Analgesic use for carbon monoxide poisoning induced headache: A randomized, controlled, double-blind, clinical trial

Purpose: To compare the effectiveness of three analgesics versus placebo in the relief of carbon monoxide (CO)-induced headache in patients with CO intoxication. Methods: This study was a prospective, randomized, double-blind and placebo-controlled trial. Patients diagnosed with CO intoxication and who had headaches were included in the study. They were divided into four groups. Patients in group 1 received 50 mg dexketoprofen i.v. in 100 mL of saline, while those in group 2 received 800 mg ibuprofen i.v. Patients in group 3 were given I g paracetamol i.v. Group 4 patients received placebo (100 mL of physiological saline. Visual analogue scale (VAS) values were recorded at onset of treatment, and subsequently at 30th, 60th, 90th and 240th min. Patients who scored 3 and below in VAS 240 were considered to have responded to treatment. Results: A total of 168 patients completed the study. Two analgesics and placebo significantly reduced VAS 240 score (p < 0.05). However, VAS 30, VAS 60 and VAS 240 values decreased significantly in the ibuprofen group, when compared to other groups (p < 0.05). Evaluation of response to treatment revealed no significant differences amongst the groups (p = 0.313). Conclusion: These results suggest that analgesics are not superior to oxygen therapy in the treatment of headaches caused by CO poisoning. However, ibuprofen + oxygen treatment may be applied in people who cannot tolerate headaches for a long time.

EFFECT OF CARBON MONOXIDE ON THE RATE OF EXCRETION OF ETHANOL BY KIDNEYS

Carbon monoxide is a toxic gas that is colourless, odourless, and has the potential to cause momentaryhypoxia by bonding with heme-inspired proteins. Because of these properties, it causes the highest number of toxications. Due to its properties, this gas causes damage to the nervous and cardiovascular system. The development of anoxia is associated with the impact on the system of oxidative phosphorylation in mitochondria and the development of oxidative stress in the body. The body produces a small amount of carbon monoxide as a result of erythrocyte breakdown. Picomolar concentrations of carbon monoxide even have anti-inflammatory, antiapoptotic,cytoprotective and antiproliferative properties. Kidney is one of the first organs,that responds to the occurrence of hypoxia, are responsible for the removal of products of metabolism and toxicants, including ethanol. For the study, the blood and urine samples were taken from patients with acute intoxication. The amount of methemoglobin in the blood was determined by spectrophotometric method. The concentration of ethanol in blood and urine was measured by gas-liquid chromatography method. The correlation analysis showed that carbon monoxide affects the rate of excretion of ethanol from the body. Among individuals under 40 years of age, there was a correlation between the level of carbon monoxide and the amount of ethanol in the blood. Among older adults this correlation was not established. A direct correlation with the level of this gas in the blood and the level of ethanol in the urine among people under 40 years of age was found. Among older individuals, the opposite was observed –a high level of methemoglobin was responsible for the decreased level of ethanol. There were no correlations between methemoglobin level and age. Comparison of the studied indices did not show any sexual differences in ethanol excretion, but there were age specific features: ethanol excretion under the influence of carbon monoxide among people under 40 years old was more accelerated.Key words:hypoxia, CO intoxication, blood, methemoglobin, kidneys. Монооксид карбону являє собою токсичний газ, який не має кольору,без запаху та здатен спричиняти миттєву гіпоксію шляхом зв’язування з гем-вмісними білками. Через такі властивості він спричиняє найбільшу кількість отруєнь. Цей газ,завдяки своїм властивостям,спричиняє ураження нервової та серцево-судинної системи. Розвиток аноксії пов’язаний із впливом на систему окисного фосфорилювання у мітохондріях та розвиткомоксидативного стресу. В організмі продукується невелика кількість ендогенного монооксиду карбону внаслідок розпаду еритроцитів. Пікомолярні концентрації монооксиду карбону навіть володіють протизапальними, антиапоптичними, цитопротекторними та антипроліферативними властивостями. Нирки є одним із перших органів, який реагує на розвитокгіпоксії, вони відповідають за видалення продуктів метаболізму й токсикантів, зокрема етанолу.Зміни у функціонуванні нирок відображаються на загальному стані організму.Для дослідження отримували зразки крові та сечі від осіб із гострою інтоксикацією. У крові спектрофотометричним методом визначали вміст метгемоглобіну, який утворювався внаслідок вдихання монооксиду карбону та відповідного потрапляння до кровоносної системи. Методом газово-рідинної хроматографії вимірювали концентрацію етанолу у крові та сечі. Розрахунок кореляційних зв’язків показав, що монооксид карбону впливає на швидкість екскреції етанолу. У осіб до 40 років спостерігалася кореляція між показником рівня метгемоглобінута вмістом етанолу у крові. У осіб старшого віку цього зв’язку не встановлено. Виявлено прямий зв’язок із рівнем цього газу у крові та рівнем етанолу в сечі у осіб до 40 років. У осіб старшого віку спостерігалася зворотня реакція–високий рівень метгемоглобінуобумовлював зниження рівня етанолу. Кореляційні зв’язки між вмістом метгемоглобіну та віком не було виявлено. Порівняння досліджуваних показників не виявило статевих відмінностей у екскреції етанолу, проте виявлено вікові особливості: екскреція етанолу в умовах впливу монооксиду карбону в осіб до 40 років була більш пришвидшена.Таким чином, можна стверджувати, що монооксид карбону обумовлює зміни у функціональній активності нирок.Ключові слова:гіпоксія, інтоксикація СО, кров, метгемоглобін, нирки.

