Under The Microscope: Hallucinogenic Drugs
Drugs of dependence may be absorbed
orally, by intravenous, subcutaneous or - rarely intramuscular injection, by smoking, or
by nasal sniffing. The routine at autopsy, in respect of obtaining samples for
toxicological analysis, is altered according to the route of administration. As
mixing of drugs and addition of non-narcotic drugs is common, itis the usual
practice to take a wide range of samples even if the primary route is known
with some degree of certainty For example, an addict dying 'on the needle'
where intravenous injection is obvious, will still have stomach contents taken for
investigation. The standard samples should be taken, as described in a previous
chapter, comprising several samples of venous blood (one with fluoride),
stomach and contents, liver and urine. In some circumstances, additional
samples such as bile, cerebrospinal fluid and vitreous humour may be taken, as
well as brain or kidney. The great advances in the analytical techniques allow
the analysis of drugs also in other biological samples, such as saliva, sweat
and hair. Hair analysis can also provide evidence of
long-term exposure to drugs (weeks, months or years), because most drugs, if
not all, incorporate in hair and are relatively stable. At least 50 mg of hair
should be collected, cutting about a pencil thickness of strands of hair as
close to the skin as possible from the back of the head, dried and stored in a
sealed plastic bag or tube at room temperature. When the drug has been
injected, then an ellipse of skin around the injection mark, extending down
through the subcutaneous tissue to the muscle,
should be excised, along with a control area of skin from another non-injected
site. These should be refrigerated, not fixed in formalin, until delivery to the
laboratory can be arranged. Full histology should always be taken, especially
if drugs have been injected, as foreign substances may be discovered as embolic
particles, especially in the lungs. Pulmonary granulomata are well-known histological features of 'mainlining' addicts taking
impure drugs intravenously, as the lung capillaries filter out coarse particulate matter used to dilute the active narcotic.
Talc is particularly prone to form granulomata,
sometimes with foreign body giant cells. Under polarized light, doubly refractile
particles may be seen in the centre of the reactive nodules. Sometimes, strands
of cotton may form foreign bodies, derived from the cloth strainer used to
filter particles crudely from the drug solution before injection.
Morphine is the major representative
of the general group of opioids, which comprise natural opium and a whole
series of chemically related derivatives. They may be taken orally or injected
and several, such as crude opium and heroin - may be absorbed by inhaling
smoke. Morphine itself is poorly absorbed from the gastrointestinal tract;
heroin can be taken via the nasal mucosa.
The group consists of opium,
morphine, heroin (diacetyl morphine), codeine (dimethyl morphine), dihydrocodeine (DF 1 18), etorphine (Immobilon),
methadone, papaverine, pethidine, dipipanone, dextrornoramide, dextropropoxyphene, pentazocine, cyclazocine,
diphenoxylate,buprenorphine, tramadol, fentanyl and many more.
The autopsy findings in deaths from
all these drugs are relatively non-specific. Toxicological analysis and expert interpretation of the results are necessary for the
proper elucidation of the deaths, but certain features can be useful pointers.
The first is the presence of injection marks. When fresh, they look just like
any other needle mark commonly seen from therapeutic or diagnostic procedures.
They are commonly on the arms, either in the classical position in the antecubital
fossa on the front of the elbow, or into one of the prominent veins of the
forearms or dorsum of the hand. The left side is favourite as most people are
right-handed, but in habitual users, sclerosis of the veins may lead to the
arms being used randomly. The veins of the dorsum of the foot may be used when
the hands and arms have become unusable because of thrombosis and scarring.
Less common sites are in the thighs but here, as with the abdominal wall, the
injections may be subcutaneous, rather than intravenous. This mode of injection
is known as 'skin-popping' and can lead to areas of subcutaneous sclerosis, fat
necrosis, abscesses and, if the injections are deeper
into the muscle, to chronic myositis.
Other external signs may be tattoos,
often bizarre and connected with the drug subculture. One
specific type is tattooing, often of
numerals, such as '13', on the buccal (inner) surface of the lower lip. Where
chronic addiction has taken its toll, the body may be emaciated, dirty and show
signs of infection, especially in the form of skin
ulceration. Rarely, there may be necrosis or even loss of phalanges from
thrombotic or septic emboli. Old injection marks, sometimes with associated bruising,
may be found, the bruising undergoing the usual spectrum of colour changes if
not recent. The veins may show overlying fibrosis where phlebitis has occurred,
or old venous thrombosis with firm cord-like vessels under the skin.
Where sudden death has occurred in
habituated addicts, there may be gross pulmonary oedema, with a plume of froth
exuding from the mouth or nostrils, suggestive of drowning. This pulmonary
oedema is sometimes a striking feature of rapid death in those who are
habituated to opioid drugs, especially heroin. It does not seem to occur in
novices to the habit, who tend to die in a different way, from a sudden primary
cardiac arrest. The oedema may be blood tinged, again causing confusion with drowning.
As with all deaths from toxic
substances, the interpretation of laboratory analytical results may present
considerable difficulties. There may be a long delay
between the administration of the drug
and death, during which time the blood, urine and even tissue levels may
decline, or even disappear. Many drugs break down rapidly in the body and their
metabolites may be the only recognizable products of their administration. In
some cases, data on lethal blood levels may be imperfectly known and great
variations in personal susceptibility may make the range of concentrations
found in a series of deaths so wide as to be rather unhelpful. As mentioned
above, some persons die rapidly after the first episode of taking a 'normal'
dose of a drug because of some ill-understood personal idiosyncrasy and here
quantitative analysis may not assist. Where habituation and tolerance has
developed, drug users may have concentrations in their body fluids and tissues far
higher than lethal levels published for non-habitues. In general, the great
usefulness of toxicological analysis is both qualitative and quantitative. The
former will show what drugs have been taken in the recent past; the length of
time that drugs or their metabolites - persist in different fluids and tissues
varies widely.
The quantitative analysis can be
useful, especially when the results reveal high levels - into the toxic or
lethal ranges. These ranges are usually obtained anecdotally from surveys of
large numbers of deaths but, as stated, can differ in terms of - minimum and
maximum values from different laboratories. The problems of idiosyncratic
sensitivity and tolerance cause such published ranges to act only as a general
yardstick and deaths that occur outside the ranges (usually off the lower end)
cannot be excluded from having been caused by the drug in question if other
factors may have been involved.
Such factors include the presence of
other drugs or alcohol, or both, delayed death and abnormal sensitivity. Thus
the analysis is not the final arbiter of the cause of death, although it is a
highly important component of the whole range of investigation. The pathologist
has the duty to correlate and interpret all known facts. He must fit the circumstances,
the presence of natural disease, trauma and other toxic substances with the
laboratory findings, to arrive at the most reasonable cause of death. The
advice of the toxicology laboratory is vital in this process, especially in
relation to known lethal ranges and the significance of metabolites, but the
analysts should not become the sole arbiter of the cause of death.
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
Komentarze
Prześlij komentarz