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Diagnosis and Treatment of Inhalation Injury in Burn Patients
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Khan Z. Shirani, Joseph A. Moylan, Basil A. Pruitt
The susceptibility of a person to carbon monoxide toxicity is greatly ininfluenced by individual variations and by physical status at the time of exposure. Patients with carbon monoxide intoxication often present with lightheadedness, increased light perception, tingling of the lips and extremities, and cherry red discoloration of the skin. The diagnosis of carbon monoxide poisoning can be made by determining the carboxyhemoglobin saturation of the blood. Carboxyhemoglobin concentrations below 10% in normal individuals are generally well tolerated, but, based on individual patient variations, carboxyhemoglobin concentrations below 5% in otherwise healthy individuals are known to have been poorly tolerated (Drinkwater et al., 1974; Aronow et al., 1974). On the other hand, patients with preexisting cardiovascular disease are extremely susceptible to carbon monoxide toxicity and may become symptomatic even at concentrations as low as 3% (Ayres et al., 1970; Aronow and Cassidy, 1975). Carboxyhemoglobin concentrations of the blood above 15% are generally considered toxic and those above 50% are usually lethal (Table 2).
Acute Lung Injury In Children Due To Chemical And Physical Agents
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Carbon monoxide (CO) is a colorless, odorless gas produced by the incomplete combustion of carbon-containing materials.188 Smoke from burning wood may contain large amounts of carbon monoxide.157 CO binds with hemoglobin with an affinity 200 to 250 times that of oxygen. The partial pressure of oxygen as measured in the blood is unaffected by the presence of carboxyhemoglobin and will be normal unless ventilation/perfusion inequalities are also present.171, 188 Carbon monoxide produces a left shift and a more hyperbolic shape to the oxygen dissociation curve impeding oxygen delivery to the tissues. At higher concentrations, CO binds to myoglobin and intracellular cytochrome oxidases blocking cellular oxidation. 157, 171, 188 Although oxygen content is reduced in cases of CO poisoning, measured percent of oxyhemoglobin may be high because of the left shift of the oxygen dissociation curve.157 Carbon monoxide poisoning may be present even when blood levels of carboxyhemoglobin are low (especially when oxygen has been administered and some time has elapsed since the exposure).151 Lactic acidosis is generally present in CO poisoning and indicates tissue hypoxia.151
Investigative Duties on Scene
Published in Kevin L. Erskine, Erica J. Armstrong, Water-Related Death Investigation, 2021
Another important factor to consider in a boating fatality is carbon monoxide poisoning. Carbon monoxide is an invisible, odorless, tasteless gas that is produced when a carbon-based fuel burns. It can make one sick in seconds, and in high concentrations, it can kill a person in just a few breaths. Check vessel ports to make sure they are clear and free of obstructions that may hinder venting of fumes. Sources of carbon monoxide on a boat may include gasoline engines, heaters, stoves, and generators. Early symptoms of carbon monoxide poisoning include eye irritation, dizziness, nausea, headache, and weakness. Interviews with fellow boaters may determine that the decedent was complaining of these symptoms.
Cardioprotective effects of hesperidin on carbon monoxide poisoned in rats
Published in Drug and Chemical Toxicology, 2021
Ramin Rezaee, Alireza Sheidary, Saeedeh Jangjoo, Sarvenaz Ekhtiary, Somayeh Bagheri, Zahra Kohkan, Madjid Dadres, Anca Oana Docea, Konstantinos Tsarouhas, Dimosthenis A. Sarigiannis, Spyros Karakitsios, Aristidis Tsatsakis, Leda Kovatsi, Mahmoud Hashemzaei
Carbon monoxide (CO) is a colorless and odorless toxic gas that competes with oxygen for binding sites of hemoglobin. It is considered the most common cause of poisoning-related mortality and morbidity worldwide (Goldstein 2008, Dindar Badem et al. 2019). CO is produced by incomplete combustion of fossil fuels and is found in motor vehicle exhaust emissions, poorly burning furnaces, charcoal burning and tobacco smoking (Satran et al. 2005, Mohamadpour et al. 2012, Eichhorn et al. 2018). Clinical manifestations of CO poisoning include injuries in the organs with great oxygen consumption, such as the brain and heart (Ghorbani et al. 2017, Tabrizian et al. 2017). Intoxication with CO causes myocardial infarction (MI), cardiomyopathy, tachycardia, dysrhythmia, hypotension, ischemia, and, in more severe cases, cardiac arrest (Goldstein 2008). Severity of cardiac poisoning is associated with the blood levels of carboxyhemoglobin (COHb) and duration of CO exposure (Kaya et al. 2016). Even a long time after CO poisoning, MI can occur, especially in patients with increased COHb concentrations (Kalay 2016).
Treatment of carbon monoxide poisoning: high-flow nasal cannula versus non-rebreather face mask
Published in Clinical Toxicology, 2021
Onder Yesiloglu, Muge Gulen, Salim Satar, Akkan Avci, Selen Acehan, Haldun Akoglu
Carbon monoxide (CO) is a colorless, odorless gas resulting from the incomplete combustion of carbon compounds. CO binds to hemoglobin competitively with oxygen (O2), causes a decrease in the oxygen content of blood and tissue hypoxia. Patients may present to the emergency department with severe symptoms ranging from ones similar to flu to coma and death. Clinical findings are non-specific such as dizziness, headache, nausea, vomiting, changes in consciousness, and can mimic many diseases. The clinical findings associated with poisoning are just loosely correlated with blood carboxyhemoglobin (COHb) levels [1].
Perfusion with carbon monoxide does not affect extracellular glutamate in dialysates of the hippocampus of freely moving mice
Published in Drug and Chemical Toxicology, 2018
Asuka Ito, Mostofa Jamal, Kiyoshi Ameno, Naoko Tanaka, Ayaka Takakura, Takanori Miki, Hiroshi Kinoshita
Carbon monoxide (CO) poisoning is a potentially fatal condition that occurs when CO gas is inhaled. CO is also formed endogenously in small amounts as a byproduct of heme degradation (Wu and Wang 2005). CO produces a range of effects on health even at very low levels (Townsend and Maynard 2002). The principal mechanism of many adverse effects of CO exposure is COHb-induced tissue hypoxia. The brain is the organ most vulnerable to CO-induced acute hypoxia, due to its high demand for oxygen and this may result in cognitive defects, especially affecting memory and learning (Piantadosi et al. 1997).