Under The Microscope: Piece By Piece One Fades Away

 

Corrosive poisons were formerly common suicidal agents, though they are now relatively rare in Western countries, probably because of the ease of obtaining less painful substances. In some parts of the world, mineral acids are still often used for homicide, assault ('vitriol-throwing') and suicide. In Malaya, reagents used in rubber production, such as formic and acetic acids, were often taken as a means of self-destruction by young women, especially Tamil rubber workers. In Britain, acids and alkalis are now almost unknown as agents of death. Even the occasional use of sulphuric 'battery acid' as a weapon of assault rarely causes death. The phenolic corrosives, however, such as carbolic acid and lysol, are occasionally encountered as suicidal agents. Toxicologically, none of these presents much problem, as the damage is often structural rather than poisonous, unless the victim survives long enough to have complications such as renal failure or chest infections. All the corrosive substances have the following features in common.

1.      There may be spillage of the fluid on the exterior of the body, corroding the skin in a pattern which may be helpful in reconstructing the posture of the victim at the time of drinking the substance. The lips may be burnt, and trickle and splash marks may run from the mouth down the chin, neck and chest. The pattern of burns at the mouth may sometimes indicate the shape of the container from which the poison was drunk, as the wide brim of a cup may mark the cheeks, while a bottleneck may sit more cleanly in the mouth. If the person was standing or sitting, then these runnels of fluid may pass down the chin onto chest and abdomen. If lying, then they may run across the face and cheeks and pass to the back of the neck. Further spillage may come from the nostrils due to spluttering and gagging. The hands may also be affected if the hands are instinctively brought up to the face.

2.      The interior of the mouth may be eroded, and the tongue swollen or shrivelled, according to the nature of the corrosive agent. The pharynx, larynx and oesophagus are all eroded, and if survival lasts more than a few minutes the glottis area may become oedematous. Spillage into the larynx and air passages may allow the respiratory mucosa to be damaged, and aspiration of liquid or vapour into the lungs can cause rapid pulmonary oedema and haemorrhages.

3.      The lower oesophagus and stomach rapidly become damaged, with discoloration, desquamation and sometimes perforation. Attempts at passing a stomach tube may themselves penetrate the softened wall of the oesophagus or stomach. If survival lasts long enough, some corrosive may pass through to damage the small intestine, but this is rare because of the time factor and spasm of the pylorus.

4.      All may cause death by pulmonary oedema from spillage into the lungs: if survival lasts a day or more, then a fulminating bronchopneumonia may be the terminal event.

The different corrosive agents have different actions on soh tissues, which can sometimes be differentiated by appearance and smell, though the mineral acids are not all that different. The phenolic compounds can usually be detected by smell alone. Strong acids act by dehydrating the tissues, coagulating the proteins and converting haemoglobin to haematin. Sulphuric acid, in concentrated form, is extremely corrosive and produces great heat in contact with water or tissues. The tissues are grey to black, rather dry and dehydrated. They may actually be charred into a blackened crust by the generated heat. The gastric lining may be grey, dark brown or black, or mixtures of all colours, depending upon the amount of altered blood in each part. Perforation may occur. The oesophagus and stomach may be grey and swollen, depending on rhe amount of acid and the amount of food already in the stomach. The tongue may be grey or black and distorted.

Nitric acid is similar, but has a brownish-yellow cast to its mucosal damage. There may be yellow or brown sharp-edged patterns on the skin burns of the face, with the usual trickle marks coming down from the corners of the mouth. Yellow fumes may arise from the stomach contents if a considerable quantity is present. The internal appearances are of yellowish-brown sloughing, though perforation seems less common than with sulphuric acid. Hydrochloric acid has similar effects, especially on mucous membranes, but is not so injurious to intact skin as sulphuric and nitric acids. The stomach may be converted into a slimy, softened mass and can perforate. The colour is greyish to black, depending on the amount of altered blood.

