HYPOSTASIS

examining the remainder was that clouding of the cornea occurred in 75 per cent of patients within 2 hours of death. They concluded that segmentation was a purely post-mortem change and any intravascular movement of blood, however irregular, was an

indication for continued resuscitation.

■ Cessation of the heart beat and respiratory movements was the primary marker of death until the advent of mechanical cardiorespiratory support as it led to immediate ischaemia and anoxia of all other tissues.

Determination of cardiac arrest may be made by prolonged auscultation of the chest to exclude heart sounds though, as in life, a feeble heartbeat may be muffled by a thick chest wall. The electrocardiograph is unchallengeable in confirming cardiac arrest.

Respiration is more difficult to confirm, especially in deep coma such as barbiturate poisoning, and prolonged listening with a stethoscope over the trachea or lung fields is necessary. All archaic procedures such as saucers of water on the chest, feathers before the nostrils and tourniquets around the fingers are only of historical interest.

The mode versus the cause of death

Confusion often arises, especially among students and younger doctors, about the distinction between the mode of death and its cause. This is particularly important in relation to the documentary certification of deaths, but the same confusion sometimes occurs among pathologists, especially those who are not habitually involved in medico- legal cases.

The mode of death refers to an abnormal physiological state that pertained at the time of death: for example, ‘coma’,

‘congestive cardiac failure’, ‘cardiac arrest’ and ‘pulmonary oedema’. These offer no information as to the underlying pathological condition and should not be used as the defini- tive cause of death unless further qualified by the more fun- damental aetiological process.

In most cases, the mode is unhelpful and immaterial in describing and understanding the cause of death, and some modal terms are quite useless, such as ‘syncope’ or ‘cardiorespiratory failure’. Even ‘bronchopneumonia’ is such a common terminal event in numerous diseases that, used alone, it conveys no information about why the patient died. The British Registrar General has recently requested that it should be omitted from death certificates, the basic condition being preferable and sufficient for statistical purposes.

In addition to the mode and cause of death, here is also themannerof death, which is not really a medical deci- sion. Manner refers to the circumstantial events, such as

‘homicide, suicide, accident or natural cause’ and is a legal or administrative categorization.

The recommendations of the World Health Organization, as given in its publication The medical certification of death, should be followed to improve both the comprehension and statistical accuracy of the cause of death. Even this booklet is inconsistent with the practice of certification in many advanced countries, in that it requests the doctor to enter the ‘manner’ of death (for example, homicide, accident or suicide) which, for example in the UK, is the pre- rogative of the legal authorities after full investigation (see Leadbeatter and Knight 1987).

POST -MORTEM CHANGES OF FORENSIC IMPORTANCE

To the forensic pathologist a number of post-mortem changes are of interest and potential usefulness, mainly in relation to the estimation of the post-mortem interval, possible interfer- ence with the body, and an indication of the cause of death.

Post-mortem hypostasis is known under a variety of older names, such as ‘lucidity’, ‘staining’ or ‘cogitation’, but the current title is most suitable as it indicates the cause.

Hypostasis occurs when the circulation ceases, as arterial propulsion and venous return then fail to keep blood moving through the capillary bed, and the associated small afferent and efferent vessels.

Gravity then acts upon the now stagnant blood and pulls it down to the lowest accessible areas. The red cells are most

FIGURE2.3 Blotchy post-mortem hypostasis, forming in the early hours after death. The patchy disposition has no significance and this usually sinks down and becomes confluent in the most dependent areas within a few more hours.

affected, sedimenting through the lax network, but plasma also drifts downwards to a lesser extent, causing an eventual post-mortem ‘dependent oedema’, which contributes to the skin blistering that is part of early post-mortem decay.

The arrival of erythrocytes in the lower areas is visible through the skin as a bluish red discoloration, ‘hypostasis’.

It often begins as blotchy patches on both lateral and dependent surfaces, but also on the upper surfaces of the legs, especially thighs. These soon coalesce and slide down to the lowest areas.

The distribution of hypostasis

The pattern of hypostasis depends on the posture of the body after death. It is most common when the deceased body is lying on its back, with the shoulders, buttocks and calves pressed against the supporting surface. This compresses

the vascular channels in those areas, so that hypostasis is prevented from forming there, the skin remaining white.

