• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.36-39
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• 2015

Copper sulfate is a copper compound used widely in the chemical and agriculture industries. Most intoxication occurs in developing countries of Southeast Asia particularly India, but rarely occurs in Western countries. The early symptoms of intoxication are nausea, vomiting, diarrhea, and abdominal cramps, and the most distinguishable clue is bluish vomiting. The clinical signs of copper sulfate intoxication can vary according to the amount ingested. A 75-year old man came to our emergency room because he had taken approximately 250 ml copper sulfate per oral. His Glasgow Coma Scale (GCS) score was 14 and vital signs were blood pressure 173/111 mmHg, pulse rate 24 bpm, respiration rate 24 bpm, and body temperature $36.1^{\circ}$ .... Arterial blood gas analysis (ABGa) showed mild hypoxemia and just improved after 2 L/min oxygen supply via nasal cannula. Other laboratory tests and chest CT scan showed no clinical significance. Three hours later, the patient's mental status showed sudden deterioration (GCS 11), and ABGa showed hypercarbia. He was arrested and his spontaneous circulation returned after 8 minutes CPR. However, 22 minutes later, he was arrested again and returned after 3 minutes CPR. The family did not want additional resuscitation, so that he died 5 hours after ED visit. In my knowledge, early deaths are the consequence of shock, while late mortality is related to renal and hepatic failure. However, as this case shows, consideration of early definite airway preservation is reasonable in a case of supposed copper sulfate intoxication, because the patients can show rapid deterioration even when serious clinical manifestation are not presented initially.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.

• The Journal of the Korean dental association
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• v.53 no.1
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• pp.47-56
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• 2015

Obstructive sleep apnea (OSA), most common respiratory disorder of sleep, is characterized by intermittent partial or complete occlusions of the upper airway due to loss of upper airway dilating muscle activity during sleep superimposed on a narrow upper airway. Termination of these events usually requires arousal from sleep and results in sleep fragmentation and hypoxemia, which leads to poor quality of sleep, excessive daytime sleepiness, reduced quality of life and numerous other serious health consequences Untreated OSAS can cause various problems such as hypertension, diabetes, stroke, cardiac disease, daytime sleepiness. Various treatments are available, including non-surgical treatment such as medication or modification of life style, surgical treatment, continuous positive airway pressure (CPAP) and oral appliance (OA). Oral appliance is known to be effective in mild to moderate OSA, also genioglossus muscle advancement (GA) or maxillomandibluar advancement (MMA) is a good option for OSA patients with muscular or skeletal problems. Although the prevalence of OSA is increasing, the proportion of the patient treated by dentist is still very law. Dentists need to understand the mechanism of OSA and develop abilities to treat OSA patients with dental problems. The purpose of this paper is to give a brief overview about OSA and the dentist's role in OSA patients.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.1
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• pp.7-11
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• 2004

Purpose: We would evaluate the cardiovascular manifestations of the patients with acute organophosphate and carbamate poisoning in the emergency department. Methods: This was retrospectively studied with the review of patient's charts, included total 38 patients were admitted during the past two years in the emergency department of Yeungnam university hospital with the diagnosis of organophosphate or carbamate poisoning. Results: Cardiovascular complications were variously developed in many patients. Electrocardiographic findings were as follows; 4 ($10.5\%$) cardiac arrhythmias included 1 cardiac arrest caused by ventricular fibrillation, 14 ($36.8\%$) sinus tachycardias, 3 ($7.9\%$) sinus bradycardias, and 17 ($44.7\%$) normal sinus rhythms. Conduction disturbances were 23 ($60.5\%$) like as prolonged QTc, 4 ($10.5\%$) ST-T changes, 2 (5.3%) first degree AV block, and 3 ($7.9\%$) right bundle branch block were shown. Other cardiovascular complications were 22 ($57.9\%$) hypertensives, 4 ($10.5\%$) hypotensives, 15 ($39.5\%$) tachycardias, 2 ($5.3\%$) bradycardias, 18 ($47.4\%$) hypoxemics, 12 ($31.6\%$) metabolic acidosis, and 9 ($23.7\%$) pulmonary edemas. Sixteen patients ($42.1\%$) needed ventilatory support because of respiratory paralysis. No patients died in hospital and 36 ($94.7\%$) patients were alive-discharged. Conclusion: Cardiovascular complications are variously in patients with acute organophosphate and carbamate poisoning. Especially, some findings included ventricular arrhythmias, QTc prolongation, hypoxemia, acidosis, and blood pressure changes are known as major precipitating factors to increase the mortality. So, intensive support and aggressive treatment are needed in patients shown various cardiovascular manifestations in the emergency department.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.781-786
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• 1995

