COHb Levels Research Articles

Association Between Near Infrared Spectroskopy (NIRS) and Normobaric and Hyperbaric Oxygen Treatment in Acute Carbon Monoxide Poisoning

Objective: Carbon monoxide (CO) is the main cause of death and morbidity associated with poisoning in developed countries. The most important mortality and morbidity cause of CO poisoning is cerebral hypoxia. Near-infrared spectroscopy (NIRS) is a useful method for assessing brain oxygenation. In this study, we aimed to evaluate the brain oxygenation of CO poisoning patients with NIRS and to investigate its benefits in patients follow up and treatment. Materials and Methods: The study was conducted as a single-center, prospective clinical trial with 33 patients who were diagnosed by measuring blood CO-Hb level or referred from other hospitals diagnosed with CO poisoning. Patients were divided into two groups as normobaric oxygen therapy (NBOT) group and hyperbaric oxygen therapy (HBOT) group according to the treatment method applied. Results: Although average cerebral saturation (ScO2) levels after treatment were higher in the NBOT group than before treatment, no statistically significant difference was found except the left frontal ScO2 values. In HBOT group, there was no difference between ScO2 values before and after treatment sessions. Conclusion: Our study concluded that NIRS may be useful in assessing brain oxygenation in CO poisoned patients, but not in determining the HBOT start-up, and not in monitoring the effectiveness of HBOT.

The relationship between intoxication severity and blood interleukin 6, interleukin 10 and CRP levels in carbon monoxide-poisoned patients

Carbon monoxide (CO) is one of the most common causes of death due to intoxications. No biochemical marker is available to evaluate the severity of CO intoxication. We measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and interleukin-10 (IL-10) levels in patients with different degrees of CO poisoning. We prospectively included 40 CO-poisoned patients admitted to emergency services. Blood samples were collected from the patients at admission (0 hour) and after treatment (six hours). While all patients received normobaric oxygen (NBO2) therapy, patients with severe CO poisoning received additional sessions of hyperbaric oxygen (HBO2) therapy. Blood samples were also collected from a group of healthy volunteers (n=40). Serum IL-6 and IL-10 levels were measured with the ELISA method while hs-CRP was quantified by turbidimetric analysis. At admission, IL-6 levels were significantly higher in the patient group compared to the control group (P=0.001), but IL-10 and hs-CRP levels were not significantly different between the groups. Compared to admission levels, IL-6 levels were higher at six hours (P=0.014). The patients were grouped according to treatment type (NBO2, HBO2) and history of syncope, but no significant differences were detected in patient subgroups regarding IL-6, IL-10 and hs-CRP levels. A weak positive correlation was found between COHb and lactate levels in patients (P=0.013; r=0.390).This study shows that IL-6 level increases in CO-poisoned patients, but it is not correlated with the severity of the intoxication.

359 Determination of the Carboxyhemoglobin Half Life in Carbon Monoxide Poisoned Patients Treated With High Flow Nasal Cannula Therapy

Acute carbon monoxide poisoning is a common environmental emergency worldwide. Treatment options are limited to normobaric oxygen therapy with a non-breather face mask and hyperbaric oxygen therapy. The aim of this study is to determine the half-life of carboxyhemoglobin with a high flow nasal cannula in adult patients admitted to the emergency department with acute carbon monoxide poisoning. Device tolerability and patient comfort with the high flow nasal cannula were also evaluated. This study was conducted between January 2017 and February 2018 in 2 academic emergency departments. Venous blood samples were obtained at 10 minute intervals to determine the rate of elimination of the carbon monoxide. Patient comfort was evaluated by verbal numeric rating scale. Device tolerability was evaluated by patient requests to change the flow rate or flow temperature. The primary outcome was the determination of the half-life of carboxyhemoglobin with a high flow nasal cannula. The secondary outcome was the device tolerability and patient comfort with the high flow nasal cannula. After excluding 6 of 39 patients, a total of 33 patients were analyzed in the study. The mean baseline COHb level of the 33 patients was 22.5% (SD 8%). The mean half-life of carboxyhemoglobin was determined as 36.76 minutes (SD 9.26 min) with a high flow nasal cannula. COHb levels were halved during the first 40 minutes in 22 (66.7%) of the study patients. Twenty of the patients did not report intolerance to a high flow, with a median verbal numeric rating score of 10. Among the 11 patients who requested a change in the flow rate, the median verbal numeric rating score was 7. After decreasing the flow rate, the median verbal numeric rating score became 9. The high flow nasal cannula is an easy, safe and comfortable method to treat acute CO poisoned patients which is effective in reducing COHb half-life. HFNC may be a promising alternative method if it is validated as effective with larger studies with clinical outcomes.

