• Journal of Chest Surgery
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• v.34 no.11
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• pp.879-882
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• 2001

advancement in the treatment of esophageal perforation due to the development of ICU care and antibiotics. There were controversies in the treatment of esophageal perforation when diagnosed after 24hrs. From 1995 to 2000, we performed a buttressed primary repair and mediastinal drainage in 6 Boerhaave\`s syndrome patients among 13 esophageal perforation patients. Two patients died(33%). They died because of pneumonia, ARDS and sepsis on 38th, 39th post-operative day respectively. Two patients had leak at the site of repair which was treated completely with conservative treatment. We report on the result of a buttressed primary repair and mediastinal drainage for 6 Boerhavve\`s syndrome patients.

• Tuberculosis and Respiratory Diseases
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• v.44 no.5
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• pp.1105-1113
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• 1997

Background : Prone position improves oxygenation in some patients with ARDS. According to some authors, prone position can also improve the deteriorated hemodynamics induced by PEEP. But these respiratory and hemodynamic effects of prone position has not yet been fully established. Methods : Twentythree consequtive patients with ARDS(M : F= 11 : 12, $62.1{\pm}20.8yrs$) were the subjects for this study. ABGA, static compliance of the respiratory system, mean arterial pressure and pulse rate were obtained in supine position and at 5min, 0.5h and 2h of prone position. Positive respiratory response was defined as 20mmHg or more increase in $PaO_2/FIO_2$ within 2h of prone position. Early of late respiratory responses were defined if the positive response was observed within of after 3 day of ARDS onset, respectively. Positive hemodynamic response was defined as 10mmHg or more increase in mean arterial pressure at 5min of prone position. Results : Fifteen patients (65%) showed positive respiratory response. In the respiratory responders, $PaO_2$ was $69.8{\pm}17.6mmHg$ in supine position, $83.2{\pm}22.6mmHg$ in prone position 0.5h, $96.8{\pm}22.7mmHg$ in prone position 2h(p<0.001), and $PaO_2/FIO_2$ was $108{\pm}41mmHg$, $137{\pm}57mmHg$, $158{\pm}50mmHg$, respectively(p=0.001). Age, sex, cause of ARDS, supine $PaO_2$ and $PaO_2/FIO_2$ were not different between the respiratory responders and the nonresponders. The respiratory responders, however, showed higher mean arterial pressure than the nonresponders($91.1{\pm}13.1mmHg$ vs. $76.0{\pm}18.7mmHg$, p=0.035), and tendency of higher survival rate(9/15 vs. 2/8, p=0.074). Static compliance of the respiratory system was decreased in prone position 0.5h($28.4{\pm}7.9ml/cm$ $H_2O$ vs. $23.8{\pm}7.6ml/cm$ $H_2O$, p=0.007). The overall rate of early response(n=23) and late response(n=11) were similar(14/23 vs. 7/11, p>0.05). But patient without early response showed late response only in 25%(1/4), while patient with early response showed late response in 85.7%(6/7)(p=0.072). Five patients(22%) showed positive hemodynamic response, two of them being respiratory nonresponders. There were no differences in the baseline mean arterial pressure or the level of PEEP applied in supine between the hemodynamic responders and the hemodynamic nonresponders. Conclusions : Prone position either improved oxygenation or increased arterial pressure in significant proportion of patients with ARDS. And the respiratory response to prone position was thought to be determined in the early stage of ARDS.

• Tuberculosis and Respiratory Diseases
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• v.42 no.1
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• pp.58-66
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• 1995

Background: Acute interstitial pneumonia is a relatively rare form of interstitial pneumonia, since the vast majority of interstitial pneumonia have a more chronic course. It corresponds to the lesion described by Hamman and Rich, as Hamman-Rich disease in 1944. Another name in the clinical literature is accelerated interstitial pneumonia, idiopathic acute respiratory distress syndrome (idiopathic ARDS), and the organizing stage of diffuse alveolar damage. Acute interstitial pneumonia differs from chronic interstitial pneumonia by clinical and pathologic features. Clinically, this disease is characterized by a sudden onset and a rapid course, and reversible disease. Method and Purpose: Five cases of pathologically proven acute interstitial pneumonia were retrospectively studied to define the clinical, radiologic, and pathologic features. Results: 1) The five cases ranged in age from 31 to 77 years old. The onset of illness was acute in all patients, it began with viral-like prodrome 6~40 days prior to shortness of breath, and respiratory failure eventually developed in all patients. In 2 cases, generalized skin rash was accompanied with flu-like symptoms. Etiologic agent could not be identified in any case. 2) All patients had leukocytosis and severe hypoxemia. Pulmonary function test of 3 available cases shows restrictive ventilatory defect, and one survived patient(case 5) has a complete improvement of pulmonary function after dismissal. 3) Diffuse bilateral chest infiltrates were present radiologically. Theses were the ground-glass, consolidation, and reticular densities without honeycomb fibrosis in all patients. The pathologic abnormalities were the presence of increased numbers of macrophages and the formation of hyaline membranes within alveolar spaces. There was also interstitial thickening with edema, proliferation of immature fibroblast, and hyperplasia of type II pneumocyte. In the survived patient(case5), pathologic findings were relatively early stage of acute interstitial pneumonia, such as hyaline membrane with mild interstitial fibrosis. 4) Of the 5 patients, four patients died of respiratory failure 14~90 days after onset of first symptom, and one survived and recovered in symptoms, chest X ray, and pulmonary function test Conclusion: These results emphasize that acute interstitial pneumonia is clinically, radiologically, and pathologically distinct form of interstitial pneumonia and should be separated from the group of chronic interstitial pneumonia. Further studies will be needed to evaluate the pathogenesis and the treatment of acute interstitial pneumonia.

