|Carbon Monoxide - A 'Silent Killer'.
Pathology of Carbon Monoxide Poisoning.
Carbon monoxide (CO),
a highly toxic gas produced by incomplete combustion of hydrocarbons,
is a relatively common cause of serious human injury.
It is a colourless, odourless and tasteless gas.
" Carbon monoxide has been responsible for many accidental poisonings in both developed and under developed countries of the world.
CO can be produced in fires, automobile engine exhausts and the incomplete combustion of organic matter.
It is a "silent killer" that initially produces a mild progressive frontal headache, drowsiness and sleep that is usually ignored as common place.
Continued low-level CO exposure for a long period of time in a confined space is cumulative and these accidental deaths occur frequently.
The incidence of carbon monoxide intoxication is increasing at a fast rate and is of even greater significance than in the past.
It all began many years ago when a bolt of lightening hit a fallen tree and produced a fire.
Severe carbon monoxide poisoning may be responsible for coma or encephalopathy, but milder intoxication may occur with nonspecific symptoms suggestive of hysteria, hyperventilation, psychosis, or viral syndrome.
Survivors of severe carbon monoxide poisoning may have permanent neurologic or neuropsychiatric disorder.
If recognition is not prompt and therapy is not quickly instituted, there may be irreparable damage to the brain with eventual death.
In the investigation of medical coma, blood is usually drawn and a reserve sample is placed in the refrigerator.
This sample may be used to detect the stable carboxyhemoglobin hours or days after the specimen has been drawn.
Many smokers and some industrial workers normally carry a level of 10% carbon monoxide saturation in the blood.
In interpreting the level of carbon monoxide one must take many factors into consideration.
- the functional integrity of the cardiovascular and pulmonary systems,
- the rate of blood flow in the vascular system,
- the number of red blood cells and total amount of hemoglobin available,
- the age of the person exposed to CO,
- physical activity at the time of exposure, and
- metabolic rate of the individual will affect the response to a given level of carbon monoxide.
- the presence of drugs such as alcohol and barbiturates will enhance the effects of carbon monoxide.
It is obvious that survival depends on the amount and length of exposure, as well as all the factors that normally govern the exchange of oxygen between the red blood cells and the parenchymal cells of the body.
Means of detection include sampling of carbon monoxide by air-sampling devices and the rapid detection of carboxyhemoglobin in the blood.
It unites with hemoglobin to form a compound, carboxyhemoglobin, which is over 200% more stable than oxyhemoglobin.
Carbon monoxide displaces normal oxyhemoglobin and interferes with the exchange of oxygen between the red blood cells and the extravascular tissue.
In fatal cases there is a cherry-red livor of the skin from the colour of the carboxyhemoglobin that is present in the superficial capillaries.
One can observe the blanching or lack of cherry-red colour over the pressure areas because of mechanical obliteration of the skin capillaries.
In cases of death not related to carbon monoxide poisoning , there is a blue discoloration of the skin (livor mortis) after somatic death.
In this instance the blue colour is caused by reduced hemoglobin.
A cherry-liver also may be caused by fluoroacetate or cyanide poisoning or by freezing.
Fluoroacetate and cyanide are cellular toxins that paralyze the metabolism of the cells so that utilization of the freed oxygen from oxyhemoglobin cannot be incorporated into the cytoplasm.
In the acute, rapidly fatal type of carbon monoxide poisoning, anatomic finding in the brain may be limited to small petechial hemorrhage of serosal surfaces and white matter of the cerebral hemispheres.
However, if the individual survives 4 to 5 days or more, gross lesions become evident and are characterized by striking hemorrhagic necrosis of the basal ganglia and lamellar necrosis of the cortical gray matter.
If there is longer survival, cystic areas develop in these regions.
In the heart the subendocardial layer of the myocardium is characterized by minute foci of necrosis. In some rare cases there may be intramural haemorrhage with myocardial rupture at the apex of the left ventricle.
Cardiac effects of carbon monoxide are caused by dual toxicity - hypoxia due to carboxyhemoglobin formation and direct effect on myocardium.
Carbon monoxide affinity to myoglobin is 60% higher than that of oxygen. Toxic effects result in arrhythmias, ventricular dysfunction, and myocardial infarction.
Carbon monoxide poisoning may cause angina and myocardial injury even in young patients with no preexisting coronary disease.
Patients with ischaemic heart disease may have symptoms of angina with carboxyhemoglobin levels as low as 5-10%. In addition to direct effects, carbon monoxide also causes nitrous oxide release, vascular smooth muscle relaxation, and hypotension.
The findings in the brain and heart are not pathognomonic for carbon monoxide poisoning and may be seen in other conditions in which acute severe hypoxia develops.
Carbon monoxide intoxications carry a high risk of immediate mortality which justify the need of early diagnosis and treatment.
Failure to diagnose carbon monoxide poisoning may result in significant morbidity and mortality and allow continued exposure to a dangerous environment.
In the emergency department , a high index of suspicion must be maintained for occult carbon monoxide exposure.
Headache, particularly when associated with certain environments, and flulike illness in the wintertime with symptomatic cohabitants should raise the index of suspicion significantly for occult carbon monoxide poisoning.
Emergency treatment of carbon monoxide poisoning begins with inhalation of supplemental oxygen and aggressive supportive care.
|Medicolegal importance of
Carbon Monoxide Poisoning:
The medicolegal aspects of carbon monoxide intoxication are of great importance when related to the public interest and safety.
Dangerous levels of carbon monoxide may accumulate when almost any heating device is defective from incomplete combustion of any carbon fuel.
If negligence on the part of manufacturer leads to illness or death from carbon monoxide intoxication, the medicolegal importance of litigation and compensation becomes obvious.
The proper investigation of a case of suspected suicide carries with it great responsibility.
At first glance it is often impossible to determine whether the death of a victim of carbon monoxide poisoning is attributable to suicide, accident, or homicide.
An exhaustive history at the scene by persons acting in the public interest (medical examiners, coroners, law enforcement officers, pathologists) is mandatory.
The importance of the classification of death as homicide or accident is obvious.
On the other hand to thoughtlessly designate a death as suicide from carbon monoxide intoxication, without proper evidence, may lead to considerable psychologic trauma to the victimís family and friends.
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Hyperbaric oxygen therapy for carbon monoxide poisoning.Undersea Hyperb Med. 2014 Jul-Aug;41(4):339-54.
Can carbon monoxide-poisoned victims be organ donors? Med Gas Res. 2014 Jul 31;4:13. doi: 10.1186/2045-9912-4-13.
Carbon monoxide poisoning and flooding: changes in risk before, during and after flooding require appropriate public health interventions.PLoS Curr. 2014 Jul 3;6
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