Under The Microscope – Shoves You Off At Once

Toxicology is a vast subject, most of it concerned with the nature, occurrence, symptomatology, biochemistry, mode of action and treatment of a wide range of poisonous substances. Many forensic medicine textbooks, especially those from Asia, devote a major part of their text to all these aspects of hundreds of toxic substances, many of which are seldom - if ever - encountered by a pathologist in most parts of the world. As the autopsy appearances of most poisons are non-specific, it seems fruitless to offer a repetitive catalogue, and therefore the descriptions selected here refer to some of those that either have specific features or are encountered more often. This chapter describes the autopsy appearances in a range of poisons that can broadly be classed as 'corrosive', even if this is not necessarily their main lethal mode of action. In addition, several toxic heavy metals will be discussed, again from the point of view of autopsy findings and relevant toxicological laboratory findings.

Cyanide is a relatively common poison, both in suicide, accident and, occasionally, homicide. It forms part of lethal toxicity of many fires in buildings, where smoke inhalation kills the majority of victims, rather than burns. Although the autopsy diagnosis of acute cyanide poisoning is rarely in doubt, toxicological analysis may be difficult to interpret because of both the destruction and production of cyanide in the dead body and even in stored blood samples awaiting analysis. Acute cyanide poisoning is most often self-administered (70 per cent in one series), in which case usually the sodium or potassium salt is swallowed. It may be accidental or industrial, in which case either salts may be involved, or it may be the free gas liberated from some commercial process. Homicidal poisoning is rare, except for the mass homicides which still occur, such as the Jonesville tragedy in Guyana, or the use of cyanide as a weapon of war against civilians in the Middle East. It has also been used for judicial execution in parts of the USA, a practice which seems to be reviving in recent years. Cyanide acts only as free hydrogen cyanide and therefore swallowed salts need to meet either water or gastric acid before liberating hydrocyanic acid, a process that takes only a few seconds. The fatal dose of cyanide is small, of the order of 150-300 mg, which allowed it to be used as hidden suicide pills by prominent Nazis at the end of the last war. Recovery has been recorded from far greater doses, however, such as 2-4g of potassium cyanide. Much depends on the purity of cyanides, as they tend to decompose in storage and old samples may contain only half the weight as active cyanide.

Cyanide acts by linking with the ferric iron atom of cytochrome oxidase, preventing the uptake of oxygen for cellular respiration. Cyanide cannot combine directly with haemoglobin, but can do so through the intermediary compound methaemoglobin. Cyanides are moderately corrosive through their alkaline nature, causing local tissue damage that is unrelated to their more general toxicity via enzyme inhibition. Externally there can be wide variations in the appearance. Traditionally, the hypostasis is said to be brick-red, due to excess oxyhaemoglobin (because the tissues are prevented from using oxygen) and to the presence of cyan- methaemoglobin. Many descriptions refer to a dark pink or even bright red skin, especially in the dependent areas, which can be confused with carboxyhaemoglobin. The few cases seen by the authors have shown a marked dark cyanotic hypostasis, perhaps caused by lack of oxygenation of the red cells by paralysis of the respiratory muscles. There may be no other external signs apart from the colour of the skin and possibly black vomit around the lips. There may be a smell of cyanide about the body, though it is well known that many persons cannot detect this, the ability being a sex-linked genetic trait. This may be of importance to pathologists and mortuary staff, as corpses dead of cyanide poisoning can present a health hazard. Internally the tissues may also be bright pink caused by the oxyhaemoglobin that cannot be utilized by the tissues - which is probably more common than the presence of cyan- methaemoglobin. The stomach lining may be badly damaged and can present a blackened, eroded surface, by altered blood staining the stripped mucosa. This is mainly because of the strongly alkaline nature of the hydrolysed sodium or potassium salts of cyanide; hydrogen cyanide itself causes no such damage. In less severe cases, the stomach lining will be streaked with dark red striae, where the rugae have been eroded while leaving the intervening folds relatively unharmed. The stomach may contain frank or altered blood from the erosions and haemorrhages in the walls. If the cyanide was in dilute solution, there may be little damage to the stomach, apart from pinkness of the mucosa and perhaps some petechial haemorrhages. There may also be undissolved white crystals or powder, with the almond-like smell of cyanide mentioned above. As death is usually rapid, little of the contents will have passed into the intestine. The oesophagus may be damaged, especially the mucosa of the lower third, though some of this may be a post-mortem change from regurgitation of the stomach contents through the relaxed cardiac sphincter after death. The other organs show no specific changes and the diagnosis is made by history smell and the reddish colour of the internal tissues, and often skin.

The usual blood, stomach contents, urine and any vomit should be submitted to the laboratory, taking particular care that the samples present no hazard to those packing, transporting or unpacking them. The laboratory should be warned in advance that a possible cyanide case is coming their way. If death was possibly caused by the inhalation of hydrogen cyanide fumes, a lung should be sent intact, sealed in a nylon (not polyvinylchloride) bag.

It is important to get the samples to the laboratory as soon as possible (in terms of days) to avoid the spurious formation of cyanide in stored blood samples. This usually occurs at room temperature so, if there is to be a delay, refrigeration is essential. ents and conversion to thiocyanate. The amount found on analysis naturally depends on the amount taken and the time between administration and death. Though the latter is usually measured in minutes, low dosage - or treatment - may allow survival for hours or even days. Assuming that no spurious cyanide is formed, any significant amount found is evidence of cyanide ingestion, which in itself is abnormal and presumably confirmatory evidence of poisoning.

Typical blood levels in one series of fatal cases following ingestion of the poison range from 1 to 53 mg/l, with an average of 12 mg/l. The spleen always has the highest tissue concentration, presumably because it contains so many red cells; in the same series, the spleen level was between 0.5 and 398 mg/l, with a mean of 44 mg/l. In another series, mean blood levels were 37 mg/l.

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