Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

We have described a spectrum of pancreatic surgery after cardiopulmonary bypass. At one end is a subclinical lesion which was manifested only by elevations in serum isoamylase levels (27 percent of patients) and increased ribonuclease levels (13 percent of patients) in asymptomatic patients followed after cardiac surgery. At the other end is a severe and often lethal necrotizing pancreatitis. Acute necrotizing pancreatitis was found at autopsy in 25 percent of 138 patients who died after cardiac surgery, and it correlated strongly with low output, acute tubular necrosis, and infarction of the liver, spleen, or bowel. It was the principal cause of death in 4 percent of these patients. In addition, 24 percent of 38 nonsurgical patients who died from cardiac failure and hypoperfusion had acute pancreatitis at autopsy, whereas acute pancreatitis was not observed in 55 nonsurgical patients who died without a significant period of low output. Acute pancreatitis was recognized postoperatively in 12 patients (0.2 percent). Three had mild pancreatitis, and all responded well to conservative therapy. In nine patients, fulminant necrotizing pancreatitis developed. Their courses were characterized by significant early postoperative hemodynamic compromise, abdominal distention, ileus, fever, and episodes of late vascular instability associated with hypocalcemia. The diagnosis of pancreatitis was usually missed because of the absence of pain, tenderness and hyperamylasemia. The diagnosis was confirmed at laparotomy in eight patients and at autopsy in one. The only two survivors among the nine with severe cases had aggressive mobilization, debridement, and wide drainage of the necrotic pancreas. We suggest that a mild subclinical injury to the pancreas may occur as a consequence of cardiopulmonary bypass and may progress to severe ischemic necrosis if hypoperfusion follows in the postoperative period, the presentation of necrotizing pancreatitis may be atypical in the cardiac surgical patient and should be considered if nonspecific abdominal symptoms are present, and aggressive debridement and drainage may be the optimal treatment for aggressive forms of this disease.
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PMID:Acute pancreatitis after cardiopulmonary bypass. 258 Apr 53

Emergency surgery is the only effective treatment of ruptured abdominal aortic aneurysms, even though morbidity and mortality rates remain high. We have studied the feasibility of left retroperitoneal aortic exposure in these cases in an effort to reduce postoperative complications. Over a 33 month period, 29 patients underwent emergency surgery for either a ruptured or symptomatic infrarenal abdominal aortic aneurysm. Of 13 patients with ruptured aneurysms, 4 underwent repair through a midline transperitoneal approach (3 deaths) whereas the remaining 9 were repaired through the retroperitoneal exposure (1 death). Supraceliac aortic clamping through the same incision prior to aneurysm exposure maintained hemodynamic integrity. The remaining 16 patients with symptomatic aneurysms were all treated through the retroperitoneal exposure (3 deaths). In the retroperitoneal groups, the cause of death was cardiac in two patients, hypertensive stroke in one, and necrotizing pancreatitis in one. Morbidity consisted of prolonged intubation, respiratory distress syndrome, and thrombophlebitis in one patient each and acute tubular necrosis in two patients. We believe that the left retroperitoneal approach is a useful option in the emergent treatment of abdominal aortic aneurysms.
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PMID:Selective use of retroperitoneal aortic exposure in the emergency treatment of ruptured and symptomatic abdominal aortic aneurysms. 340 Aug 6

Forty-four cases of acute necrotic haemorrhagic pancreatitis are studied. Fourteen cases were treated medically by peritoneal dialysis, 20 were treated surgically of which 16 had been medically treated by peritoneal dialysis. Fifteen died or 34%. Forty-one patients, 93.1% presented 8 major complications on admission and 2 complications were observed during the course of medical treatment (pulmonary shock and high digestive haemorrhage). The post surgical complications are excluded from this study. We report in order of frequency; effusion of the large peritoneal cavity (37 cases : 84%), hypocalcaemia less than or equal to 8 mg% (21 cases : 47.7%), renal insufficiency defined by a creatinaemia greater than or equal 2 mg% (17 cases : 38.6%), state of shock (13 cases : 29.5%), severe neurological disorders (11 cases : 25%), peritoneal haemorrhage (3 cases : 4.5%), disseminated intravascular coagulation (1 case : 2.2%), acute rabdomyolysis (1 case : 2.2%). Certain cases are particularly derogatory : pulmonary shock : 2 cases -- 2 deaths (100%); hypocalcaemia less than or equal to 7 mg/ : 6 cases -- 5 deaths (83.3%); acute tubular necrosis : 8 cases -- 6 deaths (75%); hypocalcaemia less than or equal 8 mg% : 21 cases -- 12 deaths (57.1%); high digestive haemorrhage : 3 cases -- 1 death (33.3%); amber known brown peritoneal effusion : 27 cases -- 12 deaths (44.4%); shock : 13 cases -- 5 deaths (38.5%). When in the same patients, less than 3 complications were present, the mortality rate was 20.8%. If more than 3 signs were observed the mortality rate rose to 53.3%. Except for pulmonary shock, six major complications were needed to give 100% mortality rate.
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PMID:[Acute necrotic hemorrhagic pancreatitis. Major complications (author's transl)]. 697 50