Sodium hydroxide in concentrated form is also a corrosive, but soft, slippery slime is the characteristic appearance and feel to tissues damaged by caustic soda. The colour is dirty white to grey. Phenol and lysol are also damaging and affect the tissues in much the same way as acids and alkalis. Carbolic acid (pure phenol) tends to stiffen the tissues and bleach them so that hard, cracked, whitish surfaces are seen on the face and skin. Internally, the same stiffness is noted in the oesophagus and stomach. Lysol is a soapy solution of phenol and cresols. It discolours the tissues a brownish purple, but is otherwise similar to phenol in its action.

Oxalic Acid and oxalate salts are not so corrosive as the mineral acids, but are poisonous and often act quickly, death occurring within minutes or the hour, from shock or hypocalcaemia. The acid is locally corrosive, but also has a systemic effect that may well be fatal even if the local damage is non-lethal. At autopsy, if an appreciable amount of either the white crystals or a strong solution has been swallowed, the local effect is a bleaching, the mucosa of mouth, pharynx and oesophagus being white, though local haemorrhage can streak this with red. The stomach contains altered blood from the damaged mucosa and is dark brown or black from acid haematin, the wall studded with acute erosions. Calcikn oxalate crystals may be seen in the stomach contents or in scrapings from the mucosa. In those who have survived the acute phase, death may be caused by abnormalities of the muscle function (including the myocardium) from the hypocalcaemia, caused by the precipitation of body calcium as insoluble calcium oxalate. More common is renal failure, death occurring 2-1 0 days later. The renal tubules suffer necrosis, primarily in the proximal convoluted tubules. This is not caused by the presence of calcium oxalate crystals, though these can be demonstrated histologically in the kidney.

Though in no sense a corrosive poison, ethylene glycol has certain features in common with oxalate poisoning and is so common relative to death from mineral acids that it cannot be omitted. The glycols are used widely as antifreeze agents in motor engines and as solvents in industry, so they are easily available. Because of their chemical inclusion in the alcohol group, they are abused as a source of intoxication, as well as being accidental and suicidal agents. At least 40-60 deaths a year are reported and this is probably an underestimate. The compounds involved are ethylene, diethylene, propylene and hexylene glycols. These do not have the same toxic effects (in fact, propylene glycol is virtually non-toxic), but ethylene glycol is the most commonly encountered. When drunk in excess of 100-200 ml, it is almost certain to be fatal unless specific treatment is given, such as dialysis and competition with alcohol. The first effects resemble drunkenness, but this passes into coma and death often within the first day. The glycol is metabolized in the body, a small but significant amount (about 1 per cent) being converted to oxalic acid, via the process glycol-glyoxal-glycolic acid-formic acid-glyoxylic acid-oxalic acid. It is not clear which of these compounds causes the most damage to the tissues. At autopsy there is no local damage, but widespread precipitation of the sheaf-like doubly refractile crystals of calcium oxalate into the tissues can be rendered visible microscopically by the use of polarized light. It is a matter of controversy whether this crystal deposition is the cause or merely a side effect of the lethal action of glycols. There may be cerebral oedema and a chemical meningoencephalitis. In the kidney there is a tubular necrosis similar to that in oxalate poisoning, and the crystals can be seen in the interstitial tissues and the tubules. Diffuse liver damage can also occur.

There is a whole range of metallic poisons, most of them from the upper reaches of the Periodic Table, accounting for their usual description as 'heavy metals'. The vast majority of toxic effects come from environmental and occupational poisoning, both chronic and acute. Acute poisoning by suicide, accident and homicide is becoming much less common, both because of the availability of other toxic agents, and because of greater awareness and controls on the environmental and industrial hazards of heavy metals. In former years, especially the nineteenth century, heavy-metal poisoning was common in homicide, but is now rarely seen in Western countries, mainly because they are now known to be easily detectable.

A constituent of all animal tissue, arsenic is the twelfth most abundant element on earth. This emphasizes the need for strict controls when making analysis for arsenic in human fluids or tissues, as the excretion of a healthy person on a diet rich in fish (especially shellfish) can exceed that seen in chronic arsenical poisoning. Similarly, where an exhumation is performed after allegations of poisoning, full control samples of soil and grave water must be taken to ensure that arsenic found in the body could not have arisen from local contamination.

