약물 유발성폐부종

성시한 ( Si Han Sung ),장혜영 ( Hye Young Jang ),임훈 ( Hoon Lim ) 대한임상독성학회 2010 대한임상독성학회지 Vol.8 No.2

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.

Pulmonary Edema after Catastrophic Carbon Dioxide Embolism during Laparoscopic Ovarian Cystectomy

이윤기,김은성,이해진 연세대학교의과대학 2008 Yonsei medical journal Vol.49 No.4

Laparoscopy is a surgical procedure used both for diagnosis and for various treatments. A rare but sometimes fatal complication of laparoscopy is pulmonary embolism with CO₂ resulting in pulmonary edema. During laparoscopic gynecological surgery in a 29-year-old woman who had previously undergone lower abdominal surgery, the end-tidal CO₂ suddenly increased from 40mmHg to 85mmHg and then decreased to 13mmHg with hemodynamic deterioration. These events are characteristic of a CO₂ embolism. When this occurred, CO₂ insufflation was immediately stopped and the patient was resuscitated. The patient's condition gradually improved with aggressive treatment, but the clinical course was complicated by bilateral pulmonary edema. This case of pulmonary edema was soon resolved with supportive management. The formation of a CO₂ embolism during laparoscopy must be suspected whenever there is a sudden change in the end-tidal CO₂. In addition, the possibility of pulmonary edema should be considered when a CO₂ embolism occurs.

재팽창성 폐부종 3례 보고-

오덕진,이영,임승평,유재현,Oh, Duck-Jin,Lee, Young,Lim, Seung-Pyeung,Yu, Jae-Hyeon 대한흉부심장혈관외과학회 1996 Journal of Chest Surgery (J Chest Surg) Vol.29 No.5

재팽창성 폐부종은 기층이나 흥수 또는 무기폐로 인해 오랜 시간동안 폐허탈이 있는 상태에서 빠른 속도로 공기나 많은 양의 흥수를 일시 에 제거함으로써 폐가 갑자기 재팽 창될때 올 수 있는 매우 드문 합 병증으로 때로는 사망에 이를 수 있는 심각한 상태에 빠지기도 한다. 재팽 창성 폐부종의 가장 중요한 요 소는 폐하탈기간(대부분 3일이상)과 음압을 사용한 급속한 재팽창이라고 생각되어진다. 본원에서는 재 팽창 폐부종 3례를 경험하였는데 2례에서는 수일동안 경과된 기층환자에서 폐쇄식 흥관삽관술 직후에 일측성으로 폐부종이 발생하였으며 산소흡입만으로 증상이 호전되 었다. 다른 1례 에서는 다량의 흥수로 폐쇄식 흥관삽술을 통해 약 2000mL의 층수를 배액한후 일측성으로 폐부종이 발생하였으며 이어 심정 지가 발생하여 심폐소생술에도 불구하고 홍관삽관술 시 행 12시간만에 사망하였다. 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.

Unexpected pulmonary edema and cardiac arrest following wedge resection of spontaneous pneumothorax -A case report-

Han Woong,Kim Gyu Seong,Lee Jong Min,Lim Chang Mook,Yang Hong Seuk,Jeong Chang Yeong,박동호 대한마취통증의학회 2022 Anesthesia and pain medicine Vol.17 No.3

BackgroundReexpansion pulmonary edema is a rare but potentially lethal complication. We report a case of suspected reexpansion pulmonary edema that led to cardiac arrest.CaseA 16-year-old male patient underwent wedge resection due to right pneumothorax. The patient showed pink frothy sputum three hours following surgery, and a chest x-ray showed right unilateral pulmonary edema. Thirteen hours following surgery, the patient continuously showed pink frothy sputum and presented with severe hypoxemia, tachypnea, and tachycardia. After transferring to the intensive care unit (ICU), he developed ventricular tachycardia. Cardiopulmonary resuscitation was performed for 32 min. Chest X-ray showed diffuse bilateral pulmonary edema. Extracorporeal membrane oxygenation was performed. During the 65 days of ICU care, the patient became mentally alert. However, follow-up echocardiography revealed severe heart failure.ConclusionsRexpansion pulmonary edema can rapidly progress to diffuse bilateral pulmonary edema. Therefore, careful observation is required for the patients who show signs of pulmonary edema after reexpansion.

