• Journal of Chest Surgery
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• v.26 no.9
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• pp.718-721
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• 1993

Reexpansion pulmonary edema[ RPE ] with hypoxemia and hypotension is a very rare complication of the treatment of lung collapse secondary to pneumothorax and pleural effusion. We experienced two cases of RPE. One is a 29 year old male with complete right pneumothorax and the other is a 20 year old female with massive right pleural effusion. Life threatening pulmonary edema was developed soon after insertion of chest tube in both. Fortunately, RPE was detected early and intensive treatment was performed. They were discharged without complication. Although RPE with hypoxemia and hypotension is rare , it is very serious and occasionally life-threatening. So, chest surgeon treating lung collapse must be aware of the possibility of RPE and make an effort to prevent the occurence of this condition.

• The Korean Journal of Pain
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• v.3 no.1
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• pp.55-58
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• 1990

A case of severe complications following intrathecal administration of 45 ml of hypertonic saline solution for the treatment of postherpetic neuralgia was presented. Transient immediate complications included were tachycardia, hypertension, neck stiffness and muscle twitch. Pulmonary edema, paralytic intestinal obstruction, and the cauda equina syndrome including sphincter disorder with atonic urinary bladder developed shortly after the injection. Tenesmus and sensory abnormality around perineum and soles were the longlasting complications.

• Journal of the korean veterinary medical association
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• v.40 no.3
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• pp.227-240
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• 2004

심부전증(Heart failure)이란 심장이 조직에서 필요로 하는 산소나 영양분을 제대로 공급하지 못하는 상태로 심장 자체의 구조적 결함이외에도 혈역학(hemodynamics)에 영향을 주는 신장 질환이나 고혈압등에 의해서도 발생한다. 심장은 커다란 펌프로 혈역학적 변화에 능동적으로 대처할 능력을 가지고 있다. 하지만 이러한 혈역학의 변화를 유발하는 원인을 제거하지 않은채 장기적으로 원인이 지속할 경우, 심장, 특히 심실은 재구성(remodeling)이 일어나게되고(좌심실의 벽이 비후되고 우심실의 벽이 얇아지는 변화) 이로인하여 심장의 혈역학 변화에 따른 보상 반응은 점차 무력화 되게된다. 이로인하여, 혈액 정체에 따른 폐부종이나 복수증 및 산소 부족에 의한 허혈성 손상이 여러 장기에 나타나게 된다. 심장 질환은 불량한 예후와 치료의 제한성때문에 그동안 수의 분야에서 간과되어왔지만, 우리나라도 애완동물의 노령화가 시작되고 있고 고급 진료에 대한 축주들의 요구가 증가하고 있어서 점파 심장 질환의 진료가 늘어갈 것으로 사료된다. 따라서 본 종설에서는 심부전증에 대한 여러 가지 병리 기전과 이에 따른 치료 방법에 대해 기술하고자한다.

• Radiation Oncology Journal
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• v.13 no.4
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• pp.321-330
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• 1995

Purpose : To evaluate whether the early pulmonary irradiation can prevent or decrease the pulmonary damage and contribute to improve ultimate survival in paraquat lung. Materials and Methods : From Jun. 1987 to Aug. 1993, thirty patients with paraquat poisoning were evaluated. Fourteen of these patients were received pulmonary irradiation(RT). All of the patients were managed with aggressive supportive treatment such as gastric lavage, forced diuresis, antioxidant agents and antifibrosis agents. Ingested amounts of paraquat were estimated into three groups(A : minimal 50cc). Pulmonary irradiation was started within 24 hours after admission(from day 1 to day 11 after ingestion of paraquat). Both whole lungs were irradiated with AP/PA parallel opposing fields using Co-60 teletherapy machine. A total of 10Gy(2Gy/fr. x 5days) was delivered without correction of lung density. Results : In group A, all patients were alive regardless of pulmonary irradiation and in group C, all of the patients were died due to multi-organ failure, especially pulmonary fibrosis regardless of pulmonary irradiation. However, in group B, six of 7 patients($86{\%}$) with no RT were died due to respiratory failure, but 4 of 8 patients with RT were alive and 4 of 5 patients who were received pulmonary irradiation within 4 days after ingestion of paraquat were all alive though radiological pulmonary change. One patient who refused RT after 2Gy died due to pulmonary fibrosis. All 3 patients who were received pulmonary irradiation after 4 days after ingestion were died due to pulmonary fibrosis in spite of recovery from renal and hepatic toxicity Conclusion : It is difficult to find out the effect of pulmonary irradiation on the course of the paraquat lung because the precise plasma and urine paraquat concentration were not available between control and irradiation groups. But early pulmonary irradiation within 4 days after paraquat poisoning with aggresive supportive treatment appears to decrease Pulmonary toxicity and contribute survival in patients with mouthful ingestion of paraquat who are destined to have reversible renal and hepatic damage but irreversible pulmonary toxicity.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.925-935
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• 1996

Background : In order to elucidate one of the pathogenic mechanisms of ARDS associated with pulmonary surfactant and oxidant injury, acute lung injury was induced by N-nitroso N-methylurethane (NNNMU). In this model, the role of phospholipase $A_2$ ($PLA_2$), surfactant, gamma glutamyl transferase (GGT) and morphology were investigated to delineate one of the pathogenic mechanisms of ARDS by inhibition of $PLA_2$ with high dose of dexamethasone. Method: Acute lung injury was induced in Sprague-Dawley rats by NNNMU which is known to induce acute lung injury in experimental animals. To know the function of the alveolar type II cells, GGT activity in the lung and bronchoalveolar lavage was measured. Surfactant phospholipid was measured also. $PLA_2$ activity was measured to know the role of $PLA_2$ in ARDS. Morphological study was performed to know the effect of $PLA_2$ inhibition on the ultrastructure of the lung by high dose of dexamethasone. Results : Six days after NNNMU treatment (4 mg/kg), conspicuous pulmonary edema was induced and the secretion of pulmonary surfactant was decreased significantly. In the acutely injured rats' lung massive infiltration of leukocytes was observed. At the same time rats given NNNMU had increased $PLA_2$ and GGT activity tremendously. Morphological study revealed bizarre shaped alveolar type II cells and hypertrophied lamellar bodies in the cytoplasm of the alveolar type II cells. But after dexamethasone treatment (20 mg/kg, for six days) in NNNMU-treated rats, these changes were diminished i.e. there were decrease of pulmonary edema and increase of surfactant secretion from alveolar type D cells. Rats given dexamethasone and NNNMU had decreased $PLA_2$ and GGT activity in comparison to NNNMU induced ARDS rats. Conclusion : Inhibition of $PLA_2$ by high dose of dexamethasone decreased pathological findings caused by infiltration of leukocytes and respiratory burst. Based on these experimental results, it is suggested that an activation of $PLA_2$ is the one of the major factors to evoke the acute lung injury in NNNMU-induced ARDS rats.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.503-516
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• 2001

Background : The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. Method : In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. Results : In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. Conclusion : A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.64 no.3
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• pp.219-223
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• 2008

Pheochromocytoma is derived from the chromaffin tissue. The typical finding of pheochromocytoma is paroxysmal hypertension accompanied with various signs and symptoms that are due to the excess of catecholamines or other bioactive substances. Yet the diagnosis is sometimes difficult to make because its clinical presentation is quite variable. Especially, hemoptysis is a very rare symptom, so the diagnosis is often missed or delayed. Without making the correct diagnosis and then subsequently administering treatment, the condition may be fatal. We herein report on a 68 year-old woman who was admitted because of abdominal pain and hemoptysis. The initial radiologic findings suggested pulmonary edema with alveolar hemorrhage. The urine catecholamine levels were elevated and she developed catecholamine-induced cardiomyopathy. We performed bronchial arterial embolization and we administered alpha blocker medication for controlling the hemoptysis and hypertension. After the temporary symptomatic improvement, her clinical course was aggravated by pneumonia and pulmonary edema. In spite of performing definitive surgery for pheochromocytoma, she died of postoperative hemodynamic instability.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.548-554
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• 1995

