Bites and burns
Brice Antao, S Irish Michael, Anthony Lander, S Rothenberg MD Steven in Succeeding in Paediatric Surgery Examinations, 2017
From the list above, select the best initial management of inhalation injury for the following scenarios. After a fire in a confined space, a 6-year-old child is brought to emergency room with respiratory distress and mild confusion. Carbon monoxide poisoning is suspected.A 3-year-old girl who was exposed to inhalation of smoke from partially combusted plastics. She is unresponsive to oxygen therapy and has persistently elevated lactate levels and mixed venous saturation.During the evaluation of an 11-year-old patient who sustained smoke inhalation injury, you notice that the child has difficulty breathing, stridor and carbonaceous sputum.
Diagnosis and Treatment of Inhalation Injury in Burn Patients
Jacob Loke in Pathophysiology and Treatment of Inhalation Injuries, 2020
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).
Chemical injuries
Jan de Boer, Marcel Dubouloz in Handbook of Disaster Medicine, 2020
The initial treatment of chemical asphyxiants includes the removal of the casualties from the source of exposure concurrent with basic and advanced life support as needed. If the exposure is not immediately lethal and ventilatory support is provided, recovery can be expected in most victims. Several of those toxins do have antidotes, which should be administered as soon as possible. Oxygen is the cornerstone of treatment, especially in carbon monoxide poisoning; consequently, the administration of 100 percent oxygen should be initiated as soon as the diagnosis is suspected. Antidote therapy in hydrogen cyanide poisoning is indicated for any patient with more than minor symptoms, as represented by restlessness, anxiety or hyperventilation23. Standard antidotes include amyl nitrite, sodium nitrite and sodium thiosulphate. However, the administration of these antidotes is quite demanding in mass casualty situations and the use of hydroxycobalamine or di-cobaltethylenediamine is more justified13,55.
The effect of preconditioning agents on cardiotoxicity and neurotoxicity of carbon monoxide poisoning in animal studies: a systematic review
Published in Drug and Chemical Toxicology, 2023
Hamed Baharara, Hanieh Ghasemi, Sara Samadi, Bahar Roohshad, Vahid Jomehzadeh, Khosrow Ravankhah Moghaddam, Amir Hooshang Mohammadpour, Omid Arasteh
The search strategy was a combination of Mesh terms and keywords that retrieve from PubMed, Embase (Emtree), and studies. According to population, intervention, comparator, outcome (PICO), the search terms were divided into three components. The population terms include carbon monoxide poisoning, carbon monoxide, carbon monoxide toxicity, carbon monoxide intoxication. The intervention included ischemic preconditioning, myocardial, ischemic preconditioning, IPC, pharmacological preconditioning, and ischemic tolerance. The outcome terms were cardiotoxicity, neurotoxicity, myocardial infarction, carbon monoxide induced heart toxicity, carbon monoxide induced cerebral injury, cardiovascular events, and neurotoxicity syndromes. The three search components combined with the Boolean logic term “AND,” while the keywords within components were combined with “OR.” The authors were not restricted in language and time during the search and identification of studies. The search strategy was re-run to retrieve the most recent studies eligible for inclusion.
Carbon monoxide poisoning mortality in the United States from 2015–2021
Published in Clinical Toxicology, 2023
It is logical to assume that residential carbon monoxide alarms would prevent poisoning. Two studies are often cited in support of carbon monoxide alarm effectiveness. In one [20], 136 New Mexico carbon monoxide deaths over 16 years were retrospectively reviewed, and study investigators determined one-half might have survived the exposure had an operational carbon monoxide alarm been present in the residence. In the other [21], a North Carolina ice storm resulted in extensive power outages and a subsequent outbreak of carbon monoxide poisonings in a county that had required carbon monoxide alarm installation in a subset of residences two years earlier. Of 124 individuals subsequently diagnosed with symptomatic carbon monoxide poisoning, 109 came from homes without reported functional carbon monoxide alarms. This included 25 of 26 with poisoning deemed to be severe, with one death. It is unknown how many undiagnosed carbon monoxide poisonings occurred or how many homes actually had functioning alarms.
TDZD-8 alleviates delayed neurological sequelae following acute carbon monoxide poisoning involving tau protein phosphorylation
Published in Inhalation Toxicology, 2020
Chenglei Su, Ningjun Zhao, Jianjiao Zou, Xianliang Yan
DNS after acute CO poisoning is still a serious disease in the world. Though hyperbaric oxygen therapy is widely used in the clinic for DNS, there is no evidence that the use of hyperbaric oxygen reduces the incidence of neurologic sequelae (Hui-Jun and Dan-Feng 2017). Several mechanisms are involved in this process, including hypoxemia, reactive oxygen species, and inflammatory reactions. However, the mechanisms have not been fully illustrated (American College of Emergency Physicians Clinical Policies Subcommittee on Carbon Monoxide Poisoning et al. 2017; Rose et al. 2017). Recently, Kilicaslan et al. (Kilicaslan et al. 2012) reported that serum Tau protein levels were significantly higher in CO poisoning patients with severe neurological symptoms. Several studies indicated that the Tau protein is involved in neuronal injuries, such as Parkinson’s disease, Alzheimer’s disease, head trauma and stroke (Alosco et al. 2019; Chen et al. 2019; Pase et al. 2019; Shi et al. 2019). Herein, we speculated that Tau protein may contribute to the development of DNS after acute CO poisoning. To our knowledge, this study is unique in investigating the relationship between DNS after CO poisoning and Tau protein in the brain.