• Journal of Chest Surgery
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• v.24 no.8
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• pp.797-801
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• 1991

Reexpansion pulmonary edema following pneumothorax, atelectasis, massive pleural effusion are clinically uncommon, but sometimes life threatening progression. Reexpansion pulmonary edema is usually ipsilateral but rarely contralateral or both. Reexpansion pulmonary edema was occurred when chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid. The pathogenesis of the reexpansion pulmonary edema is unknown but is probably mutifactorial. The etiological factors of the reexpansion pulmonary edema are chronicity of the lung collapse, technique of the reexpansion, airway obstruction, loss of the surfactant, and pulmonary artery pressure changes. In the treatment of the chronically collapsed lung, physician must be remembered the possible events, and to prevent of the complication.

• Journal of Veterinary Clinics
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• v.33 no.2
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• pp.113-115
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• 2016

A 6 month-old castrated male Yorkshire terrier (weighing 1.0 kg) was presented with acute respiratory distress. Diagnostic imaging studies found post-obstructive pulmonary edema sequel to upper airway obstruction by a rubber plug lodged at thoracic esophagus. The rubber plug was removed endoscopically. After removal of this rubber plug with conventional therapy for pulmonary edema, the clinical condition of dog was stabilized. To the best knowledge of authors, this is the first case report describing postobstructive pulmonary edema in a dog in Korea.

• Near Infrared Analysis
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• v.2 no.1
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• pp.43-53
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• 2001

A non-invasive spectroscopic method is presented for the measurement of pulmonary edema. Both early diagnosis and quantitative edema estimates were investigated. The spectroscopic determination of pulmonary edema involved the acquisition of diffuse reflectance spectra in the near-infrared (NIR) region with change in water concentration - water is the main constituent of edema fluid. Pulmonary edema was induced into the excised perfused lungs of seven animals by elevating the hydrostatic pressure. Estimates of edema were ascertained from a partial least squares regression of the measured spectral response. Actual edema was determined from the change (increase) in total lung weight. Estimates in relative lung weight increases due to in vitro edema were made with the near infrared spectra. The results revealed that fluid accumulation produced spectral changes in the O-H and C-H absorptions as well as scattering changes in the spectra. Histology of the lung was used to verify the presence or absence of interstitial and alveolar edema. Results demonstrated that near infrared spectroscopy might provide a new tool for clinical assessment of pulmonary edema.

• Journal of Chest Surgery
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• v.28 no.1
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• pp.81-84
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• 1995

Re-expansion pulmonary edema following pneumothorax or hemothorax is clinically uncommon but occasionally life threatening. Clinical details are given of two patients.Ipsilateral pulmonary edema were developed after chest tube insertion due to spontaneous pneumothorax in case I and after evacuation of postoperative hemothorax in case II. The patients were treated with frequent bronchial toilet.The administration of colloid solution and diuretics was effective. The possible mechanisms underlying the edema are discussed.Both increased time of collapse and suction tended to correlate with reexpansion edema.The present two cases provided evidence for longstanding lung collapse and immediate application of suction.

• Journal of Chest Surgery
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• v.7 no.1
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• pp.1-8
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• 1974

Acute pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution index was determined from pressure volume curves in excised lungs. Surface activity was also investigated with measurements of maximum and minimum surface tension and stability index on saline extracts of same lungs. The results were as follows. 1. The expansion index of excised lung in which pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution was ignificantly decreased as compared with the normal control of $0.86{\pm}0.017$ to $0.74{\pm}0.03$, $0.71{\pm}0.081$and $0.76{\pm}0.02$, respectively. 2. The deflation curves of excised lungs in which pulmonary edema was induced were significantly decreased as compared with the normal controls. 3. The minimum surface tension of excised lung in which pulmonary edema was induced was significantly increased in each groups and stability index was significantly decreased as compared with the normal controls 0.78 to $0.35{\pm}0.039$, $0.29{\pm}0.02 $ and $0.31{\pm}0.083$, respectively. 4. The decrease of pulmonary surface activity in acute pulmonary edema was in proportion to the degree of pulmonary edema regardless of their etiology.

