Chest
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Tube thoracostomy is a standard therapy for a number of pulmonary disorders. The procedure is associated with a certain incidence of morbidity related to the technique of insertion, the patient population selected, and the length of time the tube remains in place. ⋯ A case of a delayed pulmonary perforation developing several days after placement of a chest tube is described with a discussion of the clinical and radiographic findings associated with this complication. A possible pathophysiologic mechanism by which this complication may have occurred is proposed.
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Congestive heart failure (CHF) has been associated with the development of restrictive ventilatory abnormalities and decreased pulmonary diffusing capacity. Whether these physiologic changes reflect permanent alterations of lung anatomy or result solely from potentially reversible alterations of lung water is not known. To examine this issue, we reviewed the pulmonary function tests (PFTs) and cardiac catheterization data from recipients of successful heart transplants prior to and 1 year after transplantation. ⋯ Diffusing capacity for carbon monoxide was decreased before transplantation and showed a small decline after transplantation from 82.3 +/- 3.2 to 76.8 +/- 2.6 percent of predicted (p < 0.05). After correction of severe CHF by cardiac transplantation, normalization of FEV1, FVC, and TLC can be anticipated. Diffusing capacity, however, may actually decline after transplantation.
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Comparative Study
Comparison of blue dye visualization and glucose oxidase test strip methods for detecting pulmonary aspiration of enteral feedings in intubated adults.
To compare the relative utility of blue dye visualization with a glucose oxidase test strip method for detecting aspiration of enteral feedings. ⋯ Inspecting tracheal secretions for blue discoloration failed to detect most episodes of enteral feeding aspiration. Glucose oxidase test strip methods should replace blue dye visualization for detecting aspiration of enteral feedings in intubated adults.
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We report a patient who received a right single lung transplant (SLT) for progressive lymphangioleiomyomatosis and required reintubation for postoperative respiratory distress. She developed hemodynamic instability due to mediastinal shift from unilateral auto-PEEP with hyperinflation of the native lung. Placement of a double lumen endotracheal tube (DLET) and institution of differential lung ventilation restored equal lung inflation and hemodynamic stability.
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To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. ⋯ Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.