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A state of Injustice - Dr Robert N Moles
Chapter Four - Medical Matters

A state of Injustice: table of contents

Also by Dr Moles - Losing Their Grip - The Case of Henry Keogh - Definition and Rule in Legal Theory

The medical issues involved in the cases discussed in this book can be complex. So that a better understanding and assessment of these cases can be made, this chapter explains some general medical principles and also describes some of the procedures in detail.

The circulatory system

The blood together with the heart and its system of blood vessels, the arteries and veins, is the transportation system of the body. It brings nutrients absorbed through the stomach, and oxygen absorbed through the lungs, to all the tissues and cells of the body. It transports the waste products away, with the kidneys acting as the waste filtration system. The blood is pumped out of the heart through the arteries and eventually into small, thin-walled capillaries. It then returns to the heart by way of the veins.

The average adult human body has about 5 litres of blood. About half the blood volume is made up of a straw-coloured liquid called plasma. The remaining half of the blood is made up blood cells which are of two main types -- red cells and white cells.

The red cells are in the vast majority. They contain haemoglobin, an iron-containing substance which gives blood its red colour, and which binds oxygen to transport it around the body.

The white cells include cells such as neutrophils which scavenge for bacteria and dead tissue. For example, where blood escapes from a blood vessel which has been damaged (as in bruising), it is the neutrophils which come along to pick up the blood which has escaped into the surrounding tissues. The white cells also include the B cells which produce antibodies in the presence of foreign substances such as bacteria and viruses. It is the white cells that contain the DNA used for typing for identification.

Blood samples tell the pathologist much about the condition of the person before and after death. The presence of alcohol, drugs or poisons can be seen from toxicological analysis of the samples. Blood spattering provides information about the location and movements of a person during an attack. The way in which the blood settles in the body (lividity) tells about the timing and circumstances of death.

It is important to appreciate that bleeding does not require a person to be alive, nor does it require the heart to be beating. It simply requires there to be fluid blood in the vessels. If those vessels are torn or damaged, then the fluid blood within them will escape, and this is what is called bleeding.

Bleeding to death

The aorta is the main artery leading from the heart. It comes from the top of the heart, like a large hose, then arches over, rather  like an inverted U-bend and goes down through the centre of the body. The bend is called the aortic arch and it is anchored quite firmly to the surrounding tissues and bones. Although the membrane surrounding the heart (the pericardium) is also firmly anchored, the heart itself is not so firmly anchored, and it hangs off the end of the aorta. If someone receives a violent blow to the chest, especially with a slightly downward momentum, the heart can be pushed downwards within the chest. With the heart moving down and the aorta firmly anchored, the aorta will tear near the top of the arch.

This type of injury is commonly found in car accidents where the driver’s chest hits the steering wheel. Such an injury could also be caused by someone stamping on the chest of another person lying on the ground. This topic is usually covered in the forensic pathology books under sections headed ‘Blunt trauma injuries of the trunk’ or ‘Blunt force injuries of the chest’.

If the aorta is ruptured in this way, the heart will pump blood into the tissues or the body cavities until it stops beating. Death would occur rapidly. However, this does not mean that there could be no external bleeding. This would depend on the nature of any cuts or damage to the tissues. Even when the heart stops beating, bleeding will result from any wounds which cut across blood vessels, organs, tissues or cavities which still contain fluid blood. If an autopsy is done before the blood has become fixed, there will be bleeding each time the pathologist makes a cut into the tissues. Indeed, as discussed in the chapter on autopsies, it is an important issue for the pathologist to distinguish post-mortem bleeding (artifactual bleeding caused by the process of the autopsy) from bleeding that has occurred before death.

It is not hard to see that it is possible for a pathologist to accidentally create signs of murder while in the process of looking for them.

