Negative pressure pulmonary edema.
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A platelet function profile that provides a concise record of platelet function tests has been developed. This format can be easily modified to meet local requirements or to include hematologic tests unique to each laboratory.
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Preliminary data from a prospective randomized study of the use of a short course of adrenocorticosteroids in 73 children with ITP demonstrates a significant advantage of moderate dose (60 mg/m2/day p.o. X 21 days) prednisolone therapy in decreasing the duration of severe thrombocytopenia in most patients. The period of risk for serious bleeding, as reflected in the Rumpel-Leede test, was also significantly reduced. The number of children who developed chronic thrombocytopenia, although small in both groups, appeared to be uninfluenced by steroid therapy. No side effects or serious complications were noted in this trial.
BACKGROUND: Premature ventricular contractions (PVC), capillary leakage, and petechial hemorrhage can occur during myocardial contrast echocardiography (MCE). The effects occur as a result of the interaction of contrast agent microbubbles and the ultrasound, but the detailed etiology of the effects is not yet clear. This study tested the hypothesis that the capillary leakage results from a physiological response to injury, which might be protracted and modulated by vasoactive drugs. METHODS: Hairless rats were anesthetized and transthoracically scanned with a diagnostic ultrasound system (GE Vingmed System V) at 1.7 MHz with 1:4 triggered frames at end systole. The scan head and rats were mounted in a 37 degrees C water bath to assure free-field conditions and placement of the heart at a similar focal distance as humans. A tail vein was cannulated for injections of Optison contrast agent, vasoactive medications, and Evans Blue dye (EB). EB was injected as a marker of capillary leakage before or after scanning. RESULTS: PVCs, petechia, and capillary leakage occurred during ultrasound exposure of microbubbles in myocardium, with no effects detected in shams. The influence of the vasoactive medications propranolol and isoproterenol on the effects did not support the hypothesis. Capillary leakage occurred during and postexposure, but diminished for EB injection 20 minutes after scanning with or without isoproterenol pretreatment. CONCLUSION: MCE induced PVCs, petechia, and capillary leakage, all of which ended immediately or within 20 minutes after the examination. Contrary to the hypothesis of a physiological mechanism, the capillary leakage appears to be primarily a mechanical effect rather than a physiological response.
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The effect of hemorrhagic shock and reinfusion of the shed blood on lung microvasculature was studied in 10 anesthetized dogs during a control, a shock (40-50 mmHg aortic pressure), and a reinfusion period. Pulmonary capillary hydrostatic and oncotic pressures decreased, whereas lung lymph flow and lymph-to-plasma albumin and globulin ratios increased with shock and with reinfusion, indicating an increased microvascular permeability. Calculated pore radius increased with reinfusion (p less than 0.05), whereas pore number increased both with shock and with reinfusion in eight dogs. Comparison of the autopsy results of these experiments with those of previous control and shock animals showed that with reinfusion there was a rise in lung wet-to-dry weight ratios and increased granulocytes by light microscopy. By electron microscopy, the granulocytes were intravascular, and there was alveolar wall edema without endothelial or epithelial damage. We conclude that the morphological changes in the lung with reinfusion are minimal and that our data are consistent with the hypothesis that granulocytes may cause the observed microvascular injury and interstitial edema.
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