Under the Microscope: Fatal Hazardous Infactions and Poisonings

Many forensic situations involve drug abusers and persons with promiscuous sexual behaviour, where the statistical risk of HIV and hepatitis infection is markedly greater than in the general autopsy population. This poses a risk to pathologists, mortuary staff, police and laboratory staff who may deal with post-autopsy samples.

All autopsies should be carried out with total precautions against infective risks, so that it does not matter what case is handled. However, this is almost impossible to achieve in a busy coroner or medical examiner practice and does not solve the problem of possibly infected material being sent out to other laboratories. A more common regime is to carry out pre-autopsy testing for HIV and hepatitis, using blood from a femoral needle puncture. The result can often be returned within hours, when a decision may be made as how to handle the autopsy - or even whether to abandon it, if the risk-benefit aspect is high. More usually, a positive result will result in the autopsy being carried out with special care, additional protective clothing, visors, masks and metal gloves, with restriction of access to observers, choice of more senior technicians and warnings sent to laboratories liable to handle samples.

In this respect, hepatitis is more of a risk than HIV infection. However, so far, about 100 health-care workers have acquired HIV infection from definite occupational exposure and one pathologist is known to have become infected from autopsy work.  Also three morticians in the USA have possibly contracted occupation-related HIV positivity.

 

The time for which a corpse remains potentially contagious with HN is variable. Infectious virus has been recovered from liquid blood held at room temperature for 2 months and virus in high concentrations has been found to remain viable for 3 weeks found 51 per cent survival of virus in plasma and monocyte fractions from infected cadavers up to 21 hours post-mortem. Other series found survival in corpses from 18 hours to 11 days after death. Virus has been recovered from the spleen after 14 days post-mortem. Refrigeration seems to make little difference to viability. Cultured blood and effusions from refrigerated bodies and obtained viable virus up to 16 days post-mortem and concluded that there was no safe maximum time at which corpses ceased to be an infective risk. In industrialized countries, it has become standard to offer post-exposure prophylaxis after significant percutaneous exposure to blood or tissues of HTV patients.

Toxicology has a number of different aspects and, in such a huge subject, various specialists have different interests. The clinical toxicologist is most concerned with diagnosis and treatment of the living patient; the analytical toxicologist has the complex task of laboratory investigation; and the pathologist is concerned with evaluating poisons as a cause or a contribution to death. Though obviously linked, these various aspects are substantially different and few people can claim to be proficient in all three. As far as the pathologist is concerned, his main task is to exclude or con- firm other non-toxic factors in the death. He has then to collect suitable samples for analysis and, when the laboratory results are available, to interpret them in the light of his knowledge of the history, clinical features and autopsy appearances.

 

The pathologist inevitably needs the expertise of the laboratory analyst and the latter's knowledge of the therapeutic, toxic and fatal levels of the substances under consideration. Such data must, however, be evaluated in the knowledge of other pathological and physiological conditions present, so that it is the pathologist, rather than the laboratory toxicologist, who should provide the final opinion upon the proximate cause of death. This does not always happen and some laboratory report forms may be seen that unequivocally - and unwisely - state that a particular drug caused the death. Where, as so often happens, the toxic levels found at post-mortem are not in a potentially fatal or even toxic range, then the pathologist should seek the advice of a din- ical toxicologist to determine whether any of the symptoms or signs during life may assist in deciding on the cause of death. As so often happens in forensic problems, the investigation of a fatal poisoning must be a cooperative effort, especially between pathologist and laboratory analyst. Even in apparently obvious cases, such as a blood saturation of 50 per cent carboxyhaemoglobin, it is not for the analyst to declare a definite cause of death, as the victim may also have had a fractured skull - but equally, the pathologist has an obligation to provide the laboratory with the best possible samples in the best possible condition, as well as good information about the circumstances of the case.

 

Many persons, including some doctors, are under the firm misapprehension that, for most toxic substances, there are relatively constant quantities that will cause death. Not only the lay public, but lawyers, police, coroners and others assume that there is a more or less linear relationship between the amount of poison that enters the body, the resulting levels in blood and tissues and the degree of disability caused - the ultimate disability being death. In addition, it is often thought. that back-calculation from blood and tissue levels can arrive at a definite assessment of how much poison was originally administered. This aspect is of particular concern to coroners and similar officers, who have to decide on motive in potential suicides, where the magnitude of any overdose may assist in distinguishing between accident and self-administration.

The pathologist has his own difficulties in respect of 'the fatal dose', as quantitative results from the laboratory have to be matched against a knowledge of published blood and tissue levels' for that substance in relation to its potential toxicity. Though numerous tables of toxic levels have been published, there is considerable variation between the levels recorded. Reasons for this are explored later. It is obvious that there is no 'fatal dose' in the sense of a single threshold concentration above which a person dies and below which he survives. Instead, there is a range of levels, the upper and lower margins of which vary from one authority to another, which encompasses most deaths - but even here there are many exceptions, instances being recorded where survival occurs well above the upper limit and death occurs below the lower margin. In such cases, the task of the pathologist is to evaluate all other non-toxicological data to see if they can modify the circumstances sufficiently to allow an accept- able explanation for the death. It is sometimes difficult to explain these concepts of great biological variation to lawyers and police officers, who expect more definite decisions, and might even feel that the is being evasive or obstructive.

Over a large number of tests, it provides a toxic level at which half the animals will be expected to die. Though the indicative value in a general sense in comparing the toxicity of one substance against another, there is no way of knowing whether the human victim of poisoning lies at the upper or lower end of the classical bell-shaped curve that characterizes most biological responses. Far more useful is the cumulative record of actual laboratory results from toxicology centres that deal with human poisoning, which progressively build up a large database of blood and tissue levels, and correlate these with records of the clinical state, toxic effects and fatal outcome. Even here the variations are wide, as the many published tables testify, but at least general guidance can be obtained.

 

Acknowledgements:

www.politie.nl  Politiekorpschef  @Janny Knol©

www.aived.nl    AIVD – @Erik Akerboom ©

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

 https://www.police-nationale.interieur.gouv.fr/ @ Stephane Folcher ©

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.

  

Komentarze

Popularne posty z tego bloga

Sitting Bull

Under The Microscope: CRASH &'CRUMPLE'