• 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.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.313-316
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• 2007

Negative pressure pulmonary edema (NPPE) during anesthetic recovery is a rare, but potentially serious complication for patients who are undergoing different surgical procedures. The proposed mechanism is the generation of high negative pressure during markedly respiratory effort and upper airway obstruction from glottis closure and laryngospasm, and this all leads to pulmonary edema. We report here on a case of a healthy 26-year-old male who immediately developed NPPE and hemoptysis following extubation after partial rib resection due to benign rib tumor; the patient was treated conservatively. We also include a review of the review literatures.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.432-435
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• 2005

An 82-year-old female non-smoker with a history of hypertension presented with increasing dyspnea, cough and some purulent sputum without fever. Upon admission, the patient was in a distressed condition. Auscultation revealed diminished breath sounds with no rales over the right lung. An examination of the heart revealed a regular rhythm and a systolic murmur radiating from the apex of the heart. There was no pitting edema in the lower extremities. The blood tests showed mild leukocytosis and an increased C-reactive protein level. The $O_2$ saturation was 98 % whilst breathing room air. The electrocardiogram demonstrated sinus tachycardia. The chest radiograph showed a moderate cardiomegaly, right lobe infiltrates, and blunting of the both costophrenic sulcus suggesting a small pleural effusion. Three days after admission, the symptoms became slightly aggravated despite being treated with empirical antibiotics for presumed community-acquired pneumonia. Transthoracic color Doppler echocardiography indicated an ejection fraction of 48 %, mild left ventricular enlargement, and moderate left atrial enlargement resulting in severe mitral regurgitation. The clinical symptoms and right pulmonary edema resolved quickly with intravenous furosemide treatment.

• Proceedings of the KOR-BRONCHOESO Conference
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• 2007.05a
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• pp.42-42
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• 2007

• Journal of Chest Surgery
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• v.37 no.2
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• pp.180-183
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• 2004

We report a case of a patient with lung cancer, which invaded the left atrium and pericardium. Right middle and lower lobectomy was performed with the use of the extracorporeal circulation. Postoperative pathologic examination revealed the stage of IIIB (T4N1MO). Although the postoperative clinical course was complicated by acute localized right sided pulmonary edema and the bronchopleural fistula, the patient recovered smoothly after the procedure of omentopexy with pedicled graft of greater omentum in closing the BPF. As of August 2003, he has been followed up for 6 years and he is healthy without any evidence of recurrence. We could not find any report concerning lung cancer resection using cardiopulmonary bypass in Korean literature and believe this is the first report, especially with long-term survival.

• Journal of Chest Surgery
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• v.34 no.3
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• pp.212-223
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• 2001

배경: 이식폐의 보존 및 재관류 동안 cyclic adenosine monophosphate(cAMP)와 nitric oxide(NO)는 폐혈관 내 순환조절을 유지하는데 있어 중심적인 역할을 한다. 그러나 내치세포내의 cAMP와 NO 모두 허혈-재관류 과정 동안에 현저하게 감소한다. 이에 저자는 low potassium dextran(LPD) 폐조본액에 cAMP의 유사체인 dibutyry1 cAMP(db-cAMP)와 NO의 공여물질인 nitroglycerin(NTG)을 첨가하여 이들의 폐보존 효과를 알아보고, 이들은 첨가한 폐보존액 들의 효과를 비교하였다. 대상 및 방법: 토끼 폐장 분리관류 모형에 실험군은 각각 6마리씩 4개군으로 단순 LPD 페보존액만 사용한 경우(I군), LPD 용액에 NTG 만 참가한 경우(II군), cAMP 만 첨가한 겨우(III군) 그리고 두가지 모두를 첨가한 경우는 IV군으로 분류하였으며, 폐보존액이 주입된 심폐블록은 영상 1$0^{\circ}C$에서 24시간 동안 보관한 다음 100% 산소농도에서 기계호흡을 하면서 신선 정맥혈로 30분 동안 재관류를 시행하였다. 재관류폐의 평가를 위해 폐기능 및 폐부종 정도를 정량 측정하였으며, 유출로 혈액으로부터 tumor necrosis factor $\alpha$(TNF-$\alpha$)와 간접적인 NO의 총량을 알기 위해 nitrite/nitrate의 양을 측정하였다. 또한 재관류가 끝난 후 광학 및 전자현미경학적 소견을 관찰하였다. 결과: 모든 실험군 중 제 IV군 의 폐보존 능력이 가장 우수하였으나, 제 II, III, IV군 사이는 통RP적으로 유의한 차이가 없었다. 제 I군은 제 II, III, IV군들에 비해 유의하게 폐기능이 가장 나쁘고 폐부종 정도가 가장 심했다(p<0.05). 제 II군은 제 III군에 비해 더 좋은 폐기능을 보였고, 폐부종 정도가 덜 하였으나 통계적은 유의성은 없었다. TNF-$\alpha$ 는 제 IV 군이 Irns에 비해 유의하게 분비량이 적었다. (p<0.05). 총 NO의 양은 제 II군과 IV 군이 제 I 군과 III군보다 유의하게 높았으나(p<0.001), 제 II군과 IV군, 제 I군과 III군 사이 비교에서 유의한 차이는 없었다. 또한 제 I 군과 III군에서는 시간이 지남에 따라 유의하게 NO의 양이 점차 감소하였다. (p<0.05). 광학 및 전자현민경 소견상 폐포 및 폐혈관 구조가 제 II, III, IV 군이 I 군에 비해 더 잘 보존되어있었다. 결론: LPD 폐보존액에 db-cAMP 및 NTG의 첨가는 폐보존 효과가 모두 우수함을 확인하였고 이들의 폐보존 효과 차이는 거의 없음을 알수 있었다. 그렇지만 이들의 병합사용이 폐혈관 항상성을 더 잘 유지시킬 수 있고 허혈-재관류 손상을 줄여 폐보존 효과를 높일 수 있을 것이라고 기대된다.

• Journal of Sasang Constitutional Medicine
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• v.12 no.1
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• pp.265-270
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• 2000

Occasionally, apoplexy is caused by functional or physiologic cardiopulmonary abnormality. In addition, theses may become the factor of aggravating apoplexy and involve complication. If patient has cardiopulmonary disease, progressing of apoplexy is commonly used to be accelerate and prognosis is deteriorative. There by the patient who has cardiopulmonary disease, should be particularly treated for cardiopulmonary disease. We got good result, during treat Soeumin cerebral vascular infarction patient who has pulmonary edema leaded from congestive heart failure, with Sasang Constitutional treatment. Therefore I reported them here. She was 68 years old, female patient. She visited our hospital for apoplexy with right side hemiparesis, dysphagia, dysphasia. After her admission into our hospital, we knew that she has congestive heart failure. The diagnosis is established. She presented with severe general edema and pulmonary edema. Although Soeumin edema usually classified as Taiyin Disease, we classified this as Shaoyin Disease, through diet, discharge, sleep, tongue and symptoms. We has prescribed Gungguichongsoyijung-tang(芎歸蔥蘇理中湯) in accordance with the principle of invigorating the Spleen and lower Yin(建碑而降陰). And her symptoms has improved.

• 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.

• 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.