• 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.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.

• 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.

• Korean Journal of Veterinary Research
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• v.62 no.3
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• pp.22.1-22.4
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• 2022

This study reports the efficacy of the vasodilator sodium nitroprusside (SNP), for treatment of acute cardiogenic pulmonary edema in dogs. For this study, the patients were divided into the SNP only treatment group, the SNP, furosemide and dobutamine treatment group, and non-SNP treatment group. Seven dogs, 6 dogs and 2 dogs were favorable responders in SNP only group, group with SNP, furosemide and dobutamine and non-SNP treatment group, each. The results of this study suggest that SNP can be an effective alternative therapy for dogs with acute cardiogenic pulmonary edema.

• Tuberculosis and Respiratory Diseases
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• v.56 no.5
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• pp.532-535
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• 2004

Acute fulminating pulmonary edema was developed in 20 year old female following an acute airway obstruction due to a burglary attack on neck with bare hands. The pathogenesis of pulmonary edema is related to the alveolar and capillary damage induced by the severe negative pressure generated by attempting to inspire against the closed upper airway. This female responded to fluid restriction and oxygen supply. To our knowledge, pulmonary edema caused by man has never been reported in the literature.

• 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.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.2
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• pp.157-160
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• 2006

Nasotracheal intubation is performed routinely in maxillofacial surgery to optimize visualization of the surgical field. The CaldwellLuc operation is an approach to the maxillary sinus through the labiogingival sulcus and canine fossa. The operation is used to treat chronic maxillary sinusitis, and involves curettage of the mucosa of the maxillary sinus and the creation of an inferior meatal antrostomy. After the operation, a nasal Foley catheter is inserted into the inferior nasal meatus for the discharge of blood and tissue fluid. Then, the nostril is packed with vaseline gauze. Before the patients awaken, they experience impaired switching from nasal to oral breathing. Pulmonary edema can result from excessive negative intrathoracic pressure caused by acute airway obstruction in patients breathing spontaneously. During anesthesia and sedation, airway obstruction can occur at the levels of the pharynx and larynx. Even in patients who are awake, alteration in the ability to change the breathing route from nasal to oral may affect breathing in the presence of an airway obstruction, causing this catastrophic event. We experienced a case in which acute pulmonary edema resulted from acute airway obstruction triggered by the patient's inability to switch the breathing route from nasal to oral during emergence from anesthesia.

• The Journal of Internal Korean Medicine
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• v.11 no.2
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• pp.1-15
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• 1990

Certain oriental medication have been shown to be effective in decreasing pulmonary vascular resistance and increasing cardiac output in primary pulmonary artery pressure secondary to pulmonary edema. So oleic acid was administered in 14 dogs in order to induce acute lung injury. And we studied the hemodynamics and blood gas changes of Pyengpaetang(50mg, 100mg) with continuous postive pressure was ventilation in pulmonary edema. The pulmonary edema group, arterial oxygenation was improved after 5 and $10cmH_2O$ PEEP(positive end expiratory pressure), but cardiovascular system was depressed. Blood pressure and cardiac output were decreased, and CVP, MP AP, PCWP were increased. In Pyengpaetang(50mg) group, mean aortic pressure was decreased and PCWP(pulmonary capillary wedge pressure) was decreased remarkably, while there was a significant increase in cardiac output. And there was improvement in $PaO_2$ and $PaCO_2$ without hemodynamic changes after applying 5cm $H_2O$ PEEP, but arterial blood gases$(PaO_2,\;PaCO_2)$ were improved, while cardiovascular effects were depressed after cm $H_2O$ PEEP. In Pyengpaetang(100mg) treated group, there was no significant hemodynamic change. But mean pulmonary arterial pressure was significantly increased, and cardiac output was decreased significantly after applying the more degree of PEEP. And blood gases were not changed significantly after applying the more degree of PEEP. The above results suggest that the effects of Pyengpaetang(50mg) group is superior to those of Pyengpaetang(100mg) group on the effects of hemodynamics and gas exchanges in acute lung injury in dogs. So we can conclude that lower degree PEEP 5cm $H_2O$ is more beneficial in Pyengpaetang(50mg) treated group.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1408-1413
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• 1997

A 68 year-old male was admitted with complaint of dyspnea and nonproductive cough which developed 6 hours after accidental inhalation of nitrogen dioxide. On admission, acute pulmonary edema and severe hypoxemia were found. With oxygen and bronchodilator therapy, diffuse alveolar consolitation and his dyspnea were improved from the following day. He was discharged at 8th hospital day with prednisolone 30mg daily for prevention of bronchiolitis obliterans. During 6 weeks of follow up, there was no evidence of bronchiolitis obliterans.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.474-483
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• 1992

Background: Regardless of its causes, acute lung injury is characterized pathophysiologically by increased pulmonary arterial pressure and the protein-rich edema. Many inflammatory mediators are known to be involved in the pathogenesis of acute lung injury, including oxygen free radicals (OFR). But the changes in pulmonary capillary pressure in the OFR-induced acute lung injury is not clear. While the pulmonary edema characterized by the movement of fluid and solutes is dependent on the pressure gradient and the alveolar-capillary permeability, the role of pulmonary capillary pressure in the development of pulmonary edema is also not well understood. Method: Male Sprague-Dawley rats were divided into 5 groups: normal control (n=5), xanthine/xanthine oxidase (X/XO)-treated group (n=7), catalase-pretreated group (n=5), papaverine-pretreated group (n=7), and indomethacin-pretreated group (n=5). In isolated perfused rat lungs, the sequential changes in pulmonary arterial pressure, pulmonary capillary pressure by double occlusion method, and lung weight as a parameter of pulmonary edema were determined. Results: Pulmonary arterial pressure and pulmonary capillary pressure were increased by X/XO. This increase was significantly attenuated by catalase and papaverine, but indomethacin did not prevent the X/XO-induced increase. Lung weight gain was also observed by X/XO perfusion. It was prevented by catalase. Papaverine did not completely block the increase, but significantly delayed the onset. Indomethacin had no effect on the increase in lung weight. Conclusion: These data suggest that increased pulmonary capillary pressure by OFR may aggravate pulmonary edema in the presence of increased alveolar-capillary permeability and this may not be mediated by cyclooxygenase metabolites.