• Journal of Chest Surgery
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• v.49 no.6
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• pp.427-434
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• 2016

Background: Recent studies have demonstrated the benefits of off-pump coronary bypass grafting over the on-pump technique in patients with chronic kidney disease (CKD). To further reduce the risk of acute kidney injury and the need for renal replacement therapy, even in patients undergoing off-pump coronary artery bypass grafting, we adopted protocol-based perioperative management for patients with CKD. Methods: From December 2012 to March 2015, 265 patients underwent isolated off-pump coronary artery bypass grafting. To analyze renal function in a stable condition, we excluded 12 dialysis-dependent end stage renal failure and 10 emergency or urgent cases. Among the remaining 243 patients, 208 patients had normal kidney function (normal group), and 35 patients had CKD (CKD group). Minimizing contrast exposure, ensuring adequate hydration, using strict drug dosage adjustment, and optimizing hemodynamic status were key elements of the protocol for the CKD group. Results: The risk of acute kidney injury was about ${\times}3$ higher in the CKD group than in the normal group (p=0.01). Estimated glomerular filtration rates and serum creatinine levels deteriorated until the third postoperative day in the CKD group. However, by adopting protocol-based perioperative management, this transient renal dysfunction recovered to preoperative levels by the fifth postoperative day without requiring renal replacement therapy in all cases. Conclusion: Off-pump coronary bypass surgery combined with this protocol-based perioperative management strategy in patients with non-dialysis-dependent CKD could mostly be performed without renal replacement therapy.

• Journal of Chest Surgery
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• v.52 no.6
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• pp.400-408
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• 2019

Background: For decades, trauma has been recognized globally as a major cause of death. Reducing the mortality of patients with trauma is an extremely pressing issue, particularly for those with severe trauma. An early and accurate assessment of the risk of mortality among patients with severe trauma is important for improving patient outcomes. Methods: We performed a retrospective medical record review of 582 patients with severe trauma admitted to the emergency department between July 2011 and June 2016. We analyzed the associations of in-hospital mortality with the baseline characteristics and initial biochemical markers of patients with severe trauma on admission. Results: The overall in-hospital mortality rate was 14.9%. Multivariate logistic regression analysis showed that the patient's Rapid Emergency Medicine Score (REMS; odds ratio [OR], 1.186; 95% confidence interval [CI], 1.018-1.383; p=0.029), Emergency Trauma Score (EMTRAS; OR, 2.168; 95% CI, 1.570-2.994; p<0.001), serum lactate levels (SLL; OR, 1.298; 95% CI, 1.118-1.507; p<0.001), and Injury Severity Score (ISS; OR, 1.038; 95% CI, 1.010-1.130; p=0.021) were significantly associated with in-hospital mortality. Conclusion: The REMS, EMTRAS, and SLL can easily and rapidly be used as alternatives to the injury severity score to predict in-hospital mortality for patients who present to the emergency department with severe trauma.

• Journal of Trauma and Injury
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• v.28 no.4
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• pp.256-261
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• 2015

Purpose: The aim of this study was to evaluate the effects of blood alcohol concentration (BAC) on the clinical parameters in trauma patients. Methods: From January 2011 to March 2013, the records of a total of 102 trauma patients with BAC data were analyzed retrospectively. The revised trauma score (RTS), injury severity score (ISS), presence of shock, use of mechanical ventilation and blood transfusion, length of hospital stay, and mortality were collected. Patients were divided into four groups in accordance with the level of BAC: group A (<100 mg/dL), B (100~200 mg/dL), C (200~250 mg/dL), and D (>250 mg/dL). Patients were also divided into two groups depending on the presence of the shock, and gender, ISS, BAC, and presence of active bleeding were compared between these two groups. Results: No statistically significant differences in the ISS, RTS, presence of active bleeding, use of mechanical ventilation, and mortality were noted between groups A to D. However, the presence of shock was significantly higher in group D. After patients with severe chest injuries had been excluded, mechanical ventilation was found to have been applied more frequently in the higher BAC groups (C and D). A logistic regression analysis of these factors showed that extremely high BAC (>250 mg/dL) was an independent indicator of shock. Conclusion: High BAC is a predicator of shock and the need for mechanical ventilation in patients with trauma, regardless of injury severity. Alcohol intoxication leads to an overestimate of the clinical condition and aggressive management for trauma patients. Thus, a guideline for the diagnosis and treatment of patients intoxicated with alcohol is necessary.

• Journal of Chest Surgery
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• v.37 no.4
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• pp.335-341
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• 2004

Traumatic cardiac injury is very rare but mortality is very high when the diagnosis and management are delayed. We reviewed our case retrospectively. Material and Method: From March 1995 to July 2003, 17 patients were diagnosed as having traumatic cardiac rupture. Five patients were stabbed, seven patients were motor vehicle accidents, four patients had fallen down, and the cause was unknown in one patient. Emergency operations were done and six patients were operated under CPB. Result: Four patients died during or after operation. The mean ICU stay period was 3.86$\pm$3.35 days and the mean hospital stay was 18.27$\pm$14.99 days. No mortality was observed in those whose vital signs were stable in the operating room. Conclusion: Preoperative vital status was very important and thoracic traumatic patient should be suspected as having cardiac injury.

