Objective: To compare the efficacy of high-flow nasal cannula oxygen therapy (HFNC) and non-rebreather face mask (NRFM) in the treatment of mild acute carbon monoxide poisoning (ACOP) in reducing carboxyhemoglobin (COHb) , and to explore the feasibility of HFNC in the treatment of ACOP. Methods: Patients with mild ACOP with COHb >10% who were admitted to the emergency department of Northern Jiangsu People's Hospital from January 2015 to December 2020 were analyzed, and those with altered consciousness, mechanical ventilation and those requiring hyperbaric oxygen therapy were excluded. The patients were divided into HFNC group and NRFM group according to the oxygen therapy used in the emergency department. The COHb decline value and COHb half-life in the two groups were observed. Results: Seventy-one patients were enrolled, including 39 in the NRFM group and 32 in the HFNC group. The baseline COHb in the HFNC group was 24.8%±8.3%, and that in the NRFM group was 22.5%±7.1%, with no significant difference between the two groups (t=1.27, P=0.094) . At 60 min, 90 min and 120 min of treatment, COHb in both groups decreased, but the COHb in HFNC group was lower than that in NRFM group at the same time point (P<0.05) . After 1 h of treatment, the COHb decrease in the HFNC group (16.9%±4.5%) was significantly higher than that in the NRFM group (10.1%±7.8%) (t=4.32, P=0.013) . The mean half-life of COHb in the HFNC group (39.3 min) was significantly lower than that in the NRFM group (61.4 min) (t=4.69, P=0.034) . Conclusion: HFNC treatment of mild ACOP can rapidly reduce blood COHb level, it is a potential oxygen therapy method for clinical treatment of ACOP.
Humans ; Carbon Monoxide Poisoning/therapy* ; Cannula ; Respiration, Artificial ; Masks ; Oxygen Inhalation Therapy/methods* ; Carboxyhemoglobin ; Oxygen/therapeutic use* ; Respiratory Insufficiency/therapy*

OBJECTIVE: This study examined the effects on mortality and cell death after biomass charcoal combustion, in which carbon monoxide (CO) emissions were reduced using a biomass combustion improver in mice. METHODS: The biomass (glycerin) charcoal (Biomass CharCoal by Pusan National University, BCCP) was generated in the Power Generation System laboratory, Pusan National University. The effects and molecular mechanisms of biomass charcoal in carbon monoxide poisoning were examined by analyzing the mouse mortality, circulating leukocytes, carboxyhemoglobin (COHb), and expression of the inflammation-related genes, and cleaved capase-3 using enzyme-linked-immunosorbent-assays, real-time polymerase chain reaction, or Western blotting. RESULTS: The mortality rates were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. The circulating leukocytes were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. On the other hand, there was no significantly difference in the levels of COHb between both mice. Interestingly, the expression of the apoptosis-related gene, cleaved-capase 3, and the inflammation and tissue necrosis-related gene and receptor for the advanced glycation end products were reduced markedly in the BCCP-exposed mice compared to the raw charcoal-exposed mice. Decreased inflammation and tissue necrotic factors could be molecular mechanisms for the decreased mortality rates after BCCP burning. CONCLUSION: Biomass charcoal (BCCP) reduced the mortality rates and inflammation and tissue necrotic factors by 30%–40%. These results suggest that the biomass charcoal (BCCP) could reduce the incidence of suicide and CO-associated delayed symptoms after charcoal burning. Furthermore, it could extend the time for rescue in suicide attempts using charcoal burning.
Animals ; Biomass* ; Blotting, Western ; Burns* ; Busan ; Carbon Monoxide Poisoning ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Cell Death ; Charcoal* ; Glycosylation End Products, Advanced ; Hand ; Incidence ; Inflammation ; Leukocytes ; Mice* ; Mortality* ; Real-Time Polymerase Chain Reaction ; Suicide