Risk factors for delayed encephalopathy following carbon monoxide poisoning: Importance of the period of inability to walk in the acute stage

Objective Delayed neurological sequelae (DNS) is a serious complication that occurs after acute carbon monoxide (CO) intoxication. The study identified factors for predicting DNS development for the purpose of improving CO intoxication treatment strategies. Methods The medical records of 65 patients admitted to Shizuoka Saiseikai General Hospital between 2004 and 2020 due to CO poisoning were retrospectively reviewed. Univariate and multivariate logistic regression analyses were performed, using a range of evaluated items as explanatory variables and the development of DNS as the response variable. Results Patients who developed DNS were found to have higher peak creatine kinase (CK) (odds ratio, 1.0003; 95% CI, 1.0001–1.0005; P<0.001), and experienced a greater number of days during which walking was impossible in the acute stage following intoxication (odds ratio, 1.011; 95% CI, 1.005–1.018; P<0.001) according to the univariate analysis. Multivariate analyses indicated that DNS development was related to the score, peak CK (U/L) + 40 × the number of days in which walking was impossible. The model demonstrated an area under the receiver operating characteristic curve (AUC) of 0.96 (95% CI, 0.91–1.00), and DNS was predicted with 100% sensitivity and 82% specificity. Conclusion An indicator that incorporates the number of days that walking is impossible for a patient could be useful in planning therapeutic strategies.

Sensitive quantification of carbon monoxide in vivo reveals a protective role of circulating hemoglobin in CO intoxication

Carbon monoxide (CO) is a gaseous molecule known as the silent killer. It is widely believed that an increase in blood carboxyhemoglobin (CO-Hb) is the best biomarker to define CO intoxication, while the fact that CO accumulation in tissues is the most likely direct cause of mortality is less investigated. There is no reliable method other than gas chromatography to accurately determine CO content in tissues. Here we report the properties and usage of hemoCD1, a synthetic supramolecular compound composed of an iron(II)porphyrin and a cyclodextrin dimer, as an accessible reagent for a simple colorimetric assay to quantify CO in biological samples. The assay was validated in various organ tissues collected from rats under normal conditions and after exposure to CO. The kinetic profile of CO in blood and tissues after CO treatment suggested that CO accumulation in tissues is prevented by circulating Hb, revealing a protective role of Hb in CO intoxication. Furthermore, hemoCD1 was used in vivo as a CO removal agent, showing that it acts as an effective adjuvant to O2 ventilation to eliminate residual CO accumulated in organs, including the brain. These findings open new therapeutic perspectives to counteract the toxicity associated with CO poisoning.

Review on Chronic Impacts of Carbon Monoxide Intoxication on Some Routine Vitreous and Blood Investigations

