• 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.

• Sleep Medicine and Psychophysiology
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• v.29 no.1
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• pp.4-8
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• 2022

Obesity hypoventilation syndrome (OHS) is defined as the triad of obesity (body mass index, [BMI] ≥ 30 kg/m²), daytime hypercapnia (PaCO2 ≥ 45 mm Hg), and sleep breathing disorder, after excluding other causes for hypoventilation. As the obese population increases worldwide, the prevalence of OHS is also on the rise. Patients with OHS have poor quality of life, high risk of frequent hospitalization and increased cardiopulmonary mortality. However, most patients with OHS remain undiagnosed and untreated. The diagnosis typically occurs during the 5th and 6th decades of life and frequently first diagnosed in emergency rooms as a result of acute-on-chronic hypercapnic respiratory failure. Due to the high mortality rate in patients with OHS who do not receive treatment or have developed respiratory failure, early recognition and effective treatment is essential for improving outcomes. Positive airway pressure (PAP) therapy including continuous PAP (CPAP) or noninvasive ventilation (NIV) is the primary management option for OHS. Changes in lifestyle, rehabilitation program, weight loss and bariatric surgery should be also considered.

• Sleep Medicine and Psychophysiology
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• v.15 no.2
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• pp.67-70
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• 2008

Overlap syndrome can be defined as a coexistence of chronic obstructive pulmonary disease (COPD) and sleep apnea-hypopnea syndrome (SAHS). The association of COPD and SAHS has been suspected because of the frequency of both diseases. Prevalence of COPD and SAHS is respectively 10 and 5% of the adult population over 40 years of age. However, a recent study has shown that the prevalence of SAHS is not higher in COPD than in the general population. The coexistence of the two diseases is only due to chance. SAHS does not affect the pathophysiology of COPD and vice versa. Prevalence of overlap syndrome is expected to occur in about 0.5% of the adult population over 40 years of age. Patients with overlap syndrome have a more profound hypoxemia, hypercapnia, and pulmonary hypertension when compared with patients with SAHS alone or usual COPD patients without SAHS. To treat the overlap syndrome, nocturnal noninvasive ventilation (NIV) or nasal continuous positive airway pressure (nCPAP) can be applied with or without nocturnal oxygen supplement.

• Clinical and Experimental Pediatrics
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• v.52 no.12
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• pp.1392-1395
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• 2009

Pulmonary vascular air embolism is a rare and, universally, almost a fatal complication of positive pressure ventilation in newborn infants. Here, we report a case of this unusual complication in a very-low-birth-weight infant who showed the clinical and radiological features of this complication along with pulmonary hypoplasia and massive hydrops. The possible pathogenesis has been discussed and a brief review of related literature has been presented.

• Tuberculosis and Respiratory Diseases
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• v.78 no.4
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• pp.455-458
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• 2015

Excessive dynamic airway collapse (EDAC) is a disease entity of excessive reduction of the central airway diameter during exhalation, without cartilage collapse. An 80-year-old female presented with generalized edema and dyspnea at our hospital. The patient was in a state of acute decompensated heart failure due to pneumonia with respiratory failure. We accordingly managed the patient with renal replacement therapy, mechanical ventilation and antibiotics. Bronchoscopy confirmed the diagnosis of EDAC. We scheduled extubation after the improvement of pneumonia and heart condition. However, extubation failure occurred due to hypercapnic respiratory failure with poor expectoration. Her EDAC was improved in response to high flow nasal oxygen therapy (HFNOT). Subsequently, the patient was stabilized and transferred to the general ward. HFNOT, which generates physiologic positive end expiratory pressure (PEEP) effects, could be an alternative and effective management of EDAC. Further research and clinical trials are needed to demonstrate the therapeutic effect of HFNOT on EDAC.

• Tuberculosis and Respiratory Diseases
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• v.48 no.2
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• pp.223-235
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• 2000

Background: Liquid ventilation is associated with decreased inflammatory response in an injured lung. This study was performed to investigate if whether perfluorocarbon(PFC) can decrease chemokine expression in airway epithelial cells. Methods: A549 cells were used for airway epithelial cells and perfluorodecalin for PFC. To expose cells to PFC, lower chamber of Transwell$^{(R)}$plate was used. This study was performed in two parts. In the first part, we examined whether PFC could decrease chemokine expression in airway epithelial cells through inhibition of other inflammatory cells. Peripheral blood mononuclear cells(PBMC's) were isolated and stimulated with lipopolysaccharide(LPS, 10 ${\mu}g/mL$) for 24 hours with or without exposure to PFC. Then A549 cells were stimulated with conditioned media(CM) containing the culture supernatants of PBMC. After 24 hours, the expressions of interleukin-8(IL-8) and RANTES were measured. In the second part of the study, we studied whether PFC could directly suppress chemokine expression in airway epithelial cells. A549 cells were stimulated for 24 hours with interleukin-l$\beta$ and/or tumor necrosis factor-$\alpha$ with or without exposure to PFC, and then the chemokine expression was measured. Northern analysis was used to measure the mRNA expression, and ELISA was used for immunoreactive protein measurements in culture supernatant. Results: 1. IL-8 and RANTES mRNA expression and immunoreactive protein production were increased significantly by CM from LPS-stimulated PBMC in A459 cells compared to with CM from unstimulated PBCM (p<0.05), but exposure of PFC had no significant effect on either mRNA expression or immunoreactive protein expression. 2. IL-8 and RANTES mRNA expression and immunoreactive protein production were increased significantly by IL-1$\beta$ and TNF-$\alpha$ in A549 cells(p<0.05), but exposure of PFC had no significant effect on neither either mRNA expression nor immunoreactive protein production. Conclusion : Decreased chemokine expression of airway epithelial cells may not be involved in decreased inflammatory response observed in liquid ventilation. Further studies on possible mechanisms of decreased inflammatory response are warranted.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.169-175
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• 1998