PURPOSE: Early prediction of treatment outcomes represents an essential step towards increased treatment efficacy and survival in patients with hepatocellular carcinoma (HCC). In this study, we performed two-dimensional electrophoresis (2-DE) followed by protein profiling to identify biomarkers predictive of therapeutic outcomes in patients with HCC who received liver-directed therapy (LDTx) involving local radiotherapy (RT), and studied the underlying mechanisms of the identified proteins. MATERIALS AND METHODS: 2-DE analysis was conducted by pooling sera from patients with a good or poor prognosis; serum proteomic profiles of the two groups were compared and analyzed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Identified proteins were confirmed via enzyme-linked immunosorbent assay. An invasion assay was performed after overexpression and knockdown of target protein in Huh7 cells. RESULTS: Levels of inter-alpha inhibitor H4 (ITIH4), fibrinogen gamma chain, keratin 9/1 complex, carbonic anhydrase I, and carbonmonoxyhemoglobin S were changed by more than 4-fold in response to LDTx. In particular, pre-LDTx ITIH4 expression was more than 5-fold higher in patients with a good prognosis, compared to patients with a poor prognosis. The migration ability of Huh7 cells was significantly suppressed and enhanced by ITIH4 overexpression and knockdown, respectively. The tumors of patients with HCC and a good prognosis expressed high levels of ITIH4, compared to those of patients with a poor prognosis. CONCLUSION: Taken together, ITIH4 may be a potential therapeutic target that could inhibit cancer metastasis, as well as a prognostic marker for patients with HCC who are receiving LDTx.
Biomarkers ; Carbonic Anhydrase I ; Carboxyhemoglobin ; Carcinoma, Hepatocellular* ; Electrophoresis ; Enzyme-Linked Immunosorbent Assay ; Fibrinogen ; Humans ; Mass Spectrometry ; Neoplasm Metastasis ; Prognosis ; Radiotherapy ; Treatment Outcome

OBJECTIVE: The evidence that hyperbaric oxygen (HBO) therapy is more effective for improving the acute neuropsychological status (ANS) of carbon monoxide poisoning than normobaric oxygen (NBO) therapy is not convincing. This is because the levels of carboxyhemoglobin (COHb) do not correlate with the clinical severity of carbon monoxide poisoning and there is no universally accepted severity scale of carbon monoxide poisoning. This paper suggests a new scale for the clinical and neurological severity of carbon monoxide poisoning, called the ANS, and assesses the effect of HBO therapy for each level of ANS compared to NBO therapy. METHODS: A total of 217 patients who had been hospitalized because of carbon monoxide poisoning from January 2009 to July 2013 were studied. ANS was suggested as a new severity scale of carbon monoxide poisoning considered in the Glasgow Coma Scale, acute neuro-psychologic signs and symptoms, or cardiac ischemia on the initial medical contact. HBO therapy is indicated in those who have a loss of consciousness, seizure, coma, abnormal findings on a neurological examination, pregnancy, persistent cardiac ischemia, level of COHb >25%, or severe metabolic acidosis (pH < 7.2). The end point is the day of discharge, and recovery is defined as a normal neuro-psychological status without any sequelae. RESULTS: The levels of troponin T and creatinine increased significantly with increasing ANS score. In the moderate to severe group (ANS 2 and 3), the recovery rate was significantly higher when treated with HBO therapy than with NBO therapy (P=0.030). On the other hand, the development of delayed neuro-psychological sequelae (DNS) did not correlate with any level of ANS, type of oxygen therapy, or recovery on discharge. CONCLUSION: In the moderate to severe poisoned group, HBO therapy is more effective for improving the ANS from carbon monoxide poisoning than NBO therapy. On the other hand, the development of DNS of HBO therapy is no more preventable than with NBO therapy. Although the level of ANS is low, the patient needs to be provided with sufficient information and a follow-up visit is recommended for any abnormal symptoms because the ANS does not correlate with the development and degree of DNS.
Acidosis ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Coma ; Creatinine ; Follow-Up Studies ; Glasgow Coma Scale ; Hand ; Humans ; Hyperbaric Oxygenation* ; Ischemia ; Neurologic Examination ; Oxygen* ; Pregnancy ; Seizures ; Severity of Illness Index ; Troponin T ; Unconsciousness

