Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to review our experience with the use of OKT3 (a murine monoclonal CD3 antibody) used as immune prophylaxis for pediatric heart transplant recipients. Orthotopic heart transplantation was performed in 18 pediatric patients, 8 girls and 10 boys, ranging in age from 17 days to 17 years. OKT3 therapy was initiated intraoperatively at a dose of approximately 0.2 mg/kg and was administered at a dose of approximately 0.1 to 0.2 mg/kg/day for a period of 11.5 +/- 2.5 days. Daily average OKT3 levels were 1132 +/- 469 ng/ml. Side effects that occurred during OKT3 therapy were fever (59%), diarrhea (24%), headaches (24%), vomiting (18%), encephalopathy (12%), pulmonary edema (6%), and rash (6%). Infections occurred in 24% of patients, all within 6 months of transplantation. In the first year after transplantation, patients experienced 3.4 +/- 2.4 episodes of mild rejection and 1.0 +/- 0.8 episodes of moderate rejection. No patient experienced severe rejection. Five of the surviving 14 patients (36%) have been weaned from chronic steroid therapy, and 42% are being maintained on alternate-day prednisone at a dose of 0.06 +/- 0.02 mg/kg/day. Coronary artery disease developed in three patients; two of whom died. Actuarial survival was 83% at 1 year and 73% at 2 years. This report shows that OKT3 prophylaxis in pediatric heart transplantation can be used with acceptable short-term adverse side effects and overall survival.
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PMID:Murine monoclonal CD3 antibody (OKT3)-based early rejection prophylaxis in pediatric heart transplantation. 832 14

An alcoholic man who was admitted with an acute onset of neck pain and confusion was diagnosed as suffering from a subarachnoid hemorrhage after rupture of an anterior communicating artery aneurysm. Additionally, he showed a bilateral 6th nerve palsy of variable extent. The postoperative course was complicated by pulmonary edema and adult respiratory distress syndrome. He died on Day 28 after admission. At autopsy, surprisingly, the concomitant diagnosis of acute thiamine-deficient encephalopathy was made. Thiamine had been given only in minimal amounts during hospitalization. We describe the striking clinicopathological features of this previously undocumented case and consider the relationship between the two central nervous diseases.
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PMID:Thiamine-deficient encephalopathy in association with aneurysmal subarachnoid hemorrhage: a case report. 847 60

Systemic inflammatory response syndrome (SIRS) is characterized by body temperature abnormalities, tachypnea or hyperventilation, tachycardia, and leukocytosis or leukopenia. Although it is typically associated with a serious infection and referred to as sepsis, SIRS can stem from noninfectious causes, as well. We report the cases of four patients with toxic serum levels of salicylate (33.5 to 67.6 mg/dL) and SIRS, and we discuss mechanisms responsible for SIRS. Our patients showed temperature disturbances (35.5 degrees C to 39.8 degrees C), noncardiogenic pulmonary edema, and mixed acid base disturbances. Other abnormalities included coagulopathy (disseminated intravascular coagulation), encephalopathy, and hypotension. All four patients recovered from SIRS, probably due to early recognition and treatment; only one patient did not survive the hospitalization. Chronic salicylate toxicity should be considered as a cause of SIRS in the absence of a source of infection, since survival appears to be dependent on prompt diagnosis and management.
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PMID:Systemic inflammatory response syndrome caused by chronic salicylate intoxication. 863 72

Hypertensive crisis is defined as an extreme elevation of arterial blood pressure, with diastolic pressure > 120 mm Hg, and represents an imminent risk to the patient. In such cases, a rapid orientating diagnosis and adequate antihypertensive treatment to avoid sequelae are needed, sometimes even before diagnostic tests are completed. Hypertensive emergencies and hypertensive urgencies can be distinguished. If the critical increase in blood pressure is associated with end-organ damage such as encephalopathy, acute left heart failure and pulmonary edema, angina pectoris, myocardial infarction or dissecting aortic aneurysm, a hypertensive emergency is present, that is an acute threat to the patient's life. A hypertensive emergency requires effective lowering of blood pressure within minutes, but not necessarily to normal range. The choice of suitable antihypertensive agents depends on clinical symptoms, contraindications, duration of pressure elevation and underlying conditions, prior cardiovascular, cerebrovascular and renal disorders. The risk of imminent end-organ damage must be weighed against the risk of rapid blood pressure lowering. In hypertensive urgencies without end-organ complications, blood pressure can be lowered more slowly over several hours, often with oral agents to avoid detrimental fall in blood pressure. The drugs of choice are mainly urapidil i.v. and nitroglycerine.
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PMID:[Therapy of hypertensive crises]. 1085 68

