• Journal of Trauma and Injury
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• v.20 no.2
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• pp.57-64
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• 2007

Purpose: Clinically, acute respiratory distress syndrome (ARDS) occurs within 72 hours after acute exposure of risk factors. Because of its high fatality rate once ARDS progresses, early detection and management are essential to reduce the mortality rate. Accordingly, studies on early changes of ARDS were started, and serum ferritin, as well the as injury severity score (ISS), which has been addressed in previous studies, thought to be an early predictive indicator for ARDSMethods: From March 2003 to March 2005, we investigated 50 trauma patients who were admitted to the intensive care unit in Dongguk University Medical Center, Gyeongju. The patients were characterized according to age, sex, ISS, onset of ARDS, time onset of ARDS, serum ferritin level (posttraumatic $1^{st}\;&\;2^{nd}$ day), amount of transfused blood, and death. Abdominal computed topography was performed as an early diagnostic tool to evaluate the onset of ARDS according to its diagnostic criteria. The serum ferritin was measured by using a $VIDAS^{(R)}$ Ferritin (bioMeriux, Marcy-1' Etoile, France) kit with an enzyme-linked fluorescent assay method. For statistical analysis, Windows SPSS 13.0 and MedCalc were used to confirm the probability of obtaining a predictive measure from the receiver operating characteristics (ROC) curve. Results: The ISS varied from 14 to 66 (mean: 33.8) whereas the onset of ARDS could be predicted with the score above 30 (sensitivity: 90.0%, specificity: 60.0%, p<0.05). On the posttraumatic $1^{st}$ day, the serum ferritin levels were measured to be from 31 mg/dL to 1,200 mg/dL (mean: 456 mg/dL), and the onset of ARDS could be predicted when the value was over 340 mg/dL (sensitivity: 80.0%, specificity: 65.0%, p<0.05). On the posttraumatic $2^{nd}$ day, the serum ferritin levels were measured to be from 73 mg/dL to 1,200 mg/dL (mean: 404 mg/dL), and the onset of ARDS could be predicted when the value was over 627 mg/dL (sensitivity: 60.0%, specificity: 92.5%, p<0.05). The serum ferritin levels and the ISS were significantly higher on the posttraumatic $1^{st}$ and $2^{nd}$ day in the ARDS group, suggesting that they are suitable indices predicting the onset of ARDS, however relationship between the serum ferritin levels and the ISS was not statistically significant. Conclusion: In this study, we discovered increasing serum ferritin levels in multiple- trauma patients on the posttraumatic $1^{st}$ & $2^{nd}$ day and concluded that both the serum ferritin level and the ISS were good predictors of ARDS. Although they do not show statistically significant relationship to each other, they can be used as independent predictive measures for ARDS. Since ARDS causes high mortality, further studies, including the types of surgery and the methods of anesthesia on a large number of patients are essential to predict the chance of ARDS earlier and to reduce the incidence of death.

• Tuberculosis and Respiratory Diseases
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• v.65 no.2
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• pp.99-104
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• 2008

Background: Acute respiratory distress syndrome (ARDS) is ultimately an inflammatory state. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are inflammatory markers. The aim of this study was to evaluate the value of the ESR, CRP and APACHE II score as prognostic factors for patient with ARDS. Methods: We retrospectively analyzed the medical records of 87 ARDS patients. The predictors (APACHE II score, ESR and CRP) and outcomes (mortality and length of the total hospital stay, the ICU stay and mechanical ventilator care) were obtained from the patients' records. The patients were grouped according to survival as the Survivor and Non survivor groups. We compared the APACHE II score, the ESR and the CRP level between the survivor group and the nonsurvivor group. We evaluated the correlation between the predictors and the outcomes. The initial ESR, CRP level and APACHE II score were checked at the time of ICU admission and the second ESR and CRP level were checked $3.3{\pm}1.2$ days after ICU admission. Results: Thirty-eight (43.7%) patients remained alive and 49 (56.3%) patients died. The APACHE II score was significantly lower for the survivor group than that for the non survivor group ($14.7{\pm}7.6$ vs $19.6{\pm}9.1$, respectively, p=0.006). The initial ESR and CRP level were not different between the survivor and non-survivor groups (ESR $64.0{\pm}37.8mm/hr$ vs $63.3{\pm}36.7mm/hr$, respectively, p=0.93, CRP $15.5{\pm}9.6mg/dl$ vs $16.3{\pm}8.5mg/dl$, respectively, p=0.68). The decrement of the CRP level for the survivor group was greater than that for the non survivor group ($-8.23{\pm}10.0mg/dl$ vs $-1.46{\pm}10.1mg/dl$, respectively, p=0.003). Correlation analysis revealed the initial ESR was positively correlated with the length of the total hospital stay and the ICU stay (correlation coefficient of the total hospital days: R=0.43, p=0.001, correlation coefficient of the ICU stay: R=0.39, p=0.014). Conclusion: The initial APACHE II score can predict the mortality of ARDS patients, and the degree of the early CRP change can be a predictor of mortality for ARDS patients. The initial ESR has positive correlation with the ARDS patients' duration of the total hospital stay and the ICU stay.