PURPOSE: This study was performed to compare clinical significance between lactate and carboxyhemoglobin (COHb) in a patient with carbon monoxide (CO) poisoning. METHODS: We conducted a 13-year retrospective study on CO poisoning patients who visited the emergency departments of the Medical Center between October 2004 and January 2016. The patients were divided into two groups according to initial lactate levels. Patients with serum lactate levels of ≤2 mmol/L were classified as the normolactatemia group (n=14), and patients with serum lactate levels of >2 mmol/L were classified as the hyperlactatemia group (n=34). General characteristics, clinical features, and laboratory findings of the two groups were compared. In addition, we compared initial lactate levels with COHb levels according to complications, neurological disorder, myocardial enzyme elevation, and abnormal Glasgow Coma Scale (GCS) score in patients with CO poisoning. We also analyzed the correlation between laboratory parameters and lactate levels. RESULTS: Forty-eight patients were enrolled in this study. The hyperlactatemia group had significantly more neurological disorders and consciousness disorders than the normolactatemia group (p<0.001), and COHb, creatine phosphokinase MB, and troponin I levels were also significantly higher in the hyperlactatemia group (p<0.001, p=0.017, and p=0.007). Lactate levels were significantly elevated in patients with elevated cardiac enzymes (p=0.001), neurological disorders (p<0.001), complications (p=0.001), and abnormal GCS score (p<0.001), whereas COHb levels were not significantly increased in all subjects. The correlation between COHb and lactate levels was weak (r=0.313, p=0.030), and a positive correlation was found between lactate and bicarbonate (HCO3), white blood cell, and troponin I (p<0.001). The diagnostic value of lactate for severe CO poisoning was analyzed using a receiver operating characteristic curve. The optimal cut-off value of lactate was 2.2 mmol/L with 83.3% sensitivity and 91.7% specificity (p<0.001). CONCLUSION: Lactate has significant diagnostic efficacy in patients with CO poisoning. It is recommended that lactate level be measured for appropriate treatment and prognostic evaluation of CO poisoning.
Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin* ; Consciousness Disorders ; Creatine Kinase ; Emergency Service, Hospital ; Glasgow Coma Scale ; Humans ; Hyperlactatemia ; Lactates ; Lactic Acid* ; Leukocytes ; Nervous System Diseases ; Poisoning ; Retrospective Studies ; ROC Curve ; Sensitivity and Specificity ; Troponin I

PURPOSE: The aim of this study was to determine the risk factors for rhabdomyolysis in patients with carbon monoxide (CO) poisoning. METHODS: This was a retrospective study on patients with CO poisoning who visited the emergency department from January 1, 2014 to December 31, 2015. We compared clinical variables between patients with and without rhabdomyolysis. RESULTS: Among 120 patients who were included to this study, 108 patients exhibited normal value of CPK (creatine phosphokinase), and 12 patients were diagnosed as rhabdomyolysis. Sources of CO, duration of CO exposure, initial GCS (Grasgow coma scale), initial systolic and diastolic blood pressure, initial body temperature and AKI (Acute kidney injury) were showed significant difference between patients who developed rhabdomyolysis and patients who did not. In addition, initial white blood cell counts, troponin I level and carboxyhemoglobin (COHb) level were more higher in rhabdomyolysis group. pH and initial bicarbonate level were more lower. Duration of CO exposure (Odds ratio, 1.011; 95% confidence interval, 1.002∼1.020, P=0.021)was found to be only risk factor for rhabdomyolysis by logistic regression analysis. CONCLUSION: Duration of CO exposure is potential risk factor of rhabdomyolysis development in CO poisoning.
Blood Pressure ; Body Temperature ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Coma ; Emergency Service, Hospital ; Humans ; Hydrogen-Ion Concentration ; Kidney ; Leukocyte Count ; Logistic Models ; Poisoning ; Reference Values ; Retrospective Studies ; Rhabdomyolysis* ; Risk Factors* ; Troponin I

OBJECTIVES: To explore the change rules of behavioral characteristics, survival time and saturation of carboxyhemoglobin （HbCO） in different CO concentration to provide experimental basis for the cases of CO poisoning death in forensic practice. METHODS: Total 160 SD rats were randomly divided into four groups. CO with the concentration of 1 250 mg/m³, 3 750 mg/m³, 6 250 mg/m³ were continuously and respectively replenished in a self-made toxicant exposure equipment until rats died from poisoning. In different CO concentration, the behavioral characteristics and survival time of poisoning rats were observed and recorded. The saturation of HbCO in heart blood was detected by spectrophotometric method. Organs such as brain, heart, lung and liver, and heart blood were obtained via autopsy and histopathological observation was performed. RESULTS: The behavioral characteristics of CO poisoning rats were limp and slow response. There were a gradual decrease of survival time and an increase of HbCO saturation in rats with the increase of CO concentration. Three rats in CO concentration of 1 250 mg/m³ group showed lower saturations of HbCO than the lethal dose and this situation hasn't been found in other groups. CONCLUSIONS The animal model of CO poisoning established under different CO concentration has the advantages such as simplicity and good repeatability, which lays a foundation to the further study for CO and other inhaled toxic gas in the research of forensic sciences.
Animals ; Carbon Monoxide Poisoning/blood* ; Carboxyhemoglobin/analysis* ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Rats ; Rats, Sprague-Dawley

