OBJECTIVETo investigate the relationship between blood nitrogen monoxide(NO) and PaO2 or PaCO2 levels in patients with severe and moderate acute carbon monoxide poisoning.

METHODThe blood levels of NO in patients with severe and moderate acute carbon monoxide poisoning was assayed with nitrate reductase method, and its correlation with the blood levels of PaO2 and PaCO2 was analyzed.

RESULTSThe blood level of NO in patients with severe and moderate acute carbon monoxide poisoning were (36.6 +/- 9.9) and (35.7 +/- 10.7) mumol/L respectively, significantly lower than that of control group[(64.9 +/- 14.3) mumol/L, P < 0.01], but there was no significant difference between moderate and severe patients(P > 0.05). The analysis of linear correlation showed that there was significant positive correlation between NO and PaO2 but not PaCO2.

CONCLUSIONAnoxia of patients with acute carbon monoxide poisoning may be an important cause to reduce NO level in blood. This study provides the basis for low NO concentration inhalation in treatments of acute carbon monoxide poisoning.

Acute Disease ; Carbon Dioxide ; blood ; Carbon Monoxide Poisoning ; blood ; Humans ; Nitric Oxide ; blood ; Oxygen ; blood

OBJECTIVE: To confirm whether formaldehyde disturb detecting carbon monoxide in blood. To give an evidence that can be used for detecting carboxyhemoglobin more accurately in carbon monoxide posioning appraises. METHODS: Blood samples came from carbon monoxide poisoning and the health were collected. Regular methods for detecting carboxyhemoglobin were used. Observing and comparing the detection results between which were spiked with methanal and no spiked one were performed. RESULTS: Methanal will affect the result of following experiments such as heating, adding NaOH, absorbed by PdCl2 and spectrophotometry. CONCLUSION The samples which contaminated by formaldehyde couldn't be used for detecting carboxyhemoglobin.
Carbon Monoxide/blood* ; Carbon Monoxide Poisoning/diagnosis* ; Carboxyhemoglobin/analysis* ; Forensic Medicine ; Formaldehyde/pharmacology* ; Humans ; Spectrophotometry/methods* ; Temperature

This study was performed to observe the changes of blood sugar levels in 200 cases with acute Carbon monoxide (CO) poisoning. Successive tests of blood sugar on the day of onset and the lst, 2nd, 3rd & 4th day after anoxic insult were done in 12 patients with acute CO poisoning. In addition, to determine the derangement of thyroid function, blood levels of triiodothyronine(T3), tetraiodothyronine(T4), thyroid-stimulating hormone (TSH) were measured on the day of admission in 29 with C0 poisoning. The blood levels of T3, T4 and TSH were within normal ranges, but over two-thirds were distributed in lower range of normal mean values. This lower tendency within normal range was especially prominent in the blood level of T3. The blood level of sugar was increased, and 79.5% was higher than the upper limit of normal range. The blood levels of T3 and T4 were significantly decreased as CO exposure time period- prolonged. There was significant negative correlation between blood T3 levels and consciousness levels. Blood TSH levels were not significantly affected in acute CO poisoning. As consciousness levels were depressed and exposure time period were prolonged, blood sugar was increased. There found a rapid increase in blood sugar, followed by a abrupt dropping, and then progressive decrease to normal level over a period of 5 days after exposure to CO. In conclusion, acute CO poisoning obviously changes the thyroidal physiology. Even though blood TSH levels were variable, there was an obvious decrease in T3. The assumed CO-induced decrease in thyroid hormone secretion is seemingly not mediated by depressed TSH secretion but thyroid hormone metabolic dysfunction or extrathyroidal cotiverslon defect The alterations of blood sugar were also found to be acute and temporal which may be the result of physiologic compensation to hypoxic state caused by CO poisoning.
Blood Glucose ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Compensation and Redress ; Consciousness ; Humans ; Physiology ; Poisoning ; Reference Values ; Thyroid Gland* ; Thyroid Hormones* ; Thyrotropin

Carbon monoxide is colorless, oolorless, tasteless and non-irritating gas produced by the incomplete combustion of carbonaceous rnaterial. It combines with hemoglobin and displaces oxygen because the affinity of hemoglobin for carbon monoxide is two hundred times greater than oxygen. Symptoma and signs of carbon monoxide poisoning include headache, nausea, vomiting, dizziness, collapse, unconsciousness, blindness, convulsion, coma and skin lesions. Recently we have observed seven patients with carbon monoxide poisoning who expressed cutaneous syrnptoms. In this work we investigated the pathogenesis of cutaneous manifestations of carbon monoxide poisoning through clinical, histologic and electronmicroscopic study. The results are summarized as follows: 1. Mental states of the patients were comatose in two, Semicomatcse in two, stuporous in two, and drowsy in one patient. In routine laboratory tests, we observed elevated blood sugar in six, elevated sorum creatinine phosphokinase in four and abnormal findings in urinalysis in all patients. 2. Cutaneous lesions were vesicobullae, plaque or swelling, erythema, gangrene and 'ulceration in order of frequency and located in the dependent areas in six caies. 3. Histopathologically, the sites of the bullae were subepidermal in four cases and intraepidermal in. one case and there was one case with ulceration. 4. In electronmicroscopic findings, secretory and ductal cells showed degenerative
Blindness ; Blood Glucose ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Coma ; Creatinine ; Dizziness ; Erythema ; Gangrene ; Headache ; Humans ; Nausea ; Oxygen ; Seizures ; Skin ; Stupor ; Ulcer ; Unconsciousness ; Urinalysis ; Vomiting

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

Based on the records of carboxyhemoglobin in blood samples stored for recent years, the stability of carboxyhemoglobin in these samples could be affected by the containers, the storage temperatures, the volumes of air above the blood, the saturation of the initial carboxyhemoglobin and preservatives added in these blood samples, among which the storage temperatures, the volumes of air above the blood and the saturation of the initial carboxyhemoglobin are the major influence factors.
Air ; Blood Preservation ; Carbon Monoxide/chemistry* ; Carbon Monoxide Poisoning/blood* ; Carboxyhemoglobin/analysis* ; Drug Stability ; Forensic Medicine ; Humans ; Specimen Handling/methods* ; Temperature

Adolescent ; Adult ; Aged ; Carbon Monoxide Poisoning ; blood ; diagnosis ; Female ; Humans ; Lactic Acid ; blood ; Male ; Middle Aged ; Prognosis ; Young Adult

Adult ; Aged ; Aged, 80 and over ; Carbon Monoxide Poisoning ; complications ; Female ; Humans ; Interleukins ; blood ; Male ; Middle Aged ; Neurotoxicity Syndromes ; blood ; etiology

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

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