• Journal of The Korean Society of Clinical Toxicology
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• v.18 no.1
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• pp.42-46
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• 2020

Tetramine toxicity due to sea snail ingestion is generally mild and has a good prognosis. Tetramine toxicity acts on the acetylcholine receptor, affecting the neuromuscular junction and autonomic nervous system. A 78-year-old female patient visited the emergency room with vomiting and dyspnea after eating sea snails. At the time of admission, the vital signs recorded were 140/80 mmHg-105/min-24/min-36.5℃, and 90% oxygen saturation. Arterial blood test revealed hypercapnia (pCO₂ 58.2 mmHg) and respiratory acidosis (pH 7.213, HCO₃^- 22.5 mmol/L), whereas other blood tests showed no specific findings. Due to decreased consciousness and hypoxia, endotracheal intubation and mechanical ventilation were administered to the patient. Successful weaning was accomplished after 12 hrs, and the patient was discharged without any further complications. Although tetramine toxicity rarely results in acute respiratory failure due to paralysis of the respiratory muscle, caution is required whilst treating the patient.

• Journal of Chest Surgery
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• v.26 no.7
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• pp.526-531
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• 1993

Sixty-one consecutive patients with coronary artery bypass graft for myocardial revascularization were retrospectively reviewed to analyze various pattern of postoperative complication and death during hospital stay from Nov. 1988 to Oct. 1992. Fortytwo of the patients were male and nineteen female. The mean age was 56 and 51 years in male and female. Preoperative diagnosises were unstable angina in 14 of patients, stable angina in 28, postmyocardial infarction state in 15, and state of failed percutaneous transluminal coronary angioplasty in 4. 141 stenosed coronary arteries were bypassed with use of 20 pedicled internal mammary artery and 124 reversed saphenous vein grafts. Postoperative complications and perioperative death were as follows: 1. Of 61 patients undergoing operation, peri and postoperative over all complication occured in 15 patients [ 25% ]; newly developed myocardial infarction in 4, intractable cardiac arrhythmia including atrial fibrillation and frequent ventricular premature contraction in 3, bleeding from gastrointestinal tract in 2, persistent vegetative state as a sequele of brain hypoxia in 1, wound necrosis in 1, left hemidiaphragmatic palsy in 3 and poor blood flow through graft in 2. 2. Operative mortality was 8%[5 patients]. 3 out of these died in operating room; 1 patient by bleeding from rupture of calcified aortic wall, 1 by air embolism through left atrial vent catheter, 1 by low cardiac output syndrome. 2 patients died during hospital stay; 1 by acute respiratory distress syndrome with multiuple organ failure, 1 by brain death after delayed diagnosis of pericardial tamponade.

• Journal of Medicine and Life Science
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• v.18 no.1
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• pp.20-23
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• 2021

Methemoglobin is generated by the oxidation of ferrous iron to ferric iron within a hemoglobin molecule. Methemoglobin is unable to bind and transport oxygen, resulting in methemoglobinemia, which can lead to fatal tissue hypoxia. The most common cause of methemoglobinemia is poisoning by oxidizing agents such as dapsone, benzocaine, and primaquine. However, methemoglobinemia can also be caused by normal dietary sources. We present two cases of methemoglobinemia that developed after a normal diet in two male patients. In this case report, the patients suddenly developed dyspnea and cyanosis after eating the same meal. They had no history of suspected poisoning, such as the use of drugs, exposure to chemicals, or gas inhalation. Their symptoms did not improve even after a high dose of oxygen was administered; further, an abnormal 'oxygen saturation gap' was observed. Because of CO-oximetry, the methemoglobin levels of the patients were 50.0% and 46.6%, respectively. We administered methylene blue (1 mg/kg), and the patients recovered completely without any complications. Emergency physicians should, therefore, be aware that methemoglobinemia can also be caused by normal dietary sources. In addition, if the source and route of contamination are unclear, an epidemiological investigation should be conducted.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.231-238
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• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.

• Clinical and Experimental Pediatrics
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• v.49 no.4
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• pp.455-459
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• 2006

The major pathogenesis of acute respiratory distress syndrome (ARDS) is an inflammatory process that results from a diversity of injuries to the body. Due to the various cytokines and vasoactive peptides released from the endothelium, the vascular permeability is increased; the migration of inflammatory cells and the leakage of plasma proteins then occur and edema develops in the alveolus. There is a hypothesis that the impairment of alveolar recruitment in ARDS is caused by a defect of the surfactant system and the resultant increase of alveolar surface tension. This has been studied in pediatric patients in ARDS; after the administration of surfactant, hypoxia, respiratory symptoms and survival chances were improved. To alleviate the major pathogenic mechanism in this disease, that is to say, inflammation of the lung, steroids have been used and studied as another treatment modality for ARDS, and it has been concluded that the administration of low dose methylprednisolone may improve patients' symptoms and survival rates. We report here on a case of a young infant admitted with ARDS, who, after the intratracheal administration of 120 mg/kg surfactant, on $PaO_2/FiO_2$ was elevated. Subsequent low doses of methylprednisolone were given, and the symptoms did not recur, and no fibrotic change was shown during the follow-up period of 2 months.