흉부대동맥궁 박리증 수술 전, 후 발생한 폐렴 및폐부종에 대한 심폐호흡물리치료 임상사례

류흥호(Hung-Ho Ryou),김호봉(Ho-Bong Kim) 대한심장호흡물리치료학회 2016 대한심장호흡물리치료학회지 Vol.4 No.1

Purpose : The purpose of this case study is find out the effect of the cardiorespiratory physical therapy on a pneumonia and pulmonary edema of thoracic aortic-arch dissection patient before and after surgery. Methods : The thoracic aortic-arch dissection patient taken a pneumonia and pulmonary edema was performed cardiorespiratory physical therapy that coughing assist, tapping, deep breathing exercise, chest mobilization and aerobic exercise(bicycle) for 4days. Result : The thoracic aortic-arch dissection patient taken a pneumonia and pulmonary edema having a dyspnea, high-fever, lot of sputum and general deconditioning is improved by the cardiorespiratory physical therapy for 4days. A dyspnea, high-fever, lot of sputum of patient subsided and general deconditioning improved, patient s chest x-ray prove cardiorespiratory physical therapy that help restore patient s pneumonia and pulmonary edema. Conclusion : The result of application of cardiorespiratory physical therapy to the pneumonia and pulmonary edema of thoracic aortic-arch dissection patient demonstrate the importance of cardiorespiratory physical therapy in an approach to the pneumonia and pulmonary edema of thoracic aortic-arch dissection patient and treatment intervention.

증례 : 신동맥협착증 환자에서 신동맥 우회재건술 후에 재발한 급성 폐부종 1예

오숙의 ( Sook Eui Oh ),이영기 ( Young Ki Lee ),이해리 ( Hae Ri Lee ),노정우 ( Jeong Woo Noh ),신상준 ( Sang Joon Shin ) 대한내과학회 2006 대한내과학회지 Vol.71 No.3

저자들은 호흡 곤란으로 내원한 환자에서 우측 신동맥의 완전 폐쇄로 신동맥 우회재건술을 시행하였던 환자에서 재발한 flash pulmonary edema 1예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다. 또한 신동맥 협착에 대해 수술적 처치를 한 후에도 드물게 재협착이 올 수 있으므로 지속적인 경과 관찰이 필요할 것으로 생각된다. Renal artery stenosis is a rare cause of acute pulmonary edema. So-called flash pulmonary edema is associated with bilateral renal artery stenosis or stenosis in a single functioning kidney. Flash pulmonary edema has been recognized as an absolute indication for vascular intervention. A 33-year old man was admitted with acute shortness of breath. Renal angiography showed occlusion of the right renal artery. He underwent a right renal artery bypass graft. However, after the renal artery bypass graft, episodes of pulmonary edema recurred. A renal angiography showed complete obstruction of the right renal artery and bypass graft. The left renal angiography showed an intact renal artery and decreased kidney size.(Korean J Med 71:322-327, 2006)

증례보고 : 단계적 양측성 경동맥소체 종양 제거술 후 발생한 급성 폐부종

기유미 ( You Mi Ki ),공명훈 ( Myoung Hoon Kong ),오혜란 ( Hye Ran Oh ),이일옥 ( Il Ok Lee ),이미경 ( Mi Kyoung Lee ) 대한마취과학회 2007 Korean Journal of Anesthesiology Vol.53 No.2

We report a case of pulmonary edema developed in a 33-year-old female who underwent two-stage bilateral carotid body tumor excision. About 1 month ago, she had undergone a left carotid body tumor excision. After the operation, her tongue was deviated to left side. Bilateral hypoglossal nerve injury was suspected. These injuries should be carefully monitored in patients who will undergo a similar procedure on both sides because a bilateral deficit of the hypoglossal nerve is poorly tolerated, resulting potentially serious pulmonary edema. In recovery room, she became pale and SpO2 was fall down. We reintubated her immediately and the pulmonary edema was treated using a supportive management. She was discharged without any signs of dyspnea or airway obstruction, but hypoglossal nerve injury remained. We discuss the possible etiology of the upper airway obstruction after the neck surgery and review the literatures associated with the pulmonary edema following upper airway obstruction. (Korean J Anesthesiol 2007; 53: 274~6)

전신마취하에 내시경점막하박리술 환자에서 기관 내 튜브 발관 후 발생한 음압성 폐부종 1예

권지혜,김태현,오효정,조은영,정진수,정형철,손용 대한소화기내시경학회 2010 Clinical Endoscopy Vol.40 No.2

Negative pressure pulmonary edema is a recognized complication of airway obstruction, particularly after endotracheal extubation. The application of oxygen therapy and continuous positive airway pressure with the administration of diuretics under a rapid diagnosis usually clears pulmonary edema. We report a case of 61-year-old man who developed negative pressure pulmonary edema following extubation after an endoscopic submucosal dissection under general anesthesia. 음압성 폐부종은 급성 또는 만성 기도 폐쇄와 연관되어 발생하는 폐부종을 말한며 조기에 진단하여 적절한 산소 공급과 이뇨제를 사용함으로써 대부분의 폐부종은 해소되며 예후는 양호한 편이다. 저자들은 특별한 심폐 질환이 없었던 61세 남자환자에서 전신 마취하에 내시경점막하박리술을 마친 후 마취 회복기에 기관 내 튜브 발관한 다음, 음압성 폐부종이 발생하여 즉시 산소마스크를 통해 보조환기와 이뇨제 치료로 합병증 없이 회복된 예를 경험하여 보고한다.

