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

Activated peripheral T-lymphocytes are increased in both pre-insulin-dependent diabetes mellitus (IDDM) patients and in recently diagnosed IDDM patients, as well as in various forms of acute stress. We studied the in vivo T-lymphocyte activation in six patients in severe diabetic ketoacidosis (DKA) prior to treatment, after 24 h of treatment and > or =5 days after admission. Five of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05). There was no correlation to the admission serum glucose, osmolality, or electrolytes. Serum pH showed a trend toward an inverse correlation, but was not statistically significant. We speculate that T-lymphocyte activation plays a role in the progression of the acute complications of subclinical brain edema and interstitial pulmonary edema of DKA. This process could also be another factor in the progression of the chronic complications of IDDM in addition to the well-established effects of hyperglycemia and hypertension.
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PMID:Acute activation of peripheral lymphocytes during treatment of diabetic ketoacidosis. 1135 83

Turner's syndrome is a condition involving total or partial absence of one X chromosome and has been associated with a number of diseases including non insulin dependent diabetes mellitus, abnormalities of glucose metabolism and hypothreosis. There have been many case reports in which Turner's syndrome is associated with type 2 diabetes, but the association with type 1 diabetes and/or life threatening complications is very rare. We present an unusual case of a patient with Turner's syndrome who has type 1 diabetes and is complicated with ketoacidosis, severe acute and recurrent pulmonary edema and rhabdomyolysis.
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PMID:Diabetic ketoacidosis associated with recurrent pulmonary edema and rhabdomyolysis in a patient with Turner's syndrome. 1139 14

Severe or complicated malaria is defined by infestation by Plasmodium falciparum into all red blood cells, especially those in the brain, causing coma and repeated convulsions; severe anemia (6 g/dl hemoglobin, 20% hematocrit); renal insufficiency (265 mcmol/l creatinine, 400 ml/day diuresis); pulmonary edema; hypoglycemia (2.2 ml/l or 0.4 g/l); shock; diffuse hemorrhaging; massive hemoglobinuria; and blood acidosis. Other possible symptoms of severe malaria are clouded thinking, changes in behavior, and inability to focus. It is most common in people with no immunity to malaria (children aged 4 and travelers in endemic zones). Pregnancy, splenectomy, corticotherapy, or poorly maintained immunity status favor severe anemia in adults. Sources of chloroquine-resistant P. falciparum have existed since 1960. Resistance has since expanded from Southeast Asia and South America to Africa, posing treatment problems. Malaria usually begins with fever (40 or more degrees Celsius), headaches, muscular pain, digestive troubles (e.g., diarrhea, nausea, or vomiting), and abdominal pain. In suspected cases of malaria, a blood sample or a thick blood smear as well as treatment (even in the absence of parasitological proof) needs to be done as soon as possible. Intravenous quinine diluted in a 5-10% glucose solution should be delivered at a rate of 24 mg/kg/day. In the case of severe jaundice, the dose should be cut in half beginning 8 hours after treatment began. If intravenous delivery is impossible, intramuscular delivery should be done. Corticosteroids, anticoagulants, and aspirin are contraindicated. In 2-4 days, oral administration (chloroquine, halofantrine, or mefloquine) is warranted. 20% of malaria-related deaths among patients who receive treatment are due to complications of the central nervous system. Protection against mosquito bites prevents malaria. Chemoprophylaxis in endemic zones should be limited to short trips to malaria zones or to pregnant women.
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PMID:[Severe malaria]. 1229 Jan 83

Enterovirus 71 (EV71) infection can lead to devastating clinical outcomes. An appreciation of the scientific relationship between cytokine response and patient mortality may help limit the risks posed by this deadly illness. We present the results of a study that compared the cerebrospinal fluid (CSF) and serum levels of interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) in 24 patients with EV71 infection. Cases in this study involved diverse manifestations or complications, including encephalitis, poliomyelitis-like syndrome, meningitis, and pulmonary edema. CSF levels of IL-6 in study patients were found to be consistently higher during the first 2 days of central nervous system (CNS) involvement than afterward. Compared with patients who did not have pulmonary edema, patients who experienced pulmonary edema had dramatically varied blood values, including IL-6, white blood cell counts, and glucose levels. Our findings suggest that the combination of CNS and systemic inflammatory response may trigger EV71-related cardiopulmonary collapse.
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PMID:Proinflammatory cytokine reactions in enterovirus 71 infections of the central nervous system. 1253 66