Drowning

While the idea that someone has drowned is familiar to everyone, the term itself can give rise to confusion. This is because ‘drowning’ explains the circumstances in which death occurs; it does not, however, explain the particular biological mechanism which has caused the death. Drowning may mean that water has filled the airways and the lungs, causing the person to suffocate. Or it might mean that the person has fallen into water, and the shock has killed them before water has entered the lungs. Someone might die because the sudden immersion in water caused them to have a heart attack. If the heart muscle stops working, or the coronary artery narrows then the blood supply to the brain, and the oxygen which is contains, ceases. This is like a mechanical failure and can cause loss of consciousness and death if the supply is not restored within a few minutes. After just a few minutes, brain damage is likely to result even if the person were to be revived. Sudden immersion can also cause the brain to stop working in another way which is more like an electrical failure. Shock or fear can affect the nervous system directly and produce vagal inhibition. This is where the nervous system stops sending the electrical signals that keep the heart and lungs working. In each of these circumstances (mechanical or electrical failure) the originating cause of the death is different, but it would be quite accurate to say in each of them that the person had drowned.

To know the cause or mechanism of death, as opposed to the circumstances giving rise to it, it is necessary to understand the body’s functioning systems and to determine the order in which they closed down.

Breathing and oxygen absorption

Human beings need to absorb oxygen continually to keep their system ticking over. They breathe in through the nose and mouth, filling the lungs with air to supply the blood and other tissues and cells with oxygen. To breathe, the diaphragm and chest muscles cause the lungs to expand and take in air. The air travels along the bronchial tubes to the alveoli, which are rather like the little branches on broccoli. The alveoli contain irregular chambers which make for a large surface area. The very thin membranes of the alveoli allow the oxygen from the air to be absorbed by the blood. The oxygen is taken into the red blood cells where it binds to the haemoglobin, and is circulated throughout the body. Likewise, the carbon dioxide that is produced by the body is sent back via a similar process to be discharged into the lungs, and then expelled from the body when we breathe out.

When this process is interrupted for any period of time, death occurs. Some cells of the body are especially sensitive to a reduction or loss of oxygen, particularly the cells of the brain and the heart. Loss of oxygen to the brain can cause permanent loss of function. Loss of oxygen to the heart can affect the muscles and produce an irregular heartbeat (arrhythmia).

Asphyxiation

In a drowning caused by asphyxiation (suffocation), the water fills the airways and obstructs the intake of air, thereby halting the oxygen absorption cycle and causing death. The crucial factor here is the blockage that prevents the intake of oxygen. What actually causes the blockage is not so important. Therefore, there will be similarities in asphyxiation cases where a pillow is placed over someone’s face, where a person has been buried alive, or where a person is immersed in any fluid or fine grains or powders. If someone falls into a silo containing grain or flour and sinks because their bodyweight takes them under the surface, they would drown just as surely as if they had fallen into water.

When a person submerged in water loses consciousness, the air in their lungs and stomach is replaced with water. As the water enters the confined spaces of the lungs, it forces the air out of them and back up through the throat and mouth. This is what is happening when we see bubbles appearing after a person has been submerged for a short time.

Drowning is sometimes classified as wet or dry drowning, although some pathologists do not like to use these expressions. Wet drowning means that the water has been taken into the system while the person has been alive, and the water in the lungs and stomach has been carried into the bloodstream. Dry drowning is where the water has not reached the lungs whilst alive. This may happen when a spasm of the larynx, for example, blocks the passage of air (and hence water) into the lungs while the person is alive.

Water absorption

If the lungs of a dead person appear to be ‘waterlogged’, a number of possibilities need to be considered.

Of immediate importance to an investigation is to determine whether the person has aspired (taken in) water as part of the process of drowning, the water seeped into the body after death has taken place, or whether the fluid in the lungs is in fact, oedema. Oedema occurs when the clear fluid (plasma) of the blood which can separate from the blood under certain conditions and which cannot, for various reasons, be returned to the veins and arteries. The excess fluid becomes dispersed in the tissues, causing swelling or weals like blisters. Oedema can affect all organs, causing swelling in the lungs and brain as well as the skin, where it looks like a weal, a blister or generalised swelling. After death, the whole body may become swollen by this leaked vascular fluid, especially the face and neck. The walls of the lungs are very thin and where additional fluid builds up in the tissues, it will pass through the thin lung membranes and drain into the lung. When oedema of the lungs occurs from heart failure, the lungs can have the same weight and appearance as if they were waterlogged from drowning.

