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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On eight separate occasions, four functionally anephric diabetic patients (on maintenance hemodialysis) experienced episodes of severe hyperglycemia with acute interstitial and alveolar pulmonary edema demonstrated clinically and by chest x-ray without electrocardiographic or enzymatic evidence of an acute myocardial lesion. Three patients had normal stress 201T1 scanning. The fourth patient, who experienced three such episodes, had normal coronary angiograms and only a mild elevation of the left-ventricular end-diastolic pressure. Clinical and chest x-ray improvement were immediate following insulin therapy and control of hyperglycemia, without phlebotomy or dialysis. Since these episodes were observed during a 1-yr period, this syndrome may be more common than suspected. It is concluded that in functionally anephric diabetic individuals: (1) pulmonary edema can be precipitated by uncontrolled diabetes; (2) endogenous fluid shifts may contribute to the cause of acute pulmonary edema; (3) clinical and radiologic improvement can be achieved with adequate insulin therapy; and (4) blood glucose levels should be monitored and controlled in diabetic patients with renal failure.
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PMID:Reversible acute pulmonary edema due to uncontrolled hyperglycemia in diabetic individuals with renal failure. 676 26

In a controlled randomized study of 328 consecutive patients admitted within 24 hours after the onset of acute myocardial infarction, 163 patients received a sodium nitroprusside infusion during 24 hours, followed by six times a day 5 mg isosorbide dinitrate for seven days and 165 patients received a glucose 5% infusion. Excluded from the study were patients with either pulmonary edema and/or cardiogenic shock, two or more previous myocardial infarctions or a systolic blood pressure of less than 95 mmHg just before entering the study. Sodium nitroprusside was titrated in such a way that systolic blood pressure was kept between 95 and 105 mmHg. Standard medical treatment for both groups was the same. CK-MB was sampled every four hours until peak value was reached. Endpoint of the study was a significant reduction in mortality within a week after starting treatment.
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PMID:Treatment of acute myocardial infarction with sodium nitroprusside during 24 hours, followed by isosorbide dinitrate. 703 72

The pathophysiology of anuric hyperglycemia is characterized by changes in extracellular fluid volume and in effective osmolality. We studied these changes in 7 anuric patients during correction (seven instances) or development (one instance) of hyperglycemia. During observations, intakes and outputs of fluids were negligible and weights did not change. Pulmonary edema, present in hyperglycemia in six instances, disappeared with normalization of glucose concentration in five instances. While glucose was rising, before study, thirst and water intake were pronounced in six instances; in three, normalization of glucose concentration uncovered true hyponatremia. For the same change in blood glucose, changes in effective osmolality were greatest in patients with anasarca.
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PMID:Hyperglycemia in advanced renal failure: sodium and water metabolism. 711 Apr 75

A case of cardiomegaly with unilateral pulmonary edema is presented. The predisposing etiologies were severe hypoglycemia and a hypertonic glucose infusion into a branch of the left lower lobe pulmonary vein. Resolution resulted following maintenance of adequate glucose levels, vigorous cardiopulmonary support, and repositioning of the catheter tip in the inferior vena cava. The pathophysiologic mechanism was direct endothelial injury with an osmotic diuresis. The role of the release of a vasoactive substance was postulated.
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PMID:Grand round series: hypoglycemia and unilateral pulmonary edema in a newborn. 735 80

Scorpion envenoming results in a severe autonomic storm with a massive release of catecholamines, increased angiotensin II and inhibition of insulin secretion. These hormonal alterations could be responsible for the pathogenesis of a variety of clinical manifestations. Under these conditions, scorpion envenoming essentially results in a syndrome of fuel-energy deficits and an inability to utilize the existing metabolic substrates by vital organs causing multi-organ system failure and death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing the cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming. The use of continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg/hr, with supplementation of potassium as needed and maintenance of fluid electrolytes and acid-based balance, has become a routine protocol in our setting for treating the victims of scorpion envenoming.
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PMID:Scorpion envenoming and the role of insulin. 780 39

Toxicological effects of fenvalerate on rat lungs by bronchoalveolar lavage (BAL) and biochemical changes in 20 workers exposed to fenvalerate were studied. The results showed that the levels of CPK, albumin, TP, AKP, ACP, alpha 1-AT, MDH, LDH, glucose, and lactic acid in BAL fluid increased significantly, with a CPK level the most sensitive one. most of the above parameters in BAL fluid changed four hours after exposure and returned basically to normal on the fourth day after exposure. Only the levels of ACP, alpha 1-AT and albumin were found increased in their blood. It showed a good linear relationship between blood and BAL levels of alpha 1-AT and ACP. Changes in some biochemical parameters were also found in workers exposed to fenvalerate, which correlated to the length of their employment. The results suggested inhalation of fenvalerate may cause alveolitis, pulmonary edema, and damage to lung cells.
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PMID:[Biochemical and toxicological studies of fenvalerate on the lung]. 813 61