Epidemics of enterovirus 71 infections caused the rapid death of many children in Malaysia in 1997 and in Taiwan in 1998. Pulmonary edema occurred in most of the fatal cases and was considered to be neurogenic. The role of the heart was rarely investigated before. Between January 1998-January 2001, 34 consecutive patients who were admitted to the intensive care unit due to enterovirus infection were studied prospectively. Patients were divided into two groups: group I with pulmonary edema, and group II without pulmonary edema. Comparisons were made between the two groups based upon demographic, neurological, and cardiovascular manifestations. Group I consisted of 11 patients (5 boys, 6 girls; mean age, 22.8 months), and group II of 23 patients (12 boys, 11 girls; mean age, 28.8 months). There were no significant differences between the two groups in comparing sex, age, body weight, neurological severity, intracranial pressure, cell count, protein and glucose levels in cerebral spinal fluid, and blood pressure. All group I patients had left ventricular dysfunction, and their ejection fractions were significantly lower than those of patients in group II (37 +/- 11% vs. 75 +/- 6%, P < 0.001). Group I heart rates were higher than those of group II (175 +/- 24 vs. 137 +/- 25, P < 0.001). In group I, 9 patients who received conventional treatment died, and the only two survivors received left ventricular assist devices. In conclusion, the pulmonary edema of fulminant enterovirus 71 infection is associated with left ventricular failure. Left ventricular function is the major determinant of outcome. Early recognition of heart failure and aggressive cardiac intervention are life-saving. Pediatr Pulmonol. 2003; 35:263-268.
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PMID:Pulmonary edema of enterovirus 71 encephalomyelitis is associated with left ventricular failure: implications for treatment. 1262 22

OBJECTIVE: The objective of this study was to analyze the incidence and significance of hepatic dysfunction after cardiac surgery in children. DESIGN: Prospective, observational study. SETTING: Pediatric intensive care unit of a university hospital. PATIENTS: The study consisted of 232 children ranging in age from newborn to 17 years with no history of liver disease. MEASUREMENTS AND MAIN RESULTS: Aspartate aminotransferase (AST), alanine aminotransferase (ALT), gammaglutamyltranspeptidase (GGT), alkaline phosphatase, total and conjugated bilirubin, blood glucose, urea, creatinine, and coagulation studies were determined at admission, at 24 and 48 hrs, and at 7 days. Hepatic dysfunction was taken as an ALT of > 100 IU/L or a moderate or high hepatic score. The statistical study included bivariate analysis and multivariate logistic regression to study the risk factors for hepatic dysfunction. Twenty-one patients (9%) showed an ALT > 100 IU/L, and 29.3% had a moderate or high hepatic score. A relationship was found between hepatic dysfunction and the type of cardiopathy (D-transposition of the great arteries and coarctation of the aorta), shock, the administration of dopamine or epinephrine, renal insufficiency, the presence of pulmonary changes (pulmonary edema, atelectasis, pulmonary hypertension, hypoxemia), hematologic disturbances (prothrombin time, kaolin-cephalin time, fibrinogen, and platelets), and the need for a greater number of transfusions of packed cells, plasma, and platelets. Compared with 7.6% of the rest of the patients (p <.001), 38% of patients with an ALT > 100 IU/L died. The hepatic score of those patients who died was 4.2 (2.3)-higher than that of the survivors at 1.5 (1.8), (p <.001). Shock and renal insufficiency were the factors most significantly related to the development of hepatic dysfunction. CONCLUSIONS: Hepatic dysfunction is an uncommon complication in children after cardiac surgery. This complication is related mainly to hemodynamic disturbances and renal insufficiency and is an indicator of poor prognosis.
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PMID:Hepatic dysfunction after cardiac surgery in children. 1279 88