Where drowning is thought to be a factor in a death, it is particularly important to retain the integrity of the organs at autopsy. All organs should be removed and weighed, especially the lungs. There are standard weights for people of different sizes and types. If the organs are heavy, tests should be conducted to determine if the cause is through water or oedema, and to exclude all other possibilities.

Haemolysis

If fresh water enters the lungs while someone is alive and the heart is still pumping, the intake of water into the blood vessels can be rapid. When this happens, the total number of red cells in the blood remains the same but the volume of liquid becomes much greater, which reduces the blood’s oxygen carrying capacity. The dilution of the blood changes its chemical balance, causing the red blood cells to swell and burst. This is called haemolysis. When the red cells burst, the haemoglobin is released and becomes ineffective. This further diminishes the capacity of the blood to carry oxygen at a time when the heart requires more oxygen, not less, because of the much greater demand put on it to circulate the extra fluid taken into the blood. The net result is likely to be heart failure.

The released haemoglobin can stain the linings of some of the blood vessels, particularly the aortic artery, which is the largest vessel extending from the top of the heart. However, caution must be exercised before making a diagnosis of heart failure due to drowning based on such staining. This is because some medications and other medical conditions can also cause haemolysis and produce this staining, and may well be a cause of death. Samples must be taken of the fluid the person is said to have drowned in, so as to assist in determining the likelihood of haemolysis. Salt (sea) water, for example, may have a different effect to fresh water. Domestic bath water may include bath salts (which include sodium chloride), oils and soaps, which if ingested could also effect the chemical balance of the blood.

In a suspected drowning where signs of oedema are present, it would be important to check for any physical obstruction of the airways, because if this was found it might mean that the person had choked to death and not drowned. Such obstructions could be caused by swallowing something which has blocked the airway or could be inhaled vomited material, or could be an allergic reaction which narrowed the airways. Removing and examining the airways and lungs should be done carefully and, if vomited material and / or some other blockage is present in the airways, then it is important to determine whether the physical blockage or the water blockage occurred first. Photographs are essential during and after the removal of the organs.

Frothing

Frothing of the mouth, is caused by fluid mixing with the mucous fluids, and is a common sign of drowning.  It is not always present in drowning deaths, and it can also occur in natural deaths. The frothing may be white or pink. The latter is from the leakage of the red blood cells into the space surrounding the lung. Normally the alveoli are open, however salt water destroys the surface tension of the lining of the lungs, causing the alveoli to collapse, and the surface fluid of the alveoli to become part of the fluid in the lungs. Rather like soap, this substance causes frothing within that fluid. Damage to the alveoli may be difficult to identify as it may not always be possible to see the frothing microscopically. This is because the process of preparing the tissue sections on the microscope slides dehydrates the sample. This same consideration can apply where there may be foreign matter (such as smoke particles or dirt) in the water within the space around the lungs. The slide preparation process is like washing, and material in the tissue sample such as vomit, smoke or dirt may be removed during that process and not show up on subsequent examination of the slides.

The diatom test

Diatoms are microscopic, unicellular algae found in all sources of fresh and salt water. They have a silica body that is hard, acid-resistant and can be seen using a microscope. Different species of diatoms have different shapes and structures and these are used to determine the species. The species (or combination of species) help identify the geographical location of the water source in a drowning death.

To detect diatoms, a section of body tissue is treated with strong acid. Because diatoms are acid resistant, they will remain after the tissue is broken down and can be put onto slides and viewed with a microscope. The number and shapes of diatoms found can be compared with diatoms from a sample of water taken at the scene. This sample should be taken as close as possible to the time at which the drowning is said to have occurred.