• The Korean Journal of Physiology
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• v.20 no.1
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• pp.53-63
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• 1986

Carbon monoxide(CO) poisoning has been one of the major environmental problems because of the tissue hypoxia, especially brain tissue hypoxia, due to the great affinity of CO with hemoglobin. Inhalation of the pure oxygen$(0_2)$ under the high atmospheric pressure has been considered as the best treatment of CO poisoning by the supply of $0_2$ to hypoxic tissues with dissolved from in plasma and also by the rapid elimination of CO from the carboxyhemoglobin(HbCO). Hydrogen peroxide $(H_2O_2)$ was rapidly decomposed to water and $0_2$ under the presence of catalase in the blood, but the intravenous administration of $H_2O_2$ is hazardous because of the formation of methemoglobin and air embolism. However, it was reported that the enema of $H_2O_2$ solution below 0.75% could be continuously supplied $0_2$ to hypoxic tissues without the hazards mentioned above. This study was performed to evaluate the effect of $H_2O_2$ enema on the elimination of CO from the HbCO in the recovery of the acute CO poisoning. Rabbits weighting about 2.0 kg were exposed to If CO gas mixture with room air for 30 minutes. After the acute CO poisoning, 30 rabbits were divided into three groups relating to the recovery period. The first group T·as exposed to the room air and the second group w·as inhalated with 100% $0_2$ under 1 atmospheric pressure. The third group was administered 10 ml of 0.5H $H_2O_2$ solution per kg weight by enema immediately after CO poisoning and exposed to the room air during the recovery period. The arterial blood was sampled before and after CO poisoning ana in 15, 30, 60 and 90 minutes of the recovery period. The blood pH, $Pco_2\;and\;Po_2$ were measured anaerobically with a Blood Gas Analyzer and the saturation percentage of HbCO was measured by the Spectrophotometric method. The effect of $H_2O_2$ enema on the recovery from the acute CO poisoning was observed and compared with the room air group and the 100% $0_2$ inhalation group. The results obtained from the experiment are as follows: The pH of arterial blood was significantly decreased after CO poisoning and until the first 15 minutes of the recovery period in all groups. Thereafter, it was slowly increased to the level of the before CO poisoning, but the recovery of pH of the $H_2O_2$ enema group was more delayed than that of the other groups during the recovery period. $Paco_2$ was significantly decreased after CO poisoning in all groups. Boring the recovery Period, $Paco_2$ of the room air group was completely recovered to the level of the before CO Poisoning, but that of the 100% $O_2$ inhalation group and the $H_2O_2$ enema group was not recovered until the 90 minutes of the recovery period. $Paco_2$ was slightly decreased after CO poisoning. During the recovery Period, it was markedly increased in the first 15 minutes and maintained the level above that before CO Poisoning in all groups. Furthermore $Paco_2$ of the $H_2O_2$ enema group was 102 to 107 mmHg and it was about 10 mmHg higher than that of the room air group during the recovery period. The saturation percentage of HbCO was increased up to the range of 54 to 72 percents after CO poisoning and in general it was generally diminished during the recovery period. However in the $H_2O_2$ enema group the diminution of the saturation percentage of HbCO was generally faster than that of the 100% $O_2$ inhalation group and the room air group, and its diminution in the 100% $O_2$ inhalation group was also slightly faster than that of the room air group at the relatively later time of the recovery period. In conclusion, the enema of 0.5% $H_2O_2$ solution is seems to facilitate the elimination of CO from the HbCO in the blood and increase $Paco_2$ simultaneously during the recovery period of the acute CO poisoning.

• Journal of Preventive Medicine and Public Health
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• v.5 no.1
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• pp.17-23
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• 1972