To determine the effects of Tityus serrulatus scorpion toxin on lung compliance and resistance, ionic equilibrium and acid-base balance over time in anesthetized and mechanically ventilated rats, we measured air flow, tracheal and esophageal pressure. Lung volume was obtained by electronic integration of airflow signal. Arterial blood samples were collected through a catheter at baseline (before) and 5, 15, 30 and 60 min after scorpion toxin injection for arterial blood gases, bicarbonate, and alkali reserve levels as well as for, sodium, potassium, magnesium, glucose, lactate, hematocrit, and osmolality analysis. Injection of the gamma fraction of the T. serrulatus scorpion venom in rats under mechanical ventilatory support leads to a continuous decrease in lung compliance secondary to pulmonary edema, but no change in airway resistance. The changes in arterial blood gases characterizing metabolic acidosis were accompanied by an increase in arterial lactate and glucose values, suggesting a scorpion toxin-induced lactic acidosis, in association with poor tissue perfusion (hypotension and low cardiac output). Moreover, scorpion toxin injection resulted in hyperosmolality, hyperkalemia, hypermagnesemia and an increase in hematocrit. The experiments have shown a clinically relevant animal model to study severe scorpion envenoming and may help to better understand the scorpion envenoming syndrome.
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PMID:Lung compliance, plasma electrolyte levels and acid-base balance are affected by scorpion envenomation in anesthetized rats under mechanical ventilation. 1531 52

Acidobasic balance and respiratory pulmonary functions were examined in 15 patients with chronic renal insufficiency during continuous ambulatory peritoneal dialysis (CAPD) using a dialysis solution containing 1.5% or 2.5% of glucose. Patients did not suffer from any pulmonary disease nor ischemic heart disease. Biochemical indicators of acidobasic balance were in reference range or on its lower margin. Respiratory pulmonary functions were in tolerance except maximum expiratory flow volume at 50% and 25% of vital capacity (MEF50 and MEF25) and except diffusion lung capacity (DLCO) which were decreased. Decrease of maximum expiratory flow could be caused by a loss of elasticity of pulmonary parenchyma and by a beginning increased resistance in peripheral pulmonary ways. Decreased DLCO was identified in majority of patients and was caused by anaemia and a minimal interstitial pulmonary edema. Use of a single peritoneal dialysis with dialysis solutions of various glucose concentrations did not have any significant effect on acidobasic balance markers nor pulmonary respiratory functions.
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PMID:[Continuous ambulatory peritoneal dialysis and respiratory pulmonary functions]. 1532 56

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.
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PMID:The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep. 1546 Mar 22

The absence of osmotic diuresis modifies the effects of hyperglycemia on body fluids in patients with advanced renal failure. To determine the relationship between clinical manifestations and abnormalities in tonicity and extracellular volume in such patients, we analyzed 43 episodes of severe dialysis-associated hyperglycemia (serum glucose exceeding 600 mg/dL) treated only with insulin. The main manifestations were dyspnea in 22 cases (pulmonary edema in 19), nausea and vomiting in 15, coma in 13 and seizures in 3, while 5 patients had no symptoms. Treatment with insulin resulted in a decrease in serum glucose value from 913 +/- 197 mg/dL to 170 +/- 78 mg/dL, an increase in serum sodium level from 125 +/- 5 to 136 +/- 5 mmol/L, and a fall in calculated serum tonicity value from 300 +/- 13 to 282 +/- 11 mmol/kg (all at p < 0.001). The ratio of the change in serum sodium level over change in serum glucose concentration was -1.50 +/- 0.22 mmol/L per 100 mg/dL. The percent increase in extracellular volume secondary to hyperglycemia developing from the prior euglycemic state and calculated from changes in serum sodium and chloride concentrations, was 10.9% +/- 4.6% (1.5% +/- 0.6% per 100 mg/dL increase in serum glucose level). All clinical manifestations dissipated after correction of hyperglycemia in 42 patients. One woman developed during treatment a fatal myocardial infarction. Dialysis patients with severe hyperglycemia may develop symptoms as a result of hypertonicity and extracellular expansion. Insulin alone may be sufficient treatment for these symptoms. The changes in serum tonicity and electrolytes during treatment are consistent with theoretical predictions.
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PMID:Serum tonicity, extracellular volume and clinical manifestations in symptomatic dialysis-associated hyperglycemia treated only with insulin. 1552 Dec 14


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