Arsenic metal is not poisonous, only its compounds. These interfere with cellular respiration by combining with the sulfhydryl groups of mitochondrial enzymes, especially pyruvate oxidase and certain phosphatases. Arsenic has a particular target in vascular endothelium, accounting for the many lesions caused by increased permeability, tissue oedema and haemorrhage, especially in the alimentary canal. Arsenical poisoning may arise from the ingestion of arsenious oxide, a tasteless white powder - from copper, sodium and potassium arsenites, arsenates of lead and calcium, arsenic sulphides and gaseous arsine (confined to industry). In forensic practice, the rare cases of arsenic poisoning are now usually from arsenious oxide or one of the arsenites. Arsenical poisoning may be acute or chronic, the latter being the presentation of most environmental and occupational toxicity. Suicides are obviously invariably acute, whereas the uncommon homicidal cases may be either acute or chronic.

If taken on an empty stomach, especially in solution, only about 150 mg may be fatal, but usually some 250-300 mg are needed as a minimum lethal dose. Much larger quantities have been survived and there is some evidence that tolerance to arsenic can be attained. With large doses, much may be vomited. Death can be rapid - within hours from 'shock' and cardiorespiratory failure - or may be delayed for many days, when hepatorenal failure is the mode of death. In chronic poisoning, no lethal dosage can be indicated, as if the ingestion exceeds the small normal excretion rate, then a cumulative build-up of arsenic will occur.

 

In acute poisoning the findings may be minimal, if death occurs within hours. There may be some mild irritation of the upper gastrointestinal tract, such as reddening of the gastric mucosa, especially along the top edges of the rugae. The description of 'red velvet' has been applied to some stomach linings in acute arsenic poisoning. There may be mucus coating and granules of the poisonous agent may be trapped on the lining - a reason for sending both contents and stomach wall for analysis, as in most suspected poisonings of any type. The intestines arc: usually normal in acute poisoning. The only other lesion commonly seen is subendocardial haemorrhage on the left ventricular waU. This, of course, is a common finding in any severe shock condition when sudden hypotension occurs. It is seen in any gross injury, with loss of blood volume, blood pressure and neurogenic shock. Head injuries and raised intracranial pressure are other conditions in which these lesions are prominent. Part of forensic mythology surrounds the alleged preservation of corpses dying from arsenic poisoning. This has been endlessly discussed, but there is no real evidence that it is true. A more likely explanation is that the dehydration from diarrhoea in chronic poisoning retards the usual moist putrefaction. Externally there may be a diffuse abnormality of the skin, with a dry, scaly, hyperkeratotic surface. Clinically, there is a 'rain-drop' punctate pigmentation, but this may not be apparent after death unless really marked. It is more common in skin flexures and over the forehead and neck. There may be some hair loss. Puffy thickening and oedema of the face has been described, suggestive of myxoedema.

There is rarely any mucosal ulceration. The contents may be copious and fluid, the usual description of 'rice- water' being applied. The large intestine may show min- imal changes or be normal: the contents may be fluid and similar to the small bowel. The liver may reveal fatty change or more severe necrosis, sometimes at the periphery of the lobule. Severe liver damage may be associated with externally apparent jaundice. The kidney is damaged in chronic toxicity, there being non-specific tubular necrosis. The myocardium may also show myofibril damage, interstitial collection of cells and sometimes fatty degeneration.

In acute poisoning, the major requirement is the stomach and contents, and preferably the small intestine, tied off at each end. Blood, urine and liver should also be taken. In chronic poisoning, especially if the diagnosis is not firmly established from circumstantial and gross autopsy findings, a much wider range of samples is needed:

-          blood from peripheral veins;

-          stomach and contents;

-           small intestine and contents;

-          sample of large bowel contents;

-           Urine;

-          bile;

-          whole liver;

-          one kidney;

-          nail clippings or whole nails;

-          hair samples -whole length of at least 20 hairs, including roots.

Arsenic levels in blood are elevated only for a short time following absorption, unless exposure is continuous. The highest concentrations of arsenic are found tissues rich in sulphydryl (SH-) groups, such as skin, hair and nails. It was formerly thought that it took a week or two for ingested arsenic to find its way into the keratinized tissues such as hair and nails.