Identification of CO Exposure, Habits, COHb Blood and Worker’s Health Complaints on Basement Waterplace Apartment, Surabaya

Carbon monoxide (CO) is a silent killer because it is tasteless, colorless, odorless, and causes of death. In the basement, pollution level from vehicle engines combustion is higher than in the ambient air. Workers in the basement potentially expose to CO that trapped while they were working. CO inhaled will form COHb on the blood. This study aims to identify CO exposure, worker habits, COHb blood, and health complaints during their working time in the basement of apartment Waterplace Surabaya. This research was a descriptive with cross-sectional design and used purposive sampling technique with 20 respondents. Data which were collected through observation and interviews. The result showed that CO measurement was below 25 ppm standard. Most characteristics of workers were male (80.0%), 21–29 years old (55.0%), working time for ≤ 12 months (55.0%) and working hours for 12 hours (55.0%). The worker’s habits mostly were smoking (80.0%), regularly consume fruit (55.0%) and vegetables (60.0%). The majority (90.0%) COHb level was above the 3.5% standard. Health worker complaints were dizziness (80.0%), impaired concentration (60.0%) and tired (55.0%) while their working time. Workers that smoking, eating fruits, and vegetables were having a blood COHb levels higher. It was concluded that the levels of CO gas below the standards while blood COHb above the standards. It was suggested to reduce smoking, to start a healthier lifestyle, and to use masker while their working time.

Red blood cell distribution width as a predictor of long-term mortality in patients with carbon monoxide poisoning

ObjectivesElevated red blood cell distribution width (RDW) is an independent prognostic factor for cardiovascular events that are major causes of mortality in patients with carbon monoxide (CO) poisoning. Due to the limited number of studies, we aimed to investigate the relationship between RDW levels and long-term mortality for these patients. MethodThis retrospective study included patients with CO poisoning, who presented to the emergency department. Baseline characteristics, laboratory results and survival status were retrieved from patients' hospital records. The severity of poisoning was determined according to COHb level and/or clinical signs and symptoms. ResultsThe study included 571 patients (median age was 37.0 years) and less than half of these patients were male (n = 206, 36.1%). There were mild-moderate CO poisoning in 389 (68.1%) patients and severe poisoning in 182 (31.9%). At a median follow-up of 6.2 years, there were 33 deaths (5.8%). Univariate cox-regression analysis demonstrated that age, gender, presence of hypertension or diabetes mellitus, levels of hemoglobin, RDW, creatinine and alanine-aminotransferase, and white-blood-cell count were potential covariates of long-term all-cause mortality. In the multivariate analysis, the median age and RDW level remained independent predictors of mortality (age, Odds ratio [OR]: 1.070 95% confidence interval [CI]: 1.030–1.110, p = 0.001; RDW, OR: 1.221 95% CI: 1.042–1.431, p = 0.013). Patients with higher RDW levels had a significantly worse prognosis in terms of mortality than with lower RDW levels (log-rank test, p = 0.003). ConclusionThis study demonstrated that RDW level is an independent predictor of long-term mortality in patients with CO poisoning.

Effect of Pressure Support Ventilation on Carboxyhemoglobin Toxicokinetic after Acute Carbon Monoxide Intoxication: a Swine Model.