Status epilepticus is common and associated with significant mortality and complications. It affects approximately 50 patients per 100,000 population annually and recurs in >13%. History of epilepsy is the strongest single risk factor for generalized convulsive status epilepticus. More than 15% of patients with epilepsy have at least one episode of status epilepticus and low antiepileptic drug levels are a potentially modifiable risk factor. Other risks include young age, genetic predisposition, and acquired brain insults. Fever is a very common risk in children, as is stroke in adults. Mortality rates are 15% to 20% in adults and 3% to 15% in children. Acute complications result from hyperthermia, pulmonary edema, cardiac arrhythmias, and cardiovascular collapse. Long-term complications include epilepsy (20% to 40%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%). Neuronal injury leading to temporal lobe epilepsy is probably mediated by excess excitation via activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and consequent elevated intracellular calcium that causes acute necrosis and delayed apoptotic cell death. Some forms of nonconvulsive status epilepticus may also lead to neuronal injury by this mechanism, but others may not. Based on clinical and experimental observations, complex partial status epilepticus is more likely to result in neuronal injury similar to generalized convulsive status epilepticus. Absence status epilepticus is much less likely to result in neuronal injury, and complications because it may be mediated primarily through excess inhibition. Future research strategies to prevent complications of status epilepticus include the study of new drugs (including NMDA antagonists, new drug delivery systems, and drug combinations) to stop seizure activity and prevent acute and delayed neuronal injury that leads to the development of epilepsy.
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PMID:Status epilepticus: risk factors and complications. 1088 37

High-altitude cerebral edema (HACE) is a potentially fatal metabolic encephalopathy associated with a time-dependent exposure to the hypobaric hypoxia of altitude. Symptoms commonly are headache, ataxia, and confusion progressing to stupor and coma. HACE is often preceded by symptoms of acute mountain sickness and coupled, in its severe form, with high-altitude pulmonary edema. Although HACE is mostly seen at altitudes above that of the Denver/Front Range visitor-skier locations, we report our observations over a 13-year period of skier-visitor HACE patients. It is believed that this is a form of vasogenic edema, and it is responsive to expeditious treatment with a successful outcome.
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PMID:High-altitude cerebral edema (HACE): the Denver/Front Range experience. 1094 41

The study was conducted in 35 cases of acute tubular necrosis of varied aetiology. Cases were divided in 2 groups, Group A--17 cases treated conservatively and Group B--18 cases managed by early haemodialysis. Criteria for early haemodialysis were blood urea < 120 mg% and serum creatinine < 7 mg%. Before starting therapy both the groups had comparable biochemical and renal parameters (p > 0.05). Overall mortality was lower in Group B as compared to Group A (22.2% Vs 29.4). Complication events such as uraemic encephalopathy, pulmonary oedema, haematemesis and malena, thrombophlebitis and vomiting were significantly lower in Group B (p < 0.05). Hospital stay was also significantly lower (p < 0.05) in Group B (18 +/- 2.5 days Vs 28 +/- 3 days), this can reduce the cost of treatment also.
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PMID:Early haemodialysis in acute tubular necrosis. 1122 83

The authors encountered a case of portal-systemic venous shunt newly diagnosed after initiation of hemodialysis. A 68-year-old Japanese woman began hemodialysis because of symptoms of uremia including loss of appetite and pulmonary edema. Loss of consciousness occurred suddenly after her ninth session of hemodialysis. No hepatic functional abnormality was found other than hyperammonemia (314 microg/dL [184 micromol/L]). Loss of consciousness subsequently occurred often after hemodialysis. Color Doppler ultrasonography and magnetic resonance angiography depicted a large shunt between the left gastric vein and left renal vein resulting in portal flow entering the systemic circulation via the renal vein. Because the shunt was large, ligation of it was performed surgically. Results of histologic examination of a liver biopsy specimen obtained intraoperatively were normal. The patient became well postoperatively. This patient's encephalopathy appeared to be caused by the flow of ammonia-rich portal venous blood into the systemic circulation via the large shunt owing to a decrease in intravenous pressure after rapid hemodialysis. Portal-systemic shunt encephalopathy should be recognized as a "new" neuropsychiatric disorder characteristic of patients undergoing hemodialysis.
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PMID:Hemodialysis-related portal-systemic encephalopathy. 1533 38

A 34-year-old woman with eclampsia and the hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome developed encephalopathy, cardiomyopathy, pulmonary edema, liver failure, and disseminated intravascular coagulation (DIC), all of which resolved. She also had retinal hemorrhages in both eyes and a hemorrhagic infarct in the left occipital lobe that resulted in a permanent right homonymous hemianopia and a persistently depressed acuity of 20/100 OS. This case is unusual in demonstrating permanent visual deficits. In nearly all cases of preeclampsia or eclampsia, visual deficits are reversible. The superimposition of the HELLP syndrome may create more neurologic damage. Clinicians should be alert to patients at risk for HELLP syndrome and manage them aggressively.
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PMID:Permanent visual deficits secondary to the HELLP syndrome. 1593 36

The case is reported of a young previously healthy female cross country runner who collapsed on completion of a cross country run. The cause of the collapse was non-cardiogenic pulmonary oedema as a manifestation of hyponatraemic encephalopathy. The concurrent occurrence of non-cardiogenic pulmonary oedema and encephalopathy due to hyponatraemia is unusual.
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PMID:Sudden collapse of a young female cross country runner. 1655 75


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