Background: Heliox is known to decrease $PaCO_2$ in patients with increased airway resistance by increasing minute ventilation and reducing work of breathing(WOB). Besides these effect, heliox is expected to decrease functional anatomic dead space owing to improvement of peak expiratory flow rate(PEFR) and enhancement of gas distribution. We investigated whether heliox can decrease $PaCO_2$ even at the same minute ventilation (VE) and WOB with $N_2-O_2$ to speculate the effect of the heliox on the anatomic dead space. Material and Method: The subjects were 8 mechanically ventilated patients with asthma or upper airway obstruction(M : F=5 : 3, $68{\pm}10$years) who were under neuromuscular paralysis. The study was consisted of three 15-minutes phases: basal $N_2-O_2$ heliox and washout Heliox was administered via the low pressure inlet of servo 900C, and respiratory parameters were measured by pulmonary monitor(CP-100 pulmonary monitor, Bicore, Irvine, CA, USA). To obtain the same tidal volume(Vt) in heliox phase, the Vt on monitor was adjusted by the factor of relative flow rate of heliox to $N_2-O_2$. Dead space was calculated by Bohr equation. Results: 1) Vt, VE, peak inspiratory pressure(PIP) and peak inspiratory flow rate(PIFR) were not different between $N_2-O_2$ and heliox. 2) PEFR was higher on heliox($0.52{\pm}0.19$L/sec) than $N_2-O_2$($0.44{\pm}0.13$L/sec)(p=0.024). 3) $PaCO_2$(mmHg) were decreased with heliox($56.1{\pm}14.1$) compared to $N_2-O_2$($60.5{\pm}15.9$)(p=0.027). 4) Dead space ventilation(%) were decreased with heliox($73{\pm}9$ with $N_2-O_2$ and $71{\pm}10$ with heliox)(p=0.026). Conclusion: Heliox decreased $PaCO_2$ even at the same VE and WOB with $N_2-O_2$, and the effect was considered to be related with the reduction of anatomic dead space.

• Tuberculosis and Respiratory Diseases
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• v.71 no.2
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• pp.126-133
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• 2011

Unilateral pulmonary artery hypoplasia (UPAH) is a rare disease in adults and is frequently accompanied by a congenital cardiac anomaly at a young age. The diagnosis is usually based on computed tomography (CT), angiography, and magnetic resonance imaging (MRI). However, no reports are available on retrograde flow in patients with UPAH. We describe a 68-year-old man with isolated UPAH and retrograde blood flow. He was admitted for dyspnea on exertion for the past 23 years. His diagnosis was delayed, as his symptoms and signs mimicked his underlying pulmonary diseases, such as emphysema and previous tuberculous pleurisy sequelae. A discrepancy was detected between the results of a ventilation-perfusion scan and the CT image. This was resolved by MRI, which showed retrograde blood flow from the right to the left pulmonary artery. Using MRI, we diagnosed this patient with isolated pulmonary artery hypoplasia and retrograde flow.

• Tuberculosis and Respiratory Diseases
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• v.72 no.2
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• pp.117-123
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• 2012

Optimal level of sedation and analgesia is important for the comfort and safety of critically ill patients. However, suboptimal sedation is relatively common in the intensive care unit (ICU) and it could cause prolonged mechanical ventilation and ICU stay, also increase delirium and ICU acquired weakness and resultant decreased survival. Therefore, accurate assessment of the level of sedation and analgesia, maintaining adequate level of sedation, and daily evaluation of each patient and following adjustment could be important treatment strategy in critically ill patients. Recently, the strategy for sedation in the ICU is changing toward the direction of lowering sedation level or even "no sedation" with concurrent use of analgesics and the use of ultra short acting analgesics could be helpful in some patients. Clinicians should be aware of the importance of algorithmic approach including daily interruption of sedative and assessment of sedation level and especially in the patients under mechanical ventilation, organizational approaches such as the 'ABCDE' bundle could improve the management of critically ill patients.

• Journal of Chest Surgery
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• v.26 no.1
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• pp.59-63
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• 1993

A clinical evaluation was performed with a population of 49 patients of chest trauma, who were diagnosed to undergo ventilator therapy, and had gone through ventilator therapy at the Department of Thoracic and Cardiovascular Surgery, Kyungpook University Hospital. One of most common causes of chest trauma was vehicle accidents [77.5%] with the prevalent age group being their forties. The common findings were multiple rib fractures [89.8%], hemopneumothrax [81.6%], lung contusion [61.2%] and flail chest [44.9%]. Their common combined injuries were the orthopedics and neurosugical injuries [86.7%]. Complications caused by chest trauma were pneumonia, respiratory failure, atelectasis, barotrauma and empyema. Pulmonary infections were commonly associated with mechanical ventilation in the long term group and were best prevented by using bronchial hygiene therapy.The mortality rate was 5.8% of the total patients and that was 38.8% of the patients, who needed ventilator therapy. The causes of death were pneumonia, respiratory failure, acute renal failure and hypovolemic shock. Mechanical ventilation has an important place in the treatment of patients with severe chest trauma.