• Tuberculosis and Respiratory Diseases
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• v.68 no.2
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• pp.62-66
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• 2010

Background: Extracorporeal membrane oxygenation (ECMO) during severe acute respiratory failure helps to recover the pulmonary function. This study evaluated our experience with veno-venous ECMO in adult patients with acute respiratory failure. Methods: From January 2007 to July 2009, ECMO was used on 54 patients. Of these 54 patients, 7 were placed on veno-venous ECMO for acute respiratory failure. The indications of ECMO were based on the lung dysfunction measured as a $PaO_2/FiO_2$ ratio <100 mm Hg on $FiO_2$ of 1.0, or an arterial blood gas pH <7.25 due to hypercapnia despite the optimal treatment. $EBS^{(R)}$, $Bio-pump^{(R)}$, and Centrifugal Rotaflow $pump^{(R)}$ were used and all cannulations were performed percutaneously via both femoral veins. When the lung function was improved, an attempt was made to wean on ECMO at moderate ventilator settings followed by decannulation. Results: Five of the 7 patients were male and the mean age was $46.3{\pm}18.3$. The causes of acute respiratory failure were 3 cases of pneumonia, 2 near-drownings, 1 pulmonary hemorrhage due to acute hepatic failure and 1 mercury vapor poisoning. The mean support time of ECMO was $17.3{\pm}13.7$ days. Of the 7 patients implanted with ECMO, 5 patients (71%) were weaned off ECMO and 3 patients (43%) survived to hospital discharge after a mean 89.6 hospital days. Conclusion: The early use of ECMO for acute respiratory failure in adults due to any cause is a good therapeutic option for those unresponsive to the optimal conventional treatments.

• Journal of Chest Surgery
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• v.25 no.9
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• pp.968-975
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• 1992

A clinical analysis was performed on 404 cases of the chest trauma who were admitted and treated at department of thoracic and cardiovascular surgery, Chung Ang University, Yong San Hospital during the past 8 years from July 1984 to April 1992. The results were as follows. 1. The sex ratio was 3: 1 with male predominence. 2. The common age groups were 3rd, 4th, 5th and 6th decades. 3. The most common chief complaint was chest pain[58.2%]. 4. Of 404 cases of chest trauma, 50 cases were resulted from penetrating injuries whereas 354 cases were from non penetrating injuries. The most common cause of the non penetrating injuries was traffic accident[234/354, 66.1%] and of the penetrating injuries were stab wound[47/50, 94%]. 5. The left thorax was the preferred site of chest trauma. 6. The range of hospital stay was from less than 1 week to over 6 weeks and the average duration was about 2 weeks. 7. The common chest trauma was rib fracture[51.6%] and others were simple contusion [18.8%], hemothorax[14.6%], hemopneumothorax[14.9%] and pneumothorax[8.7i]. The rib fracture was prevalent between 4th to 9th rib laterally. 8. There were 92 cases of associated injuries which were bone fracture[66/92, 71.7%], head injury[17/92, 18.5%] and abdominal injury[9/92, 9.8%]. 9. The methods of treatment were conservative management[58.6%], closed tho-racostomy[23.3%], open thoracotomy[3.4%] and others. 10. There were 28 cases[6.9%] of complication, such as pneumonia, atelectasis, emp-yema, respiratory failure and others. 11. The overall mortality was 2.5%[10 cases] and causes of death were hypovolemic shock, acute renal failure, adult respiratory distress syndrome, sepsis and multiple organ failure.

• Journal of Chest Surgery
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• v.25 no.12
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• pp.1508-1515
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• 1992

Between 1975 and 1992, forty five patients with trachea stenosis received tracheoplasty for relief of obstruction. The causes of airway problem are brain contusion[19 cases, 40%], cerebrovascular disease[3 cases, 7%], drug intoxication[8 cases, 18%], psychotic problem[2 cases, 4%], trachea tumor[3 cases, 7%], adult respiratory distress syndrome[9 cases, 20%] and direct trauma[1 case, 2%]. Direct causes of trachea stenosis were complications of tracheostomy[36 cases, 80%], complications of nasotracheal intubation[5 cases, 11%], tumor[3 cases, 6%] and trauma[1 case, 2%]. Thirty one patients underwent the sleeve resection and end-to-end anastomosis. Five patients performed a wedge resection and end-to-end anastomosis. Forteen patients received the Montgomery T-tube for relief of airway obstruction. Four patients have done simple excision of granulation tissue. Two, subglottic stenosis patients were received Rethi procedure[anterior division of cricoid cartilage, wedge partial resection of lower thyroid cartilage and Montgomery T-tube molding] and the other subglottic stenosis patient underwent permanent trachea fenestration. Including cervical flexion in all patients postoperatively, additional surgical techniques for obtain tension-free anastomosis were hyoid bone release technique in two cases, and hilar mobilization, division of inferior pulmonary ligament and mobilization of pulmonary vessel at the pericardium were performed in one case. Cervical approach was used in 39 cases, cervicomediastinal in 12 cases and transthoracic in one case. Complications of tracheoplasty were formation of granulation tissue at the anastomosis site[3 cases], restenosis[9 cases], trachea-innominate artery fistula[2 cases], wound infection[2 cases], separation of anastomosis[2 cases], air leakage[3 cases], injury to a recurrent laryngeal nerve[temporary 8 cases, permanent 2 cases] and hypoxemia[1 case]. Surgical mortality for resection with primary reconstruction was 6.7%, with one death due to postoperative respiratory failure and two deaths due to tracheo-innominate artery fistula.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.547-557
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• 1996