• Journal of Chest Surgery
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• v.48 no.4
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• pp.289-293
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• 2015

A 38-year-old male was admitted with symptoms of upper respiratory infection. Despite medical treatment, his symptoms of dyspnea and anxiety became aggravated, and bilateral lung infiltration was noted on radiological imaging studies. His hypoxemia failed to improve even after the application of endotracheal intubation with mechanical ventilator care, and we therefore decided to initiate venovenous extracorporeal membrane oxygenation (VV ECMO) for additional pulmonary support. On his twentieth day of hospitalization, hypotension and desaturation (arterial saturated oxygen <85%) developed, and right ventricular failure was confirmed by two-dimensional echocardiography. Therefore, we changed from VV ECMO to venoarteriovenous (VAV) ECMO, and the patient ultimately recovered. In this case, right ventricular dysfunction and volume overloading were induced by long-term VV ECMO therapy, and we successfully treated these conditions by changing to VAV ECMO.

• 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.

• The Korean Journal of Physiology
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• v.28 no.1
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• pp.71-77
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• 1994

In the animal model of acute respiratory distress syndrome (ARDS) induced by N-nitroso-N-methylurethane (NNNMU) the secretory activity of alveolar type H cells during acute alveolar injury was investigated by determining phospholipid and pulmonary surfactant associated proteins in crude surfactant. The mechanism of the secretory change was studied by determination of DNA and RNA levels in the lung tissue. After induction of acute alveolar injury with NNNMU, pulmonary hemorrhage, atelectasis and gross hypertrophy were observed. Seven days after NNNMU treatment the level of total DNA in lung homogenate was increased markedly indicating that a hypertrophy was induced by cellular proliferation. Although the total DNA level increased, the RNA/DNA ratio was gradually decreased after NNNMU treatment. Seven days after NNNMU treatment the RNA/DNA ratio returned to the normal control level. During the acute alveolar injury, phospholipid and surfactant associated proteins were reduced significantly as compared with the control, implying that the secretory activity of alveolar type II cells was altered during acute alveolar injury induced by NNNMU. The protein content in crude surfactant during peak injury(7 days after NNNMU) was decreased significantly but phospholipid/protein ratios were identical in both control and NNNMU treatment groups. SDS-PAGE of proteins in crude pulmonary surfactant showed a decrease in major surfactant associated protein(M.W. 38,000) during acute alveolar injury. The present study may suggest that while alveolar type H cells proliferate markedly, transcription of alveolar type ll cell gene was inhibited by an unknown mechanism such as DNA methylation induced by NNNMU. Such an inhibition of transcriptional activity is thought to be associated with the decreased secretory activity of alveolar type ll cells, which may lead to pulmonary atelectasis and edema during the acute alveolar injury.

• Journal of Chest Surgery
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• v.50 no.1
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• pp.8-13
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• 2017

Background: Extracorporeal membrane oxygenation (ECMO) has been successfully used as a method for the interhospital transportation of critically ill patients. In South Korea, a well-established ECMO interhospital transport system is lacking due to limited resources. We developed a simplified ECMO transport system without mechanical ventilation for use by public emergency medical services. Methods: Eighteen patients utilized our ECMO transport system from December 2011 to September 2015. We retrospectively analyzed the indications for ECMO, the patient status during transport, and the patient outcomes. Results: All transport was conducted on the ground by ambulance. The distances covered ranged from 26 to 408 km (mean, $65.9{\pm}88.1km$) and the average transport time was $56.1{\pm}57.3minutes$ (range, 30 to 280 minutes). All patients were transported without adverse events. After transport, 4 patients (22.2%) underwent lung transplantation because of interstitial lung disease. Eight patients who had severe acute respiratory distress syndrome showed recovery of heart and lung function after ECMO therapy. A total of 13 patients (70.6%) were successfully taken off ECMO, and 11 patients (61.1%) survived. Conclusion: Our ECMO transport system without mechanical ventilation can be considered a safe and useful method for interhospital transport and could be a good alternative option for ECMO transport in Korean hospitals with limited resources.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.369-379
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• 1998