Carbon monoxide (CO) poisoning has increased rapidly in South Korea and may cause a variety of clinical effects. The most common complications are neurologic and neuropsychological disturbances. However, in rare cases, CO poisoning may also be associated with acute kidney injury and non-traumatic rhabdomyolysis. Here, we report a case of acute kidney injury and rhabdomyolysis complicating CO poisoning. A 32-year-old woman was admitted to our emergency department with dyspnea and confused consciousness after exposure to CO during a suicide attempt involving charcoal briquettes. Laboratory findings revealed a carboxyhemoglobin (COHb) level of 44.8%, a blood urea nitrogen level of 20.5 mg/dL, a serum creatinine level of 1.4 mg/dL, and a creatine phosphokinase level of 8,688.3 IU/L. Acute kidney injury and rhabdomyolysis complicating CO poisoning were diagnosed. This case was managed with normobaric oxygen therapy and hydration. The patient recovered completely with respect to renal function and muscle enzyme level, and COHb level returned to 0%.
Acute Kidney Injury* ; Adult ; Blood Urea Nitrogen ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Charcoal ; Consciousness ; Creatine Kinase ; Creatinine ; Dyspnea ; Emergency Service, Hospital ; Female ; Humans ; Korea ; Oxygen ; Poisoning ; Rhabdomyolysis* ; Suicide

Carbon monoxide intoxication is the most prevalent cause of death from carbon monoxide poisoning. We herein report the case of a 56-year-old man who was found unconscious and smelled of smoke after exposure to carbon monoxide from a heater. He scored 5 on the Glasgow Coma Scale, and had respiratory insufficiency and elevated troponin I, creatine kinase-MB fraction and carboxyhaemoglobin levels. He was treated by mechanical ventilation. After regaining consciousness, brain magnetic resonance imaging showed diffusion restriction in the left occipital lobe; there was a loss of vision (right temporal hemianopsia), which improved by the follow-up session. Carbon monoxide intoxication may cause neurologic and cardiac sequelae, and the initial treatment includes oxygen therapy. Acute carbon monoxide poisoning can cause serious injury to the brain, heart and other organs; the most severe damages that could be inflicted to the brain include cerebral ischaemia and hypoxia, oedema, and neural cell degeneration and necrosis.
Brain ; physiopathology ; Brain Ischemia ; physiopathology ; Carbon Monoxide ; chemistry ; Carbon Monoxide Poisoning ; physiopathology ; Carboxyhemoglobin ; chemistry ; Creatine Kinase, MB Form ; blood ; Diffusion ; Glasgow Coma Scale ; Humans ; Hyperbaric Oxygenation ; Hypoxia ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Myocardial Ischemia ; physiopathology ; Stroke ; physiopathology ; Troponin I ; blood

OBJECTIVE: Acute carbon monoxide poisoning has important clinical value because it can cause severe adverse cardiovascular effects and sudden death. Acute carbon monoxide poisoning due to charcoal is well reported worldwide, and increased use of charcoal in the restaurant industry raises concern for an increase in occupational health problems. We present a case of carbon monoxide poisoning induced cardiomyopathy in a 47-year-old restaurant worker. MATERIALS AND METHODS: A male patient was brought to the emergency department to syncope and complained of left chest pain. Cardiac angiography and electrocardiography were performed to rule out acute ischemic heart disease, and cardiac markers were checked. After relief of the symptoms and stabilization of the cardiac markers, the patient was discharged without any complications. RESULTS: Electrocardiography was normal, but cardiac angiography showed up to a 40% midsegmental stenosis of the right coronary artery with thrombotic plaque. The level of cardiac markers was elevated at least 5 to 10 times higher than the normal value, and the carboxyhemoglobin concentration was 35% measured at one hour after syncope. Following the diagnosis of acute carbon monoxide poisoning induced cardiomyopathy, the patient's medical history and work exposure history were examined. He was found to have been exposed to burning charcoal constantly during his work hours. CONCLUSIONS: Severe exposure to carbon monoxide was evident in the patient because of high carboxyhemoglobin concentration and highly elevated cardiac enzymes. We concluded that this exposure led to subsequent cardiac injury. He was diagnosed with acute carbon monoxide poisoning-induced cardiomyopathy due to an unsafe working environment. According to the results, the risk of exposure to noxious chemicals such as carbon monoxide by workers in the food service industry is potentially high, and workers in this sector should be educated and monitored by the occupational health service to prevent adverse effects.
Angiography ; Burns ; Carbon Monoxide Poisoning ; Carbon Monoxide* ; Carbon* ; Carboxyhemoglobin ; Cardiomyopathies* ; Charcoal* ; Chest Pain ; Constriction, Pathologic ; Coronary Vessels ; Death, Sudden ; Diagnosis ; Electrocardiography ; Emergency Service, Hospital ; Food Services ; Humans ; Male ; Middle Aged ; Myocardial Ischemia ; Occupational Health ; Occupational Health Services ; Reference Values ; Restaurants* ; Syncope