Hundreds of deaths occur each year from atmos- pheric lightning, especially in tropical countries.
A lightning strike from cloud to earth may involve property, animals or humans. Huge electrical forces are involved, producing millions of amperes and phenomenal voltages. Some of the lesions caused to those who are struck directly or simply caught close to the lightning strike are electrical, but other will be from burns and yet others result from the
‘explosive effects’ of a compression wave of heated air leading to ‘burst eardrums’, pulmonary blast in- jury and muscle necrosis/myoglobinuria. All kinds of bizarre appearances may be found, especially the partial or complete stripping of clothing from the victim, which may arouse suspicions of foul play.
Severe burns, fractures and gross lacerations can occur, along with the well-known magnetization or even fusion of metallic objects in the clothing. The usual textbook description is of ‘fern or branch-like’
patterns on the skin – the so-called Lichtenberg
Figure 17.19 Multiple electrical marks/burns on the hand, associated with scorching and blistering.
Figure 17.20 Multiple burns from high-voltage (multi-kilovolt) electrical supply lines. The ‘crocodile skin’ is caused by arcing of the current over a considerable distance.
(a)
(b)
240 V Metal
Spark
240 V
Fused nodule of keratin
Pale areola Pale zone Collapsed blister
with raised edge and pale
areola
Figure 17.18 Electrical mark on the skin: collapsed blister formation following fi rm contact (a) and a ‘spark burn’ across an air gap.
17 Heat, cold and ele ctrical tr auma
figure (Figure 17.21) – but others claim that such marks are not seen. Red streaks following skin creases or sweat-damped tracks are more likely, although many bodies are completely unmarked.
■ Further information sources
Arturson MG. The pathophysiology of severe thermal injury. Journal of Burn Care and Rehabilitation 1985; 6:
129–46.
Ayoub C, Pfeifer D. Burns as a manifestation of child abuse and neglect. American Journal of Diseases in Children 1979; 133: 910–14.
Busche MN, Gohritz A, Seifert S et al. Trauma mechanisms, patterns of injury, and outcomes in a retrospective study of 71 burns from civil gas explosions. Journal of Trauma 2010; 69: 928–33.
Celik A, Ergün O, Ozok G. Pediatric electrical injuries: a review of 38 consecutive patients. Journal of Pediatric Surgery 2004; 39: 1233–7.
Cherrington M, Olson S, Yarnell PR. Lightning and Lichtenberg fi gures. Injury 2003; 34: 367–71.
D’Souza AL, Nelson NG, McKenzie LB Pediatric burn injuries treated in US emergency departments between 1990 and 2006. Pediatrics 2009; 124: 1424–30.
Hussmann J, Kucan JO, Russell RC, Bradley T, Zamboni WA.
Electrical injuries – morbidity, outcome and treatment rationale. Burns 1995; 21: 530–5.
Kauvar DS, Wolf SE, Wade CE, Cancio LC, Renz EM, Holcomb JB Burns sustained in combat explosions in Operations Iraqi and Enduring Freedom (OIF/OEF explosion burns). Burns 2006; 32: 853–7.
Lund CC, Browder NC. The estimation of areas of burns.
Surgery, Gynaecology, Obstetrics 1944; 79: 352–358.
Madea B, Tsokos M, Preuβ J. Death due to hypothermia, Chapter 1. In: Tsokos M (ed.) Forensic Pathology Reviews, Volume 5. Totowa, NJ: Humana Press, 2008; p. 3–21.
Maquire S, Moynihan S, Mann M et al. A systematic review of the features that indicate intentional scalds in children.
Burns 2008; 34: 1072–81.
McCance KL, Huether SE. Pathophysiology. The Biologic Basis For Disease in Adults and Children, 6th edn.
St Louis, MO: Mosby Inc., 2009.
Moritz AR, Henriques FC. Studies of thermal injury II. The relative importance of time and surface temperature in the causation of cutaneous burns. American Journal of Pathology 1947; 23: 695–720.
Nixdorf-Miller A, Hunsaker DM, Hunsaker JC 3rd.
Hypothermia and hyperthermia medico-legal investigation of morbidity and mortality from exposure to environmental temperature extremes. Archives of Pathology and Laboratory Medicine 2006; 130: 1297–304.
Roeder RA, Schulman CI. An overview of war- related thermal injuries. Journal of Craniofacial Surgery 2010;
21: 971–5.
Rothschild MA. Lethal hypothermia. Paradoxical undressing and hide-and-die syndrome can produce very obscure death scenes, Chapter 11. In: Tsokos M (ed.) Forensic Pathology Reviews, Volume 1. Totowa, NJ: Humana Press, 2004; p. 263–72.
Ryan CM, Schoenfeld DA, Thorpe WP et al. Objective estimates of probability of death from burn injuries.
New England Journal of Medicine 1998; 338: 362–6.
Selvaggi G, Monstrey S, Van Landuyt K, Hamdi M, Blondeel P. Rehabilitation of burn injured patients following lightning and electrical trauma. NeuroRehabilitation 2005; 20:
35–42.
Shkrum MJ, Ramsay DA. Forensic Pathology of Trauma:
Common Problems for the Pathologist. Totowa, NJ:
Humana Press, 2007.
Suominen PK, Vallila NH, Hartikainen LM, Sairanen HI, Korpela RE. Outcome of drowned hypothermic children with cardiac arrest treated with cardiopulmonary bypass.
Acta Anaesthesiologica Scandinavica 2010; 54: 1276–81.
Vege A. Extremes of temperature. In: Payne-James JJ, Corey T, Henderson C, Byard R (eds). Encyclopedia of Forensic and Legal Medicine, Volume 2 Oxford: Elsevier Academic Press, 2005; pp. 300–3.
Wick R, Gilbert JD, Simpson E, Byard RW. Fatal electrocution in adults – a 30-year study. Medicine, Science, and the Law 2006; 46: 166–72.
Figure 17.21 The ‘Lichtenberg fi gure’ and lightening fatalities.
Note the fern-like branching pattern of skin discoloration on the chest.
Chapter
■ Introduction
Drugs and alcohol influence lives in many ways.
The heroin- and crack-dependent addict arrested for robbery, the recreational cocaine user sus- pended following drug screening at work, the stu- dent arrested for driving under the influence of drugs and alcohol, and the chronic alcoholic dying in police custody because of unrecognized alcohol withdrawal are all examples of how drug abuse can have huge impacts on individuals. However, this impact may well be low compared with the number of cancer patients dying in pain because they have been treated with inadequate doses of pain reliev- ers as a result of their physicians fearing legal pro- ceedings against them. Doctors treating patients dying of severe pain risk being accused of illegal prescribing or, even more tragically, being charged with euthanasia because post-mortem drug testing demonstrates blood concentrations said to exceed the ‘therapeutic range’ (although what a therapeutic range in a cadaver might constitute is hard to say).
One of the key tasks faced by forensic practition- ers is to determine the role that a specific drug (or drugs) plays in instances of impairment and death.
This task is made complicated by a series of issues, many of which arise simply because physicians,
toxicologists and lawmakers fail to understand the basic issues of forensic science, and the way these issues may interplay in complex legal, clinical and pathological matters. As a consequence, the inter- pretation of forensic evidence is often based more on anecdote and intuition than controlled scientific studies. Inadequate or bad science, or the misinter- pretation of established sciences can lead to wrong legal decisions. Faulty and unjust conclusion can only be avoided if the limitations of the science are understood.
Stories of exotic poisonings give rise to plots that fascinate television viewers but which, more often than not, can pose vexing problems for foren- sic scientists. Fortunately, they are uncommon.
Detailed knowledge of exotic poisons is a skill not much in demand today. What is required is the ability to recognize (and manage) the common complications of commonly abused drugs, such as stimulants, opiates, cannabinoids, hallucinogens, solvents, some anaesthetics and some prescrip- tion medications. With each edition of this book the molecular mechanisms of addiction and drug abuse have become clearer. At the same time, our ability to measure drug concentrations in any tissue has become ever more precise. The problem is to determine what those measurements signify.
■ Introduction
■ Principles
■ Definitions
■ Testing matrices
■ Interpretation
■ Further information sources
Principles of toxicology
18
1 8 Principle s of toxicolo gy
■ Principles
The term ‘toxic’ can be applied in different ways.
Some use the term synonymously with ‘poisonous’, meaning to imply that ingestion of a particular sub- stance will cause death. Others mean only to imply that some sort of illness will result if the substance is ingested. The definition of ‘lethal dose’ is more precise, but now that the molecular mechanisms of many poisons are known, the relevance of this concept is not as important as it once was. Drug sensitivity and resistance vary from individual to individual (if for no reason other than their size).
Thus ‘lethal dose’ is said to represent the dose of that drug at which all subjects given the drug will die, and that dosage will be expressed in grams, micrograms or milligrams per kilogram.
The abbreviation LD50 specifies the dose at which 50% of those who take a particular dose will die. The LD50 depends partly on the mode of drug administration, because the route of ingestion determines exactly how much drug is ultimately absorbed into the system. Put another way, the route of ingestion determines bioavailability. A drug injected intravenously is 100% bioavailable because the entire dose of drug enters the circulation. The amount absorbed after oral ingestion is variable. A 10 mg dose of morphine given intravenously would be expected to result in a peak plasma concentration of between 100 and 200 nanograms per mililitre. But if that same amount were given by mouth the peak plasma concentration would be only a fraction of that seen after intravenous injection. Because of anatomic and metabolic differences, the LD50 for any particular drug varies from experimental animal to experimental animal, and in no case can results obtained from the study of experimental animals be directly extrapolated to humans. The process of extrapolation from animals to humans is so unreliable that courts in many different countries have held that animal studies alone do not suffice to prove causation in humans.
The issue of receptor physiology is extremely important. Drugs exert their effects by binding with receptors. How well a particular drug will bind to a receptor determines how effectively it will act (or how toxic it will be). It does not help much to know that opiates bind to the mu (μ) receptor.
What matters is how effectively any particular opiate binds to the receptor, and receptor-binding ability is altered by many factors. On a weight for
weight basis, oxycodone is many times more pow- erful than morphine, simply because it is a better fit for the binding site on the μ receptor than is morphine. Receptors are subject to mutation. More than 140 different mutations have been identified within the μ receptor itself. Mutations cause recep- tors to change shape. Structural distortions of the receptor make some drugs fit better while others fit worse. The actual result cannot be predicted with- out knowledge of the mutation and the structure of the receptor, but this knowledge is never avail- able to Coroners or forensic toxicologists as they have neither the facilities nor the budget to study receptor or enzyme genetic composition. How may this be important in clinical practice? An example could be the patient who asks for a ‘stronger’ pain medication not because he or she is a drug seeker, but because they carry a mutation that prevents the current pain reliever from binding normally to the μ receptor.