Diatoms can enter the bloodstream of a drowning person if the lungs fill with so much water that the alveoli break. This allows the water (and any diatoms contained in it) into the bloodstream. The presence of diatoms in lung tissue alone cannot discriminate between drowning and immersion in the water after death. Diatoms can also be present in the air and enter the lungs by being inhaled. Thus, to show conclusively that water has been taken into the system whilst the person was alive and while the heart was still beating, rather than just passively draining into the lungs after the person died some other way, it is necessary to test organs other than the lungs for the presence of diatoms. This means that tests should be conducted on organs such as the kidneys and the bone marrow. Finding diatoms in enclosed tissue such as bone-marrow indicates that the drowning caused the death. The test, however, is often of limited usefulness because of the low numbers of diatoms in some waters and the very small number of diatoms recovered from the body. It is critical that control samples be processed to check for contamination which could be caused, for example, from diatoms in the reagents and the water used in the laboratory. [1] To be meaningful, the species of diatoms found in the body tissue must also be found at the site of the drowning. If there is no site sample, a diatom test on the tissues alone would not be likely to provide any useful information. [2]

Death by drowning

How long does it take for a drowning person to die? Experience shows that it varies from immediately to much longer and may well depend on the definition of death. For someone to be pronounced dead, it usually will be reported that the eyes are fixed and the pupils dilated, and that there is no respiration or pulse. When blood is not circulating, brain damage occurs fairly quickly through lack of oxygen. If this situation continues for any period of time, the brain is irreparably damaged. The heart can continue to pump after breathing has ceased, but the blood will not be conveying oxygen. When the lungs fill with water there is (in effect) complete asphyxiation. Although the heart can beat, if the airway can’t be cleared, death is inevitable. If the airway is blocked, attempts can be made to remove the blockage by either sucking it out or dislodging it. If this can’t be done, the airway can be pierced below the blockage to get air into the lungs. A hollow tube (tracheotomy tube) or needle is inserted through an incision below the blockage. In emergencies it has been done by inserting the plastic tube of a ballpoint pen.

Electrocardiograms record the electrical activity associated with the heartbeat. Where there is no beat, the heart is said to be asystolic or straightline (as it shows on a monitor). Where there is an irregular beat, the heart is said to be suffering from arrhythmia, and in extreme cases it will be in a state of fibrillation. Fibrillation is where the heart muscle is twitching, but not moving enough to pump blood. It may be possible to get the heart muscle beating properly again by using a defibrillator to apply an electrical shock across the chest. It is often thought that the defibrillator is used when the heart has stopped beating. It is in fact only possible to get the heart beating again where it is fibrillating. Another way of doing this is to use manual cardio-pulmonary resuscitation (CPR) to keep the heart and airflow going.

Diagnosis of drowning

In some instances the autopsy findings on a person who has died by drowning may be no different to those found in other forms of death by asphyxiation. When death has been rapid, and the deceased immersed only for a short time, there may be few, if any, external signs of drowning. [3] When positive evidence of drowning (say from an eye-witness) is lacking a ‘diagnosis by exclusion’ is all that can be made. This means that when all other reasonable causes have been excluded, and macroscopic, microscopic and toxicologic examinations have revealed nothing, then the pathologist might attribute the death to something which reasonably could be inferred without there being specific physical signs of it.

Allergies

An allergy is an inappropriate or excessive immune response to antigens. [4] An antigen is a substance that stimulates the production of antibodies when it enters the body. It is the role of the antibodies to bind to the antigens to remove them from the system, hopefully before they cause any harm. Antigens which trigger allergic reactions are called allergens. Common allergens include pollen (particularly ryegrass pollen in the Adelaide area), house dust-mites, penicillin, insect stings, yeasts and moulds, and foods such as shellfish and eggs.

Allergens and hypersensitivity

People who suffer from an allergy are said to be hypersensitive to the particular allergen. Hypersensitivity begins with the process of sensitisation, which is the initial exposure to an allergen that leads to the production of antibodies, specifically, large antibodies called IgE (immunoglobulin E). The IgE antibodies are made in the B cells, a type of white blood cell. People who make a lot of IgE antibodies tend to have allergic reactions more than those who do not. The tendency to produce IgE antibodies in response to specific allergens may be genetically determined.

Mast cells and histamine

There is a time lag between initial contact with an allergen and the production of antibodies. Because of this, it might be that the first exposure to the allergen does not produce any observable symptoms of the reaction that is beginning to take place. The IgE antibodies produced from this first contact become attached to the cell membranes of what are called mast cells, millions of which are in the tissues lining the surfaces of the body in the skin, ears, lips, eyes, nose, mouth, lungs and intestines. Once the IgE antibodies are bound to the mast cells the system is prepared for the next exposure to the same allergen. When the next exposure happens, the antibodies already bound to the mast cells will bind the allergen immediately, which stimulates the mast cells to release histamine and other chemicals that they contain into the surrounding tissues. These chemicals attract scavenger cells to the area which then release their own chemicals, extending and exaggerating the responses initiated by the mast cells. This is called an allergic reaction.