• Journal of The Korean Society of Clinical Toxicology
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• v.8 no.2
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• pp.113-121
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• 2010

Purpose: Drug-induced non-cardiogenic pulmonary edema has been reported on in a drug case series. For most of the agents that cause pulmonary edema, the pathogenic mechanisms that are responsible for the pulmonary edema remain unknown. We report here on the cases of suspected drug-induced pulmonary edema and we analyze the clinical characteristics. Methods: We reviewed the medical records of 1,345 patients who had drug adverse effects and drug poisoning from January 2005 to July 2010, and 480 of these patients were admitted to the EM Department. Among them, 17 patients developed abnormal chest radiological findings and they were analyzed for any clinical characteristics, the initial symptoms, securing the airway and the clinical results. Results: Seventeen patients out of 480 (3.54%) developed drug-induced abnormal chest radiographic pulmonary edema; they displayed initial symptoms that included mental change (41.2%), dyspnea (17.6%), vomiting (11.8%), etc, and some displayed no symptoms at all (11.8%). Only 3 patients out of the 11 who died or had severe pulmonary edema were able to obtain an advanced airway prior to their arrival to the EM Department. Clinical recovery was generally rapid and this was mostly completed within 6 hours. The mortality rate was 11.8% (2 of 17 patients), and the causative drugs were found to be propofol (35.3%, 6 of 17 patients), multiple drugs (41.2% or 7 out of 17) and one patient each with ephedrine, ethylene glycol, doxylamine and an unknown drug, respectively. Conclusion: Drug-induced pulmonary edema and deaths are not uncommon, and recovery is typically rapid with few long-term sequelae when drug administration is discontinued. Oxygen therapy and securing the airway must be performed during transportation for patients with pulmonary edema.

• Journal of Chest Surgery
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• v.29 no.5
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• pp.581-584
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• 1996

Reexpansion pulmonary edema is a rare complication of the treatment of lung collapse secondary to pneumothordx, pleural effusion, or atelectasis but occasionally life threatening. Generally, reexpansion pulmonary edema is believed to o cur only when a chronically collapsed lung is rapidly reexpanded by evacuation or large amounts of air or fluid. This complication is heralded by tachypnea, unilateral rales, and profuse expectoration of frothy secretion within several hours of reexpansion. Increased dur- ation of pneumothorax and the use o( suction are important factors in the generation of reexpansion pulmonary edema. We had experienced 3 cases of reexpansion pulmonary edema. In the two cases the pneumothorax had been present for several days, and, after insertion of a chest tube, pulmonary edema developed unilaterally but improved with supplemental oxygen. In the third case, massive pleural effusion was present. and, after insertion of a chest tube, pulmonary edema developed unilaterally, followed by cardiac arrest. He died of pulmonary edema inspire of resuscitation.

• Journal of Yeungnam Medical Science
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• v.21 no.1
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• pp.114-119
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• 2004

This report concerns an unusual case of acute postoperative pulmonary edema without any apparent causes in a 45-year-old man. The patient was subjected to the removal of a previously placed device on the left tibia, and the excision of a benign mass on the right forearm. Unexpected acute bilateral pulmonary edema occurred immediately after the completion of the procedures. The etiologies were reviewed in relation to the patient's condition and clinical manifestations. Fluid overloading was excluded as a cause in view of the patient's perioperative state and postoperative chest X-ray results. We could not find any symptoms of upper airway obstruction during emergence from general anesthesia. We had doubts about tourniquet or fentanyl-induced pulmonary edema, but these factors were not sufficient to bring about pulmonary edema in this case. To our knowledge, the cause of acute pulmonary edema in this case is indeterminate.

• Journal of Chest Surgery
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• v.28 no.5
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• pp.510-512
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• 1995

Reexpansion pulmonary edema following treatment of pneumothorax and pleural effusion is a rare complication. However, because of possibility of its fatal outcome, physicians must be aware of this complication and every effort must be made to prevent its occurrence. We experienced 5 cases of reexpansion of pulmonary edema. One was complete tension pneumothorax and became death despite of intensive management. Remained four were 3 pneumothoraces and 1 pleural effusion and discharged without event, fortunately.

• Tuberculosis and Respiratory Diseases
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• v.51 no.2
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• pp.161-165
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• 2001

Acute bilateral reexpansion pulmonary edema after pleurocentesis is a rare complication. In one case, bilateral reexpansion pulmonary edema after unilateral pleurocentensis in sarcoma was reported. Various hypotheses regarding the mechanism of reexpansion pulmonary edema include increased capillary permeability due to hypoxic injury, decreased surfactant production, altered pulmonary perfusion and mechanical stretching of the membranes. Ragozzino et al suggested that the mechanism leading to unilateral reexpansion pulmonary edema involves the opposite lung when there is significant contralateral lung compression. Here we report a case of bilateral reexpansion pulmonary edema and acute respiratory distress syndrome after a unilateral pleurocentesis of a large pleural effusion with contralateral lung compression and increased interstitial lung marking underlying chronic liver disease.