Under The Microscope: It 'nearly' killed me!

 

Death from alcoholic poisoning is not uncommon and can  occur at blood levels in excess of about 300mg1100ml. Some deaths could be  attributed to alcohol at even lower concentrations. Death  can be caused either by the direct depressive effects upon  the brainstem, mediated via the respiratory centres - or  through secondary events such as aspiration of vomit. the use of 'aspiration of vomit' as  a cause of death must be used with great caution unless there -  is ante-mortem eyewitness evidence. The major exception  to this proviso is in acute alcoholism, where if copious  inhalation of stomach contents right down to the secondary  bronchi is confirmed, then in the absence of significant  natural disease, injury or other toxicity, a high blood-alcohol. level may reasonably be incriminated as the probable cause.

Many such fatalities occur during police custody, when considerable outcry, publicity and disciplinary investigations are the usual outcome. Drunken persons are often involved in fatal trauma, which may be of many types. The majority of homicides are triggered by the aggressive behaviour engendered by alcohol. Road accidents, either caused by drunken drivers (often upon themselves) or by drunken pedestrians walking into  traffic, 'are commonly related to alcoholic vulnerability. Falls  are extremely frequent and often fatal. Drunken persons may  fall down stairs or steps and suffer head injuries. Falls from  high places are less common, but do occur from drunken  carelessness or unsteady gait. Death from burns or carbon monoxide poisoning may  occur in drunken persons who smoke when intoxicated.  A common scenario is for a drunk to go to bed and fall  asleep whilst smoking, the cigarette igniting the bedclothes.  Sometimes, a gas, electric or kerosene heater may be knocked  over during drunken staggering, which again starts a  fatal fire. Drowning is seen occasionally, especially in river or dockland areas. A typical happening is for a drunken sailor to  return to his ship late at night, and fall from a bridge or  gangway into the water. Death is sometimes not caused by  drowning but by sudden vagal cardiac arrest from the shock  of hitting cold water or having cold water suddenly flood  the pharynx and larynx. The drunken state seems to sensitize  the victim to such vasovagal shock, perhaps because of the  marked cutaneous vasodilatation encouraged by alcohol.

The pathological features of this condition are extensive and  can only be surveyed briefly here. In this context, chronic  alcoholism refers to the steady, regular abuse of drink, rather  than intermittent 'binge' drinking, which gives the tissues  time to recover between bouts of acute alcoholism.  At autopsy, there may be signs of general neglect and  malnutrition, but many chronic alcoholics are obese or  even oedematous, the latter because of chronic heart failure. The specific lesions are in the liver, heart and brain,  though they may be difficult to identify as unequivocally  caused by alcohol. The early stages of liver damage cause  fatty change, usually with enlargement.

The normal weight,  according to the sex and build, is between 1300 and  16OOg, but a fatty liver may be well in excess of 2000g. The surface is pale and greasy, though this may not be  a uniform change, especially in early or less severe cases.  Patchy yellowish areas may be visible within normal hepatic  parenchyma.  If the abuse continues, then the fatty change may eventually give way to fibrosis, the liver surface becoming rippled  beneath its capsule. Such cirrhosis is fairly fine, with nodules  of the order of 5-10 mm in diameter. In the later stages the  liver becomes smaller and contracts to a hard, greyish-yellow  block of only 800-1200 g.

Without a history of long-term alcohol abuse, it is difficult or impossible to be definite about the aetiology purely on autopsy appearances, though suspicion may be strong. A similar liver may develop as a sequel to hepatitis - and less often as an end result of certain dietary or metabolic defects. The spleen may be enlarged and firm: and portal varices may be present at the gastro-oesophageal junction, but these are both manifestations of portal hypertension and do not assist in determining the precise aetiology of the hepatic fibrosis. A useful index of liver damage and the progression or remission of alcoholic impairment is the level of the enzyme y-glutamyl transpeptidase in the serum.

Normal levels are less than 36 units, whereas liver damage can elevate this by a factor of many times. Alcoholic cardiomyopathy is certainly a real entity and can be diagnosed clinically. Whether it can be definitely identified on histological appearances alone is a matter of dispute. The heart is enlarged and shows patchy fibrosis with a variable mixed cellular infiltrate, hypertrophy of muscle fibres, patchy necrosis, hyalinization, oedema and vacuolization. Nuclear enlargement and polymorphism complete the range of changes, but none of these are specific, being found in hypertensive heart disease, coronary stenosis and other types of myocarditis. Combined with a definite history of chronic alcoholism, however, these relatively non-specific changes can be ascribed to alcohol if other causes can be excluded.

More specific myocardial damage has  been caused by cobalt added to commercial beers and several  outbreaks are on record. Systemic fat embolism has also been  recorded in victims of alcoholic fatty liver. Microinfarcts in  myocardium and brain are possible, though this aspect has  so far been rather neglected in research. Fat stains are not  usually employed in routine investigations and it is not  known how the victims of a fatty liver compare with control subjects in respect of diffuse target organ embolism.

 

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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