Transcatheter arterial chemoembolization(TACE) was performed in a 61 year old male patient with hepatocellular carcinoma with 10 cc of Lipiodol and 50 mg of doxorubicin. Three days later, he complained of dyspnea and dry cough. The arterial blood gas study revealed moderate hypoxemia and hypocarbia. The chest PA showed acute pulmonary edema with bilateral pleural effusion. To rule out the possibilities of acute respiratory failure caused by infection, pulmonary embolism or congestive heart failure, we performed several laboratory studies. The blood and sputum culture studies revealed negative results for bacterial growth. The echocardiogram was normal. The abdominal CT scan and MR imaging revealed no thrombus or mass lesion in the inferior vena cava. So we concluded pulmonary oil embolism induced by lipiodol as the cause of acute lung injury. Four weeks later, clinical symptoms and chest x-ray were markedly improved with conservative care. We report a case of acute lung injury after TACE with lipiodol and doxorubicin, with review of literatures.

• Journal of Yeungnam Medical Science
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• v.35 no.1
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• pp.84-88
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• 2018

A 33-year-old woman visited the emergency department presenting with fever and dyspnea. She was pregnant with gestational age of 31 weeks and 6 days. She had dysuria for 7 days, and fever and dyspnea for 1 day. The vital signs were as follows: blood pressure 110/70 mmHg, heart rate 118 beats/minute, respiratory rate 28/minute, body temperature $38.7^{\circ}C$, and oxygen saturation by pulse oximetry 84% during inhalation of 5 liters of oxygen by nasal prongs. Crackles were heard over both lung fields. There were no signs of uterine contractions. Chest X-ray and chest computed tomography scan showed multiple consolidations and air bronchograms in both lungs. According to urinalysis, there was pyuria and microscopic hematuria. She was diagnosed with community-acquired pneumonia and urinary tract infection (UTI) that progressed to severe sepsis and acute respiratory failure. We found extended-spectrum beta-lactamase producing Escherichia coli in the blood culture and methicillin-resistant Staphylococcus aureus in the sputum culture. The patient was transferred to the intensive care unit with administration of antibiotics and supplementation of high-flow oxygen. On hospital day 2, hypoxemia was aggravated. She underwent endotracheal intubation and mechanical ventilation. After 3 hours, fetal distress was suspected. Under 100% fraction of inspired oxygen, her oxygen partial pressure was 87 mmHg in the arterial blood. She developed acute kidney injury and thrombocytopenia. We diagnosed her with multi-organ failure due to severe sepsis. After an emergent cesarean section, pneumonia, UTI, and other organ failures gradually recovered. The patient and baby were discharged soon thereafter.

• Journal of The Korean Society of Clinical Toxicology
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• v.6 no.2
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• pp.130-133
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• 2008

In South Korea, attempted suicide by paraquat (PQ) intoxication is fairly common, and is lethal by pulmonary fibrosis and hypoxemia. However, the treatment of PQ poisoning is primarily supportive management. To increase the survival rate associated with PQ intoxication, many treatments have been developed. Here, we treated a case of PQ intoxication with steroid pulse therapy. A 23-year-old man was admitted to the hospital because of PQ intoxication. He drank two mouthfuls of Gramoxon (24% commercial paraquat). His vital signs were stable, but he had a throat infection, and navy blue urine in the sodium dithionite test. Standard treatment, including gastric lavage with activated charcoal was performed, and emergent hemoperfusion with a charcoal filter was initiated 11 h after PQ ingestion. Pharmacotherapy was initiated 18 h after PQ ingestion with the administration of 5 mg dexamethasone. On day 10, chest PA showed pulmonary fibrosis. Therefore, we initiated steroid pulse therapy, with 1g methylprednisolone in 100 mL of D5W administered over 1 h repeated daily for 3 days, and 1 g cyclophosphamide in 100 mL of D5W administered over 1 h daily for 2 days. On day 15, dexamethasone therapy was initiated. On day 30, pulmonary fibrosis was improved. Thus, if pulmonary fibrosis becomes exacerbated after dexamethasone therapy during the subacute stage, pulse therapy with methylprednisolone and cyclophosphamide could be helpful.

• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.42-49
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• 1999

Background: In patients with chronic obstructive pulmonary disease(COPD). it is well known that hypoxemia increases the frequency of VPB, which is associated with the poor prognosis such as sudden death. The aim of this study is to evaluate the effect of short and long-term low flow oxygen therapy on the development of VPBs in patients with COPD by correcting the hypoxemia. Method: In 19 patients with COPD, oxygen saturation and VPB's were monitored by pulse oxymeter and 24-hour Holter EKG, with room air and oxygen saturation and VPB's were monitored on the 1st and on the 8th day during oxygen therapy with nasal prong (2L/min). Results : The arterial oxygen saturation was significantly higher on the 1st day of oxygen therapy compared with breathing room air, and was also higher on the 8th day of oxygen therapy than on the 1st day. We found that there was significant correlation between the lowest value of the arterial oxygen saturation and the mean value of the arterial oxygen saturation. The number of VPB's per hour was significantly lower on the 1st day of oxygen therapy compared with breathing room air, and also lower on the 8th day of oxygen therapy than on the 1st day. Our results showed positive correlation between the decrease in the frequency of VPB's and the increase in the lowest arterial oxygen saturation, even though correlation was not significant(p=0.056). Conclusion: With oxygen therapy, the arterial oxygen saturation was increased and the number of VPB's was decreased. Long-term oxygen therapy more than 7days, would be helpful to decrease the number of VPB' s in patients with COPD.

• The Korean Journal of Pain
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• v.5 no.1
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• pp.37-43
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• 1992

Postoperative hypoxemia in the absence of hypoventilation occurs more often after thoracic or upper abdominal surgery than lower abdominal operations or surgery on extremities. Although the factors which produce postoperative alveolar collapse have not been fully evaluated, the dominant factor of postoperative hypoxemia is shunt of blood passing collapsed alveoli and the postoperative pain is associated with restriction of depth of breathing, sighing and movement. In 1979, the first successful clinical usage of epidurally administered morphine for control of postoperative pain was reported by Behar and associates. This study was carried out for twenty patients who received posterolateral thoracostomy with bleb resection between May 1990 and May 1991 and who were primary spontaneous recurrent pneumothoraxes under general endotracheal anesthesia. For the relief of post-thoracotomy pain following of the general anesthesia, we selected ten patients as control group which were treated intermittently IM with injection of pethidine(50 mg) according to the conventional method and another ten patients as study group which were managed with thoracic epidural analgesia. The tip of the catheter was inserted to T4-5 epidural space through T12-L1 or L1-2 interspinous region before the induction of the general anesthesia and then the epidural analgesics(0.25% bupivacaine 15 ml+morphine 3 mg) was injected once a day via the catheter until 4 th POD in the study group. The epidural catheters were removed at postoperative 4 th day in study group. Clinical observations were done about vital signs, ABG, tidal volume, FVC and occurence of adverse effects during postoperative 2hr, 8hr, 1st day, 2nd day, 7th day in both groups. The results were as follows; (1) The values of $V_T$ and FVC were significantly improved in study group(85% and 66%) as compared with control group(76% and 61%) during the postoperative 4 day of the epidural analgesia. (2) After the end of the epidural analgesia(7th POD), the values of FVC were improved invertly rather in control group(98%) than study group(84%). It suggested that the reduction of FVC in study group were caused by the raised pain sensitivity following the end of epidural analgesia. (3) The side effects of epidural analgesia such as transient urinary retention(2 cases), itching sensation(1) and headache(1) were noted.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.231-238
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• 1999

Background: Nocturnal hypoxemia occurs in patients with chronic obstructive pulmonary disease(COPD) and the detection and treatment of nocturnal hypoxemia should be part of the management of COPD patients. We performed this study to evaluate the factors influencing to sleep related arterial oxygen desaturation($SaO_2$) in patients with COPD. Methods: Resting and exercise cardiopulmonary function test, polysomnography, and $SaO_2$ during resting, exercise and sleep were measured in 12 patients with COPD. Results: The $SaO_2$ fell twice as much during sleep as during maximal exercise($13.1{\pm}9.3%$ fall in nocturnal $SaO_2$ vs. $6.4{\pm}3.3%$, p<0.05). Fall in nocturnal $SaO_2$ was well correlated with mean exercise $SaO_2$(r=-0.78, p<0.05), minimum exercise $SaO_2$(r=-0.90, p<0.01), and resting $SaO_2$(Cr=-0.82, p<0.05). Lowest sleep $SaO_2$ was well correlated with mean exercise $SaO_2$(r=0.80, p<0.05), lowest exercise $SaO_2$(r=0.90, p<0.01), and resting $SaO_2$(r=0.84, p<0.05). Conclusion: Resting and exercise $SaO_2$ was well correlated with nocturnal $SaO_2$, but exercise study add no additional information to predicting the nocturnal oxygen desaturation in patients with COPD.