• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.33 no.3
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• pp.156-159
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• 2022

The coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus-2 has upended the world of otolaryngology. After COVID-19 infection, patients experience various complication of symptoms due to injury of the larynx and lung/ respiratory system. Regardless of the patient's severity, patients can experience several complications including dysphonia, vocal cord paralysis/paresis and sensory neuropathy. An emerging role for otolaryngologists in the coming weeks and months is the management of laryngeal complications of COVID-19. This review is intended to describe laryngeal complications in patients recovering from COVID-19 infection.

• The Korean Journal of Emergency Medical Services
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• v.9 no.1
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• pp.89-93
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• 2005

Penetrating chest trauma by stab injury may result in massive hemothorax from damage to single or multiple intrathoracic organs such as heart, aorta, internal mammary artery, intercostal artery or pulmonary parenchyme. Prognosis of massive hemothorax necessitating emergency thoracotomy is fatal especially so if there exists concomitant underlying compromise of cardiopulmonary function. A 56 year old man with destroyed left lung due to old pulmonary tuberculosis was stabbed in right parasternal lesion through third intercostal space. Intubation with cardiopulmonary resuscitation and closed thoracostomy were performed to resuscitate from cardiac asystole from hemorrhagic shock and acute respiratory distress. Midsternotomy was made to expose active bleeding foci in right mammary artery, subclavian vein, intercostal artery and anterior segment of right upper lung showing severe bullous change and pleural adhesion. Postoperative care included ventilator support, inotropic instillation and cautious, balance fluid therapy ; successful extubation was done on third postoperative day and patient was discharged on tenth postoperative day without any complication.

• Applied Microscopy
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• v.33 no.1
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• pp.1-16
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• 2003

As is well known that N-nitroso-N-methylurethane (NNNMU) causes acute lung injury (ALI) in experimental animals. And ALI caused by NNNMU is very similar to ARDS in human being in its pathology and progress. In its context, we investigated the pathogenetic mechanism of ARDS associated with oxidative stress by neutrophils in Sprague-Dawley rat model of NNNMU-induced ALI. NNNMU had increased lung weight/body weight ratio (L/B ratio), lung myeloperoxidase (MPO) activity, protein content and number of neutrophils in bronchoalveolar fluid (BALF) compared with those of control rat (p<0.001, respectively). In contrast, the amount of pulmonary surfactant in BALF was decreased by NNNMU (p<0.001). Morphologically, light microscopic examination denoted pathological findings such as formation of hyaline membrane, infiltration of neutrophils and perivascular cuffing in the lungs of NNNMU-treated rats. In addition, ultrastructural changes such as the necrosis of endothelial cells, swelling and vacuolization of lamellar bodies of alveolar type II cells, and the degeneration of pulmonary surfactant were identified after treatment of NNNMU. Very interestingly, cerium chloride electron microscopic cytochemistry showed that NNNMU had increased the production of cerrous-peroxide granules in the lung, which signified the increased production of hydrogen peroxide in the lung. Collectively, we conclude that NNNMU causes acute lung leak by the mechanism of neutrophilic oxidative stress of the lung.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.437-450
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• 2006

Background : Acute respiratory distress syndrome (ARDS) is characterized by severe inflammatory pulmonary edema of unknown pathogenesis. To investigate the pathogenesis of ARDS associated with neutrophilic oxidative stress, the role of phospholipase $A_2$ ($PLA_2$) was evaluated by the inhibition of calcium channel. Methods : In Sprague-Dawley rats, acute lung injury (ALI) was induced by the instillation of E.coli endotoxin (ETX) into the trachea. At the same time, diltiazem was given 60 min prior to tracheal instillation of ETX. Parameters of ALI such as lung and neutrophil $PLA_2$, lung myeloperoxidase (MPO), BAL neutrophils, protein, surfactant were measured. Production of free radicals from neutrophils was measured also. Morphological studies with light microscope and electron microscope were carried out and electron microscopic cytochemistry for detection of free radicals was performed also. Results : Diltiazem had decreased the ALI parameters effectively in ETX given rats and decreased the production of free radicals from neutrophils and lung tissues. Morphological studies denoted the protective effects of diltiazem. Conclusion : Diltiazem, a calcium channel blocker, was effective in amelioration of ALI by the suppression of neutrophilic oxidative stress mediated by $PLA_2$ activation.

