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Identifying and managing adverse environmental health effects: 6. Carbon monoxide poisoning.

Carbon monoxide poisoning is an enigmatic illness. The symptoms are often non-specific or masked by an exacerbation of an underlying illness, such as congestive heart failure, that has been triggered by carbon monoxide inhalation. The effects can range from mild, annoying symptoms relieved by removal of the source to severe morbidity with profound central nervous system dysfunction, acute complications and delayed sequelae. Estimates suggest that about one-third of nonfatal cases of carbon monoxide poisoning go undetected and undiagnosed. We present a case of residential carbon monoxide poisoning to illustrate these points and to demonstrate the usefulness of a simple tool based on the CH2OPD2 mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs) that physicians can use to obtain an environmental exposure history. We outline the clinical management of carbon monoxide poisoning and provide strategies and resources to prevent exposure.

Adolescent↗

An interesting cause of pulmonary emboli: acute carbon monoxide poisoning.

Carbon monoxide poisoning, a public health problem of considerable significance, is a relatively frequent event today, resulting in thousands of hospitalizations annually. A 70-year-old lady was seen in the emergency department with a provisional diagnosis of carbon monoxide poisoning. The previous night, she slept in a tightly closed room heated with coal ember. She was found unconscious in the morning with poor ventilation. She had a rare presentation of popliteal vein thrombosis, pulmonary emboli, and possible tissue necrosis with carbon monoxide poisoning. Oxygen treatment with low-molecular-weight heparin (nadroparine) and warfarin therapy resulted in an improvement in both popliteal and pulmonary circulations. In conclusion, the presence of pulmonary emboli should be sought in patients with carbon monoxide poisoning.

Aged↗

Carbon monoxide poisoning.

Carbon monoxide poisoning has received little attention in th pediatric literature, although it is not uncommon in children. With the advent of alternative energy sources, such as woodburning stoves, one might predict an increase in its incidence over the next few years. Carbon monoxide poisoning is well described in the adult medical, surgical, neurologic, and psychiatric literature. It can cause a severe encephalopathy and have cardiovascular, pulmonary, muscular, renal, cutaneous, visual, and auditory manifestations. In this review a case of severe carbon monoxide poisoning with complications is presented.

Acute Kidney Injury↗

[Cardiologic aspects of carbon monoxide poisoning].

Carbon monoxide poisoning causes tissue hypoxia because of reduced transfer and altered release of oxygen by hemoglobin. Considering many case histories, we realized that symptoms and clinical signs of acute poisoning are mostly neurologic: coma, headache, dizziness, vomiting. On the contrary, it seems that myocardium, the other organ which mostly requires O2, is attacked in a "silent way". ECG in 5 patients with accidental carbon monoxide poisoning underlined that cardiac rate increased (3 of them presented tachyarrhythmias by atrial fibrillation) and the presence of more or less important alteration of ventricular repolarization like "subendocardial lesion". Simple hyperbaric oxygen treatment determined the regression of the rhythm disorder and of the abnormalities of ventricular repolarization. The only patient who had not the restoration of sinus rhythm had chronic atrial fibrillation.

Adult↗

[Family practitioner and carbon monoxide poisoning].

Carbon monoxide poisoning is not easily identifiable. It is the first cause of death by accidental poisoning in Europe. The family practitioner, who has not been made aware of this problem, incurs the risk of diagnostic indecision or of involuntary personal poisoning. Since symptomatology is non specific, the general practitioner answering housecalls is sometimes confronted with an urgent medical problem linked to the complications of this intoxication (coronary, neurological problems...), without having ways of documenting its origin of the poisoning or any means to protect himself. Through direct contact with his patients' environment, the family practitioner, being made sensitive to this problem, can certainly contribute to care and aftercare of the patient suffering from carbon monoxide poisoning, but also to the prevention of this public health problem often called "the silent killer".

Carbon Monoxide Poisoning↗

Pathophysiology and treatment of carbon monoxide poisoning.