Background: Cardiogenic pulmonary edema increases nonspecific airway responsiveness in humans and animals. Increased extravascular lung water from overt pulmonary edema to subclinical interstitial edema is a common finding in patients with chronic renal failure. Several studies carried out to assess pulmonary function disturbances in this condition have documented a reduction in forced expiratory volume that usually reverses after hemodialysis, suggesting airway edema as the underlying mechanism. This interstitial edema may also lead to nonspecific bronchial hyperresponsiveness. We hypothesized that patients with chronic renal failure may present nonspecific bronchial hyperresponsiveness due to subclinical interstitial pulmonary edema. Methods: We studied 18 chronic renal failure undergoing regular hemodialysis 3 times a week(New York Heart Association Class II) without concomittent disease. These patients were checked pulmonary function test and metacholine provocation test before hemodialysis and same procedure was repeated if responsive, after hemodialysis. Results: 1) 12 out of 18 patients before hemodialysis were reactive in metacholine provocation test(66.7%) before hemodialysis. This airway hyperresponsiveness were decreased after hemodialysis. 2) Pulmonary function was improved after hemodialysis and change in $FEV_1$ was correlated with change in weight(r=-0.62, p<0.01). 3) There was a close correlation between log $PD_{20}$ and $FEF_{25}$, which is one of the variables of the peripheral airways(r=0.58, p<0.05). Conclusion: We speculated interstitial pulmonary edema may play a significant role in bronchial hyperresponsiveness and lung function impaired in patients with chronic renal failure.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.274-279
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• 1996

Pulmonary veno-occlusive disease is a rare cause of pulmonary hypertension in which the primary abnormality is obliterative obstruction of pulmonary veins, especially venules. Clinicaly, we should suspect this disease in the case of congestive cardiac failure with pulmonary hypertension, chronic interstitial pulmonary edema, and normal or elevated wedge pressure on cardiac catheterization. We experience a case of pulmonary hypertension due to pulmonary veno-occlusive disease. A 55-years -old woman developed progressive dry cough and dyspnea for 3 months. Physical examination showed normal heart sounds, diffuse crackles in the whole lung fields. The liver was not palpable and pitting edema was absent. The diagnosis was made by chest HRCT, 2-D echocardiography, normal pulmonary capillary wedge pressure on cardiac catheterization, and confirmed by thoracoscopic lung biopsy. This patient was treated with vasodilator(calcium antagonist) and with mild symptomatic improvement. We reported a case of pulmonary veno-occlusive disease with review of literatures.

• Radiation Oncology Journal
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• v.9 no.1
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• pp.117-122
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• 1991

Malignant small round cell tumor (SRCT) of the thoracopulmonary region appears to originate in the soft tissues of the chest wall or the peripheral lung. A differential diagnosis of poorly differentiated small round cell tumors which include Ewing's sarcoma of bone and soft tissue, embryonal rhabdomyosarcoma, Askin tumor, neuroblastoma, peripheral neuroectodermal tumor, small cell osteogenic sarcoma and Iymphoma are often difficult by light microscopy alone. In recent, by the extensive studies electron microscopic examination, histochemical study, immune-chemical study, cytogenetics and gene analysis, these tumors may be derived from the primitive and pluripotential cells, differentiating into mesenchymal, epithelial and neural features in variable proportions. Treatment for SRCT of thoracopulmonary region is not determined because of massive involvement of the lung, pleura or soft tissues of the chest wall resulted in a dismal outcome despite aggressive surgery, irradiation and chemotherapy.