• Tuberculosis and Respiratory Diseases
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• v.52 no.2
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• pp.166-173
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• 2002

Transient peripheral eosinophilia occurs in several disorders, such as allergic diseases, cancer, and parasitic infections. However, in most cases, their presence is not accompanied by tissue destruction or organ dysfunction. In certain disease states, eosinophils can accumulate in any organ in the body and cause tissue destruction as a result of the eosinophil infiltration or the toxic effects of the degranulated proinflammatory products. Idiopathic hypereosinophilic syndrome is a rare disorder characterized by persistent eosinophilia of an unknown origin, usually associated with a dysfunction of organs such as the heart, lung, skin, and nervous system. Idiopathic hypereosinophilic syndrome usually has an indolent course over a period of several months. However, in some cases, they have grave symptoms if vital organs such as heart and lung are infiltrated. Here we report a case of idiopathic hypereosinophilic syndrome presenting acute pulmonary edema involving the heart, bone marrow, and lung with a review of the relevant literatures.

• Sleep Medicine and Psychophysiology
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• v.22 no.1
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• pp.30-34
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• 2015

Obesity hypoventilation syndrome (OHS) is characterized by severe obesity, excessive daytime sleepiness, hypoxemia and hypercapnea. Because OHS mimics pulmonary hypertension or cor pulmonale, clinicians should recognize and treat this syndrome appropriately. A 58-year-old female visited the emergency room because of dyspnea. She was obese and had kyphoscoliosis. The patient also experienced snoring, recurrent choking during sleep and daytime hypersomnolence which worsened after gaining weight in the recent year. The arterial blood gas analysis showed she experienced hypoxemia and hypercapnea not only during nighttime but also daytime. We suspected OHS and the patient underwent polysomnography to confirm whether obstructive sleep apnea was present. During the polysomnography test, sleep obstructive apnea was observed and apnea-hypopnea index was 9.2/hr. The patient was treated with bilevel positive airway pressure therapy (BiPAP). After BiPAP for 4 days, hypoxemia and hypercapnia were resolved and she is currently well without BiPAP. We report a case successfully treated with clinical improvement by presuming OHS early in a patient who had typical OHS symptoms, even while having other conditions which could cause hypoventilation.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1382-1389
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• 1997

Hantavirus pulmonary syndrome(HPS) is a systemic disease that is caused by a newly discorved and characterized virus of the Hantavirus genus, which is most frequently referred to as the sin nombre virus. The clinical syndrome resembles other hantavirus syndromes worldwide, except that it is characterized by a brief prodromal illness followed by rapidly progressive, noncardiogenic edema, and that it is more deadly than any previously recognized hantavirus infection. The clinical manifestations of HPS are characterized by four clinical phases : prodrome, pulmonary edema and shock, diuresis, and convalescence. Mortality is greatest in the first 24 hours of the pulmonary edema and shock phase of the illness. These phases are strikingly similar to the clinical phases of Hemorrhagic fever with renal syndrome(HFRS) induced by Hantaan virus, except that HPS has not been associated with renal failure and Disseminated intravascular coagulation(DIC). We here report a case of hantavirus pulmonary syndrome developed in a 58 year-old man. He had a flu-like illness followed by the rapid onset of respiratory failure due to noncardiogenic pulmonary edema. HPS was diagnosed by clinical manifestations, identification of high titer antibody to Hantaan virus antigen and histologic finding of transbronchial lung biopsy (TBLB) specimen. The patient was treated with mechanical ventilation and initial corticosteroid pulse therapy resulting in successful outcome.