Though other heavy metals have declined in forensic importance over the past century, thallium has several times been used homicidally in recent years, sometimes for multiple poisonings. Thallium is used as a rat killer and widely employed in industry, especially in glass manufacture. It has curious aspects in relation to forensic pathology, in that it can be seen radiologically in the intestine and deposited in the liver, so in the rare event of a pathologist suspecting thallium poisoning, X-rays of the body should be taken before autopsy. The other unique aspect is that it is probably the only homicidal agent to be confirmed after cremation. The fatal dose is somewhere about 1 g, depending upon the type of thallium compound employed, as there are several different salts available, such as the acetate, sulphate or nitrate. The estimates vary from 6 to 40 mgl/kg body weight, with an average of about 12 mgl/kg.

Autopsy appearances are variable and non-specific, but pallor and streaking of a pale, degenerate myocardium have been recorded. Hair loss is one of the clinical signs that arouses suspicion of thallium poisoning, as it was formerly used as a depilatory. This effect begins about a week after administration, but may not be noticeable for twice that time. Large tufts tend to come away, rather than a general thinning. Loss of the outer third of the eyebrows is said to be a significant sign, though these are also the areas that are lost in hypothyroidism. Examination of the roots of surviving hairs may show a black coating, caused not by the thallium itself, but by an excess of melanin. Liver necrosis and renal tubular necrosis are non-specific findings in those who survive for some time.

 

Acknowledgements:

www.aived.nl    AIVD – @Erik Akerboom ©

www.politie.nl  Politiekorpschef  @Janny Knol©

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

 

Bibliography:

 

1.    Criminal Investigations – Crime Scene Investigation.2000

 

2.    Forensic Science.2006

 

3.    Techniques of Crime Scene Investigation.2012

 

4.    Forensics Pathology.2001

 

5.    Pathology.2005

 

6.    Forensic DNA Technology (Lewis Publishers,New York, 1991).

 

7.    The Examination and Typing of Bloodstains in the Crime Laboratory (U.S. Department of Justice, Washington, D.C., 1971).

 

8.    „A Short History of the Polymerase Chain Reaction". PCR Protocols. Methods in Molecular Biology.

 

9.    Molecular Cloning: A Laboratory Manual (3rd ed.). Cold Spring Harbor,N.Y.: Cold Spring Harbor Laboratory Press.2001

 

10.   "Antibodies as Thermolabile Switches: High Temperature Triggering for the Polymerase Chain Reaction". Bio/Technology.1994

 

11.   Forensic Science Handbook, vol. III (Regents/Prentice Hall, Englewood Cliffs, NJ, 1993).

 

12.   "Thermostable DNA Polymerases for a Wide Spectrum of Applications: Comparison of a Robust Hybrid TopoTaq to other enzymes". In Kieleczawa J. DNA Sequencing II: Optimizing Preparation and Cleanup. Jones and Bartlett. 2006

 

13.   Nielsen B, et al., Acute and adaptive responses in humans to exercise in a warm, humid environment, Eur J Physiol 1997

 

14.   Molnar GW, Survival of hypothermia by men immersed in the ocean. JAMA 1946

 

15.   Paton BC, Accidental hypothermia. Pharmacol Ther 1983

 

16.   Simpson K, Exposure to cold-starvation and neglect, in Simpson K (Ed): Modem Trends in Forensic Medicine. St Louis, MO, Mosby Co, 1953.

 

17.   Fitzgerald FT, Hypoglycemia and accidental hypothermia in an alcoholic population. West J Med 1980

 

18.   Stoner HB et al., Metabolic aspects of hypothermia in the elderly. Clin Sci 1980

 

19.   MacGregor DC et al., The effects of ether, ethanol, propanol and butanol on tolerance to deep hypothermia. Dis Chest 1966

 

20.   Cooper KE, Hunter AR, and Keatinge WR, Accidental hypothermia. Int Anesthesia Clin 1964

 

21.   Keatinge WR. The effects of subcutaneous fat and of previous exposure to cold on the body temperature, peripheral blood flow and metabolic rate of men in cold water. J Physiol 1960

 

22.   Sloan REG and Keatinge WR, Cooling rates of young people swimming in cold water. J Appl Physiol 1973

 

23.   Keatinge WR, Role of cold and immersion accidents. In Adam JM (Ed) Hypothermia – Ashore and Afloat. 1981, Chapter 4, Aberdeen Univ. Press, GB.