Carbon monoxide (CO) is a toxic gas produced as a result of incomplete combustion of organic materials. The source of CO production is very common especially in nations that depend on power generating sets for electricity. Chronic disease is non-communicable and usually takes a longer time to manifest. Examples are kidney failure, diabetes mellitus, hypertension, cancer, and cardiac arrest. These diseases are now very common in society, not sparing the youthful population that was rare ab initio. The major difficulty in the containment of chronic diseases is the inability to establish a definitive causative agent. The definite causative agent is important in public health and management of chronic diseases. Preventive medicine is anchored on establishing the causative agent of a disease. Without knowing the causative agent of a disease, the path to prevention becomes very cumbersome. The knowledge of the causative agent of a disease is the bedrock of preventive medicine and public health. Several reasons such as lifestyle modification, hereditary, climate change, nutrition or aging have been adduced as the cause of chronic diseases. These reasons are quite weak and not definite. The exact causative agent(s) of chronic diseases is a conundrum that needs a deliberate study and review so as to enhance definite diagnosis, preventive measures and appropriate therapeutic intervention. Measurement of biochemical and haematological parameters are employed in disease diagnosis and management. Alterations of these parameters are used to identify chronic diseases and also form part of an alarm system of a potential breakdown of the normal functioning of the body. The effect of chronic CO intoxication on these parameters could be of importance in establishing causative agent(s) of diseases that are for long opaque and non-definite. This review was therefore designed to interrogate various narratives, meta-analysis, and researches on this subject. Explicit knowledge of the pattern or presentation of biochemical and haematological parameters arising from chronic CO intoxication could be of great importance in preventive medicine, disease diagnosis and appropriate therapeutic intervention.

Highly sensitive quantification of carbon monoxide (CO) in vivo reveals a protective role of circulating hemoglobin in CO intoxication

Carbon monoxide (CO) is a gaseous molecule known as the silent killer. It is widely believed that an increase in blood carboxyhemoglobin (CO-Hb) is the best biomarker to define CO intoxication, neglecting the important fact that CO accumulation in tissues is the most likely direct cause of mortality. There is no reliable method other than gas chromatography to accurately determine CO content in tissues. Here we report the properties and usage of hemoCD1, a synthetic supramolecular compound composed of an iron(II)porphyrin and a cyclodextrin dimer, as an accessible reagent for a simple colorimetric assay to quantify CO in biological samples. The assay was validated in various organ tissues collected from rats under normal conditions and after exposure to CO by inhalation. The kinetic profile of CO in blood and tissues after CO treatment suggested that CO accumulation in tissues is prevented by circulating Hb, revealing a protective role of Hb in CO intoxication. Furthermore, hemoCD1 was used in vivo as a CO removal agent, showing that it acts as effective adjuvant to O2 ventilation to eliminate residual CO accumulated in organs, including the brain. These findings open new therapeutic perspectives to counteract the toxicity associated with CO poisoning.

Highly sensitive quantification of carbon monoxide (CO) in vivo reveals a protective role of circulating hemoglobin in CO intoxication

Carbon monoxide (CO) is a gaseous molecule known as the silent killer. It is widely believed that an increase in blood carboxyhemoglobin (CO-Hb) is the best biomarker to define CO intoxication, neglecting the important fact that CO accumulation in tissues is the most likely direct cause of mortality. There is no reliable method other than gas chromatography to accurately determine CO content in tissues. Here we report the properties and usage of hemoCD1, a synthetic supramolecular compound composed of an iron(II)porphyrin and a cyclodextrin dimer, as an accessible reagent for a simple colorimetric assay to quantify CO in biological samples. The assay was validated in various organ tissues collected from rats under normal conditions and after exposure to CO by inhalation. The kinetic profile of CO in blood and tissues after CO treatment suggested that CO accumulation in tissues is prevented by circulating Hb, revealing a protective role of Hb in CO intoxication. Furthermore, hemoCD1 was used in vivo as a CO removal agent, showing that it acts as effective adjuvant to O2 ventilation to eliminate residual CO accumulated in organs, including the brain. These findings open new therapeutic perspectives to counteract the toxicity associated with CO poisoning.

Carbon monoxide intoxication in geriatric patients: How important are lactate values at admission?

Purpose: The aim of this study was to investigate the demographic and clinical characteristics and treatment modalities of elderly patients with carbon monoxide (CO) intoxication. The secondary aim was to evaluate the importance of plasma lactate values in the diagnosis of acute CO intoxication in geriatric patients. Methods: Data on geriatric patients who were admitted to the emergency department of Atatürk University Medical Faculty between January 2013 and April 2016 were analyzed retrospectively. Results: Of the 197 cases included in the study, 97 were in the intoxication group and 100 were in the control group; 82.5% of the intoxication cases had mild neurological symptoms and 17.5% had severe neurological symptoms. Carboxyhemoglobin levels were significantly higher in patients with severe neurological symptoms ( p = 0.031). All patients with severe neurological symptoms received hyperbaric-oxygen therapy ( p < 0.001). In the intoxication group, lactate levels were significantly higher than in the control group ( p = 0.001). The specificity for lactate 4 mmol/L and above was found as 98.0% with a positive predictive value and negative predictive value of 84.5% and 53.3%, respectively. Conclusion: High initial lactate levels may be a guide for cases with nonspecific symptoms in geriatric patients with suspected CO intoxication.