Carbon monoxide poisoning is the leading cause of poisoning deaths in the US, and published reports of carbon monoxide related morbidity and mortality can vary widely. Common morbidity involves myocardial and/or neurologic injury including delayed neurologic sequelae. The pathophysiology of this entity is complex, involving hypoxic stress on the basis of interference with oxygen transport to the cells and possibly impairing electron transport. Carbon monoxide can also affect leukocytes, platelets and the endothelium, inducing a cascade of effects resulting in oxidative injury. Carboxyhemoglobin levels are valuable for confirming carbon monoxide exposure but cannot be used to stratify severity of poisoning, predict prognosis, or indicate a specific treatment plan. Oxygen therapy is the key treatment of carbon monoxide intoxication, and hyperbaric oxygen has been shown to interdict and improve clinical outcome in some patients. Immediate treatment with a high fraction of inspired oxygen and careful clinical evaluation are mandatory. Timely referral for hyperbaric oxygen is indicated for patients with any history of unconsciousness, cardiovascular instability or ischemia, and persistent mental and/or neurologic deficits. Hyperbaric oxygen should also be considered in certain other patient subsets.

Animals↗

Management of carbon monoxide poisoning.

Carbon monoxide poisoning is a major cause of illness and death in the United States. Most cases result from exposure to the internal combustion engine and to stoves burning fossil fuels. Most cases of accidental exposure are preventable if proper precautions are taken; however, when cases arise, their presenting signs and symptoms are nonspecific and often lead to a misdiagnosis resembling a flu-like viral illness. As a result, the incidence of acute CO poisoning is underestimated. The effects of CO poisoning are due to tissue hypoxia, with the CNS and the heart being the most susceptible target organs due to their high oxygen needs. Prolonged hypoxia due to high CO levels may lead to cardiac arrhythmias or arrest (or both) and a variety of neurologic sequelae. Treatment is directed toward the relief of tissue hypoxia and the removal of CO from the body. Severity of poisoning can be divided into three levels based on CO levels in the blood. Administration of normobaric 100 percent oxygen is the therapy of choice for most cases, while hyperbaric oxygen therapy is reserved for severe poisonings.

Carbon Monoxide Poisoning↗

An unusual case of carbon monoxide poisoning.

Carbon monoxide, a gas originating from incomplete combustion of carbon-based fuels, is an important cause of human deaths. In this paper, we describe an unusual carbon monoxide poisoning in a dwelling without obvious sources of combustion gases, for which two adults had to be treated in a hyperbaric chamber. Carbon monoxide readings were taken in the house and in the neighboring homes. Methane gas and nitrogen oxide levels were also monitored in the house air. Soil samples were collected around the house and tested for hydrocarbon residues. The investigation revealed the presence of a pocket of carbon monoxide under the foundation of the house. The first readings revealed carbon monoxide levels of 500 ppm in the basement. The contamination lasted for a week. The investigation indicated that the probable source of contamination was the use of explosives at a nearby rain sewer construction site. The use of explosives in a residential area can constitute a major source of carbon monoxide for the neighboring populations. This must be investigated, and public health authorities, primary-care physicians, governmental authorities, and users and manufacturers of explosives must be made aware of this problem.

Adult↗

Neuroimaging, cognitive, and neurobehavioral outcomes following carbon monoxide poisoning.

Carbon monoxide is a colorless, odorless gas produced as a byproduct of combustion. Carbon monoxide is the leading cause of poisoning injury and death worldwide. Morbidity following CO poisoning includes neurologic sequelae, neuropathologic abnormalities on brain imaging, neurobehavioral changes, and cognitive impairments. It is estimated that as high as 50% of individuals with carbon monoxide poisoning will develop neurologic, neurobehavioral, or cognitive sequelae. Carbon monoxide related cognitive impairments included impaired memory, attention, executive function, motor, visual spatial, and slow mental processing speed. Given the high rate of brain related morbidity and the fact that the majority of carbon monoxide is avoidable, awareness and prevention of carbon monoxide poisoning is warranted.

Brain Injuries↗

[Neurologic and psychiatric sequelae of carbon monoxide poisoning].