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.487-499
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• 2000

Background : Acute lung injury is an hypoxic respiratory failure resulting from damage to the alveolar-capillary membrane, which can be developed by a variety of systemic inflammatory diseases. In this study the therapeutic effects of intra-tracheal pulmonary surfactant instillation was evaluated in the intratracheal endotoxin induced acute lung injury model of a rat. Methods : Twenty Sprague-Dawley rats were divided into 4 groups, and normal saline (2 ml/kg, for group 1) or LPS (5 mg/kg, for group 2, 3, and 4) was instilled into the trachea respectively. Either normal saline (2 ml/kg, for group 1 & 2, 30 min later) or bovine surfactant (15 mg/kg, 30 min later for group 3, 5 hr later for group 5) was instilled into the trachea. The therapeutic effect of intratracheal surfactant therapy was evaluated with one chamber body plethysmography (respiratory frequency, tidal volume and enhanced pause), ABGA, BAL fluid analysis (cell count with differential, protein concentration) and pathologic examination of the lung. Results : Intratracheal endotoxin instillation increased the respiration rate decreased the tidal volume and int creased the Penh in all group of rats. Intratracheal instillation of surfactant decreased Penh, increased arterial oxygen tension, decreased protein concentration of BAL fluid and decreased lung inflammation at both times of administration (30 minute and 5 hour after endotoxin instillation). Conclusion : Intratracheal instillation of surfactant can be a beneficial therapeutic modality as discovered in the acute lung injury model of rats induced by intratracheal LPS intillation. It deserves to be evaluated for treatment of human acute lung injury.

• Tuberculosis and Respiratory Diseases
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• v.60 no.5
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• pp.564-570
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• 2006

Toxic gases and soot deposition as a consequence of smoke inhalation can cause direct injury to the upper and lower airways and even to the lung parenchyma. A delay in proper and prompt therapy can be detrimental to critically ill burn patients with an inhalation injury. Therefore, serial chest radiography is an important diagnostic tool for pulmonary complications during treatment. The radiographic findings of the chest include normal, consolidation, interstitial and alveolar infiltrates, peribronchial thickening, atelectasis, cardiogenic and non-cardiogenic pulmonary edema, and a pneumothorax as acute complications of smoke inhalation. In addition, bronchiectasis, bronchiolitis obliterans and pulmonary fibrosis can occur as late complications. We encountered a case of 44-year-old male who presented with acute lung injury after an inhalation injury. He required endotracheal intubation and mechanical ventilation due to respiratory failure. He was managed successfully with conservative treatment. Later, a cavitary lesion of the left upper lobe was observed on the chest radiography and computed tomography, which was complicated by massive hemoptysis during the follow-up. However, the cavitary lesion disappeared spontaneously without any clinical consequences.

• Tuberculosis and Respiratory Diseases
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• v.49 no.5
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• pp.614-623
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• 2000

Background : Diffuse alveolar hemorrhage (DAH) is rare but often fatal. To determine the clinical manifestations of DAH, its etiology, clinical course and prognosis were studied. Method : A retrospective analysis was performed in 21 patients that were diagnosed as DAH. Diagnosis of DAH was based on the presence of the "classical triad" of hemoptysis, anemia, and rapidly progressive infiltrates on chest X-ray and a finding of bronchoalveolar lavage or lung biopsy. Results : Thirteen patients (61.9%) had collagen vascular diseases (CVDs) as underlying disease and 10 patients had systemic lupus erythematosus. Females were more prevalent in CVD than in non-collagen vascular disease (NCVD). Otherwise, there were no significant differences between the two groups in terms of clinical manifestations. Dyspnea (95.2%), cough (76.2%), hemoptysis (61.9%), and fever (33.0%) were frequent symptoms. The initial creatinine level was higher in CVD than in NCVD ($3.27{\pm}3.15$ mg/dl vs. $1.19{\pm}0.94$ mg/dl, p=0.030). The corresponding drop in hemoglobin level was $2.69{\pm}1.26$ g/dl. Maximal drop in hemoglobin preceded the progression of infiltrates on the chest radiograph by $1.38{\pm}4.22$ days. The mortality rate was higher in the patients with NCVD than in those with CVD (50.0% vs. 23.1%). Conclusion : The DAH can occur not only in patients with CVD but also in those with NCVD. Higher creatinine level CVD in patients is associated with renal involvement in conjunction with DAH. The maximal drop in hemoglobin preceeding the progression of infiltrates on the chest radiograph suggests that the drop in hemoglobin is important for diagnosing DAH.

• Membrane Journal
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• v.15 no.3
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• pp.224-232
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• 2005

The use of the lung assist device (LAD) would be well suited for acute respiratory failure (ARF) patients, combining the simplicity of mechanical ventilation with the ability of extracoporeal membrane oxygenators (ECMO) to provide temporary relief for the natural lungs. This study's specific attention was focused on the effect of membrane vibration in the LAD. Quantitative experimental measurements were performed to evaluate the performance of the device, and to identify membrane vibration dependence on blood hemolysis. We tried to decide upon excited frequency band of limit hemolysis when blood hemolysis came to through a membrane vibration action. The excited frequency of the module type 5, consisted of 675 hollow fiber membranes, showed the maximum gas transfer rate. We concluded that the maximum oxygen transfer rate seemed to be caused by the occurrence of maximum amplitude and the transfer of vibration to hollow fiber membranes. It was excited up to $25{\pm}5$ Hz at each blood flow rate of module type 5. We found that this frequency became the 2nd mode resonance riequency of the flexible in blood flow. Blood hemolysis was low at the excited frequency of $25{\pm}5$ Hz. Therefore, we decided that limit hemolysis frequency of this LAD was $25{\pm}5$ Hz.