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

We treated two cases of diabetes mellitus who developed acute pulmonary edema following accidental aspiration of sweetened water for emergency treatment, when they had fallen into hypoglycemic coma following an overdose of injectable insulin. Although they showed hypoxemia and radiological examinations revealed pulmonary edema, they improved by giving only oxygen and antibiotics in a few days. The osmotic pressure of the sweetened water in each case was approximately 2,600 mOsm and 1,900 mOsm. We suppose that the pathogenesis of the pulmonary edema was due to the sweetened water causing water within the pulmonary vessels to permeate into the alveoli.
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PMID:Acute pulmonary edema caused by accidental aspiration of sweetened water in two cases of diabetes mellitus. 986 63

The acute complications of diabetic ketoacidosis in children and adolescents are well recognized but not completely understood. Clinical studies have focused primarily on brain edema. We have investigated the prevalence and course of interstitial pulmonary edema in patients with severe diabetic ketoacidosis all of whom had uneventful clinical courses. High resolution computed tomography scans of the lungs were analyzed by determining the Hounsfield attenuation level and then converting to physical density values. All seven patients had evidence of interstitial pulmonary edema on the first scan, which was performed within 1 h of hydration and prior to receiving insulin; six of the seven patients had increased pulmonary density 6-8 h into treatment, and all had complete resolution of the interstitial changes at discharge. Our study suggests that subclinical interstitial pulmonary edema may be a frequent occurrence in children and adolescents with severe diabetic ketoacidosis and may very well be present prior to treatment. The study also supports the philosophy of cautious rehydration and the close monitoring of children and adolescents with diabetic ketoacidosis until a more complete understanding of this pathophysiologic event is achieved.
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PMID:Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. 987 65

The use of perinatal steroid therapy, first introduced in 1972 is effective in precocious maturation of human lungs. Antenatal corticosteroid therapy results in reduction of fetal mortality, respiratory distress syndrome, intraventricular hemorrhage in preterm babies. These benefits extend to a broad range of gestational age. They comprise the interval between 24 and 34 weeks of human pregnancy and are not limited by the infant's gender or race. The beneficial effects of corticosteroids are the best pronounced after more than 24 hours from the beginning of the treatment. Noteworthy is that therapy less than 24 hours of duration may also improve outcomes. In the presence of premature rupture of membranes, or better with intact membranes, antenatal corticosteroids reduce frequency of RDS, IVH and finally mortality and morbidity. Review of meta-analyses based on randomized trials supports general option that premature infants whose mothers received corticosteroids before delivery are less likely to develop RDS and its complications. Recent data showed that benefits derived from ANS are additive to those of surfactant therapy, rendering the latter more effective. Followup of children up to 12 years of age indicate that ANS do not impair physical growth or psychomotor development. Short-term adverse effects including maternal infection, maternal pulmonary edema were not clearly demonstrated. Pulmonary edema has not been reported when ANS were used alone (i.e. not in combination with betamimetic tocolytics). No long-term unwanted effects on maternal adrenal function have been observed. There is no serious maternal risk resulting from immunosuppressive effect of corticosteroid therapy on maternal immune system. Although glucocorticoid therapy is likely to provoke insulin resistance, and thereby deterioration in diabetic control, and potentially causes cortisol resistance in the fetal lung, the results of scarce randomized trials are not conclusive. In any rate strict control of maternal diabetes mellitus reduces incidence of RDS. Current available data are not indicative of higher risk of fetal mortality in association with maternal hypertensive disease and ANS. In conclusion, most randomized trials of ANS has provided a positive evidence of efficacy and safety of this highly cost effective therapy in most common clinical situations. However, further trials and more precise estimates are justified on ANS treatment specifically related to blood glucose control and evidence concerning the promotion of fetal lung maturity in babies of women with diabetes mellitus. Although benefits of the corticosteroid therapy are beyond any doubts, more experience is needed to assess the effect of ANS on maternal and/or fetal infection in presence of premature rupture of membranes. And finally, further assessments are required on antenatal corticosteroids with dose regimens in patients with multifetal gestation, more common after wide use of techniques of the assisted human reproduction.
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PMID:[Intrauterine stimulation for fetal respiratory system maturation; benefits and risks]. 1114 22