Carbon monoxide intoxication may result in neuropsychiatric abnormalities that can be overlooked or not fully appreciated. The authors describe two female patients who developed troublesome cognitive and emotional problems following carbon monoxide poisoning and stress the value of the precise neuropsychological testing and prolonged clinical observation in such cases.

Adult↗

Carbon monoxide poisoning.

Carbon monoxide poisoning is a significant cause of illness and death. Its protean symptoms probably lead to a gross underestimation of its true incidence. Low levels of carbon monoxide aggravate chronic cardiopulmonary problems, and high levels are associated with cardiac arrhythmias and cerebral edema. Patients who survive acute poisoning are at risk of delayed neurologic sequelae. The measurement of carboxyhemoglobin levels does not reveal the tissue levels of carbon monoxide but is useful in determining therapy. Treatment includes the monitoring and management of cardiac arrhythmias and oxygenation. Hyperbaric oxygenation is beneficial, but there are currently no definite criteria for its use.

Carbon Monoxide Poisoning↗

Carbon monoxide poisoning.

Carbon monoxide is a common domestic and industrial poison which may be lethal. Survivors can develop permanent neuropsychiatric disability. The mechanisms of toxicity are poorly understood and the traditional criteria used to determine the severity of the poisoning have low predictability. Oxygen is the recommended antidote to carbon monoxide, but it appears that oxygen under hyperbaric conditions repeated either daily or as indicated by the patient's condition may be required to provide an effective dose. A reliable marker of the severity of carbon monoxide poisoning is urgently needed so that trials of alternative regimens can proceed.

Carbon Monoxide Poisoning↗

Carbon monoxide poisoning.

Carbon monoxide (CO) poisoning is common and frequently unrecognized since the signs and symptoms are relatively nonspecific. CO poisoning causes tissue hypoxia. Additionally, various animal studies have demonstrated that CO interferes with myoglobin, P450, and other enzyme function; causes lipid peroxidation through neutrophil activation; produces oxidative stress manifested by peroxynitrate deposition in endothelium; binds to cytochrome aa3, disrupting intracellular oxygen utilization; can cause neuroexcitotoxicity; and contributes to hippocampal cellular death through apoptosis. Emergency treatment for CO poisoning is 100% oxygen. Hyperbaric oxygen therapy (HBO2) is accepted in CO poisoning, although data from randomized clinical trials regarding the efficacy of HBO2 in CO poisoning is conflicting. CO poisoning, even when treated with supplemental oxygen can leave the patient with permanent neurocognitive or affective problems. Unfortunately, there appears to be no marker or constellation of signs or symptoms at presentation that predicts long-term outcome following CO poisoning. Given the neurocognitive sequelae following CO poisoning, increased awareness and prevention of CO poisoning is imperative.

Apoptosis↗

Acute hydrocephalus following carbon monoxide poisoning.

Carbon monoxide remains a significant cause of poisoning in children. Cerebral edema is often the cause of significant morbidity and mortality in exposed children. While lesions of the basal ganglia have been well documented, the advent of neuroimaging has allowed antemortem demonstration of infarctions of the globus pallidus and putamen with carbon monoxide intoxication. Acute hydrocephalus following carbon monoxide poisoning has been a rare occurrence. We report a 2 year 6 month-old boy who, to our knowledge, represents the first reported case in which repeat computed tomography documented the evolution of hydrocephalus due to carbon monoxide exposure in a child.

Acute Disease↗

Diagnosis and treatment of carbon monoxide poisoning.

Carbon monoxide (CO) poisoning is a common occurrence in today's society. Most such poisonings are a direct consequence of inhaling the toxic byproducts of combustion. Exposure to toxic amounts of CO occurs most often during inhalation of automobile exhaust or smoke resulting either from faulty heating systems or industrial accidents. CO poisoning is associated primarily with injury to the brain and the heart because the gas binds to hemoglobin and interferes with these organs' need for a continuous supply of oxygen. Prompt recognition of CO poisoning and treatment of the patient with oxygen are essential to prevent long-term damage and delayed neurologic sequelae.

Carbon Monoxide Poisoning↗