In an experimental study on carbon monoxide (CO) exposure in swine, we aimed to compare the influence of oxygen therapy using a non-rebreathing mask (NRM) to continuous positive airway pressure (CPAP) and two pressure support ventilation (PSV) devices on the decrease of the terminal elimination half-life of carboxyhemoglobin (COHb t1/2). This was the primary outcome. Eight spontaneously breathing pigs were sedated by propofol and exposed to 940ppm CO several times (n = 25) to obtain COHb levels of 30%. CPAPb (high flow open system, CPAP Boussignac® [7.5 cmH2O]), PSV-Vy (open system, Vylife Boussignac®), and PSV-Leg (closed system, Legendair® [inspiratory/expiratory airway pressure 12/4 cmH2O]) devices were used in a randomized order and compared to NRM (O2 at 15lmin-1) and atmospheric air (AA). The primary outcome was COHb t1/2. Multiple comparisons were performed using Dunn's tests. Median FiO2 and minute ventilation were significantly higher in the PSV-Leg group than the NRM group (p < 0.05). Median COHb t1/2 was 251, 85, 82, 93, and 58min for AA, NRM, CPAPb, PSV-Vy, and PSV-Leg, respectively. All the interventions were superior to AA in terms of CO elimination (p < 0.001), but there was no statistically significant difference between CPAP or PSV and NRM. There was only a trend between PSV-Leg and NRM (p = 0.18). The median AUCs for ln (COHb) × time (h) were 170, 79, 83, 100, and 64 for AA, NRM, CPAPb, PSV-Vy, and PSV-Leg respectively, with a statistically significant difference only between AA and PSV-Leg (p = 0.002). In conclusion, in our study on CO intoxication in swine, the use of the closed PSV-Leg system led to the shortest COHb t1/2. These results suggest that PSV-Leg can be more efficient than NRM in eliminating CO and support the design of a clinical study to assess this hypothesis.

Camera-based pulse-oximetry - validated risks and opportunities from theoretical analysis.

Camera-based pulse-oximetry has recently shown to be feasible, even when the signal is corrupted by noise and motion artifacts. Earlier work showed that using three instead of the common two wavelengths improves robustness of the measurement, however without a thorough investigation on the optimal wavelength selection. We therefore performed a search to identify these wavelengths to further improve the robustness of the measurement. Besides motion, it is empirically known that there are several other factors that influence the measurement leading to falsely-low or falsely-high SpO2 readings. These factors include the presence of dyshemoglobins or other species. In this paper, we use a theoretical skin-model to study how these factors influence the measurement, and how a proper wavelength selection can reduce the impact on the measurement. Additionally, we show that adding a third wavelength does not only improve robustness, but can also be exploited to create a reliability index for the measurement. Finally, we show that the presence of dyshemoglobins in arterial blood can not only be detected but also quantified. We illustrate this by comparing the estimated COHb levels of a small group of smokers and non-smokers, which typically have different CO-levels.

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice.

There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning.

Inhaled Carbon Monoxide: From Toxin to Therapy.

Carbon monoxide (CO) is usually recognized as a toxic gas that can be used to assess lung function in the pulmonary function laboratory. The toxicity of CO relates to its high affinity for hemoglobin and other heme molecules, producing carboxyhemoglobin (HbCO). Despite that blood HbCO levels are commonly measured in patients with CO poisoning, the clinical presentation often does not correlate with the HbCO level, and clinical improvement in the patient's condition does not correlate with HbCO clearance. In patients with CO poisoning, administration of 100% O2 is standard practice. If available, hyperbaric O2 can be used, although this is controversial. Measurement of exhaled CO might be useful to estimate HbCO, such as in smoking cessation programs, but assessment of HbCO using pulse oximetry can be misleading. Endogenous CO is generated as the result of heme oxygenase activity. It is becoming increasingly recognized that the results of heme oxygenase activity, specifically CO production, might have important physiologic functions. These include effects on vascular function, inflammation, apoptosis, cell proliferation, and signaling pathways. Given the abundance of basic science supporting a therapeutic role for CO, clinical trials are exploring this potential.