반복적인 급성 폐부종으로 나타난 신동맥 협착의 내과적 치험

한선숙 ( Han Seon Sug ),최대희 ( Choe Dae Hui ),이성원 ( Lee Seong Won ),이희영 ( Lee Hui Yeong ),김우진 ( Kim U Jin ),이상현 ( Lee Sang Hyeon ),정해혁 ( Jeong Hae Hyeog ) 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.4

Renal artery stenosis is a rare cause of acute pulmonary edema. So-called flash pulmonary edema is associated with bilateral renal artery stenosis or stenosis in a single functioning kidney. Most patients have co-morbid cardiovascular disease and a renovascular etiology is overlooked. Flash pulmonary edema has been recognized as an absolute indication for vascular intervention. However, our case could be treated with medical treatment directiong a complete inhibition of renin-angiotensin system. A 81-year old man was admitted with acute shortness of breath. During that admission, despite the dialysis therapy for renal insufficiency, he had four severe episodes of acute pulmonary edema requiring mechanical ventilation. CT angiography showed bilateral renal artery stenosis. After administration of ACE inhibitor, angiotensin receptor blocker, and spironolactone, there was no further attack of pulmonary edema. (Korean J Nephrol 2003;22(4):474-478)

실험적 중추성 폐부종으로 인한 폐 및 시상하부 병변에 대한 Phentolamine의 효과

이춘장,백민우,김달수,허춘웅,하영수,강준기,송진언 대한신경외과학회 1982 Journal of Korean neurosurgical society Vol.11 No.3

This experiment was performed to define the participation of a discrete hypothalamic neural structure in the genesis of pulmonary edema and the effect of alpha-adrenergic blockade. Fifty adult cats weighing 2.5 to 4.0㎏, were used in this study. The components of the pathophysiological systemic changes, lung weight, and histopathological changes of lung and hypothalamus were studied in groups of animals when intracranial pressure(ICP) was raised to 200㎜H₂O or 300㎜H₂O for 2 hours by intraventricular infusion with normal saline. We have also observed the effect of the alpha-adrenergic blockade(phentolamine) in the neurogenic pulmonary edema which was produced by elevated intracranial pressure. The animals were divided into 5 groups : The normal control group was comprised in 10 normal cats. Control and phentolamine treated animal groups which had an elevated ICP of up to 200㎜H₂O consisted of 10 cats each. Control and phentolamine treated animal groups which had an elevated ICP of up to 300㎜H₂O consisted of 10 cats each. The results obtained were as follows : 1) In the animal groups of elevated ICP to 200㎜H₂O or 300㎜H₂O, there were hemodynamic systemic changes which were neurogenically mediated and caused an immediate elevation in blood pressure of 30㎜Hg to 60㎜Hg. The hemodynamic data of the animals that had an elevated ICP of up to 300㎜H₂O were significantly more deviated from normal control values than the 200㎜H₂O ICP groups. The hemodynamic responses of the phentolamine treated animal with elevated ICP of up to 200 and 300㎜H₂O were less deviated from normal control values. 2) The lung weights of the animals with an elevated ICP of up to 200 and 300 ㎜H₂O were significantly heavier than the normal control value(p<0.05) and the lung weights of the animals with an elevated ICP of 300 ㎜H₂O were significantly heavier than those with an ICP of 200 ㎜H₂O(p<0.01). The lung weights of the phentolamine treated animal groups were significantly lighter than the control group but showed little increase in the lung weight when compared to the normal value. 3) By controlling the elevated ICP above 200 ㎜H₂O in the experimental animals we have confirmed gross and microscopic appearances of hemorrhagic pulmonary edema. Histopathological changes of the phentolamine treated animals were significantly less sever than in the control groups. 4)By elevating ICP above 200㎜H₂O in the experimental animals, we have confirmed discrete bilateral hemorrhagic spots of the anterior hypothalamus, preoptic region induced by increased intracranial pressure. Histopathological change of the phentolamine treated animals with the elevated ICP were significantly less severe than of the control groups. 5) This experimental model may define the specific particification of the hypothalamus in the pathophysiological pathogenesis of neurogenic pulmonary edema. These results suggest that the lungs are directly affected by the intense sympathetic discharge evoked by release phenomenon from the sympathoinhibitory influence of the hypothalamus, and pulmonary edema was effectively eliminated by alpha adrenergic blockade.