Background : An excessive accumulation of neutrophils in lung tissue has been known to play an important role in mediating the tissue injury among the adult respiratory distress syndrome, idiopathic pulmonary fibrosis and cystic fibrosis by releasing toxic oxygen radicals and proteolytic enzymes. Therefore, it is important to understand a possible mechanism of neutrophil accumulation in lung tissue. In many species, exposure to hyperoxic stimuli can cause changes of lung tissues very similar to human adult respiratory distress syndrome and neutrophils are also functioning as the main effector cells in hyperoxic lung injury. The purpose of the present study was to examine whether neutrophils function as a key effector cell and to study the nature of possible neutrophil chemotactic factors found in bronchoalveolar lavage fluid from the hyperoxia exposed rats. Methods : We exposed the rats to the more than 95% oxygen for 24, 48, 60 arid 72 hours and bronchoalveolar lavage(BAL) was performed. Neutrophil chemotactic activity was measured from the BAT- fluid of each experimental groups. We also evaluated the molecular weight of neutrophil chemotactic tractors using fast performance liquid chromatography and characterized the substances by dialyzer membrane and heat treatment. Results : 1) The neutrophil proportions in bronchoalveolar lavage fluid began to rise from 48 hours after oxygen exposure, and continued to be significantly increased with exposure times. 2) chemotactic index for neutrophils in lung lavages from rats exposed to hyperoxia was significantly higher in 48 hours group than in control group, and was significantly increased with exposure time. 3) No deaths occured until after 48 hours of exposure. However, mortality rates were increased to 33.3 % in 60 hours group and 81.3 % in 72 fours group. 4) Gel filtration using fast performance liquid chromatography disclosed two peaks of neutrophil chemotactic activity in molecular weight of 104,000 and 12,000 daltons. 5) Chemotactic indices of bronchoalveolar lavage fluid were significantly deceased when bronchoalveolar lavage fluid was treated with heat ($56^{\circ}C$ for 30 min or $100^{\circ}C$ for 10 min) or dialyzed (dialyzer membrane molecular weight cut off : 12,000 daltons). Conclusion : These results suggested that the generation of neutrophil chemotactic factor and subsequent neutrophil influx into the lungs are playing an important roles in hyperoxia-induced acute lung injury. Neutrophil chemotactic factor in the lung lavage fluids consisted of several distinct components having different molecular weight and different physical characteristics.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.617-628
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• 1998

In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.

• The Korean Journal of Nuclear Medicine
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• v.18 no.1
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• pp.45-53
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• 1984

The purpose of this study is to observe the changes of pulmonary capillary permeability and various hemodynamic parameters before and after Positive End-Expiratory Pressure(PEEP) in Adult Respiratory Distress Syndrome (ARDS). Using a canine oleic acid induced ARDS model, we measured the pulmonary capillary permeability with a slope of lung: heart radioactivity ratio, hemodynamic parameters with Swan-Ganz catheter and blood gas tensions. 1) In normal and ARDS dogs, the PEEP didn't significantly influence the slope of lung: heart radioactivity ratio. But in ARDS group the slope index was increased compaired with that of control group (p<0.05). 2) Also in ARDS group, $PaO_2$ was significantly decreased, and $PaCO_2,\;PvCO_2$, MPAP, $AaDO_2$, Qs/Qt were significantly increased compared with those of control group (p<0.05). 3) In normal dogs, the PEEP didn't influence blood pH or gas tension, $AaDO_2$, Qs/Qt, or hemodynamics. 4) In ARDS dogs, however, the PEEP significantly increased $PaO_2$ and decreased $AaDO_2$, Qs/Qt (p<0.05).

