Electrophysilogical analysis and interpretation of isopotential surface maps data.
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Three cases of delayed development of pleural effusion under tension, 20 to 30 years after therapeutic pneumothorax, are described. A sudden increase in dyspnea and the radiographic findings of increasing opacity, a change from hypovolemia to hypervolemia of the hemithorax, and mediastinal shift should alert one to this delayed complication. Careful thoracentesis to decompress intrapleural tension effusion can relieve the dyspnea and improve hypoxemia. The potential risks of creating excessive negative intrapleural pressure are presented.
In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a 24Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.
Prior to the antituberculous drugs era, plombage was commonly performed for the management of pulmonary tuberculosis. However, this procedure has been associated with a variety of early and late complications depending on the technique as well as the material used. We report a rare case of severe tracheal compression as a late complication of plombage and a review of the literature.
We describe a 29-yr-old male, status post-bilateral lung transplant, who developed unilateral negative pressure pulmonary edema induced by chest tube suction in association with bilateral bronchial anastomotic strictures. We conclude that negative pressure pulmonary edema may occur secondary to high levels of negative pressure applied to the intrapleural space via chest tubes in the presence of partial large airway obstruction. Post-lung transplant patients may be especially at risk because of compromised lymphatic drainage.
A 68-year-old woman was found to have synchronous soft-tissue sarcoma of the anterior chest wall and adenocarcinoma of the breast. During her initial interview, she denied prior radiation therapy. On further questioning, it was learned that the patient had been treated for tuberculosis, as a young woman, by the induction of a pneumothorax that was monitored by repeated chest fluoroscopies. Biologically important doses of ionizing radiation can be given as an incidental part of a variety of medical treatments. The importance of searching for atypical radiation exposures, particularly in patients with unusual tumor presentations, is stressed.
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OBJECTIVE: The purpose of this study was to determine if a small pneumothorax would influence the pleurodesis resulting from talc instillation. METHODS: Sixty rabbits received an intrapleural injection of 400 mg/kg talc slurry. One half also received 10 mL of air intrapleurally after the talc. Ten rabbits in each group were killed 2, 14, and 28 days after instillation. RESULTS: Two days after the injection, the mean volume of air in the animals that had received the air was 7.5+/-0.4 mL. There was no air present in any other rabbits. The volume of pleural fluid and the pleural fluid glucose, protein, cell count, and differential were similar in both groups on day 2, while the LDH level was significantly higher in the air group (p<0.05). The degree of gross adhesions and microscopic fibrosis was similar in both groups and increased with time. CONCLUSIONS: A small pneumothorax does not decrease the efficacy of talc pleurodesis in our experimental model. These results suggest that the presence of a small amount of intrapleural air is not a contraindication to talc pleurodesis in humans.
STUDY OBJECTIVES: Collapse therapy for pulmonary tuberculosis involved placement of various materials to occupy space and keep the lung collapsed. Complications are encountered decades later. PATIENTS AND METHODS: Between 1980 and 1997, we treated 31 patients with a history of pulmonary tuberculosis in whom collapse therapy had been used and who later developed complications related to their treatment. Pyogenic empyema was present in 24 patients, pleural calcifications with bronchopleural fistula was present in 3 patients, pleural calcification with nonresolvable pneumothorax was present in 1 patient, and migration of a foreign body with formation of subcutaneous mass occurred in 3 patients. All patients with empyema were treated with antibiotics and tube drainage of pus. In addition, Lucite balls were extracted in 4 patients, lung decortication was performed in 6 patients, thoracoplasty was performed in 2 patients, and fenestration was performed in 16 patients. Bronchopleural fistulas were closed with sutures and reinforced with intercostal muscle flap in three patients; in one patient with pleural calcification and nonresolvable pneumothorax, tube drainage was attempted. In three patients with subcutaneous mass due to paraffin migration, paraffin was extracted. RESULTS: Pulmonary decortication (six patients) and thoracoplasty (two patients) resulted in elimination of empyema. Extraction of Lucite balls resulted in lung expansion and elimination of empyema in three of four patients; draining sinus remains in one patient. Fenestration resulted in elimination of empyema in 12 of 16 patients, with 3 patients with residual draining sinuses and 1 patient with remaining empyema. All bronchopleural fistulas closed with intercostal muscle flap remained closed. Following extraction of paraffin blocks, infection developed in one patient. During the follow-up period, three patients died, all of unrelated causes. CONCLUSIONS: Delayed complications of collapse therapy for tuberculosis should be treated without delay. Pressure on adjacent structures or their erosion presents danger and mandates immediate extraction; however, there is no need for routine removal of every residual plombe. Further increase in the number of multiple-drug resistant strains may force the return of collapse therapy.
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STUDY OBJECTIVES: Pneumothorax following ultrasound-guided thoracentesis is rare. Our goal was to explain the mechanisms of pneumothorax following ultrasound-guided thoracentesis in a setting where pleural manometry is routinely used. METHODS: We reviewed the patient records and procedure reports of 401 patients who underwent ultrasound-guided thoracentesis. When manometry was performed, pleural space elastance was determined. A model assuming dependence of the pleural space elastic properties on respiratory system elastic properties was used to isolate cases with presumed normal pleural space elastance. Elastance outside mean +/- SD x 2 of the isolated sample was considered abnormal. Four radiographic criteria of unexpandable lung were used: visceral pleural peel, lobar atelectasis, basilar pneumothorax, and pneumothorax with ipsilateral shift. RESULTS: There were 102 diagnostic thoracenteses, 192 therapeutic thoracenteses with pleural manometry, and 73 therapeutic thoracenteses without manometry. There was one pneumothorax that occurred from lung puncture and eight unintentional pneumothoraces, all of which showed radiographic evidence of unexpandable lung. Four of eight unintentional pneumothoraces had abnormal elastance; none had excessively negative pleural pressure (< -25 cm H(2)O). CONCLUSIONS: Unintentional pneumothoraces cannot be prevented by monitoring for symptoms or excessively negative pressure. These pneumothoraces were drainage related rather than due to penetrating lung trauma or external air introduction. We speculate that unintentional pneumothoraces are caused by transient, parenchymal-pleural fistulae caused by nonuniform stress distribution over the visceral pleura that develop during large-volume drainage if the lung cannot conform to the shape of the thoracic cavity in some patients with unexpandable lung. These fistulae appear to be pressure dependent, and the resulting pneumothoraces rarely require treatment. Drainage-related pneumothorax is an unavoidable complication of ultrasound-guided thoracentesis and appears to account for the vast majority of pneumothoraces occurring in a procedure service.
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