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 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

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

OBJECTIVETo investigate the changes in serum level of high mobility group protein B1 (HMGB1) in patients with delayed encephalopathy after acute carbon monoxide poisoning and the clinical significance of these changes.

METHODSThirty-four patients with delayed encephalopathy after acute carbon monoxide poisoning (delayed encephalopathy group), 30 normal controls (control group), and 32 cases of acute carbon monoxide poisoning without delayed encephalopathy (carbon monoxide poisoning group) were recruited in this study. The serum HMGB1 level was determined by enzyme-linked immunosorbent assay. The correlation between serum HMGB1 level and scores of the activity of daily living scale (ADL), Information-Memory-Concentration Test (IMCT), and Hasegawa dementia scale (HDS) was determined.

RESULTSIn the acute stage of carbon monoxide poisoning, the serum HMGB1 level of delayed encephalopathy group was significantly higher than those of the carbon monoxide poisoning group and the control group (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level in the convalescent stage was significantly lower than that in the acute stage (P < 0.05); ADL score was higher and HDS and IMCT scores were lower in the acute stage than in the convalescent stage (P < 0.01). In the delayed encephalopathy group, serum HMGB1 level was positively correlated with HDS and ADL scores in both acute stage and convalescent stage (correlation coefficients: 0.612, 0.607, 0.609, and 0.612, P < 0.01).

CONCLUSIONHMGB1, as an important late mediator of inflammation, is involved in the inflammatory reaction in delayed encephalopathy, and is positively correlated with HDS and ADL scores, indicating that it can be used as one of the major indicators in monitoring carbon monoxide poisoning.

Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; blood ; etiology ; Carbon Monoxide Poisoning ; blood ; complications ; Female ; HMGB1 Protein ; blood ; Humans ; Male ; Middle Aged

OBJECTIVEBy explore the role of serum soluble Fas (sFas) in occurrence and progression of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).

METHODSEnzyme-linked immunosorbent assay (ELISA) was used to detect serum sFas levels in 40 patients with DEACMP in acute stage and convalescent stage, with 36 healthy elderly subjects as the control group.

RESULTSSerum sFas levels of the patients with DEACMP in both the acute and convalescent stages showed no significant difference from those in the control group (P=0.737 and 0.137, respectively), nor was any significant difference found between the patients in acute and exacerbation stages (P=0.059).

CONCLUSIONSerum sFas is not involved in the occurrence and progression of DEACMP.

Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; etiology ; Carbon Monoxide Poisoning ; blood ; complications ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; fas Receptor ; blood

Carbon monoxide (CO) is a well-known chemical asphyxiant, which causes tissue hypoxia with prominent neurological injury. Therapeutic hypothermia (TH) has been shown to be an effective neuroprotective method in post-cardiac arrest patients. A 26-year-old man presented to the emergency department with severe CO poisoning. On arrival, the patient was comatose. His vital signs were blood pressure, 130/80 mm Hg; heart rate, 126/min; respiratory rate, 26/min; body temperature, 36degrees C; and O2 saturation, 94%. Initial carboxyhemoglobin was 45.2%. Because there was no available hyperbaric chamber in our local area, he was intubated and treated with TH. The target temperature was 33 +/- 1degrees C for 24 hours using an external cooling device. The patient was then allowed to reach normothermia by 0.15-0.25degrees C/hr. The patient was discharged after normal neurological exams on day 11 at the hospital. TH initiated after exposure to CO may be an effective prophylactic method for preventing neurological sequelae.
Anoxia ; Blood Pressure ; Body Temperature ; Carbon ; Carbon Monoxide ; Carbon Monoxide Poisoning ; Carboxyhemoglobin ; Coma ; Emergencies ; Heart Rate ; Humans ; Hypothermia ; Hypothermia, Induced ; Respiratory Rate ; Vital Signs

OBJECTIVETo explore the changes and the clinical significance of 5-hydroxytryptamine (5-HT), dopamine (DA) levels in serum and cerebrospinal fluid (CSF) of patients with delayed encephalopathy (DEACMP) after acute carbon monoxide poisoning.

METHODSThe dynamic detection of 5-HT and DA levels in serum and CSF from 42 patients with DEACMP was performed with high performance liquid chromatography (HPLC). The condition changes of patients with DEACMP were analyzed with three types of scales: the activity of daily living scale (ADL), information memory concentration test (IMCT) and Hasegawa's dementia scale (HDS); these changes were compared with those from 38 other encephalopathy patients and 38 non-encephalopathy patients, respectively.

