-ischaemic HTK (histidine-tryptophan-ketoglutarate-Bretschneider solution) perfusion, on microvascular consequences of 4 or 6 h ischaemia and 2 h of reperfusion. Intravital microscopy was applied to examine capillary perfusion and leucocyte-endothelium interactions. The cremaster muscle was subjected to 4 or 6 h of cold (4 degrees C) or warm (33-34 degrees C) ischaemia and 2 h of reperfusion. Measurements were performed at baseline, prior to HTK perfusion and ischaemia, and at 0, 1 and 2 h after blood flow restoration. Hypothermia completely prevented the 50% reduction in capillary perfusion that was observed previously at start of reperfusion after 4 h warm ischaemia. After 6 h of warm ischaemia, perfusion resumed in only 45% of capillaries and remained at this low level during reperfusion. In contrast, only a slight decrease (< 10%) in capillary perfusion was observed after 6 h of cold ischaemia. Pre-ischaemic HTK perfusion had no beneficial effect on tissue perfusion. Both hypothermia and HTK attenuated the significant increase in venular leucocyte-vessel wall interactions, which was observed after 4 h of warm ischaemia in a previous study. Combined application of both interventions had no additional effects. After 6 h of warm ischaemia, no increase in leucocyte-vessel wall interactions was observed, possibly due to venular flow reduction. In conclusion, hypothermia preserves capillary perfusion and prevents an increase in leucocyte-vessel wall interactions during reperfusion after muscle tissue ischaemia. Preischaemic perfusion of the vasculature with HTK does not improve the effects of cold storage on tissue perfusion, but attenuates the inflammatory response independently of temperature effect.
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PMID:Effect of hypothermia and HTK on the microcirculation in the rat cremaster muscle after ischaemia. 1561 71

An 11-year-old male was admitted to our hospital because of high-grade fever, repetitive seizures, and prolonged impairment of consciousness (Glasgow coma scale E1, M5, V1). His seizures were repetitive complex partial seizures that expanded from the unilateral face to the corresponding side of the body. He sometimes developed secondary generalized seizures. While most seizures lasted 1 or 2 min, intractable seizures also frequently (about 5 times/h) occurred. We diagnosed him as encephalitis/encephalopathy, and treated him with artificial respiration, thiamylal sodium, mild hypothermia therapy, steroid pulse therapy, massive gamma-globulin therapy, etc. Afterwards, he had sequelae, such as post-encephalitic epilepsy (same seizures continued to recur), hyperkinesia, impairment of immediate memory, change in character (he became sunny and obstinate), dysgraphia, and mild atrophy of the hippocampus, amygdala, and cerebrum. However, he could still attend a general junior high school. He was diagnosed as acute encephalitis with refractory, repetitive partial seizures (AERRPS). In this case, he was positive for autoantibody to glutamate receptor Gluepsilon2 IgG or IgM in an examination of blood and spinal fluid, and we presumed that this may have influenced his sequelae. In this case, a combination of mild hypothermia therapy, steroid pulse therapy, and massive gamma-globulin therapy was effective.
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PMID:A case of acute encephalitis with refractory, repetitive partial seizures, presenting autoantibody to glutamate receptor Gluepsilon2. 1619 11

Cold-water immersion can include aspects of both hypothermia and near drowning. We present a case of a 22-year-old active duty service member who became a victim of cold-water immersion in Alaska. His rescue by the U.S. Coast Guard and subsequent treatment in a small community emergency room are reviewed using a case management format. Care of the cold-water immersion patient with limited resources is highlighted and the potential complications of cold-water immersion are emphasized. Disturbances in acid base balance, pulmonary function, and cardiac rhythm are discussed. Changes in some of the hematological indices seen in the cold-water immersion patient are reported for the first time.
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PMID:Cold-water immersion in a 22-year-old service member. 1676

An increase in the histamine concentration in the brain has been demonstrated to provide protective effects against ischemia/reperfusion brain injury. Since hypothermia and barbiturates are also regarded to protect ischemic brains, effects of postischemic treatments were compared in gerbils between mild hypothermia and intraperitoneal administration of L-histidine, a precursor of histamine. Furthermore, effects of thioperamide, a histamine H(3) receptor antagonist, were evaluated in histidine-treated gerbils after 60 days. Transient forebrain ischemia for 4 min at 37 degrees C provoked severe neuronal damage in the hippocampal CA1 pyramidal cells after 7 days. Postischemic hypothermia (33 degrees C) for 3 h under pentobarbital anesthesia alleviated neuronal death, and the number of preserved neurons was 77+/-56/mm (mean+/-S.D., n=14). The effect of L-histidine injected three times, immediately, 6 h, and 24 h after reperfusion (1,000 mg/kg, i.p., each), was more prominent than that of hypothermia, and the number of preserved neurons was 142+/-55/mm (n=14). When the histologic outcome was evaluated after 60 days, most neurons were damaged in both the hypothermic and histidine groups. The improvement of the histologic outcome was observed even after 60 days in animals injected with thioperamide, immediately and 6 h after reperfusion (5 mg/kg, s.c., each), with three injections of l-histidine. The number of preserved neurons was 133+/-88/mm (n=10), while that in the hypothermic group was 7+/-15 (n=10). Activation of the central histaminergic system provides beneficial effects against cerebral ischemia.
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PMID:A comparison of protective effects between L-histidine and hypothermia against ischemia-induced neuronal damage in gerbil hippocampus. 1691 39

Hypothermia is generally defined as a core body temperature less than 35 degrees C (95 degrees F), and is one of the most common environmental emergencies encountered by emergency physicians. A 32-year-old male hunter was admitted to the hospital with altered mental status. He remained unconscious, Glasgow Coma Scale (GCS) score was recorded as 5/15, and pupils were dilated and unreactive. His vital signs showed a heart rate of 48 beats/min, respiratory rate of 10 breaths/min, blood pressure of 95/50 mm Hg, and rectal temperature of 31 degrees C. An electrocardiogram (ECG) was obtained and showed marked sinus bradycardia and J waves. His finger-stick glucose was 85. He was intubated. After 3 h of active rewarming, his temperature was 34 degrees C, and the repeat ECG showed near-complete resolution of the J waves and acceleration of the sinus rate to 68 beats/min. At the same time, emergency head computed tomography (CT) scan showed subarachnoid hemorrhage (SAH) and subdural hemorrhage. The patient died on the third day of admission. In this case we want to indicate that J waves and obtunded state could be due to either SAH or hypothermia, and SAH could have been missed if initial obvious hypothermia had been believed to cause all symptoms.
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PMID:The Osborn wave in accidental hypothermia. 1739 90


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