A rapid and massive inflammation of the affected tissues may result. The severity of the reaction depends on the individual’s sensitivity and the bodily location involved. If allergen exposure occurs in the skin, the responses may be restricted to that area. It often appears as localised redness and / or swelling and involves itching or hives (urticaria). An allergic reaction in the nose causes a runny nose (rhinitis) and sneezing. When this is combined with irritation of the eyes (conjunctivitis) it is called hay fever.

Anaphylactic shock

If, however, an allergen enters the bloodstream, as with a bee-sting for instance, it can rapidly come into contact with the mast cells throughout the entire body and the response could be a systemic (whole body) reaction. This is known as anaphylactic shock. It can be swift and lethal. In anaphylactic shock the mast cells throughout the body release histamine into the blood vessels. As a result, the linings of the blood vessels become more porous, and plasma (the clear fluid part of the blood) leaks out into the surrounding tissues. This quickly produces swelling and oedema in the outer layer of the skin. Raised welts, blisters or hives may appear on the surface of the skin, especially on the face where the tissue is soft. The histamine causes the blood vessels to expand to allow the white cell reaction to speed up. The white cells are important to the healing process.

However, if this process gets out of control, the oversupply of histamine can cause real problems. Extensive and rapid expansion of the blood vessels occurs. The heart tries to keep the blood pressure up but as the space in the ‘pipes’ through which the blood flows may double in size, so it has to pump faster and harder. This produces a sudden fall in blood pressure that can lead to circulatory collapse (heart attack).

The histamine may also cause the smooth muscles along the respiratory passageways to contract or spasm. As these muscles tighten up, they narrow the air passages and make breathing extremely difficult. The combination of breathing difficulties, increase of heart rate and loss of circulatory pressure can cause either or both systems to stop.

Certain drugs and diagnostic reagents can also directly trigger mast cell histamine release. [5]

Anaphylaxis may occur rapidly or slowly. Many of the symptoms of anaphylaxis can be prevented by the prompt administration of antihistamines. People with a susceptibility to this can carry a puffer or inhaler which will deliver an antihistamine dose directly to the airways. As its name implies, the antihistamine blocks the effect of the histamine that has been released into the system. The treatment of anaphylactic shock in a hospital setting involves antihistamine, corticosteroid and epinephrine injections. [6] It may also require adrenaline and intravenous fluids, plus artificial ventilation. Intubation (passing a tube into the trachea) may also be necessary to deal with the problem of airway swelling.

Systemic anaphylaxis is characterised by an appearance of a generalised flush, weakness, anxiety, dizziness, palpitations, tingling of the fingers or toes or of the tongue, hives (urticaria), swelling of the lips, tongue, neck and face (angio-oedema), nausea and vomiting, and uterine and gastro-intestinal cramps. Vomiting occurs in 10 to 15 per cent of people with anaphylaxis. The entire range of symptoms can develop within seconds or within minutes of contact with or administration of the drug or particular allergen to which the individual is sensitive. [7]

If not treated, the reaction may progress to respiratory distress, over-contraction of the muscles, (hyper-peristalsis), irregular heart beat (arrhythmia), cardio-vascular collapse (heart attack), seizures, coma and death. Death can occur within 30 minutes. [8]

Most anaphylactic reactions are due to insect stings, food allergies or pharmaceuticals. [9] Penicillin and even aspirin can produce these problems. [10] In a drug-induced allergy, the reaction is most likely to occur at the start of a new course of treatment, or with a previously used drug which may not have caused allergic symptoms at earlier times. However, anaphylactic hypersensitivity can exist for many years in the absence of any known exposure to the drug.