• Tuberculosis and Respiratory Diseases
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• v.59 no.6
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• pp.690-695
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• 2005

Nitric acid is an oxidizing agent used in metal refining and cleaning, electroplating, and other industrial applications. Its accidental spillage generates oxides of nitrogen, including nitric oxide (NO) and nitrogen dioxide ($NO_2$), which cause chemical pneumonitis when inhaled. The clinical presentation of a nitric acid inhalation injury depends on the duration and intensity of exposure. In mild cases, there may be no symptoms during the first few hours after exposure, or the typical symptoms of pulmonary edema can appear within 3-24 hours. However, in cases of prolonged exposure, progressive pulmonary edema develops instantaneously and patients may not survive for more than 24 hours. We report a case of a 44-year-old male who was presented with acute respiratory distress syndrome after nitric acid inhalation. He complained of cough and dyspnea of a sudden onset after inhaling nitric acid fumes at his workplace over a four-hour period. He required endotracheal intubation and mechanical ventilation due to fulminant respiratory failure. He was managed successfully with mechanical ventilation using positive end expiratory pressure and systemic corticosteroids, and recovered fully without any deterioration in his pulmonary function.

• Journal of Life Science
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• v.20 no.4
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• pp.474-480
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• 2010

Rutin, a group II phospholipase $A_2$ ($PLA_2$) inhibitor, was tested on interleukin-1 (IL-1) induced acute lung injury (ALI) in male Sprague-Dawley rats. Rutin did not alter the increased lung myeloperoxidase activity by IL-1. However, the number of neutrophils in bronchoalveolar lavage fluid (BALF) and IL-1 induced lung leak were decreased by rutin (p<0.001). Simultaneously, rutin decreased lung $PLA_2$ activity, which was increased by IL-1 (p<0.001). The reduction of neutrophilic respiratory burst by the inhibition of $PLA_2$ was confirmed by group II $PLA_2$ inhibitors such as rutin, manoalide and scalaradial. The increased level of cytokine-induced neutrophilic chemoattractant (CINC) in BALF by IL-1 was not affected by rutin. Ultrastructural changes of ALI and increased generation of free radicals in the lung by IL-1 were found, and rutin ameliorated these pathological findings. Taken together, rutin seems to be effective in decreasing IL-1 induced ALI through inhibition of group II $PLA_2$.

• Tuberculosis and Respiratory Diseases
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• v.62 no.2
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• pp.105-112
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• 2007

Background: Oxidative stress may play an important role in the pathogenesis of endotoxin-induced acute lung injury (ALI). This study evaluated the therapeutic effect of ${\alpha}$-lipoic acid, a nonenzymatic antioxidant, in a rat model of lipopolysaccharide (LPS) induced ALI. Materials and Methods: ALI was induced in Sprague-Dawley rats by instilling LPS (E.coli, 3mg/Kg) into the trachea. The rats were classified into the control, control+${\alpha}$-lipoic acid, LPS, and LPS+${\alpha}$-lipoic acid groups.The lung lavage neutrophil count, cytokine-induced neutrophil chemoattractant (CINC), lung myeloperoxidase (MPO), and cytokine concentrations (TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and IL-10) were measured at 2 h and 6 h after LPS administration. Results: The total cell and neutrophil counts of the LPS+${\alpha}$-lipoic acid groups were significantly lower than the LPS groups. The protein concentration in the BAL fluid was similar in the LPS groups and LPS+${\alpha}$-lipoic acid groups. The TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 concentrations in the BAL fluid were not decreased by the ${\alpha}$-lipoic acid treatment in the LPS treated rats. Conclusions: Although ${\alpha}$-lipoic acid decreased the level of LPS-induced neutrophil infiltration into the lung, it could not attenuate the LPS-induced ALI at the dose administered in this study.