When the body lies for a sufficient time on the side or face, the hypostasis will distribute itself accordingly, again with white pressure areas at the zones of support.

If the body remains vertical after death, as in hanging, hypostasis will be most marked in the feet, legs and to lesser extent in the hands and distal part of the arms. In addition to pallor of the supporting areas, any local pressure can exclude hypostasis and produce a distinct pattern in contrast to the discoloured area. Examples include the irregular linear marks made by folds in rumpled bedlinen, the pattern of fabric from coarse cloth, the pressure of tight belts, brassière straps, pants’ elastic and even socks. According to Bonte et al.(1986), when electrocution takes place in water (usually a bathtub), the hypostasis is sharply limited to a horizontal line corresponding to the water level.

FIGURE2.4 Post-mortem hypostasis in the normal distribution. The pale areas are the result of pressure against a hard supporting surface.

FIGURE2.5 Post-mortem hypostasis in a death from hanging. The discoloration of the skin is in the legs and hands, due to the vertical posture after death.

The colour of hypostasis

The usual hue is a bluish red, but variation is wide. This depends partly on the state of oxygenation at death, those dying in a congested, hypoxic state having a darker tint as a result of reduced haemoglobin in the skin vessels. This is an unsure indicator of the mode of death, however, and no reliance can be placed on a cyanotic darkening of the hypostasis to indicate a hypoxic death in the sense of

‘asphyxia’. Many natural deaths from coronary or other disease have markedly dark hypostasis. Often the colour of the hypostasis varies from area to area on the same body. Sometimes a rim of lighter colour may be seen along the margin of the lower darker area and sometimes there is a def- inite contrast between a bluish zone and a pink margin. This may appear and change as the post-mortem interval lengthens. Often the whole area of hypostasis is pink or bright red.

When death has been due to hypothermia or exposure to cold in the agonal period, such as drowning, the colour may assist in confirming the cause of death; again this is relatively non-specific because bodies exposed to cold after death (especially in mortuary refrigeration) may turn pink after an initial stage of normal bluish-red tint.

The mechanism is not understood, but is obviously a result of oxyhaemoglobin forming at the expense of the darker reduced haemoglobin. This is understandable in hypothermia, where the reduced metabolism of the tissues fails to take up oxygen from the circulating blood, but its frequent forma- tion in the post-mortem period is difficult to explain.

Several researchers have investigated the colour of hypostasis in relation to time since death. Schuller et al.

(1987) noted an increasing paleness between 3 and 15 hours post-mortem, measuring this as a change in wave- length from 575nm at 3 hours at an average rate of 2nm per hour. Vanezis (1991) has used tristimulus colorimetry to study colour changes and secondary shifting of hypostasis, and claimed that there is a linear relationship between the fading colour and time during the first 2 hours after death, following which changes are unpredictable. Inoue et al.(1994) have also described measurement of hypostatic colour as a measure of time since death.

It may sometimes be noticed that originally bluish hypostasis becomes pink along the upper part of the horizontal margin, the lower parts remaining dark, so a quanti- tative change probably occurs, the haemoglobin being more easily re-oxygenated where the erythrocytes are packed less densely in the upper layers of hypostasis.

Other changes in the colour of hypostasis are more useful.

The best known is the ‘cherry-pink’ of carboxyhaemoglobin, which is a unique colour and is often the first indication to the pathologist of carbon monoxide poisoning. Cyanide poisoning is said to have its own characteristic dark blue–pink hue,

but it is really an index of the congested, cyanotic, mode of death and, if the pathologist was not already aware of the potential cause from the history – and perhaps the odour of cyanide – it is doubtful whether hypostasis would be a primary indication of the nature of the death. The hypostasis may be a brownish red in methaemoglobinaemia and may be various shades in aniline and chlorate poisoning. In deaths from septic abortions where Clostridium perfringensis the infecting agent, a pale bronze mottling may sometimes be seen on the skin, though this is not confined to the areas of hypostasis.

Skin haemorrhages, varying in size from small petechiae to large blotches and even palpable blood blisters may develop in areas of hypostasis. The most common place is the back of the shoulders and neck, though they may appear on the front of the chest, even on a body lying on its back.