In South Australia in one year recently, there were two rapid deaths from anaphylactic shock caused by bee-stings.  In highly sensitive people, just having the substance on the skin or in the air may produce a similar response. There are examples of sensitised people developing the reaction by merely being in a restaurant where the allergen has been included in a sizzling dish which has been carried past their table. Anaphylactic reaction to the presence of peanuts is not uncommon.

Diagnosis of sudden anaphylactic death

Anaphylaxis has long been recognized by forensic pathologists as a cause of sudden death. [11] However, diagnosis at autopsy is complicated by the relatively non-specific and inconstant pathologic findings seen in these cases. [12] If the death is the result of asphyxia the findings would be similar to those seen in other types of asphyxia, including drowning, but often there are no specific visual autopsy findings that indicate an allergic death. [13]] This reflects the rapidity and mode of death, which is often the result of shock, rather than asphyxia. Where this shock is established within minutes of the start of the reaction, there may be no time for other features to occur. It is possible, however, to confirm the diagnosis of anaphylactic shock by testing for elevated levels of tryptase in the blood serum. [14] Tryptase is an enzyme which is released from the mast cells at the same time as the histamine. In contrast to histamine, however, it is relatively stable in serum and can therefore be measured in autopsy samples, including after storage at –20 degrees C. [15] A study in the United Kingdom has shown that the absence of specific findings at autopsy does not exclude a finding of anaphylaxis and thus the possibility of anaphylaxis should be considered in all cases of sudden unexpected death. [16]

Epilepsy

Epilepsy is a discharge of electricity within the brain that causes the body to convulse. It often leaves no visible signs within the brain to be found at autopsy. It may be possible to infer an epileptic seizure from cuts or bruises on the body, especially from a cut to the tongue, which is why it is prudent to look for evidence of trauma (bite marks) to the tongue.

Where an epileptic fit occurs in a person in a potentially dangerous situation, such as when driving a car, in a bath or while swimming, it may result in death. While the traumatic cause of death (the injuries resulting from the car crash) will be evident at autopsy, there will be no evidence of the epileptic fit that caused the driver to crash.

Diagnosis of epilepsy

As for drowning, the diagnosis of epilepsy is a diagnosis by exclusion.

In chronic cases of epilepsy where there have been repeated attacks, it may be possible to take samples of tissue from the correct areas of the brain and show damage to the neurones, but in the case of a first attack this can’t be done. Where a dead person is known to be epileptic, it might be possible to attribute the death to epilepsy without seeing specific physical signs of it.

Time of death

There are several methods for estimating the time of death, all of which are subject to variables that affect their accuracy.

Body cooling

The cooling of a body after death is known as algor mortis. The temperature of the body when found and the rate at which it is cooling can be used to estimate a time of death. [17] The temperature, which is measured in the rectum or alternatively in the liver via an abdominal stab, is taken as soon as possible after death, with further recordings being taken at regular intervals afterwards.  This information can then be used in calculations [18] or, better, applied to a nomogram which is a mathematical diagram which relates temperatures with times and body weights to help determine a time of death. [19] To calculate as accurately as possible, it is necessary to know the ambient (air) temperature in the room where the deceased is found, and also the temperature outside the room and outside the building, to help calculate the rate at which the temperatures have changed. Likewise, the temperature of water in baths, pools, rivers or the sea in which a body is found needs to be recorded.

A number of variables affect the accuracy of a time of death calculated by body cooling. Some, such as the size of the person and the amount of clothing they were wearing at the time of death, can be measured and factored in. Others, such as the person’s temperature at the time of death and any changes in the ambient conditions since their death, are unknown and have to be assumed. [20]

Environmental factors, such as the humidity, whether the area is open or closed, and how windy, wet or otherwise it is, should be noted. The value of temperatures and other information recorded at the scene is that they are always available for later review and evaluation by an expert. [21]

Lividity

If a body lies undisturbed for some time after death, the blood, without the heart to pump it around the system, settles at the lowest parts of the body producing areas of discolouration under the skin. These areas, which can be seen through the skin, turn red and then purplish as the blood pools and changes colour. This is called lividity (also livor mortis or hypostasis). Those parts of the body which are in contact with the ground will show white patches (blanching) because the pressure of the body on the ground stops the blood from settling in those areas. This means that if a body is discovered some time after death, the pattern of discolouration and blanching can help the pathologist to understand fairly accurately the way in which the body was lying after death.