Beginning in 1981, Prapokklao Regional Hospital in Chantaburi, Thailand, admitted all pregnant women with malaria to the obstetrics unit so midwives and obstetricians could learn how to better detect early signs or symptoms of malaria. Prior to 1981, they treated these women with quinine hydrochloride in a 500 ml 5% dextrose drip for 8 hours. They failed to detect hypoglycemia and pulmonary edema, however, resulting in many deaths. After 1981, they used 20 mg/kg quinine hydrochloride in a 250 ml 5% dextrose drip in 4 hours then 10 mg/kg quinine hydrochloride in a 250 ml 5% dextrose drip at the same rate at 8 hour intervals. Once the patient could take the drug orally, they administered 600 mg quinine sulfate at 8 hourly intervals for 7 days. They measured blood bilirubin levels and performed renal function tests on admission and on days 2 and 5. They monitored blood sugar levels on admission, at hourly intervals during intravenous quinine treatment, and every 4 hours during oral quinine treatment. Clinicians encouraged women who could drink to drink glucose syrup during quinine treatment. If, during treatment, a patient experienced unconsciousness or convulsions or blood sugar levels fell below 60 mg/dl, they would administer 100 ml of 50% glucose. If bilirubin levels remained high or a patient became jaundiced on day 2, clinicians monitored bilirubin on days 3 and 4. If levels increased, they reduced the dose 33% until the situation improved. They recorded urinary output hourly and measured central venous pressure. If the patient had normal pressure, but urinary output was less than 30 ml/hour, clinicians prescribed a diuretic. They kept patients in a propped-up position to reduced the likelihood of pulmonary edema. They monitored fluid intake and output and, in severe cases, central venous pressure. They allowed just enough fluid intake to maintain the pressure at 10-12 mm H20 and urine output at no less than 30 ml/hour. These efforts reduced maternal deaths in the unit from 341 to 54/100,000 live births (1981 - 8 deaths; 1986 - no deaths).
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PMID:Malaria in pregnant women: action for survival. 818 99

The effect of trehalose, a non-reducing disaccharide which stabilizes and protects membranes, in the preservation of canine lungs was examined when Euro-Collins solution was basically used as a preservant. In group I, five lungs were perfused and preserved in an Euro-Collins solution modified by replacing the glucose with 35.0 g/L of trehalose. Five control lungs (group II) were perfused and preserved with Euro-Collins solution containing 35.0 g/L glucose. In both groups, no vasodilators were used. After preservation for 12 hours, left lung allotransplantation was performed. At 10, 40, 70, and 130 minutes after reperfusion, the right pulmonary artery was clamped for 10 minutes and four parameters were measured: arterial oxygen tension, mean pulmonary arterial pressure, peak inspiratory pressure, and wet/dry weight ratios. The transplanted lung was also examined histologically. At 10, 40, 70, and 130 minutes after reperfusion, oxygen-tension levels from group I were 263.2 +/- 19.2, 283.4 +/- 14.0, 277.5 +/- 19.9 and 264.9 +/- 26.2 mmHg, respectively. In group II, the corresponding values were 191.2 +/- 33.9, 188.0 +/- 40.3, 153.4 +/- 40.0 and 134.7 +/- 49.4 mmHg, respectively. At 70 and 130 minutes the difference were significant (p < 0.05). All transplanted lungs from group I showed normal histology, whereas four dogs in group II developed severe pulmonary edema and one had a partially edematous lung. These findings suggest that simple substitution of trehalose for glucose has a beneficial effect on preservation of canine lung for 12 hours.
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PMID:Effects of trehalose in preservation of canine lung for transplants. 836 58

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

The effects of ventilation at positive end-expiratory pressure (PEEP) on extravascular lung water (EVLW) and cardiopulmonary function were studied in dogs with experimental severe hydrostatic pulmonary edema, which was generated by inflating a left atrial balloon and simultaneously injecting warm 5% glucose solution into the pulmonary artery. The EVLW was measured by the double indicator dilution method using heat and sodium ions. All the dogs were ventilated at zero end-expiratory pressure (ZEEP) until the EVLW had increased by 200-300% (maximal edema), when they were divided into two groups, one of which (n = 6) was ventilated at a PEEP of 10 cm H2O throughout the 4 hr study period (PEEP group) and the other (n = 6) was maintained at ZEEP during their survival period (ZEEP group). All the dogs in the PEEP group survived ventilation for 4 hr, whereas all those in the ZEEP group died within 3 hr, (2 within 1 hr, 1 between 1 and 2 hr and 3 between 2 and 3 hr). The EVLW of the PEEP group remained unchanged throughout the 4 hr study period, whereas that of the ZEEP group showed a tendency to increase. The arterial oxygen tension (PaO2) increased significantly throughout the 4 hr period of ventilation in the PEEP group but tended to decrease in the ZEEP group. In conclusion, PEEP improves gaseous exchange, but does not decrease the EVLW in dogs with experimental severe hydrostatic edema.
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PMID:Effect of positive end-expiratory pressure on extravascular lung water and cardiopulmonary function in dogs with experimental severe hydrostatic pulmonary edema. 874 Dec 68


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