Under the Microscope: CARBON MONOXIDE POISONING


  

As always, an adequate history may give the clue to the cause of death. Where the circumstances are obvious, such as a death in a car with a tube leading from the exhaust, the pathologist's attention will be directed towards carbon monoxide from the outset. There are many other circumstances, however, in which the history may be obscure, and only the vigilance of the pantologist and his staff will pick up the possibility of this type of toxicity. In fact, many a case has first been recognized by the mortuary technician who commented on the colour of the skin or tissues. A number of fatal monoxide poisonings have already been certified as 'natural causes' by uncritical clinicians (especially in general practice) when in fact carbon monoxide poisoning, either suicidal or accidental, was the true reason for the death. Failure to examine the body fully is the usual cause, as the pink coloration may only be noticeable in the areas of postural hypostasis not normally visible in a body in bed, though the sides and back of the neck are reasonably accessible even to cursory examination.

At autopsy the most striking appearance of the body is the colour of the skin, especially in areas of post-mortem hypostasis. The classical 'cherry-pink' colour of carboxy- haemoglobin is usually evident if the saturation of the blood exceeds about 30 per cent. Below this, familiarity and good lighting are needed and below 20 per cent, no coloration is visible. As these low concentrations are rarely fatal, however, little is lost. Sometimes, darker cyanosis tends to mask the skin colour, but the margins of the hypostasis and the internal tints are usually apparent.

When the victim is anaemic, the colour may be faint or even absent because insufficient haemoglobin is present to display the colour. In racially pigmented victims the colour may obviously be masked, though may still be seen on the inner aspect of the lips, the nail-beds, tongue, and palms and soles of the hands and feet. It is also seen inside the eyelids, but rarely in the sclera. Rarely, there may be blistering of the skin of dependent areas, such as the calves and buttocks, and around wrists and knees, similar to the so-called 'barbiturate blisters'. These are not specific to carbon monoxide toxicity and are the result of cutaneous oedema in any profound coma where there is total immobility and lack of venous return from muscle movement. As most carbon monoxide deaths are relatively rapid, such blisters are rare. Internally the most noticeable feature is again the colour. Blood and muscle will be pink as a result of carboxyhaemoglohin and carboxymyoglobin. In relatively low concentrations, in poor light and in some artificial lighting in autopsy rooms, the cherry-pink colour may be difficult to see. It can be enhanced by diluting the blood with water against a white background, as in a porcelain sink or an enamel scale-pan, when the pinkness will be more evident.

The pinkness of hypothermia or refrigeration is a different colour. Unfortunately, some pathologists have a red-colour visual impairment, which makes it difficult for them to differentiate between subtle changes in redness, so laboratory is always required for objective confirmation and quantification of the monoxide concentration. Other suggestive indications of carbon monoxide are that, when tissues are placed in formol saline for preservation of histology, they do not decolourize as quickly as normal tissues and remain pink for a long period. If carbon monoxide poisoning is suspected at autopsy, a quick test is to add a few drops of blood to some 10 per cent sodium hydroxide solution on a white tile or in a tube against a white background. The normal blood will immediately become brownish-green but, if significant monoxide is present, the colour will remain pink, as no methaemoglohin is formed. One has to bear in mind though, that unlike adult blood, fetal blood up to the age of 6 months is more resistant to alkali and the colour change can take hours to develop.

None of these rather idiosyncratic tests can replace proper laboratory investigation, however. Blood should be taken for analysis in the usual way, preferably from a peripheral vein. In contrast to most toxicological investigations, even foul samples can still be useful for carboxyhaemoglobin estimations. Heart blood, blood from body cavities and even from bone marrow when the bones are split open, can still provide valid material for estimating the percentage of haemoglobin converted to carboxyhaemoglobin.

When a body has been badly damaged by fire, fluid blood may be hard to obtain, so that any sanguineous body fluid or bone marrow can provide material for analysis. If analysis is to be delayed more than a day, it is recommended that fluoride be added as a preservative. There are no other autopsy features in acute deaths, which form the majority seen by forensic pathologists. Where survival occurs there are a number of neurological lesions that follow severe carbon monoxide exposure. Necrosis and cavitation of the basal ganglia in the brain, notably the putamen and globus pallidus, has been known for well over a century. Within about 5 days, histological changes occur here, with 'gitterzellen' scavenging cellular debris, the foam cells and microglia presenting an appearance characteristic of tissue breakdown in the central nervous system. There may also be damage in the substantia nigra of the brainstem. In delayed deaths, petechiae and ring-shaped haemorrhages may occur in the cerebral white matter.

Carbon monoxide has an affinity for haemoglobin that is between 200 and 300 times greater than oxygen. Therefore even small concentrations of monoxide in the inspired air will progressively displace oxygen from the erythrocytes and this will lower the oxygen-carrying capacity of the blood. It was formerly thought that all the toxic properties of carbon monoxide lay in this hypoxic action, but more recently it has been shown to interfere with other ferroproteins such as myoglobin and various enzymes including members of the cytochrome family.

The major effect is undoubtedly the reduction in oxygen transport and, for this reason, it is the percentage saturation of the total available haemoglobin that is important rather than an absolute quantity of carboxyhaemoglobin in the blood. Anaemic persons will not show the external cherry- pink colour if insufficient haemoglobin is available for the monoxide component to become visible. It is the residual non-combined haemoglobin still available for oxygen trans- port that is important in maintaining life. For example, an anaemic person with only 8g/ 1100 ml of haemoglobin having four of those occupied with carbon monoxide (50 per cent saturation) is in much worse a state than a person with a total of 14 g of which four are monoxide-occupied. There are many tables available that relate saturation levels to the clinical symptoms. There is a wide margin of variation in these, as there is with lethal levels.

Old people may die at relatively low concentrations, such as 30 per cent and, in some cases, no other cause can be found when the ~carboxyhaemoglobin level is only 25 per cent. This may be the result of anaemia, so that there is less reserve for oxygen carrying when part of the haemoglobin is occupied by monoxide. In many cases, the senile myocardium is already in a fragile state and any extra hypoxia will cause it to fail. Infants also seem to die at relatively low levels, perhaps because their higher respiration rate allows a more rapid absorption.

. Carboxyhaemoglobin is stable and can be detected even in putrefied bodies a long time after death, as long as sophisticated laboratory techniques are used. Monoxide cannot enter a body post-mortem to any significant extent. Bodies burnt after death do not absorb any monoxide and thus a significant level (more than 10 per cent) in a body from a fire means that respiration must have been proceeding whilst the conflagration was in progress.

A minor source of local carboxyhaemoglobin and myohaemoglobin is gunshot wounds, where the propellant gases (which are rich in the compound) are blown into the wound from contact or short-range discharges. The tissues absorb monoxide, especially around the entrance wound. It has been claimed that this is a way of differentiating the entrance from the exit wound, but in fact the whole track of the missile(s) may be sheathed in a zone of monoxide trvs- fer into blood and muscle from a near-discharge, though theoretically there should be a gradient of concentration from one end of the track to the other.

 

Acknowledgements:

www.aived.nl    AIVD – @Erik Akerboom ©

www.politie.nl  Politiekorpschef  @Janny Knol©

www.politie.nl WEB Politie - @Henk van Essen©

 

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