• Journal of Chest Surgery
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• v.43 no.6
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• pp.675-680
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• 2010

Background: The aim of this study was to identify the distinguishing clinicoradiologic findings of traumatic tracheobronchial injury. Material and Method: Between January 2003 and December 2009, six patients who underwent surgical repair for traumatic tracheobronchial injury due to blunt trauma were included in this study. We evaluated the mechanism of the injury, the coexisting injuries, the time until the making diagnosis and treatment, the diagnostic methods, the anatomic location of the injury and the surgical outcomes. Result: The mechanisms of injury were traffic accident and crushing forces. The frequent symptoms were subcutaneous emphysema, dyspnea and pain, and the common radiologic findings were pneumothorax, mediastinal emphysema, rib fracture and lung contusion. Only 2 patients were diagnosed by chest CT and the others were not diagnosed preoperatively. The location of injury was the trachea in 2 patients and the bronchial tree in 4 patients. There was no postoperative mortality or anastomotic leak; however, vocal cord palsy occurred in one patient. The most distinguishing sign was persistent lung collapse even though the chest tube was connected with negative pressure. Conclusion: Although it was not easy to diagnose traumatic tracheobronchial injury without a clinical suspicion, the distinguishing clinical symptoms and CT findings could help to make an early diagnosis without performing bronchoscopy.

• Journal of Chest Surgery
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• v.30 no.1
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• pp.116-118
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• 1997

Endobronchial lipomas Are rare lesions that usually obstruct a major bronchus and cause irreversible pulmonAry damage distally. They are histologically benign tumors. But they can produce pulmonary damage or irreversible bronchiectasis if dignoses or tr atments are delayed. Whenever possible, the treatment of choice is resection by means of bronchoscopy. If endoscopic removal is not possible or lf the nature of the tumor is unclear, surgery is necessary. with lobectomy or pneumonectomy being required in most cases due to the extensively damaged pulmonary parenchyma . We present a case of endobronchial lipoma causing bronchial obstruction and peripheral organizing pneumonia with its clinical features. diagnosis find treatment methods.

• Journal of Chest Surgery
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• v.36 no.1
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• pp.39-42
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• 2003

Endobronchial lipomas are rare benign tumors that arise from the lung. They partially or totally obstruct the bronchial lumen, producing a variable degree of collapse, irreversible bronchiectasis, and pulmonary damage. Although bronchoscope, CT and MR are reported to be helpful in establishing the diagnosis, CT is highly specific and sensitive in detecting fatty tumor. They may be removed by endoscope or thoracotomy or lobectomy. We present a case of endobronchial lipoma completely obstructing the right middle lobe and postobstructive irreversible pulmonary change with review of literatures.

• Korean Journal of Bronchoesophagology
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• v.15 no.2
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• pp.75-80
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• 2009

A 44 year-old nonsmoker female presented to our hospital with persistent cough with sputum for three months. She had been diagnosed as pneumonia and treated with antibiotics in a local hospital but was transferred to our hospital because of no symptomatic improvement. We performed flexible bronchoscopy and found an ovoid and smooth surfaced mass obstructing the bronchus of right middle lobe. The biopsy specimen revealed a benign tumor composed of spindle cells without dysplasia consistent with leiomyoma. There was no evidence of leiomyoma in uterus. The right middle lobectomy and bronchoplasty were performed and the patient was healthy twelve months later. Primary endobronchial leiomyoma is a rare benign tumor of the lung. Herein we report a case of primary endobronchial leiomyoma diagnosed during treatment of pneumonia.

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1243-1246
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• 1998

Tracheobronchial injuries are uncommon. Except for the cervical region, most tracheobronchial injuries are due to blunt chest trauma in Korea. The depth of the tracheobronchial trees renders these structures relatively safe from stab wound. We experienced a case of left main bronchial laceration with azygos vein tear following stab wound in the back of right chest firstly in Korea. The patient was a 24 years old male. A routine chest radiography showed a knife in chest at emergency room. We didn't remove the knife at emergency room. This patient was carried to operation room in 30 minutes after arrival of our hospital without computed tomography and bronchoscopy. The operation was performed through standard right posterolateral thoracotomy and then the knife was removed. The left main bronchus and azyos vein were lacerated obliquely. The penetrated azygos vein was ligated and the laceration of the left main bronchus was repaired. Postoperative course was uneventful.