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

The thiazolidinediones are an important class of insulin-sensitizing agents used for the treatment of type 2 diabetes. Similar to other antidiabetic agents, use of the thiazolidinediones is limited by adverse drug reactions. Specifically, use of the thiazolidinediones is associated with a triad of fluid retention, edema, and weight gain. In premarketing clinical trials, edema was reported to occur infrequently with minimal severity. However, several published cases from postmarketing data demonstrate that thiazolidinedione-induced fluid retention, exhibited by the initial onset of peripheral edema and weight gain, can progress to a more severe form of pulmonary edema that is refractory to diuretic therapy with resolution of symptoms only through discontinuation of the offending thiazolidinedione. In clinical practice, the occurrence of edema secondary to a thiazolidinedione drug may occur more frequently than reported. Two cases presented in this report illustrate a different outpatient management approach that enables both desired glycemic control and minimal fluid retention while using the thiazolidinediones.
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PMID:Management of rosiglitazone-induced edema: two case reports and a review of the literature. 1239 45

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called noninsulin-dependent diabetes mellitus) is not as rare as was once thought. This article reviews data about precipitating events, pathogenesis, carbohydrate, lipid and ketone, water and electrolyte metabolism in this hyperglycemic crisis. The review discusses diagnostic procedures, laboratory evaluation, differential diagnosis and treatment: replacement of fluid and electrolytes, low-dose insulin therapy and recommendations for use of bicarbonate. A discussion of complications management of diabetic ketoacidosis (hypoglycemia, hypokalemia, cerebral edema, hyperchloremic metabolic acidosis, pulmonary edema, adult respiratory distress syndrome), mortality rate and prevention are included in this review.
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PMID:[Diabetic ketoacidosis]. 1247 77

Thiazolidinediones represent an established class of insulin sensitizing agents for treating noninsulin-dependent diabetes mellitus. Darglitazone, a thiazolidinedione approximately 200x more potent than ciglitazone, was evaluated in preclinical safety assessment studies using rats (1, 5, and 50 mg/kg/day) and cynomolgus monkeys (50, 75, and 100 mg/kg/day). Darglitazone was a potent adipogenic agent in rats, causing hyperplastic/hypertrophic changes and firmness of white and perirenal, dorsal thoracic (TBAT), and interscapular brown adipose tissue (BAT). Progressive changes in BAT size, morphology, firmness, and fatty acid composition preceded clinical signs of impaired respiration and the subsequent development of a dose-dependent, life-threatening hydrothorax. The characteristics of the pleural effusate were consistent with lymphatic fluid. These adverse effects were ameliorated/reversed upon drug withdrawal and were insulin-dependent since rats rendered totally insulinopenic by streptozotocin pretreatment did not develop TBAT changes or hydrothorax. Although the effects of darglitazone on BAT changes were consistent with enhanced sensitivity to endogenous glucocorticoids, adrenalectomy, and dietary dehydroepiandrosterone administration were without a protective effect. Treated monkeys also developed white and BAT hyperplasia/hypertrophy, peripheral edema, and hydrothorax-related morbidity/mortality. Both species developed reversible, dose-related reductions in red blood cell parameters and follicular atresia. Peripheral and pulmonary edema are purportedly a multifactorial process involving vasodilatation, increased endothelial permeability, and/or plasma volume expansion due to reduced renal sodium excretion. Moreover, profound alterations in TBAT hypertrophy/hyperplasia/firmness may lead to discrete hydrothorax by restricting normal thoracic lymphatic drainage. Similar effects on adipose tissue, hemodilution, and edema (peripheral and pulmonary) were observed clinically with darglitazone and/or several other structurally similar/dissimilar PPAR-gamma agonists.
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PMID:Mechanism and implications of brown adipose tissue proliferation in rats and monkeys treated with the thiazolidinedione darglitazone, a potent peroxisome proliferator-activated receptor-gamma agonist. 1262 51