Decreased blood pressure associated with in-vehicle exposure to carbon monoxide in Korean volunteers

BackgroundCarbon monoxide (CO) is one of the primary components of emissions from light-duty vehicles, and reportedly comprises 77% of all pollutants emitted in terms of concentration. Exposure to CO aggravates cardiovascular disease and causes other health disorders. The study was aimed to assess the negative effects by injecting different amounts of CO concentration directly to human volunteers boarding in the car.MethodsHuman volunteers were exposed to CO concentrations of 0, 33.2, and 72.4 ppm, respectively during the first test and 0, 30.3, and 48.8 ppm respectively during the second test while seated in the car. The volunteers were exposed to each concentration for approximately 45 min. After exposure, blood pressure measurement, blood collection (carboxyhemoglobin [COHb] analysis), medical interview, echocardiography test, and cognitive reaction test were performed.ResultIn patients who were exposed to a mean concentration of CO for 72.4 ± 1.4 ppm during the first exposure test and 48.8 ± 3.7 ppm during the second exposure test, the COHb level exceeded 2%. Moreover, the diastolic blood pressure was decreased while increasing in CO concentration after exposure. The medical interview findings showed that the degree of fatigue was increased and the degree of concentration was reduced when the exposed concentration of CO was increased.ConclusionAlthough the study had a limited sample size, we found that even a low concentration of CO flowing into a car could have a negative influence on human health, such as change of blood pressure and degree of fatigue.

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Objectives: Carbon monoxide (CO) is a colorless and odorless gas responsible for poisoning mortality and morbidity in the United States. At this time, there is no reliable method to predict the severity of poisoning or clinical prognosis following CO exposure. Whole blood cells, such as peripheral blood mononuclear cells (PBMCs) and platelets, have been explored for their potential use to act as sensitive biomarkers for mitochondrial dysfunction which may have a role in CO poisoning.Design: The objective of this study was to measure mitochondrial respiration using intact cells obtained from patients exposed to CO as a potential biomarker for mitochondrial inhibition with results that can be obtained in a time frame useful for guiding clinical care. This was a prospective, observational pilot study performed from July 2015 to July 2016 at a single academic tertiary care center that is the location of the region’s only multi chamber hyperbaric.Measurements: Clinical characteristics, patient demographics, mitochondrial respiration and outcomes were recorded.Main results: There were 7 patients enrolled with a mean COHb level 26.8 ± 10 and with a mean lactate of 1.1 ± 0.4 mmol/L. All 7 CO exposures were related to heat generators used during winter months with two deaths. There was a positive correlation between maximal respiration and COHb levels with both high maximal respiration and high spare respiratory capacity correlating with a high COHb level. There was a subset of PBMCs (n = 4) that were analyzed for Complex IV (cytochrome c oxidase) activity.Conclusions: In this pilot study, measurements can be performed in an appropriate timeline for clinical care with potential to serve as a prognostic marker. Further work is necessary to develop high-resolution respirometry as a clinical tool for assessing the severity of illness and guiding therapy.

Hemoglobin Kirklareli (α H58L), a New Variant Associated with Iron Deficiency and Increased CO Binding

Mutations in hemoglobin can cause a wide range of phenotypic outcomes, including anemia due to protein instability and red cell lysis. Uncovering the biochemical basis for these phenotypes can provide new insights into hemoglobin structure and function as well as identify new therapeutic opportunities. We report here a new hemoglobin α chain variant in a female patient with mild anemia, whose father also carries the trait and is from the Turkish city of Kirklareli. Both the patient and her father had a His-58(E7) → Leu mutation in α1. Surprisingly, the patient's father is not anemic, but he is a smoker with high levels of HbCO (∼16%). To understand these phenotypes, we examined recombinant human Hb (rHb) Kirklareli containing the α H58L replacement. Mutant α subunits containing Leu-58(E7) autoxidize ∼8 times and lose hemin ∼200 times more rapidly than native α subunits, causing the oxygenated form of rHb Kirklareli to denature very rapidly under physiological conditions. The crystal structure of rHb Kirklareli shows that the α H58L replacement creates a completely apolar active site, which prevents electrostatic stabilization of bound O2, promotes autoxidation, and enhances hemin dissociation by inhibiting water coordination to the Fe(III) atom. At the same time, the mutant α subunit has an ∼80,000-fold higher affinity for CO than O2, causing it to rapidly take up and retain carbon monoxide, which prevents denaturation both in vitro and in vivo and explains the phenotypic differences between the father, who is a smoker, and his daughter.