The blood eventually becomes fixed in position, so the pattern of colouring and blanching will remain, even if the body is moved subsequently. If the pattern of discolouration and blanching is not consistent with the way in which the body is lying on the ground (or other surface) when discovered, then it can be inferred that it has been moved some time after death. This is why colour photographs of the body at the scene and at the autopsy are so important.

Lividity is usually apparent about one hour after death, but may be noticeable as soon as half an hour, depending on the conditions. [22] If a person were to die in a warm bath, then the process may be speeded up, because the blood vessels would be dilated (expanded) and so hasten the draining effect of the blood. It appears earlier in asphyxial (suffocation) deaths. It is usually complete within 8 to12 hours. [23]

Rigor mortis

Rigor mortis is the stiffening of the muscles after death. [24] The muscles of the body need a continuous supply of the chemical adenosine triphosphate (ATP) to enable them to contract. The production of ATP stops at death, but it is still used by the muscles. When the ATP is used up, the other chemicals present in the muscles combine and set to produce the stiffening known as rigor mortis. [25] A number of factors affect the rate at which rigor develops. Strong exercise or increased temperatures prior to death will speed up the use of any ATP that is still in the muscles after death, and thus speed up the process of rigor after death. Cold or freezing will delay the onset of the rigor, as well as prolonging its presence. Rigor gradually disappears as the body begins to decompose. Usually rigor appears within 2 to 4 hours of death, fully develops in 6 to 12 hours, and is gone after about 36 hours.

Insect infestation

After the first 24 to 48 hours of death, the processes of rigor, temperature and lividity become less useful in determining a time of death as decomposition progresses. This is where the study of insects becomes most helpful. By understanding the life-cycle of insects attracted to a decomposing body, a specialist may be able to determine a time of death. The blowfly is the most common of these insects, especially where a body has been in the open. Eggs or live maggots may be laid on the body, and then develop as maggots which leave the body and, when a metre or so away, burrow into the ground to pupate. It is important to examine the ground in the vicinity of the body to see if this has occurred. Any investigation of insect infestation requires the advice of a specialist forensic entomologist.

Stomach contents

An examination of the gastric contents can sometimes be used to give an estimate of the time interval between eating and death. If the time the deceased last ate is known or can be found out from witnesses, for example, then this time interval can be used in combination with other factors found at autopsy to indicate an approximate time of death.

‘Normal’ stomach emptying times range from less than an hour to 6 hours. [26] There are a number of factors affecting these times, and in a death investigation many of these are imponderables. No precise estimate is therefore ever practicable, and evidence of time of death derived in this way must be treated with great reserve.

There are some obvious factors that need to be taken in to account in making such estimates. They include the size and type of meal – the larger the meal, the longer the emptying time – and the types of food (liquid or solid) and the specific food involved. Others factors are not so obvious and some certainly not easily determined. They include the energy value of the food, the age of the deceased, the ‘normal’ emptying time of the stomach of the deceased (which usually isn’t known or knowable), and their physical, mental and emotional states in the interval between eating and death and at the time of death (also often not known or knowable). Delayed emptying of the stomach is well recognized in shock, trauma and unconsciousness. Fear and anxiety also may cause great delay. [27]

Estimates of time of death can be expected to cover a range of some hours. [28] The degree of imprecision is considered by some specialists to be unacceptable and that as such it is liable to mislead the investigator and the court. [29] The stomach is a poor ‘forensic clock’. [30]

Endnotes

1. AJ Peabody, ‘Diatoms and drowning – a review’, Medicine, Science and the Law, no. 20, 1980, pp. 254–61.

AJ Peabody, ‘Diatoms in forensic science’, Journal of the Forensic Science Society, no. 17, 1977, pp. 81–7.

