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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nutritional therapy can be impaired if imbalances in water and electrolyte status have led to gross disorders of the cardiovascular, pulmonary, renal, metabolic, and central nervous systems. Restauration and maintenance of the functional extracellular fluid volume is the primary therapeutic goal in water and electrolyte resuscitation. Hyper- and hypoosmolar disturbances are automatically corrected by intrinsic regulatory mechanisms. Potassium deficiency or overload, or potassium disequilibrium between the intracellular and extracellular space can lead to dangerous cardiac arrhythmias. Hyper- and hypokalemia usually develop within days or even weeks and should not be corrected within a few hours. If life threatening hyperkalemia develops during acute renal failure, 20 ml 10% calcium gluconate solution can be given intravenously in order to avoid ventricular fibrillation or cardiac arrest. The discrimination between prerenal disease, acute tubular necrosis and other causes of acute renal failure is based on special investigations, such as urinary osmolality, urinary sodium concentration, clearance of creatinine, osmolar solutes, free water, and fractional sodium excretion. The clinical examination of a patient should be the basis of assessing his water and electrolyte state. Laboratory findings which are in disagreement with the clinical state have to be repeated, critically interpreted, but not completely rejected. Third space losses make fluid balance difficult.
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PMID:[Imbalances of the water and electrolyte status]. 393 12

Acute renal tubular necrosis occurred in this 19-year-old white female after severe hypotension developed as the result of massive pulmonary emboli and failure of the right side of the heart. This previously healthy young girl was 19 days into her first cycle of an oral estrogen-progestogen agent. Upon admission to the hospital she was in critical condition, and 4 hours after admission cardiopulmonary resuscitation was necessary. 34 days after admission she developed ventricular tachycardia during a cardiac catheterization. Hemodialyses were instituted twice, with ventricular fibrillation occurring during the first procedure, which required cardiac defibrillation. Hemiparesis of the left side developed after this episode. She was discharged after 58 days with some left-sided weakness. After 9 months the pulmonary lesions had cleared and her electrocardiogram was normal.
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PMID:Acute renal tubular necrosis; a complication of pulmonary thromboembolism. 1227 13

Patient maintenance after successful cardiopulmonary resuscitation starts with decreasing the neurological damage despite serious difficulties such as hypoxic ischemic infarcts and reperfusion infarcts. Therapeutic hypothermia is the most rejoicing method in use to prevent neurological damage. Here, we discuss about a 35-year-old woman resuscitated for 20 minutes in hospital who was followed because of postpartum cardiomyopathy. Sudden onset of ventricular fibrillation subsequent to ventricular tachycardia was the underlying cause of cardiac arrest. To prevent neurological damage, therapeutic hypothermia was used, and she was cooled for 24 hours. After therapeutic hypothermia, her Glasgow coma score was 15, fortunately no sequela appeared. Although we were successful to prevent neurological damage, rhabdomyolysis arose secondary to therapeutic hypothermia. As a result, the intubation process was prolonged, and acute tubular necrosis due to myoglobinuria was occurred. Despite all complications patient faced, she was discharged on her 31th day; without sequela and with no need for hemodialysis; under medical therapy.
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PMID:Rhabdomyolysis Secondary to Therapeutic Hypothermia After Cardiopulmonary Resuscitation: A Rare Complication. 2629 13