• Journal of Chest Surgery
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• v.38 no.6 s.251
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• pp.450-453
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• 2005

Broncholithiasis is uncommon in patients with silicosis. Bronchoesophageal fistula complicated by broncholithiasis is especially rare and only one case has been reported in Korea. Surgical treatment of broncholithiasis should be as conservative as possible to preserve the adequate pulmonary function. Meticulous dissection and division of the fistula with the interposition of viable tissues will prevent recurrence, We report a rare case of bronchoesophageal fistula complicated by broncholithiasis in a patient with silicosis.

• Tuberculosis and Respiratory Diseases
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• v.52 no.4
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• pp.355-366
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• 2002

Background : The heat shock protein (HSP) 70 families are known to protect cells against the irreversible tissue injury induced by stress and to induce the recovery of cell function during stress. Heat pretreatment was reported to decrease the acute lung injury (ALI) of rats induced by lipopolysaccharide (LPS). However, the role of heat shock with LPS co-treatmenton ALI is unclear. The purpose of this study was to investigate the effect of heat treatment, which was given immediately after the beginning of ALI induced by LPS intratracheally administered in rats. Methods : Either saline (saline group) or LPS was intratracheally instilled without heat treatment (LPS group). In addition, heat was conducted 18 hours prior to the instillation of LPS (pre-treatment group) and conducted immediately after instillation of LPS (co-treatment group). Six hours after the LPS or saline treatment, blood, bronchoalveolar lavage (BAL) fluid and lung tissue samples were obtained. The myeloperoxidase (MPO) activity and the heat shock protein expression in the lung tissue, the differential counts of the polymorphonuclear leukocytes (PMN) in the BAL fluids, and the LDH, protein, $IL-1{\beta}$, $TNF-{\alpha}$ and IL-10 levels in BAL fluid and serum were measured. Results : 1) The MPO activity, the differential PMN counts in the BAL fluid, BAL fluid and serum cytokines were higher in the LPS, the heat pre-treatment and co-treatment group than those of the saline group (p value <0.05). 2) The MPO activity and the protein level in the BAL fluid from the heat co-treatment group were similar to those of the LPS group. 3) The serum $TNF-{\alpha}$ level of the heat co-treatment group was significantly higher than that of the LPS group (p=0.01). Conclusion : Heat shock response administered immediately after a LPS instillation did not attenuate the ALI in this model.

• Tuberculosis and Respiratory Diseases
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• v.45 no.3
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• pp.553-564
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• 1998