Pengaruh ekstrak melon terhadap kadar HbCO pada tikus Wistar jantan yang dipapar asap rokok

Background: Smoking is something that is usual for most Indonesian society, especially adult males. According to Riskesdas, smoking behavior of the population trends to increase. A previous study suggested that exposure to cigarette smoke produce CO bond to hemoglobin. Melon (Cucumis melo) contains antioxidants that prevent tissue damage.Objective: Analyze differences in levels HbCO Wistar male rats in treated and untreated extracts of melon.Method: The research was a laboratory experiment with the post test control group design and complete random design. The subjects were 25 male Wistar rats aged 3 months. Subjects were divided into 5 groups and each group received treatment for 28 days. Data of level HbCO was collected and analyzed by Anova One Way test at 95% confidence level.Results: The results showed a difference between the average levels of HbCO male Wistar rats (p value=0,000) treated and untreated extracts of melon.Conclusion: Melon extracts effect on decreasing the levels of HbCO due to exposure to cigarette smoke. There were differences in levels of male Wistar rats HbCO on treated and untreated extracts of melon and be given at a dose of 250 IU/day.

Interaction between endogenous carbon monoxide and hydrogen sulfide in the mechanism of gastroprotection against acute aspirin-induced gastric damage

Acetylsalicylic acid (ASA) is mainly recognized as painkiller or anti-inflammatory drug. However, ASA causes serious side effects towards gastrointestinal (GI) tract which limits its usefulness. Carbon monoxide (CO) and hydrogen sulfide (H2S) have been described to act as important endogenous messengers and mediators of gastroprotection but whether they can interact in gastroprotection against acute ASA-induced gastric damage remains unknown.In this study male Wistar rats were pretreated with 1) vehicle (saline, i.g.), 2) tricarbonyldichlororuthenium (II) dimer (CORM-2, 5mg/kg i.g.), 3) sodium hydrosulfide (NaHS, 5mg/kg i.g.), 4) zinc protoporphyrin (ZnPP, 10mg/kg i.p.), 5) D,L-propargylglycine (PAG, 30mg/kg i.g.), 6) ZnPP combined with NaHS, 7) PAG combined with CORM-2 or 8) 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10mg/kg i.p.) combined with CORM-2 or NaHS and 30min later ASA was administered i.g. in a single dose of 125mg/kg. After 1h, gastric blood flow (GBF) was determined by H2 gas clearance technique and gastric lesions were assessed by planimetry and histology. CO content in gastric mucosa and COHb concentration in blood were determined by gas chromatography and H2S production was assessed in gastric mucosa using methylene blue method. Protein and/or mRNA expression for cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), heme oxygenase (HO)-1, HO-2, hypoxia inducible factor-alpha (HIF)-1α, nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), cyclooxygenase (COX)-1 and COX-2, inducible nitric oxide synthase (iNOS) and interleukin (IL)-1β were determined by Western blot or real-time PCR, respectively.ASA caused hemorrhagic gastric mucosal damage and significantly decreased GBF, H2S production, CO content, mRNA or protein expression for CSE, 3-MST, HO-2 and increased mRNA and/or protein expression for CBS, HO-1, Nrf-2, HIF-1α, iNOS, IL-1β, COX-2 in gastric mucosa and COHb concentration in blood. Pretreatment with CORM-2 or NaHS but not with PAG decreased ASA-damage and increased GBF. ZnPP reversed protective and hyperemic effect of NaHS but PAG failed to affect CORM-2-induced gastroprotection. CORM-2 elevated CO content, mRNA or protein expression for HO-1, Nrf-2, and decreased expression of CBS, HIF-1α, COX-2, IL-1β, iNOS, the H2S production in gastric mucosa and COHb concentration in blood. NaHS raised mRNA or protein expression for CSE, COX-1 and decreased mRNA expression for IL-1β and COHb level in blood.We conclude that CO is involved in gastroprotection induced by H2S while beneficial protective action of CO released from CORM-2 in gastric mucosa seems to be H2S-independent. In contrast to H2S, CO ameliorates hypoxia, regulates Nrf-2 expression but similarly to H2S acts on sGC-dependent manner to restore gastric microcirculation and exhibit anti-inflammatory activity in gastric mucosa compromised by ASA.

