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