2. NI Hendrey, ‘Diatoms and drowning – a review’, (letter), Medicine, Science and the Law, no. 20, 1980, 289.2

3. VD Pluckenham, Lectures on forensic medicine and pathology, 5th edn, University of Melbourne, 1982, p.204

4. FH Martini, Fundamentals of anatomy and physiology, 5th edn, Prentice-Hall, New Jersey, 2001, pp. 788–9.

5. JW Yunginger, DR Nelson, DL Squillace, RT Jones, KE Holley, BA Hyma, L Biedrzycki, KG Sweeney, WQ Sturner & LB Schwartz , ‘Laboratory investigation of deaths due to anaphylaxis’, Journal of Forensic Sciences, no. 36, 1991, pp. 857–65.

6. See Martini, ref. 4.

7. Ibid.

C Delage & NS Irey, ‘Anaphylactic deaths: a clinicopathological study of 43 cases’, Journal of Forensic Sciences, no. 17, 1972, pp. 525–40.

8. AT Bennett & KA Collins, ‘An unusual case of anaphylaxis’, American Journal of Forensic Medicine and Pathology, no. 22, 2001, pp. 292–5.

9. Ibid.

10. LB Schwartz, DD Metcalfe, JS Miller, H Earl & T Sullivan, ‘Tryptase levels as an indicator of mast-cell activation in systemic anaphylaxis and mastocytosis’, New England Journal of Medicine, no. 316, 1987, pp. 1622–6.

11. See Delage & Irey, ref. 7.

12. VW Weedn, ‘Anaphylactic deaths’, Journal of Forensic Sciences, no. 33, 1988, pp. 1108–9.

B Randall, J Butts & JF Halsey, ‘Elevated post-mortem tryptase in the absence of anaphylaxis’, Journal of Forensic Sciences, no.40, 1995, pp. 208–11.

13. See Bennett & Collins, ref. 8.

14. See Schwartz et al, ref. 10.

15. See Yunginger et al, ref. 5.

16. RSH Pumphrey & IS Roberts, ‘Postmortem findings after fatal anaphylactic reactions’, Journal of Clinical Pathology, no. 53, 2000, pp. 273–6.

17. VJ DiMaio & D DiMaio, Forensic pathology, 2nd edn, CRC Press, Boca Raton, Florida, 2001, pp. 28–30.

18. TK Marshall, ‘The use of body temperature in estimating the time of death and its limitations’, Medicine, Science and the Law, no. 9, 1969, pp. 178–82, 184–5 (figures).

19. C Henssge, ‘Death time estimation in case work: I. The rectal temperature time of death nomogram’, Forensic Science International, no. 38, 1988, pp. 209–6.

20. See Marshall, ref. 18.

21. University of Dundee, Forensic Medicine, <www.dundee.ac.uk/forensicmedicine/llb/timedeath.htm>

22. See DiMaio, ref. 17, pp. 21–5.

J Dix & M Graham, Time of death, decomposition and identification: An atlas, CRC Press, Boca Raton, Florida, 2000, pp. 4–6.

23. See Plueckhahn, ref. 3, p. 117.

24. See DiMaio, ref. 17, pp. 26–8.

See Dix & Graham, ref. pp. 2–4.

25. See DiMaio, ref. pp. 26–8.

See also Dix & Graham, ref. 22, pp. 2–4.

26. See DiMaio, ref. 17, p. 37.

EF Rose, ‘Factors influencing gastric emptying’, Journal of Forensic Sciences, no. 24, 1979, pp. 200–6.

27. See DiMaio, ref. 17, pp. 37–9;

See also Rose, ref. 28 below and Horowitz & Pounder  ref. 30 below.

TH Howells, T Khanam, L Kreel, Seymour, B Oliver & JAH Davies, ‘Pharmacological emptying of the stomach with metoclopramide’, British Medical Journal, no. 2, 1970, pp. 558–60.

28. M Horowitz & DJ Pounder, ‘Gastric emptying: forensic implications of current concepts’, Medicine, Science and the Law, no. 25, 1985, pp. 201–14.

29. FA Jaffe, ‘Stomach contents and the time of death. Reexamination of a persistent question’, American Journal of Forensic Medicine and Pathology, no. 10, 1989, pp. 37–41.

30. M Horowitz & DJ Pounder, ‘Is the stomach a useful forensic clock?’, Australian and New Zealand Journal of Medicine, no. 15, 1985, pp. 273–6.

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