Effects of pre‐fire age and health status on vulnerability to incapacitation and death from exposure to carbon monoxide and smoke irritants in Rosepark fire incident victims

SummaryAge‐related decline and illness increase susceptibility to smoke and toxic fire gases, with incapacitation and death likely for lower exposures. Carbon monoxide (CO) in non‐burned fire fatalities as %COHb indicates the fatal ‘dose’ of toxic effluents (including CO and other toxic species). The elderly and infirm should be overcome earlier during a fire, with lower post‐mortem blood %COHb levels than younger fatalities. The Rosepark care home incident involved 18 elderly casualties (average age 85 years, range 61–99) with a variety of illnesses. Post‐mortem reports and health records provided %COHb concentrations at death or time of rescue, age and pre‐fire health status. To examine effects of health status on susceptibility, heart, circulation, lungs and general health conditions were classified on a 0–5 severity scale for each condition. Scores for each subject were plotted against age or %COHb and examined for trends. No increase in susceptibility to incapacitation was found for survivors. %COHb in fatalities (range 48–82% average 63% COHb) was similar to published levels for young adults (average 61% COHb). There was no increasing susceptibility with age or severity of lung or ‘other health’ conditions, but some trend with severity of cardiovascular disease, especially heart disease (statistically significant 5% level). Copyright © 2016 John Wiley &amp; Sons, Ltd.

GAMBARAN LAMA PAJANAN DENGAN KADAR HbCO DALAM DARAH PADA PETUGAS RETRIBUSI TERMINAL PURABAYA BUNGURASIHSURABAYATAHUN 2015

Bus station activity, transportation operations creates high pollution of carbon monoxide (CO) which is so dangerous for retribution officers of Purabaya bus station, Bungurasih. HbCO level can be affected by long exposure. This research aims to describe exposure to carbon monoxide tested through HbCO in the blood of retribution officers of Purabaya Bus Station Bungurasih.This is a descriptive research with cross sectional approach and uses x Blood Gas analyzer method. Sample of the research was 12 retribution officersworkingin morning and afternoon shift. Data was analyzed by descriptive tabulation in the form of table.Interview was conducted to determine characteristics of the retribution officers of Purabaya Bus station, Bungurasih.Results showed that retribution officers possessed averageHbCO level of 11.94%, exposure duration per day of &gt; 8 hours was 66.7% and 41.7% officers had smoking habit of ½ - 2 packs/day.It is concluded that HbCO level in officers blood washigher than normal level( &gt; 5%). Improvement is needed in all aspects; all employees working outdoors are recommended to wear mass to filter gases or pollutants in which is harmful for health. They are recommended not to smoke when working. Manager of bus station also needsto do planting in bus station area.

Feedback Response to Selective Depletion of Endogenous Carbon Monoxide in the Blood.