• Journal of Chest Surgery
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• v.32 no.3
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• pp.270-275
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• 1999

Background: In the patients with thoracic injury, we suspect simultaneous cardiac contusion or concussion. We analyzed the patients with possible cardiac injury by electrocardiography, serum creatine kinase (CK), creatine kinase isoenzyme fraction (CK-MB) screening, followed by two dimentional echocardiogram (2-DE) to access the severity of injury. Material and Method: From January 1997 to April 1998, 15-month retrospective study of suspicious myocardial injury was undertaken in including 24 patients admitted for suspected cardiac injury. All patients with history or signs of blunt chest injury were checked serially and the serial CK, CK-MB fraction, electrocardiography (EKG) analysis screening were followed by 2-DE. Result: The age range was between 20-40 years and were predominant male patients in(M:F=3:1). Most common causes of injury were traffic accidents, 15 patients(62.5%). Associated injuries involved multiple rib fractures, sternal fracture and such. EKG findings on the cardiac concussion were within normal limits, EKG findings on the cardiac contusion were nonspecific ST and T wave abnormality. In cardiac contusion patients, CK-MB fraction did not increase significantly on admission but on 2nd, 3rd, 4th hospital days, it increased significantly (p=0.0080, 0.0130, 0.0130). The average admission days were 9.22 in concussion and 26.18 in contusion patients(p=0.0075). Most common complication was the adult respiratory distress syndrome(7 cases), 5 out of the patients with ARDS were mechanically ventilated. There were no deaths. Conclusion: We believe the serial checks of CK-MB, EKG and subsquent two-dementional echocardiographic sector scanning are presently the most sensitive indicators available for structural and functional cardiac injury.

• Journal of Chest Surgery
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• v.31 no.5
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• pp.481-487
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• 1998

The surgical management of acute type B dissection is controversial. The complexity of the repair usually requires a period of aortic cross-clamping exceeding 30 minutes, which can cause ischemic injury of the spinal cord. Several forms of distal perfusion have been considered for use to prevent this injury. To determine the safety and efficacy of a graft replacement with cardiopulmonary bypass in reparing acute dissection of descending thoracic aorta, we retrospectively reviewed our surgical experience treating 8 patients who had aortic dissection secondary to atherosclerosis, trauma, and carcinoma invasion. Cardiopulmonary bypass was performed with two aortic cannulas for simultaneous perfusion of the upper and lower body and one venous cannula for draining venous blood from the right atrium or inferior vena cava. Although aortic cross-clamp time was relatively long (average, 117.8 minutes; range, 47 to 180 minutes) in all cases, there was no neurologic deficit immediately after graft replacement for the aortic lesion. Two patients(25%) of relatively old age died on the postoperative 31st and 41st days, respectively, because of delayed postoperative complications, such as pulmonary abscess and adult respiratory distress syndrome. Although any of several maneuvers may be appropriate in managing dissection of the descending aorta, graft replacement with cardiopulmonary bypass during aortic cross-clamping may be a safe and effective method for the treatment of acute dissection of the descending thoracic aorta.

• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.46-53
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• 1996

Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.462-474
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• 1994

Background : In acute lung injury, activated neutrophils play an important role in tissue damage. For neutrophils to participate in lung inflammation, chemotactic factors released from mononuclear phagocytes are needed to bring these cells to the local site of inflammation, with interleukin-8 (IL-8) being one of the most specific and important chemotactic factors for neutrophils. IL-8 also induces the expression of adhesion molecules and activates neutrophils to release various inflammatory mediators. Lipopolysaccharide(LPS) is one of the most important causes of adult respiratory distress syndrome and can cause release of many inflammatory cytokines including IL-8 leading to acute lung injury. But little is known about the regulatory mechanism of LPS-induced IL-8 gene expression in mononuclear phagocytes. Method : Human alveolar macrophages(HAM) and peripleral blood monocytes(PBMC) were isolated from healthy volunteers. Time and dose relationship of LPS-induced IL-8 mRNA expression was observed by Northern blot analysis. To evaluate the regulatory mechanism of LPS-induced IL-8 gene expression, pretreatment of actinomycin D(AD, $5{\mu}g/ml$) and cycloheximide(CHX, $5{\mu}g/ml$) was done and Northern blot analysis for IL-8 mRNA and ELISA for immunoreactive IL-8 protein in culture supernatant were performed. Results : 1) In HAM, dose and time dependent LPS-induced IL-8 mRNA expression was observed with peak mRNA level at 8 hours post-stimulation. 2) In PBMC, dose and time dependent LPS-induced IL-8 mRNA expression was also observed with peak mRNA level at 4 hours post-stimulation. 3) AD decreased expression of LPS-induced IL-8 gene expression at both mRNAand protein levels in both types of cells. 4) CHX decreased expression of LPS-induced IL-8 gene expression at protein level in both cell types but in HAM, superinduction of IL-8 mRNA was observed while decreased expression of IL-8 mRNA was observed in PBMC. Conclusion : Time and dose dependent LPS-induced IL-8 gene expression was observed in mononuclear phagocytes which is at least partly regulated pretranslationally. LPS-induced IL-8 mRNA expression in HAM needs no de novo protein synthesis and may be under the control of a labile repressor protein while de novo protein synthesis may be needed in PBMC.