Background: Platelet-activating factor(PAF) might play an important role in the development of acute respiratory distress syndrome. Since PAF induced lung injury is similar to changes of acute respiratory distress gyndrome, and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of PAF on the regulation of surfactant protein A, B and C mRNA accumulation Method: The effects of PAF on gene expression of surfactant protein A, B and C in 24 hours after intratracheal injection of PAF in rats. Surfactant protein A, B and C mRNAs were measured by filter hybridization. Results: The accumulation of SP-A mRNA in PAF treated group was significantly decreased by 37.1 % and 41.6%, respectively compared to the control group and the group treated with Lyso-PAF(p<0.025, p<0.01). The accumulation of SP-B mRNA in PAF treated group was decreased by 18.7% and 32.2 %, respectively compared to the control group and the group treated with Lyso-PAF but statistically not significant. The accumulation of SP-C mRNA in PAF treated group was significantly decreased by 30.7% and 38.5%, respectively compared to the control group and the group treated with Lyso-PAF(p<0.l, p<0.01). Conclusion: These findings represent a marked inhibitory effects of platelet-activating factor on surfactant proteins expression in vivo. This supports, in turn, 'platelet-activating factor might be related to pathogenesis of acute respiratory distress syndrome.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Tuberculosis and Respiratory Diseases
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• v.65 no.4
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• pp.301-307
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• 2008

Background: The triggering receptor expressed on myeloid cells-1 (TREM-1) is an activating receptor that is expressed on the surface of neutrophils and mature monocytes when stimulated with several microbial components, which can amplify the inflammatory response. This study analyzed the prognostic value of the sTREM-1 levels in patients with acute respiratory distress syndrome (ARDS). Methods: The bronchoalveolar lavage (BAL) fluid and blood was collected prospectively from 32 patients with ARDS, 15 survivors and 17 nonsurvivors. An enzyme-linked immunosorbent assay was performed to measure the sTREM-1. The following data was obtained: APACHE II score, Clinical Pulmonary Infection Score (CPIS), BAL fluid analysis, C-reative protein. Mortality in the ICU was defined as the end point. Results: The serum sTREM-1 level was significantly higher in the nonsurvivors than survivors ($54.3{\pm}10.3pg/ml$ vs. $22.7{\pm}2.3pg/ml$, p<0.05). The sTREM-1 level in the serum, but not in the BAL fluid, was an independent predictor of the ICU mortality (OR: 22.051, 95% CI: 1.780~273.148, p<0.016), and a cut-off value of ${\geq}33pg/ml$ yielded a diagnostic sensitivity of 71% and specificity of 93%. Conclusion: The serum sTREM-1 level may be a useful predictor of the outcome of ARDS patients.

• Journal of Biomedical Engineering Research
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• v.24 no.5
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• pp.391-399
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• 2003

Intravascular oxygenation represents an attractive. alternative support modality for therapy originated with acute respiratory distress syndrome(ARDS). However. the clinical study concluded that more gas exchange was needed for intravascular oxygenation to be clinically effective in ARDS treatment. In this study, we tried to enhance gas exchange on the VIVLAD using microencapsulation of hemoglobin and perfluorocarbon emulsion(PFC emulsion). Blood gas measurements were performed by collecting blood samples from the arterial and venous sides of the circuit, and processing them in a blood/gas analyzer. The function of hemosome. blood/hemosome mixed solution. and blood/PFC emulsion mixed solution were tested by an oxygen dissociation curve using a blood/gas analyzer. As a result, it was shown that the oxygen transfer of hemosome and blood/hemosome mixed solution were higher than that of whole blood. Also. it showed that the carbon dioxide transfer of whole blood/PFC emulsion mixed solution was higher than that of others. Therefore, we determined that hemosome and PFC emulsion could increase oxygen transfer and carbon dioxide transfer. respectively.