The physiological roles of endogenous carbon monoxide (CO) have not been fully understood because of the difficulty in preparing a loss-of-function phenotype of this molecule. Here, we have utilized in vivo CO receptors, hemoCDs, which are the supramolecular 1:1 inclusion complexes of meso-tetrakis(4-sulfonatophenyl)porphinatoiron(II) with per-O-methylated β-cyclodextrin dimers. Three types of hemoCDs (hemoCD1, hemoCD2, and hemoCD3) that exhibit different CO-affinities have been tested as CO-depleting agents in vivo. Intraperitoneally administered hemoCD bound endogenous CO within the murine circulation, and was excreted in the urine along with CO in an affinity-dependent manner. The sufficient administration of hemoCD that has higher CO-affinity than hemoglobin (Hb) produced a pseudoknockdown state of CO in the mouse in which heme oxygenase-1 (HO-1) was markedly induced in the liver, causing the acceleration of endogenous CO production to maintain constant CO-Hb levels in the blood. The contents of free hemin and bilirubin in the blood plasma of the treated mice significantly increased upon removal of endogenous CO by hemoCD. Thus, a homeostatic feedback model for the CO/HO-1 system was proposed as follows: HemoCD primarily removes CO from cell-free CO-Hb. The resulting oxy-Hb is quickly oxidized to met-Hb by oxidant(s) such as hydrogen peroxide in the blood plasma. The met-Hb readily releases free hemin that directly induces HO-1 in the liver, which metabolizes the hemin into iron, biliverdin, and CO. The newly produced CO binds to ferrous Hb to form CO-Hb as an oxidation-resistant state. Overall, the present system revealed the regulatory role of CO for maintaining the ferrous/ferric balance of Hb in the blood.

Myocardial Infarction in a Young Patient After Acute Exposure to Carbon Monoxide.

Carbon monoxide (CO) is an odorless, colorless, clear gas that attaches to the hemoglobin (Hb). Its affinity for Hb is approximately 200 times higher than that of oxygen, and CO blocks the capacity of Hb to carry oxygen (1). One of the most important effects of CO is tissue hypoxia, especially in the parts of tissues with the highest demand for oxygen and the lowest metabolic stores, such as the brain and heart, which are therefore more vulnerable. CO intoxications are usually expressed as neurological events, but cardiological events can also occur (2). Myocardial injury may arise via electrical, functional, and morphological changes in the heart through severe general tissue hypoxia; there may be a direct toxic effect on the myocardial mitochondria promptly after exposure, or this may be delayed for several days (3). CO can induce a tendency toward coronary vasospasm and thrombus formation by slowing the bloodstream, increasing the permeability of the vessel walls, and increasing platelet aggregability and polycythemia; these factors are also responsible for myocardial damage in patients with CO poisoning (4). In addition, oxygen radical formation and subsequent lipid peroxidation, as well as induction of cellular apoptosis, are also potential explanations for the cardiotoxicity of CO (2, 5). Cardiac involvement encompassing angina attack, myocardial infarction, heart failure, cardiogenic shock, and arrhythmias, such as ventricular extrasystoles, atrial fibrillation, bradycardia, and atrioventricular block in CO poisoning was first noted by Lippi (5). However, 50% or more of the circulating form of carboxyhemoglobin can lead to patchy myocardial necrosis, a CO-Hb level of ≥ 25% is considered an indication for the use of hyperbaric oxygen or advanced treatment (6, 7). Acute myocardial infarction (AMI) is a clinical condition occurring suddenly but resulting from a long-term decrease in the amount of oxygen present in the myocardium. Its most common cause is atherosclerotic disease of the coronary arteries. AMI associated with CO poisoning occurs very rarely. In this letter, a young person who did not have known coronary atherosclerotic disease and had AMI due to exposure to CO is presented with the aim of drawing attention to the fact that CO poisoning which occurs commonly throughout the world may lead to AMI. A 27-year-old male patient lost consciousness while struggling against fire in the workplace and entered cardiac arrest. After undergoing resuscitation by the 112 emergency service, he was brought to emergency intubated with unconscious and admitted. Upon admission to the hospital, ventilation with 100% oxygen was continued. The patient’s Glasgow coma score was 4, and noradrenaline infusion was initiated owing to hypotension. Arterial blood gas analysis was performed, and a CO-Hb value of 22% was detected. On initial electrocardiogram (ECG), ventricular tachycardia and other alterations were observed. The patient was diagnosed with anteroseptal AMI. Emergency angiographic and primary percutaneous interventions were performed; it was observed that Left anterior descending (LAD) as completely obstructed, (Figures 1 and 2) and a stent was placed (Figures 3 and 4). The patient further stabilized and was prepared for and transferred to hyperbaric oxygen therapy. Thorax computed tomography (CT) was taken and pneumothorax and trachea rupture was observed, probably due to resuscitation. No intervention was considered necessary except for chest tube insertion by the Chest Surgery Department The patient was extubated on the 11th day after admission to intensive care unit and transferred to the infectious diseases clinic. Identifying cardiotoxicity in patients with CO poisoning can be difficult. This report of a rare case should remind physicians