• Journal of Chest Surgery
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• v.26 no.6
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• pp.441-451
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• 1993

Protective effect of superoxide dismutase[SOD] and substrates on acute ischemic and reperfused myocardium was assessed by cardiac microdialysis. 30 Rabbits were divided into 4 groups; normal control group [group I, n=5], ischemic group [group II, n=5], SOD treated group [group III, n=10], and substrates treated group [group IV, n=10]. After a microdialysis apparatus was implanted in rabbit myocardium, coronary artery was occuluded for 5 minutes and reperfusion was performed for 30 minutes. Hemodynamic changes, CK-MB isoenzyme level and adenine ring compound level in effluent dialysates [equilibrated with interstitial fluid], and ultrastructural changes of myocardial cell were analysed. Systolic blood pressure at 10 and 30 minutes after reperfusion was higher in group III and IV than in group II [p<.05]. Also percent recovery of systolic blood pressure in group III [p<.01] and IV [p<.02] was higher than in group II. CK-MB isoenzyme level in effluent dialysates was peaked at 10 minutes after reperfusion, thereafter decreased in group II, III and IV. At 30 minutes after reperfusion, its level was lower in group III and IV than in group II[p<.05]. Adenine ring compound level in effluent dialysates increased till 10 minutes after reperfusion and progressively decreased. At 10 and 30 minutes after reperfusion, its level was lower in group III and IV than in group II without significance. Degree of myocardial damage was estimated by scoring of mitochondrial injury. Group I was within normal range and most severe injury was seen in group II. And the score of mitochondrial injury in group III and IV was lower than in group II. In conclusion, SOD and substrates[KMP solution] had protective effect on stunned myocardium. The microdialysis appratus was a good device for studying stunned myocardium, and cardiac microdialysis might be a unique technique for analysis of regional intramyocardial interstitial fluid.

• Journal of Chest Surgery
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• v.22 no.6
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• pp.901-913
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• 1989

This study was investigated under the postulation that activation of intracellular calcium- calmodulin complex during ischemia-reperfusion leads to myocardial injury. The protective effects of calcium channel blocker, diltiazem and calmodulin inhibitors, trifluoperazine, flunarizine and calmidazolium from ischemic injury in rat hearts were observed by using Langendorff apparatus when the antagonists were infused for 3 min in the beginning of ischemia. Thereby, an increase in resting tension developed during 30-min ischemia was analyzed with regard to [1] the degree of cardiac functional recovery following 60-min reperfusion, [2] changes in biochemical variables evoked during 30-min ischemia. The results obtained were as follows: l. In the ischemic group, the resting tension was increased by 4.1*0.2 g at 30-min ischemia. However, the increase in resting tension was markedly reduced not only by pretreatment with diltiazem [3.3 p M] but also with calmodulin inhibitors, trifluoperazine [3.3 p M], flunarizine [0.5 p M] and calmidazolium [0.5 p M], respectively. 2. Recovery of myocardial contractility, +dF /dt and coronary flow were much reduced when evoked by reperfusion in the ischemic group. These variables were significantly improved either by pretreatment with diltiazem or with calmodulin inhibitors. 3. The resting tension increment evoked during ischemia was significantly inversely correlated with the degree of cardiac function recovered during reperfusion. 4. Following 30-min ischemia, the production of malondialdehyde and release of lysosomal enzyme were much increased in association with a decrease in creatine kinase activity. 5. The increases in malondialdehyde production and release of free lysosomal enzyme were suppressed by pretreatment with calmodulin inhibitors as well as diltiazem. Likewise, the decrease of creatine kinase activities was prevented by these calcium antagonists. With these results, it is indicated that a increase in resting tension observed during ischemia has an inverse relationship to the cardiac function recovered following reperfusion, and further, the later may be significantly dependent on the degree of biochemical alterations occurred during ischemia such as decrease in creatine kinase activity, increased production of malondialdehyde and increased release of free lysosomal enzyme. Thus it is concluded that calmodulin plays a pivotal role in the process of ischemic injury.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.51-59
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• 1995

This study was designed to test whether or not 1) ischemia-reperfusion attenuates endothelium-dependent relaxation of coronary arteries and 2) preconditioning protects the arterial endothelium from ischemia-reperfusion injury. In anesthetized open chest rabbits, branches of the left circumflex artery were exposed to different combinations of the experimental conditions; ischemia (15 minutes), ischemia (15 minutes)-reperfusion (10 minutes), preconditioning ischemia, and pre-conditioning fellowed by ischemia-reperfusion. Preconditioning consisted of 3 occlusions of 2-min duration, each followed by n 5-min reperfusion. Rings of the artery exposed to the experimental condition and of normal left anterior descending coronary artery were prepared and suspended for isometric force measurement in organ chambers containing Krebs Ringer bicarbonate solution. The rings were contracted with 29.6 mM KCI. Ischemia alone did not attenuate endothelium-dependent relaxation by acetylcholine. However, ischemia-reperfusion significantly impaired endothelium-dependent relaxation. Endothelium-independent relaxation by sodium nitroprusside was not impaired by ischemia-reperfusion and the constrictive response to acetylcholine was not altered in reperfused rings without endothelium, compared with control rings. Arterial rings exposed to preconditioning followed by ischemia-reperfusion exhibited impaired endothelium-dependent relaxation by acetyl-choline. However, although preconditioning not fellowed by ischemia-reperfusion, attenuated endothelium-dependent relaxation at low concentrations of acetylcholine, the magnitude of the impairment by preconditioning followed by ischemia-reperfusion was significantly less than that of the impairment by ischemia-reperfusion alone. These data demonstrate that ischemia-reperfusion significantly attenuates endothelium-dependent relaxation by producing endothelial dysfunction and preconditioning Protects the endothelium of coronary arteries from ischemia-reperfusion injury.