Background: The immediate hoot response to LPS is the production of proinflammatory cytokines that act as intercellular mediators in inflammatory reactions, including acute lung injury. These "early response" cytokines transmit signals from recognition cells to target or effector cells. This host response is further amplified by the expression of leukocyte chemoattractants, growth factors, and adhesion molecules, resulting in an array of proinflammatory events. This experiment was performed to define the lung origin of proinflammatory cytokines, such as TNF-$\alpha$, IL 6 in early periods of endotoxin induced acute lung injury (ALI). Method: The healthy male Sprague-Dawley, weighted 150 - 250g, were divided into saline control (NC) and endotoxemia-induced ALI (ETX-), and leukopenic endotoxemia-induced ALI (CPA-ETX-Group) which was induced by cyclophosphamide, 70 mg/kg i.p. injection. Acute lung injury was evoked by LPS, 5 mg/kg, intravenously administered. Bronchoalveolar lavage was performed at 0, 3, 6 h after LPS-treated to estimate the influx of phagocytes and concentration of total protein, and cytokines as TNF-$\alpha$ and IL 6 by a bioassy using MIT method. We also examined the localization of TNF-$\alpha$ and IL 6 protein in endotoxemia-challenged lung tissue by immunohistochemical stain (IH). Results: The total cell, macrophage and PMN count in BALF were elavated in ETX group compared to NC(p<0.05). In CPA-ETX group, total cell and macrophage count in BALF were not changed compared to NC. but PMN count was markedly reduced and it took part in less than 0.1 % of total BAL cells (p<0.01). The protein concentration in BALF were significantly increased in ETX and CPA-ETX group Compared to NC (p<0.05), but there was significant difference between ETX- and CPA-ETX group only at 6 h (p<0.05). This observation suggested that even if PMNs are involved in the pathogenesis of acute lung injury, their role cannot be viewed as essential The concentration of TNF-$\alpha$ and IL 6 in BALF was significantly increased in the ETX- and CPA-ETX group compared to NC. There was no difference between ETX- and CPA-ETX group. In IH, anti-TNF-$\alpha$- and anti-IL 6 antibody was strongly localized at interstitial monocytes and alveolar macrophages in endotoxemia-challenged lung tissue. From above point of view, activated alveolar macrophage/monocyte considered as a prominent source of proinflammatory cytokines in endotoxemia-challenged lung injury. Conclusion: The prominent source of proinflammatory cytokines in early periods of endotoxemia-induced lung injury will be the activated resident macrophages like an alveolar macrophage and interstitial monocytes. The pulmonary macrophage/monocyte will impact the initiation and continuance of lung injury without PMNs's certain inflammatory role, particularly in endotoxemia-induced acute lung injury.

• Biomedical Science Letters
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• v.3 no.2
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• pp.139-150
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• 1997

In order to investigate the effect of aging and the $H_2O$$_2$ localization in association with histological, ultrastructural, and cytochemical studies in lung tissue after interleukin-1$\alpha$(IL-1) induced lung injury, an acute lung injury was induced by instillation of IL-1 into the trachea. Both of 4- and 20-months-old male rats, protein contents in IL-1 treated branchoalveolar lavage increased significantly compared to each control rats. Acute lung injury occured by oxidative stress because neutrophils accumulated in vascular lumen and formed the adhesion with endothelial cells. As these cause, tissue proteins were exuded and leukocytes migrated into the alveolar lumen. Neverthless in these lung injury $H_2O$$_2$ localization of IL-1 treated 20 months rats was not different compared to IL-1 treated 4 months rats. After all aging was not a factor to accelate IL-1 induced lung injury. Based on these results, it is suggested that neutrophil infilteration might be an important cause in acute lung injury, and aging is not a factor to change the acute lung injury by oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.58 no.3
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• pp.276-284
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• 2005

Backgraound : There have been many reports on the pathogenesis of sepsis-induced acute respiratory distress syndrome(ARDS) but, the precise mechanism has not been elucidated. This study examined the protective effect of an inhibition of platelet activating factor(PAF) remodeling and the adhesion molecule on the oxidative stress of the lungs in rats with an endotoxin induced acute lung injury(ALI). Methods : ALI was induced in Sprague-Dawley rats by instilling an E-coli endotoxin into the trachea. Ketotifen and fucoidan were used respectively to inhibit PAF remodeling and adhesion molecule. The lung leak index, lung myeloperoxidase(MPO) activity, bronchoalveolar lavage(BAL) fluid neutrophil count and lyso PAF acetyltransferase activity(AT), were measured and an ultrastructural study and cytochemical electron microscopy were performed. Results : The lung leak index, lung MPO activity, BAL fluid neutrophil count and lyso PAF AT activity was higher in the endotoxin-treated rats. In addition, severe destruction of the pulmonary architecture and increased hydrogen peroxide production were identified. These changes were reversed by ketotifen. However, fucoidan did not appear to have any protective effects. Conclusion : The inhibition of PAF remodeling appeared to be effective in decreasing the endotoxin-induced ALI. In addition, this effect might be derived from the inhibition of neutrophilic oxidative stress. However, the inhibition of the adhesion molecules by fucoidan appeared to be ineffective in decreasing the endotoxin-induced ALI.