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)

Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.
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PMID:Alcoholic detosis. 80 36

Investigation of the clearance of proteins from the air spaces is important for an understanding of the resolution of pulmonary edema and also because of current interest in delivery of therapeutic peptides via the distal air spaces. Few experimental studies have examined the size dependence for alveolar clearance of large macromolecules; there have been no human studies. In anesthetized rabbits, we measured clearance of cyanocobalamin and different-sized human proteins instilled into the air spaces. After 8 h, the amounts of instilled tracer recovered in the lungs were [57Co]cyanocobalamin, 19.4 +/- 3.0% (Stokes radius 0.65 nm); 125I-labeled insulin, 64.6 +/- 3.9% (1.2 nm); 131I-labeled albumin, 87.0 +/- 4.0% (3.5 nm); and 125I-labeled immunoglobulin G, 91.8 +/- 3.3% (5.5 nm) (P < 0.05). Sieving of different-sized proteins occurred across the alveolar epithelial barrier because tracer concentrations in air space lavage fluid after 8 h were decreased more for the smaller tracers than the larger ones. Size selectivity for alveolar protein clearance in humans with resolving alveolar edema was investigated by measuring the changes in albumin and total protein concentration. The fraction of total protein concentration made up of albumin was greater in the edema fluid than in the plasma initially. The albumin fraction decreased with time in 9 of 10 patients with resolving edema, from 0.62 +/- 0.2 to 0.58 +/- 0.10 (P < 0.05) after 10 +/- 5 h. Thus both rabbit studies and human studies provide evidence for size-dependent clearance of protein from the air spaces of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clearance of different-sized proteins from the alveolar space in humans and rabbits. 144 74

Thorough assessment of the patient and good understanding of potential complications enhance patient care and safety. Correction of volume depletion and maintenance of a strict fluid balance chart is essential to avoid complications of congestive cardiac failure, cerebral or pulmonary oedema, renal failure and further dehydration. Careful monitoring of electrolytes and administration of supplements should be undertaken to prevent instability. Regular monitoring of blood glucose levels and careful insulin administration should be undertaken to prevent fluctuations in blood glucose levels. Any possible source of infection should be identified and treated as prescribed. Good basic nursing care for the patient and support and counselling for the patient and his family are essential components of holistic care.
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PMID:Hyperosmolar non-ketotic hyperglycaemia. 164 76

Besides general complications of immunosuppression such as increased susceptibility to opportunistic infections or malignancy, individual immunosuppressive agents are associated with specific side effects. Nephrotoxicity is the major side effect of cyclosporine (CsA). Various attempts have been made to minimize this toxicity, such as monitoring drug blood levels, modifying the protocol, and coadministering other agents. Other side effects caused by CsA are hepatotoxicity, hyperkalemia, hypertension, tremor, gum overgrowth, and hirsutism. Azathioprine (AZA) causes dose-related bone marrow suppression, commonly leading to leukopenia. Careful monitoring of complete blood cell count and dosage adjustment according to white blood cell count are usually adequate to prevent serious leukopenia. The side effects of corticosteroids are numerous and include slow wound healing and de novo insulin-dependent diabetes mellitus. Many complications are dose related, and with low dosage or discontinuation of steroids, their frequency rapidly decreases. Antilymphoblast and antithymocyte globulins (P-ALG) are foreign antibodies and may cause allergic-type reactions such as fever, chill, and hypotension. The initial side effect of monoclonal antibody (muromonab-CD3, OKT3) is similar to that of P-ALG. It includes high fever, shaking chills, headache, rigors, and hypotension. To prevent it, acetaminophen, an antihistamine, and a steroid usually are administered before injection. Because this agent is also associated with high frequency of pulmonary edema, it should not be given to any patient who has more than 3% body weight gain during the week prior to therapy. In rare case, it causes aseptic meningitis or encephalopathy, which is manifested by fever, severe headache, and seizure.
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PMID:Complications associated with immunosuppressive therapy and their management. 174 17