Carbon Monoxide poisoning is one of the most serious Public health problems in Korea. The incidence rate. officially reported has been known to be the highest in the world. This high incidence is mainly due to the wide prevalence of anthracite coal briquette as the domestic fuel for unique Korean heating system called 'ondol,' The coal briquette gas contains around 3-5% of Carbon Monoxide. A nation-wide effort to eliminate or reduce this serious hazards has produced little effect and the most hospitals are offering very ineffective measures such as oxygen inhalation through nasal catheter. Author has believed that this preventable accident should be approached by the secondary preventive measure because of our socio-economic status do not allow us optimistic results from primary preventive measure as far as the problem of CO poisoning is concerned. Author has treated 466 patients during 30 months period by Hyperbaric Oxygenation at Seoul National University Hospital. The results found are as follows. 1. Female has a higher incidence rate than male and the age group between 15-29 years showed highest incidence. 2. The recovery time depends on the time when the patients arrived at hospital. Earlier the arrival time, shorter the recovery time. 3. Some objective signs are representing typical physiological response to tissue hypoxia. 4. Therapeutic effectiveness of Hyperbaric Oxypenation is confirmed by such indices as recovery rate, Admission rate and average stay in hospital. Futher, these results are cocordant with other reports on the clinical value of Hyperbaric Oxygenation in the treatment of CO poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.1
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• pp.26-32
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• 2016

Purpose: Aspiration pneumonia is an important complication of drug intoxication with decreased mental status. The purpose of the study is to investigate the risk factors of aspiration pneumonia in the patients of benzodiazepine overdose with or without co-ingestion of other drugs. Methods: A retrospective chart review of patients who visited the emergency department between January 2012 and December 2014 was conducted. Demographic data, time from ingestion to visit, initial vital signs, symptoms, mental status, medical history, laboratory results, chest radiological findings and co-ingested medications were recorded. Multiple logistic analyses were performed to verify the association between variables and the development of aspiration pneumonia. Results: A total of 249 patients presented to the emergency department with benzodiazepine overdose. Aspiration pneumonia had developed in 24 patients (9.6%). Univariate analysis revealed time from ingestion to visit was longer, Glasgow coma scale score was lower, hypoxia was presented, leukocytosis was shown, types of ingested drugs was high, less activated charcoal was applied and tricyclic antidepressants was taken in patients that developed aspiration pneumonia. Time from ingestion to visit (odds ratio (OR) 1.121, 95% confidence interval (CI), 1.057-1.189, p=0.000), GCS score (OR 0.724. 95% CI, 0.624-0.839, p=0.000), oxygen saturation (OR 0.895, 95% CI, 0.835-0.959, p=0.002), and co-ingestion of TCA (OR 4.595, 95% CI, 1.169-18.063, p=0.029) were identified as risk factors of morbidity of aspiration pneumonia upon multiple logistic regression analysis. Conclusion: Time from ingestion to visit, low GCS score, low oxygen saturation and co-ingestion of TCA were risk factors of the development of aspiration pneumonia in benzodiazepine overdose patients.

• Journal of Oral Medicine and Pain
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• v.40 no.2
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• pp.63-71
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• 2015

Purpose: To investigate the relationship between headache and sleep by evaluating sleep quality, daytime sleepiness, and specific features related to sleep-disordered breathing (SDB). Methods: One hundred one subjects with headache and 118 healthy controls were enrolled. To collect various information on headache attacks, headache group completed self-reported questionnaire about the characteristics of headache attacks and the migraine disability assessment (MIDAS) questionnaire. The subjective quality of sleep was evaluated in all of the subjects using the Pittsburgh sleep quality index (PSQI) and Epworth sleepiness scale (ESS). In addition, the following specific features of sleep were evaluated in 28 subjects selected randomly from each group: apnea-hypopnea index (AHI), prevalence of SDB, nocturnal oxygen saturation (SaO2), and oxygen desaturation index (ODI) as measured using a portable monitoring device. Results: The global PSQI and the prevalence of poor sleeping (global PSQI >5), ESS scores and the prevalence of daytime sleepiness (ESS score >10) were significantly higher in the headache group (both p<0.0001, respectively). The mean scores on the numerical rating scale and the MIDAS were significantly higher in the poor-sleeper group than in the good-sleeper group (p=0.0347 and p=0.0016, respectively). The global PQSI and prevalence of daytime sleepiness were significantly higher in the chronic-headache group than in the acute-headache group (p=0.0003 and p=0.0312, respectively). Conclusions: There is a significant association between headache and sleep. Especially, severity and chronicity of headache were significantly associated with sleep quality and daytime sleepiness.

• Journal of Chest Surgery
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• v.34 no.10
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• pp.792-796
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• 2001

Chronic pulmonary artery thromboembolism is a relatively rare phenomenon causing hypoxia and pulmonary hypertension that eventually leads to respiratory failure and right heart failure. Patients with acute pulmonary artery thromboembolism are generally treated with antithrombotics and thrombolytics. However, in cases with chronic pulmonary artery thromboembolism the fibrinized thrombus is so strongly adhered to the pulmonary artery wall that medical treatment becomes ineffective and surgical treatment must then be considered. We report a 47year old patient, with a history of repeated admission due to unresolved chronic obstructive pulmonary disease and chronic pulmonary artery thromboembolism at a local hospital, who underwent a successful endarterectomy of pulmonary artery thromboemboli using intermittent total circulatory arrest.