RESULTSBefore treatment, the serum 5-HT and DA levels [(662.61 ± 178.50) and (155.74 ± 60.32) nmol/L, respectively] of DEACMP group were both significantly lower than those [(914.08 ± 198.04) and (225.70 ± 48.53) nmol/L] of non-encephalopathy group (P < 0.05); the serum DA level of DEACMP group was also significantly lower than that [(243.57 ± 66.94) nmol/L] of other encephalopathy group (P < 0.05); the serum 5-HT level of DEACMP group was not significantly different from that [(729.54 ± 299.87) nmol/L] of other encephalopathy group (P > 0.05). After treatment, the serum 5-HT and DA levels [(714.08 ± 170.47) and (192.18 ± 33.07 nmol/L, respectively)] of DEACMP group elevated to various extent, but only serum DA level was significantly higher than that before treatment (P < 0.05). Before treatment, the CSF 5-HT and DA levels of DEACMP group were significantly lower than those of non-encephalopathy group and those of other encephalopathy group (P < 0.05). After treatment, the CSF 5-HT level (232.44 ± 54.28 nmol/L) was similar to normal level and significantly higher than that before treatment (P < 0.05); the CSF DA level [(56.83 ± 12.85) nmol/L] of DEACMP group increased only slightly (P > 0.05). In DEACMP group, ADL score (50.64 ± 7.23), HDS score (8.55 ± 8.08) and IMCT score (4.95 ± 7.30) before treatment were significantly different from those (8.5 ± 8.08, 4.95 ± 7.30 and 15.64 ± 10.90) after treatment (P < 0.01). In DEACMP group, there wasa negative correlation between DA level changes and HDS score changes, when the DA levels and HDS scores before treatment were compared with those after treatment (P < 0.05).

CONCLUSIONThe dynamic changes of 5-HT and DA levels in serum and CSF of patients with DEACMP consisted basically with the patient's condition change. The dynamically detected 5-HT and DA levels can be used as the biological indicators to reflect the condition change and treatment effects of DEACMP patients.

Adult ; Aged ; Aged, 80 and over ; Brain Diseases ; blood ; cerebrospinal fluid ; etiology ; Carbon Monoxide Poisoning ; blood ; cerebrospinal fluid ; complications ; Case-Control Studies ; Dopamine ; blood ; cerebrospinal fluid ; Female ; Humans ; Male ; Middle Aged ; Neurotoxicity Syndromes ; blood ; cerebrospinal fluid ; etiology ; Serotonin ; blood ; cerebrospinal fluid

Adult ; Aged ; Carbon Monoxide Poisoning ; blood ; pathology ; Creatine Kinase ; blood ; Female ; Humans ; Male ; Middle Aged ; Myocardium ; pathology ; Natriuretic Peptide, Brain ; blood ; Peptide Fragments ; blood ; Troponin I ; blood ; Young Adult

OBJECTIVETo investigate the startup detail of circulation dysfunction and its role in the progress of delayed neuropsychologic sequelae (DNS) after carbon monoxide (CO) poisoning with comparison with the model of ischemia-reperfusion.

METHODSThe ischemia-reperfusion rat model was established by Pulsinelli-Brierley method, and the CO poisoning rats model by i.p. injected with CO repeatedly respectively, and the rats were identified with DNS following the experiment of pathology and the ethnology.

RESULTSThe whole blood viscosity, plasma viscosity, hematocrit and fibrinogen increased significantly immediately after reperfusion, and recovered gradually with the ischemia-reperfusion rat model. The whole blood viscosity decreased significantly immediately after CO treated i.p. Especially at low shear rate, the hematocrit also declined remarkably in the early stage after CO treatment. But 1day later, these parameters turned to the trend of the ischemia-reperfusion rats. There was a prominent elevation of both indexes until the 14th day following CO injection i.p.

CONCLUSIONThere are significantly sustained hyper-coagulation and hyper-viscosity with circulation in rats after CO poisoning compared with ischemia-reperfusion model during the period of DNS, which might contribute to increase cerebral circulation resistance, blocked blood flow, and deteriorate hypoxemia in progression of DNS.

Animals ; Blood Circulation ; Carbon Monoxide Poisoning ; physiopathology ; Disease Models, Animal ; Hemorheology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology