Survival period after wounding
Mainly as a result of the pioneering work of Jyrki Raekallio in Finland, the histochemical sequence of events in wounds has been actively pursued in recent years. Some techniques need frozen sections, others can be carried out on fixed tissue. Estimations of histamine or serotonin are usually ‘tube’ methods, rather than microscopic, though some fluorescent techniques have been developed. Betz and his co-workers have also published extensively on the immunohistochemistry of wound dating.
At the present time these methods still remain mainly in the realm of the research laboratory, apart from a few enthusiasts who employ them in casework. For the histo- chemical novice, it would be unwise to put such procedures into evidence without first gaining extensive experience of control material. Experience emphasizes that strictly standard conditions are required for the production of such histochemical sections, the end result depends largely on laboratory procedures – ‘change your technician and you change the answer’.
A list of standard procedures for some of these reactions is given in Appendix 1.
The following are some of the histochemical wound changes described by Raekallio and others:
■ In a wound through the skin surface there is a central zone 0.2–0.5 mm wide that will become necrotic and in which enzyme activity rapidly decreases. This may be termed ‘negative vital reaction’. Immediately beyond this layer, is a 0.1–0.3 mm zone of reaction and eventual repair, where a number of enzymes and other substances become increased in concentration during the reparative process, compared to the normal level in the areas outside the wound. Enzymatically, this can be called ‘positive vital reaction’, as no such zone develops in a post-mortem wound.
■ Within one hour after injury, esterases and adenosine triphosphatase increase in the positive zone. At around 2 hours, aminopeptidase activities increase and, at 4 hours, acid phosphatase activity increases. Alkaline phosphatase activity is delayed another hour or so though, of course, all these times are relative and subject to the usual biological variability.
■ Where death occurs at some stage of this process, the enzyme pattern is ‘frozen’ at that point and post-mortem changes do not substantially alter the reactions within a few days after death, especially if autolysis is kept at bay by refrigeration. Senility, severe illness and cachexia, as well as widespread multiple injuries, may distort the usual pattern by reducing the ability to produce these reparative enzymes. In contused wounds, the reactions are less useful than in cutaneous injuries, as the damage is more diffuse and there are no definite ‘zones’.
In all wounds, lack of reaction cannot be taken as indisputable proof of a post-mortem origin, though, if the opposite occurs, positive increase in the outer zone must only be the result of a vital reaction. Other enzymes have been used for wound dating: the review by Janssen (1984) in his authoritative book on forensic histology should be consulted for details, as well as the work of Betz.
■ Tissue cathepsins are said to increase almost immediately if the stroma is damaged, being demonstrable within 5–10 minutes. Two other substances are of use in establishing that wounds are ante-mortem and giving some idea as to their age. Both are produced during the inflammatory response that accompanies tissue damage – histamine and serotonin (5-hydroxytryptamine). They tend to be complementary to the enzymes, as they appear soon after infliction, within the hour or so before adenosine triphosphatase and esterases become detectable.
These vasoactive amines appear in maximum concentration about 10 minutes (serotonin) and 20–30 minutes (histamine) after wounding. One of the first demonstrations of this forensic aid was by Fazekas and Varagos-Kis (1965), who showed that a ligature mark in hanging revealed increased serotonin; presumably the hanging was atypical and the victim took 10 minutes to die which is rather unusual. For the employment of the test in human autopsy work, about 2 grams of skin freed from subcutaneous fat are sampled, together with a similar control sample from a nearby normal area of skin from the same corpse. This is to allow for the markedly different amounts found in different people and, indeed, in the same persons at different times.
To establish that a wound was ante-mortem rather than inflicted after death, the level of histamine in the wound must be at least 50 per cent greater than the control sample – and, for serotonin at least, twice the concentration of the control skin.
SURVIVAL PERIOD AFTER
A person who has his brainstem destroyed by a penetrat- ing injury, or his aortic arch completely transected, will be inactive and clinically dead almost immediately. It would not necessarily be the case if his frontal lobes were damaged or his abdominal aorta was crushed by a railway wheel.
Extraordinary instances of survival in both these latter instances are on record.
An opinion should always err on the side of caution in expressing opinions on this subject, as victims can do far more than might be expected after injury. The author (BK) once dealt with a homicide in which the victim was stabbed through the heart, yet ran more than a quarter of mile before collapsing.
A wound in the left ventricle can partly seal itself by the con- traction of the muscle around the defect and collapse may only occur when sufficient blood has leaked into the pericardium to form a tamponade. Wounds of the right ventricle are often more rapidly fatal as, although the pressure of contained blood is less, the thinner wall is not so effective in preventing the leak.
Head injuries can present many paradoxical instances of prolonged survival, depending partly on what part of the brain is injured. As mentioned, frontal lobes seem remarkably resistant to damage and it is often the generalized head impact, rather than focal damage to this area, that causes most harm. For example, a Finnish man who committed suicide made a home movie of himself firing a pistol into his brain.
There was immediate collapse but, just at the end of the 4-minute film, the victim opened his eyes and raised his head, finally dying some uncertain time after the spool ran out.
In the more usual stabbing, head injury, cut throat or shooting, the pathologist must try to assess the nature and severity of the physical damage, and relate that to the age, health and environment of the victim. This is naturally an imprecise exercise. A senile old lady, or someone with severe cardiac or respiratory disease, is less likely to survive multiple injuries for as long as a robust young person – though if the nature of the injury is grossly life-threatening, these factors will make little difference.
A cut artery will lose blood faster than a vein of the same general size, especially if it is only partly severed so that it cannot retract. Other factors, such as the possibility of air embolism occurring in a cut jugular vein, might alter the usual pattern of expected events. The heart is less vulner- able than great thoracic vessels in many stab wounds, as mentioned above. Many wounds of the ventricles are sur- vivable. The author (BK) has twice been warned by police of an imminent autopsy on victims admitted for emer- gency surgery – only to hear later that, thankfully, they had walked out of the hospital after a successful operation. One had a through-and-through stab wound of the left ventricle that transfixed the heart from front to back.
Where a wound has transected a major coronary artery, then prolonged survival is unlikely, as is one that interrupts a
major branch of the conducting system. Other than injuries to the brain or to a large blood vessel, most other injuries can rarely be declared to have caused sudden death or rapid loss of function. In criminal cases, it may be a point of some impor- tance to decide whether the victim could have continued fighting, have run away, have resisted, or even have inflicted injuries on someone else before collapsing and dying. It is dif- ficult to swear that at least some activity was not possible in the great majority of instances. In the adrenaline response of
‘fight or flight’, the shock element of pain is greatly sup- pressed – many soldiers have been quite unaware of having sustained severe or lethal wounds until they notice the blood or the battle is over. Thus the usual ‘shock’ effect may be damped down considerably in an assault and only the sheer physical and haemodynamic sequelae of the injury will even- tually lead to a slowing down, then collapse and death. In the interval, injured victims may be able to perform normal physical activity, sometimes to an astonishing degree, albeit followed by sudden deflation of their capacity for exercise.
As in most aspects of forensic medicine, it is unwise of the doctor to be too definite about these matters – the old forensic aphorism ‘Seldom say never – seldom say always’ is even more true here than usual.
Most issues of this nature revolve around periods of a few minutes, the perimortal or agonal time when few morphological signs are available. The more sophisticated enzyme and serotonin techniques mentioned elsewhere in this chapter may give some clue about the survival period, but are rarely unequivocal enough to be used as hard forensic evidence. If survival is longer, then both gross and histolog- ical changes of ‘vital reaction’, such as thrombosis, inflam- mation, infection and healing may be useful, but they usually require hours or even days of survival to appear.
The accepted wisdom of wound dating is that polymorph leucocytes begin to appear in wounded tissue within a few minutes, but it has been shown that this can happen even several hours after death, as all leucocytes do not become immobile with cardiac arrest. A good, conventional inflam- matory response must be a vital reaction, however, though several hours survival is needed for it to be convincing. The author (BK) has seen a dramatic red flare caused by post- mortem burning at least 30 minutes after undoubted death from strangulation.
Another problem with differentiating ‘ante-mortem’ from
‘post-mortem’ injuries is the definition of the moment of death. Again, lawyers, judges and coroners tend to assume that death is an event, whereas, in reality, it is a process (Chapter 2). Though in most criminal or accidental deaths the moment of death is conventionally – and reasonably – taken to be the moment of cardiac arrest, and thus collapse of blood pressure and cerebral circulation, the cells of the body are still alive and remain so for a variable time – only minutes
in the case of neurones, but leucocytes and muscle cells sur- vive for many hours, and connective tissue cells, such as fibroblasts, for days. Thus, it is unreasonable to expect dra- matic changes within minutes in skin wounds, etc., until pro- gressive hypoxia alters biochemical processes and enzyme activity. Leucocytes may be motile for more than 12 hours and can aggregate around chemotactically active material, such as gastric contents aspirated into the air passages. This makes the ‘vital reaction’ a dubiously valid phenomenon in the perimortal period. Much more research is needed into the histology, histochemistry and biochemistry of the perimortal period to clarify these issues, but in the mean time, less dog- matic reliance must be held upon the old criteria of ‘ante-’
and ‘post-’ mortem phenomena and the ‘vital reaction’.
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