Increasing evidence suggests that neurohumoral manifestations of heart failure may lead to insulin resistance, predisposing patients with heart failure to the development of glucose intolerance or worsening of existing diabetes. Theoretically, insulin-sensitizing thiazolidinediones (TZDs) should be beneficial in this patient population. A 74-year-old man with well-compensated systolic dysfunction and longstanding type 2 diabetes mellitus treated with glyburide began therapy with rosiglitazone 4 mg/day, which was increased to 8 mg/day after 1 month. Two weeks later he was seen with a 5-kg weight gain, shortness of breath, bibasilar rales, +S3 gallop, and increased jugular venous distention. Twelve days later symptoms worsened, with pulmonary edema on chest radiograph, continued weight gain, and +4 pitting edema resistant to oral diuretics. The patient was admitted to the hospital for exacerbation of heart failure. Five days after discharge he was readmitted for similar symptoms, including an 11.8-kg weight gain. He reported adherence to drug therapy and diet. Rosiglitazone was immediately discontinued and 11 days later the man's weight stabilized to 79 kg and remained between 79 and 80 kg 2 and 3 months after discharge. This case demonstrates that TZDs may precipitate weight gain and pulmonary and peripheral edema in patients with stable heart failure. Earlier reports documented similar symptoms in patients without a history of heart failure. Although current recommendations state that TZDs should not be administered to patients with New York Heart Association class III or IV disease, practitioners should be aware that these adverse effects also may occur in patients with milder forms heart failure as well as those without heart failure.
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PMID:Possible heart failure exacerbation associated with rosiglitazone: case report and literature review. 1288 8

Thiazolidinediones, also called glitazones, are insulin sensitisers that act as agonists of the peroxisome proliferator-activated receptors-gamma (PPARgamma). After the withdrawal of troglitazone due to hepatotoxicity, only pioglitazone and rosiglitazone can be used for treating patients with type 2 diabetes mellitus, either as monotherapy or in combination with metformin or with sulphonylureas (or glinides). The combination of glitazones with insulin is also appealing, as it allows improvement of glycaemic control while decreasing the daily insulin requirement. Insulin dosage has to be adjusted regularly to avoid hypoglycaemic episodes. However, some concerns have been raised about such combined glitazone-insulin therapy because it may favour weight gain due to both enhanced adipogenesis and fluid retention. Such adverse effects are commonly observed in all diabetic individuals receiving glitazones, whatever the mode of use, but they appear to be exacerbated in insulin-treated patients. Body fat gain is a major drawback of treatment with adipogenic compounds such as glitazones. However, some evidence suggests that the fat is redistributed in a favourable direction, that is, from visceral to subcutaneous depots, although no long-term follow-up is yet available. An estimated 2-5% of patients receiving glitazone monotherapy and 5-15% receiving concomitant insulin therapy experience peripheral oedema. Some anecdotal cases of pulmonary oedema have also been reported, especially in insulin-treated patients, although the actual incidence of this complication is unknown. All glitazones increase the intravascular volume by approximately 6-7% in a dose-dependent manner. Rather than a direct effect on cardiac or renal function, fluid retention and tissue oedema seem to be part of a vascular 'leak' syndrome. Such a phenomenon may have greater consequences in patients with type 2 diabetes treated with insulin because such patients are usually older, have had the disease long-term and have worse cardiac or renal function. Additionally, glitazones may potentiate the renal effects of insulin on sodium and water retention. Regardless of the mechanism, it is conceivable that additional fluid retention caused by glitazones may alter the already precarious volume status in patients with underlying cardiac or renal dysfunction, thus leading to oedema and congestive heart failure. Thus, it is prudent to either avoid glitazones or use them cautiously in individuals with impaired cardiac function. Further studies are clearly needed to define the mechanisms of fluid retention associated with glitazone use and to determine the safety of cautious use of these new insulin sensitisers in insulin-treated patients with type 2 diabetes.
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PMID:Combined thiazolidinedione-insulin therapy: should we be concerned about safety? 1536 73

The edematogenic properties of insulin have long been documented, although they have been underestimated despite current trends toward intensive insulin therapy. Insulin treatment has been associated with weight gain, mild or moderate edema, and, rarely, generalized edema and cardiopulmonary congestion. In addition, the use in recent years of thiazolidinediones, which improve insulin sensitivity, has been associated with weight gain and peripheral edema, which can progress to pulmonary edema, particularly when thiazolidinediones are used in combination with insulin. This article attempts to raise awareness about the overlooked edematogenic action of insulin. In addition, the potential role of edema-provoking properties of insulin in the development of vascular complications in patients with diabetes is discussed.
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PMID:The edematogenic properties of insulin. 1538 8


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