착화탄 연소에 의한 일산화탄소 중독사에서 자살입증에 관한 사례연구

Carbon monoxide (CO) intoxication, arising from CO from an ignited charcoal briquette (ICB), is a popular means of committing suicide in Korea. Most CO intoxications are related to suicide attempts; however, the possibility of a homicide disguised as a suicide cannot be ruled out. Therefore, forensic investigation of the deceased and the crime scene is crucial to confirm that the deceased committed suicide. Detection of the components of an ICB on the objects suspected of being contacted by the deceased, such as the hands, nostrils, and doorknobs, is essential for linking the crime scene to the victim in the case of suicides by ignited ICBs. The traces from an ICB were analyzed by investigating the morphological characteristics and obtaining elemental compositions. The ICBs were completely different from blackened wood, as detected by discriminant analysis with the elements of carbon and oxygen. We analyzed one case of CO intoxication to demonstrate an excellent procedure for verifying whether a suicide occurred with an ICB. We employed SEM-EDX for the analysis of an ICB, microscope-FT/IR and pyrolysis-GC/MS for a partly burnt resin-type substance, GC/MS for diphenhydramine (a sleeping drug), and GC/TCD for the CO-Hb level. We detected traces of an ICB on the hands, nostrils, and doorknobs, which were all discriminated into an ICB group. Detection of ICB traces from the nostrils could indicate that the deceased started the fire themselves to commit suicide. The partially burnt black material was analyzed as an acrylronitrilestyrene polymer, which is normally used to make bags for carrying or wrapping and could be assumed to have been used to transport the ICB. Diphenhydramine, a sleeping drug, was detected at a level of 2.3 mg/L in the blood, which was lower than that in fatal cases (8-31 mg/L; mean 16 mg/L). A CO-Hb level of 79% was found in the blood, which means that the cause of death was CO intoxication. The steps shown here could represent an ideal method for reaching a verdict of suicide by CO intoxication produced by burning an ICB in a sealed room or a car.

Analysis of patients presenting to the emergency department with carbon monoxide intoxication

ObjectivesCarbon monoxide is a potentially fatal form of poisoning. The exact incidence is unclear, due to cases being undiagnosed or reported as fewer than the real number. Hyperbaric oxygen therapy (HBOT) is of proven efficacy in the treatment of CO intoxication.The purpose of this study was to describe the general characteristics of carbon monoxide (CO) intoxications presenting to the emergency department and to investigate troponin I values and the effectiveness of hyperbaric oxygen therapy (HBOT) in these patients. Material and methodsPatients presenting to the emergency department with CO intoxication over one year and patients with such intoxications receiving HBOT were examined retrospectively. ResultsOne hundred seventy-one patients were included; 140 (81.9%) were poisoned by stoves, 18 (10.5%) by hot water boilers and 10 in (5.8%) by fires. COHb levels were normal in 49 of the 163 patients whose values were investigated, and were elevated in 114 patients. Mean COHb value was 16.6. Troponin I values were investigated in 112 patients. These were normal in 86 patients and elevated in 26. Mean troponin I value was 0.38 ng/ml. One hundred twenty-three of the 171 patients in the study were discharged in a healthy condition after receiving normobaric oxygen therapy, while 48 patients received HBOT. Forty-two (87.5%) of the patients receiving HBOT were discharged in a healthy condition while sequelae persisted in five (10.4%). One patient died after 15 session of HBOT. ConclusionAlthough elevated carboxyhemoglobin confirms diagnosis of CO intoxication, normal levels do not exclude it. Troponin I levels may rise in CO intoxication. No significant relation was observed between carboxyhemoglobin and receipt of HBOT. A significant correlation was seen, however, between troponin I levels and receipt of HBOT.