Thirty patient suffering from acute necrotic hemorrhagic pancreatitis and treated from admission by peritoneal dialysis were studied. According to developments, 4 groups are defined. The first group consisted fo 14 patients treated only by peritoneal dialysis, 3 died. The second group consisted of 7 patients whose peritoneal dialysis was interrupted during hospitalization and who underwent differed surgery. The third group consisted of 5 patients who were operated during the period of peritoneal dialysis, all died. Finally, the fourth group consisted of 4 patients who were dialysed for a short period before emergency surgery, there were no deaths. Peritoneal dialysis, associated with other therapeutic measurements resulted in early improvement of abdominal and toxaemic signs such as shock and functional renal insufficiency. Acute tubular necrosis, observed in 5 patients was reversible in two. Six out of eleven were weaned from assisted ventilation. This allowed the spontaneous resorption of peripancreatic necrotic masses in four cases. Nevertheless it did not prevent the development of new necrotic masses in 5 other cases nor peritoneal infection, seen in 4 cases. It is ineffective in the development of shock lung which followed in 2 cases, during the course of treatment. In all, 11 patients survived by medical peritoneal dialysis only. Of the 30 patients, 19 survived or 63.4%. If the period between the first digestive signs and the installation of the peritoneal dialysis is less than or equal to 7 days, as seen in 21 cases, 15 patients survived or 71.5%.
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PMID:[Peritoneal dialysis treatment for acute necrotic hemorrhagic pancreatitis (author's transl)]. 733 48

Acute renal failure (ARF) incidence varies depending on whether the intensive care unit only or also general and specialist medicine departments are considered. In some cases, however, such as after major cardiosurgical operations, ARF can occur in up to 30% of patients. Most of ARFs in intensive care units are secondary to acute tubular necrosis occurring because of a multi-organ dysfunction syndrome. Factors most often associated with acute renal damage are: advanced age, volume depletion, arterial hypotension, massive bleeding, and sepsis. ARF often leads to complications for the following pathologies: serious liver disease, pancreatitis, pre-existing renal dysfunction, great burns, and cardiosurgical and vascular operations on large vessels. Among the so-called 'iatrogenic factors', contrast media and aminoglycosides are definitely the main cause of a rapid deterioration of renal function. Mortality is low for the isolated forms of ARF,whereas it peaks to 0-80% in multi-organ failures where co-existing pathologies often dominate. The mortality rate over the past 20 years has not changed, although pharmacological supports and especially dialysis instruments have improved. Patients are now older and older, affected by multiple pathologies and with poor recovery capacity. Mortality is higher among elderly patients, while toxic forms (from contrast media or from myoglobinuria) result generally in better outcomes. Patients with acute renal damage and oliguria have a worse prognosis than non-oliguric patients. Finally, some unfavorable prognostic factors include the prolonged use of high dose inotropic drugs, mechanical ventilation, cardiac failure and a septic state.
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PMID:[Epidemiology of acute renal failure]. 1706 24

The most severe complication of ischemia-reperfusion injury following lower limb arterial surgery is reperfusion syndrome. Therefore, our aim was to describe the extent of muscle damage and the reperfusion syndrome-related remote organ lesions in detail, through a well-documented case of long-lasting infrarenal aorta thrombosis. After urgent revascularization, several clinical signs of multiple organ dysfunction were detectable, including the circulatory, urinary, respiratory, gastrointestinal, and hemostatic systems. Upon histological examination, intraoperative muscle biopsy showed severe muscle damage. Muscle fiber viability was assessed with a special nitroblue tetrazolium staining-based viability test developed by our team; the obtained results indicated significant degree of muscle damage before this was confirmed by conventional histological methods. Thorough postmortem examination confirmed the presence of remote organ damage. The pathological findings included acute tubular necrosis, myocardial and jejunal infarctions, ischemic pancreatitis, and diffuse alveolar damage with hyaline membrane formation in the lungs and focal centrilobular liver necrosis. By using special staining techniques, the presence of myoglobin and lipofuscin deposits was confirmed in the kidney samples. In this paper, we present a patient who developed all major complications following long-lasting arterial occlusion. We also introduce a novel method to assess the degree of ischemic injury, which may be suitable in the near future for the rapid detection of irreversible muscle injury. Therefore, the mortality of the disease might be reduced.
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PMID:Rapidly progressing fatal reperfusion syndrome caused by acute critical ischemia of the lower limb. 2385 Jan 81