• Tuberculosis and Respiratory Diseases
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• v.61 no.5
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• pp.479-483
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• 2006

Acute fibrinous and organizing pneumonia (AFOP) is a histological pattern consisting of prominent intra-alveolar fibrin and organizing pneumonia, with out hyaline membranes or prominent eosinophilia. The clinical manifestations of AFOP resemble those of acute lung injury such as acute interstitial pneumonia (AIP). However, the classic histological patterns of AFOP differ from diffuse alveolar damage (DAD), bronchiolitis obliterans with organizing pneumonia (BOOP) or acute eosinophilic pneumonia (AEP). The characteristic intra-alveolar fibrin ball and lack of classic hyaline membrane are the predominant histological features of AFOP. Although some reports suggest that its clinical course is less catastrophic than DAD, the clinical entity that distinguishes AFOP from DAD has not been established. We present a case of pathologically demonstrated AFOP in a 79-year-old man. The radiological findings of our case were similar to those of DAD, presented with diffuse bilateral lung infiltrations. However, despite the rapid development of respiratory failure, the patient had a better response and outcome to steroid therapy than what would be expected for DAD.

• Tuberculosis and Respiratory Diseases
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• v.67 no.2
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• pp.95-104
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• 2009

Background: The pathophysiologic mechanisms of early acute lung injury (ALI) differ according to the type of primary insult. It is important to differentiate between direct and indirect pathophysiologic pathways, and this may influence the approach to treatment strategies. NF-$\kappa$B decoy oligodeoxynucleotide (ODN) is a useful tool for the blockade of the expression of NF-$\kappa$B-dependent proinflammatory mediators and has been reported to be effective in indirect ALI. The purpose of this study was to investigate the effect of NF-$\kappa$B decoy ODN in the lipopolysaccharide (LPS)-induced direct ALI model. Methods: Five-week-old specific pathogen-free male BALB/c mice were used for the experiment. In the preliminary studies, tumor necrosis factor (TNF)-$\alpha$, interleukine (IL)-6 and NF-$\kappa$B activity peaked at 6 hours after LPS administration. Myeloperoxidase (MPO) activity and ALI score were highest at 36 and 48 hours, respectively. Therefore, it was decided to measure each parameter at the time of its highest level. The study mice were randomly divided into three experimental groups: (1) control group which was administered 50 ${\mu}L$ of saline and treated with intratracheal administration of 200 ${\mu}L$ DW containing only hemagglutinating virus of Japan (HVJ) vector (n=24); (2) LPS group in which LPS-induced ALI mice were treated with intratracheal administration of 200 ${\mu}L$ DW containing only HVJ vector (n=24); (3) LPS+ODN group in which LPS-induced ALI mice were treated with intratracheal administration of 200 ${\mu}L$ DW containing 160 ${\mu}g$ of NF-$\kappa$B decoy ODN and HVJ vector (n=24). Each group was subdivided into four experimental subgroups: (1) tissue subgroup for histopathological examination for ALI at 48 hours (n=6); (2) 6-hour bronchoalveolar lavage (BAL) subgroup for measurement of TNF-$\alpha$ and IL-6 in BAL fluid (BALF) (n=6); (3) 36-hour BAL subgroup for MPO activity assays in BALF (n=6); and (4) tissue homogenate subgroup for measurement of NF-$\kappa$B activity in lung tissue homogenates at 6 hours (n=6). Results: NF-$\kappa$B decoy ODN treatment significantly decreased NF-$\kappa$B activity in lung tissues. However, it failed to improve the parameters of LPS-induced direct ALI, including the concentrations of tumor necrosis factor-$\alpha$ and interleukin-6 in BALF, myeloperoxidase activity in BALF and histopathologic changes measured by the ALI score. Conclusion: NF-$\kappa$B decoy ODN, which has been proven to be effective in indirect models, had no effect in the direct ALI model.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.424-428
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• 1994

Many organic and nonorganic agents can cause chemical pneumonitis. Chemical pneumonitis induced by inhalation of acetic acid is a rare clinical condition. As acetic acid is a water soluble agent, it causes chemical irritation to respiratory tract and causes variable symptoms. We experienced a case of acute lung injury due to inhalation of acetic acid fume. A 56-year-old male patient was admitted due to dyspnea with vomiting for one day. After he inhaled acetic acid fume in occupational situation, he had chest tightness, chilling sense, and productive cough. Our case was good response to oxygen inhalation, antibiotics, and systemic steroids.