• Journal of Chest Surgery
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• v.33 no.2
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• pp.125-131
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• 2000

Background: Hyperinflation during lung ischemia has been known to improve pulmonary functions after reperfusion which may be exerted through a pulmonary vasodilation and avoidance of atelectasis by an increased surfactant release and been known whether the improvement of pulmonary function was the effect of hyperinflation itself or the oxygen content in inflation gas. Therefore we attempted to clarify the effect of hyperinflation with oxygen in pulmonary inflation gas during warm ischemia on pulmonary function after reperfusion to solve the problem of ischemia-reperfusion injury after lung transplantation. Material and Method: sixteen mongrel dogs were randomly divided into two groups: the left lung was inflated to 30-35 cm H2O with 100% oxygen in oxygen group and 100% nitrogen in nitrogen group. The inflated left lung was maintained with warm ischemia for 100 minutes. Arterial and mixed venous blood gas analysis and hemodynamics were measured before ischemia and 30, 60, 120, 180 and 240 minutes afer reperfusion. Lung biopsy was taken for the measurement of lung water content after the end of reperfusion. Result: In oxygen group arterial oxygen tension the difference of arterial and mixed venous oxygen tension and the difference of alveolar-arterial oxygen tension at 30-minute after reperfusion were not significantly different from those before ischemia and were stable during the 40hour reperfusion. However in nitrogen group these values were significantly deteriorated at 30-minute after reperfusion. there was no significant difference between two groups in hemodynamic data peak airway pressure and lung water content. Conclusion : The results indicated that the oxygenation one of the most important pulmonary functions was improved by pulmonary inflation with 100% oxygen during warm ischemia but the hemodynamics were not. Oxygen as a metabolic substrate during warm ischenia was believed to make the pulmonary tissues to maintain aerobic metabolism and to prevent ischemic damage of alveoli and pulmonary capillary.

• Journal of Chest Surgery
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• v.30 no.2
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• pp.213-218
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• 1997

Pseudoaneurysm of the thoracic aorta is potentially fatal. However, reports of such cases are rare even in large series. We report four cases of thoracic aortic pseudoaneurysm who underwent surgical repair, The causes were considered as infection in two cases (VSD repair, descending thoracic aortic aneurysm resection) and blunt chest trauma by traffic accident in two patients. The pseudoaneurysms developed on ascending aorta suspected as sites of arterial and cardiolplegic needle insertion in one patient. The others were located at descending thoracic aorta immediatly below the left subclavian artery. One patient died of sepsis associated with bile peritonitis and others were followed up from 10 to 18 months with specific morbidity. This study suggest that the incidence of pseudoaneurysm of the thoracic aorta followed by open heart or aorctic surgery can be repaired succesfuly and careful inspection of associated injury is very important in cases of traumatic thoracic pseudoaneurysm.

• Archives of Plastic Surgery
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• v.38 no.3
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• pp.323-325
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• 2011

Purpose: Breast implant ruptures and displacement are problematic complications after augmentation mammoplasty. The authors report a patient whose cohesive silicone gel implant ruptured and migrated into the pleural cavity after augmentation mammoplasty. Methods: A 23-year-old female had received augmentation mammoplasty at a local clinic a week before visiting our hospital. When the patient's doctor performed a breast massage on the sixth postoperative day, the left breast became flattened. The doctor suspected a breast implant rupture and performed revision surgery. The implant, however, was not found in the submuscular pocket and no definite chest wall defect was found in the operative field. The doctor suspected implant migration into the pleural cavity, and after inserting a new breast implant, the doctor referred the patient to our hospital for further evaluation. The patient's vital signs were stable and she showed no specific symptoms except mild, intermittent pain in the left chest. A CT scan revealed the ruptured implant in the left pleural cavity and passive atelectasis. Results: The intrapleurally migrated ruptured implant was removed by video-assisted thoracic surgery (VATS). There were no adhesions but there was mild inflammation of the pleura. No definite laceration of the pleura was found. The patient was discharged on the first day after the operation without any complications. Conclusion: Surgeons should be aware that breast implants can rupture anytime and the injury to the chest wall, which may displace the breast implant into the pleural cavity, can happen during submuscular pocket dissection and implant insertion.