Externally there can be wide variations in the appearance. Traditionally, the hypostasis is said to be brick-red, due to excess oxyhaemoglobin (because the tissue are prevented from using oxygen) and to the presence of cyanmethaemoglobin. 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 author have shown a marked dark cyanotic hypostasis, perhaps caused by lack of oxygenation of the red cells by paralysis of the respiratory muscle. There may be no other external signs apart from the color of the skin and possibly black vomit around the lips11.
There may be a smell of cyanide about the body, and a distinct odor of bitter almonds about the viscera especially in the skull cavity and the brain10. Though it is well known that many persons cannot detect this, so the telltale odor of bitter almonds cannot be used as a guide because 40% to 60% of the population is unable to dettect cyanide by smell. The ability being a sex-linked genetic trait1-13.
This may be of importance to pathologists and mortuary staff, as corpes dead of cyanide poisoning can present a health hazard. Reported that a pathologist became ill and was temporarily disabled shortly after conducting an autopsy on a suicide who has swallowed a massive amount of potassium cyanide. Presumably he had inhaled hydrogen cyanide from the stomach contents when examining the viscera11.
The materials usually saved for toxicologic examination are the stomach contents, lungs, brain and visceral organ like the liver. If the poison is inhaled, the lung will show a high hydrocyanic acid content than the stomach contents. If poison is ingested most of it will be in the stomach, and the lungs will giv only a small amount3,10.
Cyanide concentrations in tissue, such as liver, lung, spleen, and heart, may be more accurate indicators of the blood cyanide intoxication levels3. cyanide appears to display first-order kinetics during the period of initial toxicity. The volume of distribution for cyanide appears to change as the blood levels of the chemical change, but these alteration probably reflect the marked intracellular sequestration of the molecule. Ingestion of cyanide results in much higher levels in the liver than does inhalation; this is useful differential point in forensic investigation3.
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 cyanmethaemoglobin.
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 hydrolyzed sodium or potassium salts of cyanide; hydrogen cyanide itself causes no such damage. The findings at autopsy are otherwise the same as described above under hydrocyanic acid10,11. In less severe cases, the stomach lining will be streaked with dark red striae, where the rugae have been eroded while leaving the interlining 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 un dissolved white crystals or powder, with the almond-like smell of cyanide mentioned above10,11.
As death usually rapid, little of the contents will have passed into the intestine. The oesophagus may be damage, 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 color of the internal tissues, and often skin.
The detection and quantitation of cyanide in the blood after decomposition is difficult. Cyanide may be produced postmortem in a body or even in a test tube, due to decomposition. In addition, if the method of analysis is not absolutely specific, other substances in the blood (sulfides) may react like cyanide, giving falsely elevated levels of cyanide5.
Pathologically no particular lesions can delineate that the lesions are principally in the central nervous system, predominantly necrosis in the white matter. Probably the most wide-spread pathologic condition attributed to chronic cyanide poisoning is tropic ataxic neuropathy following cassava consumption4 .
Case report12 : (because the small number of victims in autopsy room at forensic department University of Indonesia, this case I downloaded from cyanide poisoning on net )
A male, 20-year-old university student, studying Chemistry. He shouted from his lodging's window that he had been poisoned, and was found in a collapsed state in his bedroom. He died two hours later in hospital At post mortem, six hours later, there was a distinct smell of almonds associated with the body. The organs of the body were congested and the stomach contents smelt strongly of almonds.The mucosa of the stomach was noted to be blue, with heavy staining of the fundus and body of the stomach, but the antrum was spared. Sometime later, a bottle with a small quantity of residual liquid was found on the premises. Toxicological analysis identified an aqueous solution of 13% sodium nitroprusside. Death was caused by cyanide poisoning. Nitroprusside contains five cyanide groups (CN) and one nitrous oxide group (NO). The latter component accounts for its therapeutic action as an antihypertensive agent. Nitroprusside in the blood reacts rapidly with haemoglobin to produce thiocyanate and cyanide, through which its toxic effects are exerted.
The reaction seen in the stomach will be familiar to all histopathologists, as it is the basis of Perl's Prussian blue reaction. In histological sections, ferric iron in the form of ferric hydroxide (Fe(OH)3)) is unmasked from compounds such as haemosiderin by acid. The ferric iron then reacts with a ferrocyanide (nitroprusside) to produce an insoluble blue compound, ferric ferrocyanide. The exact source of the ferric ions in the stomach mucosa is unknown (possibly altered blood). Antral sparing from coloration occurs as a result of its relative lack of acid secreting cells. Histology of the mucosa showed autolysis, and the positioning of the blue staining was difficult to assess, although most staining appeared to be superficial.
Interestingly, the first person to find the victim did not smell the typical "bitter almond" scent of cyanide. Ballantyne reported that the typical smell of cyanide was not present in the tissues of cadavers victim to this poison. However, this study used a single pathologist1. Certain individuals cannot detect the smell of cyanide and, anecdotally, 1 in 6 people are not capable of identifying its odor. Cyanide anosmia appears to be more prevalent in males, although its exact genetic basis is not fully understood.
The case was reported in 1931 in the British Medical Journal (1931, ii, 344) by Professor Fowweather, and is part of the collection at the University of Sheffield's Department of Forensic Pathology.