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-37-year-old woman in shock condition was transferred to our hospital after cardiopulmonary resuscitation for ventricular fibrillation. She was unconscious and suspected of suffering ischemic brain damage, with pathologic reflexes and weak brain stem reflexes. Brain CT scan showed cerebral edema without hemorrhage or infarction and an electroencephalograph revealed slow alpha-theta waves. Chest CT scan and echocardiogram showed ascending aortic aneurysm with sever aortic regurgitation. An emergent operation was performed for progression of heart failure. There were no distortion or dilatation of the sinus of Valsalva and annuloaortic ectasia and aortic valve leaflets were almost normal. We considered that the aortic valve dysfunction was cause by dilatation of the sinotubular junction. Ascending aortic and aortic valve replacement were carried out to shorten cardiopulmonary bypass time and to prevent the progression of brain damage. Mild hypothermia was employed as a neuroprotective procedure for three days after surgery. The patient's neurological symptoms, which were right hemiparesis, facial apraxia and motor aphasia, improved and she was discharged from the hospital on foot without any neurological complications on the 47th postoperative day and returned to work after two months.
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PMID:[An unconscious patients with ascending aortic aneurysm accompanied by aortic regurgitation successfully treated by emergency operation after cardiopulmonary resuscitation]. 1159 40

Wernicke encephalopathy (WE) was first described by Carl Wernicke in 1881. WE is caused by thiamine deficiency. Alcoholism is the most common etiologic factor associated with WE in the United States, but it can occur in any patient with a nutritional deficiency state such as hyperemesis gravidarum, intestinal obstruction, and malignancy. WE is a clinical diagnosis. The common findings include mental status changes, ocular dysfunction, and a gait apraxia, present in only 10% of cases. Only a few cases of WE are diagnosed before death. Approximately 80% of patients with untreated WE have development of Korsakoff syndrome, which is characterized by memory impairment associated with confabulation. The initial clinical diagnosis of WE is critical, keeping in mind that the classic triad of symptoms is often absent. Recognition of nutritional deficiency and any portion of the classic triad should prompt treatment. Additionally, hypothermia, hypotension, and coma should raise clinical suspicion for the disease. Primary treatment includes timely administration of thiamine, for which the route and dosage remain controversial. Clinical judgment should be exercised in diagnosis and treatment (dosage, frequency, route of administration and duration) in all cases of WE. Overdiagnosis and overtreatment may be preferred to prevent prolonged or persistent neurocognitive impairments given the excellent safety profile of thiamine. Further prospective research is warranted to better understand the disease biology, risk factors, and treatment recommendations.
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PMID:Wernicke Encephalopathy-Clinical Pearls. 3117 Nov 16