 

24.   Keatinge WR and Evans M, The respiratory and cardiovascular responses to immersion in cold and warm water. QJ Exp Physiol 1961

 

25.   Keatinge WR and Nadel JA, Immediate respiratory response to sudden cooling of the skin. J Appl Physiol 1965

 

26.   Golden F. St C. and Hurvey GR, The “After Drop” and death after rescue from immersion in cold water. In Adam JM (Ed). Hypothermia – Ashore and Afloat, Chapter 5, Aberdeen Univ. Press, GB 1981.

 

27.   Burton AC and Bazett HC, Study of average temperature of tissue, of exchange of heat and vasomotor responses in man by means of bath coloremeter. Am J Physiol 1936

 

28.   Adam JM, Cold Weather: Its characteristics, dangers and assessment, In Adam JM (Ed).Hypothermia – Ashore and Afloat, Aberdeen Univ. Press, GB1981.

 

29.   Modell JH and Davis JH, Electrolyte changes in human drowning victims.Anesthesiology 1969

 

30.   Bolte RG, et al., The use of extracorporeal rewarming in a child submerged for 66 minutes. JAMA 1988

 

31.   Ornato JP, The resuscitation of near-drowning victims. JAMA 1986

 

 

 

32.   Conn AW and Barker CA: Fresh water drowning and near-drowning — An update.1984;

 

33.   Reh H, On the early postmortem course of “washerwoman’s skin at the fingertips.” Z Rechtsmed 1984;

 

34.   Gonzales TA, Vance M, Helpern M, Legal Medicine and Toxicology. New York, Appleton-Century Co, 1937.

 

35.   Peabody AJ, Diatoms and drowning – A review, Med Sci Law 1980

 

36.   Foged N, Diatoms and drowning — Once more.Forens Sci Int 1983

 

37.   "Microscale chaotic advection enables robust convective DNA replication.". Analytical Chemistry. 2013

 

38.   Sourcebook in Forensic Serology, Immunology, and Biochemistry (U.S. Department of Justice, National Institute of Justice, Washington, D.C.,1983).

 

39.   C. A. Villee et al., Biology (Saunders College Publishing, Philadelphia, 2nd ed.,1989).

 

40.   Molecular Biology of the Gene (Benjamin/Cummings Publishing Company, Menlo Park, CA, 4th ed., 1987).

 

41.   Molecular Evolutionary Genetics (Plenum Press, New York,1985).

 

42.   Human Physiology. An Integrate. 2016

 

43.   Dumas JL and Walker N, Bilateral scapular fractures secondary to electrical shock. Arch. Orthopaed & Trauma Surg, 1992; 111(5)

 

44.   Stueland DT, et al., Bilateral humeral fractures from electrically induced muscular spasm. J. of Emerg. Med. 1989

 

45.   Shaheen MA and Sabet NA, Bilateral simultaneous fracture of the femoral neck following electrical shock. Injury. 1984

 

46.   Rajam KH, et al., Fracture of vertebral bodies caused by accidental electric shock. J. Indian Med Assoc. 1976

 

47.   Wright RK, Broisz HG, and Shuman M, The investigation of electrical injuries and deaths. Presented at the meeting of the American Academy of Forensic Science, Reno, NV, February 2000

48. Broor SL, Kumar A, Chari ST, et al. 1989. Corrosive oesophageal strictures following acid ingestion: clinical profile and results of endoscopic dilatation.

49. Baud FJ, Barriot P, TOGS V, et al. 199 1. Elevated blood cyanide concentrations in victims of smoke inhalation.

50. Blackwell M, Robbins A. 1979. Arsine (arsenic hydride) poisoning in the workplace.