The efficacy of insulin administration in reversing haemodynamic changes in pulmonary oedema in victims of poisonous scorpion sting is assessed by a study based on animal experiments in which insulin administration reversed metabolic and electrocardiographic changes induced by scorpion envenomation. Six previously healthy children aged 18 months to 11 years were admitted to hospital five to 17 hours after scorpion sting. Frusemide for raised central venous pressure and pulmonary oedema, crystalloid infusion for reduced central venous pressure, and hydrocortisone and dopamine for hypotension were used as standard therapy. Insulin (0.3 units g-1 of glucose) was administered when the standard therapy failed to produce an improvement, and at the earliest sign of haemodynamic instability. Reversal of pulmonary oedema and haemodynamic changes, and attainment or normal respiratory rate, blood pressure and central venous pressure, were observed. It is concluded that insulin administration may be useful in reversing haemodynamic changes and pulmonary oedema in victims of scorpion stings.
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PMID:Insulin reverses haemodynamic changes and pulmonary oedema in children stung by the Indian red scorpion Mesobuthus tamulus concanesis, Pocock. 181 42

A randomized, single-blind controlled study intended to assess the potential benefits of intravenous amiodarone in anterior myocardial infarction is presented. Three hundred nineteen patients entered the study, 159 received amiodarone infusion, and 160 received glucose-insulin-potassium (GIK) infusion. Basal characteristics were similar in the two experimental groups, who were randomized on a consecutive basis. Exclusion criteria were shock or pulmonary edema, hypotension, inferoposterior infarction, bradycardia, antrioventricular block, severe diabetes, and other major diseases. Patients aged 27 to 70 years, with a Q-wave anterior infarction, initiated 12-40 hours earlier at the time of admission, entered the trial. Other entry criteria were heart rate higher than 80 beats/min and systolic blood pressure higher than 100 mmHg. Amiodarone was administered in saline infusion 10-20 mg/kg, within 4 to 10 hours, through a central vein. GIK infusion consisted of 150-300 g of glucose, 25-50 IU of insulin, and 80-120 mEq of KCl in 1000 cc of water at a rate of 1.5-2.0 ml/g/hour. Both groups received digitalis, nitrates, sedatives, and diuretics as needed. Although individually the major endpoints of death, reinfarction, and sustained supraventricular and ventricular arrhythmias did not differ significantly, each was less in the amiodarone group than in the control, and the sum of all adverse events was significantly lower for the amiodarone patients (p less than 001). Heart failure and conduction disturbances were not different in the two groups. This study shows that amiodarone, with its vasodilating and antiarrhythmic properties, may be beneficial in acute anterior infarction, but further studies on larger populations will be necessary in order to show a reduction of mortality rate.
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PMID:Intravenous amiodarone in acute anterior myocardial infarction: a controlled study. 248 93

The authors observed 53 cases of diabetic ketoacidosis treated with low doses of insulin. Mean age of the patients was 41 +/- 17 years, duration of diabetes mellitus 7.5 +/- 6.4 years. Ketoacidosis was due to: infections in 36%, other diseases in 7%, and cessation of insulin therapy in 25% of cases. Ketoacidosis was a first sign of diabetes mellitus in 19% of cases while causative factor was not detected in 13% of cases. At the admission to hospital mean blood pH was 7.02 +/- 0.15, mean bicarbonate concentration 6.17 +/- 3.45 mM/l, and glycaemia 40.6 +/- 16.8 mM/l. Therapy of ketoacidosis was complicated by hypopotassemia in 1 patient and transient hypoglycaemia in another patient. Five patients (9.6%) died. Infections, myocardial infarction, acute pancreatitis, pulmonary edema, and disseminated intravascular coagulation were the causes of deaths.
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PMID:[Analysis of the cause of death in diabetic ketoacidosis based on 5 years of personal observation]. 251 62

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

To assess the effect of diabetes on outcome after acute myocardial infarction (MI), we compared a cohort of 228 type II (non-insulin-dependent) diabetic patients who had sustained acute MI with a similar number of nondiabetic patients with MI. Thirty-day mortality was greater in the diabetic group (27 vs. 17%). However, diabetic patients were older and had more cardiovascular disease before MI. Analyses accounting for such baseline risk revealed a complex effect of diabetes. The relative risk (RR) of dying from MI due to diabetes was greatest among patients with lowest baseline risk (RR 7.3) and least among those at highest baseline risk (RR 0.83). These effects were most striking with transmural MI, which was highly lethal for those with diabetes. Analyses with pulmonary edema as the endpoint support the significant risk conferred by diabetes and its interaction with baseline risk. Diabetes is a risk factor for poor outcome after MI, particularly among patients whose pre-MI cardiovascular status otherwise appears normal.
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PMID:Diabetic myocardial infarction. Interaction of diabetes with other preinfarction risk factors. 291 99

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.
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PMID:Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis. 297 Oct 75


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