They are more common in cyanotic, congestive types of death and become more pronounced as the post-mortem interval lengthens. Their importance is in not being mistaken for the so-called signs of ‘asphyxia’. They appear in the most gross form when a body dies or is left with the head downwards: the confluent petechiae and ecchymoses may be so marked that they virtually blacken the face and neck.

The timing and permanence of hypostasis

Too much has been claimed in the past for the usefulness of hypostasis as an indicator of the time of death and post-mortem disturbance of the body. The phenomenon appears at a variable time after death – indeed, it may not appear at all, especially in infants, old people or those with anaemia. It may be so faint as almost to escape detection.

Hypostasis can appear within half an hour of death or it may be delayed for many hours. Its variability is such that it is useless for any estimation of the time since death.

It is claimed that hypostasis can sometimes be observed in the living if the heart action is failing or if venous return is impaired by the immobility of deep coma. The latter is certainly associated with skin blistering caused by dependent oedema.

Once hypostasis is established, there is controversy about its ability to undergo subsequent gravitational shift. If the body is moved into a different posture, the primary hypostasis may either:

■ remain fixed

■ move completely to the newly dependent zones or

■ be partly fixed and partly relocated.

Thus if a corpse is found with the hypostasis in an obviously inappropriate distribution related to the present posture, it must have been moved after death. This fact may

Hypostasis

have important significance in the investigation of criminal deaths, such as the return of the culprit or some other per- son to the scene. It may also migrate either partly or completely, however, thus negating its diagnostic usefulness.

Older theories about ‘fixation’ of the staining after a certain time are not tenable, as there is no constant interval when this occurs.

Mallach (1964) analysed data including onset, confluence, maximum intensity, displacement and shifting, taken from publications between 1905 and 1963. These are summarized in Table 2.1, ‘thumb pressure’ meaning displacement by thumb pressure. Table 2.2 shows the variable opinions on hypostasis culled from standard textbooks.

A considerable amount of research has been devoted to the investigation of clotting of post-mortem blood, its subsequent lysis and inhibition of coagulation by fibrinolysins, but this cannot be translated into practice. Formerly, it was held that if a body had remained in its original posture for a certain minimum length of time, the blood would coagulate in the hypostatic areas, so that secondary shifting could not then occur if the body was moved. This is not true in the majority of instances, as there may be partial or complete secondary gravitation at any time – at least, until true staining of the tissues due to haemolysis begins as part of early decomposition, which is not until the second or third day in temperate conditions.

Suzutani et al.(1978) examined 430 bodies by pressure on hypostatic areas, finding that the colour could not be squeezed out in 30 per cent where death had occurred 6–12 hours previously. More than 50 per cent were fixed after 12–24 hours and no fading occurred in 70 per cent of those

dead for more than 1–3 days. However, in a significant number, hypostasis was still mobile for at least 3 days.

Fechner et al. (1984) found no linear relationship between fixation and time of death and also observed vari- ations in fixation according to storage temperatures.

TABLE2.1 Hypostasis related to the time of death (hpm) as derived from previous literature

Standard

Limits

Stage Mean deviation Lower Upper

Beginning 0.75 0.5 0.25 3

Confluence 2.50 1.0 1.00 4

Maximum 9.50 4.5 3.00 16

Thumb pressure 5.50 6.0 1.00 20

Complete shifting 3.75 1.0 2.00 6

Incomplete shifting 11.00 4.5 4.00 24

TABLE2.2 Time of onset of hypostasis as stated by previous authors

Reference Onset Maximum

Adelson 30 min–4 h 8–12

Polson, Gee, Knight 30 min–2 h 6–12

Spitz and Fisher 2–4 h 8–12

Taylor (ed. Simpson) 0 h 12

Taylor (ed. Mant) 1 h 12

Gradwohl (ed. Camps) 20–30 min 6–12

Glaister, Brash – 8–12

DiMaio 30 min–2 h 8–12

Sydney Smith 0 h 12

Mant 0 h 12

Gordon and Shapiro ‘few’ h 12

FIGURE2.6 Extensive confluent skin haemorrhages may occur within the dependent hypostasis. They worsen as the post-mortem interval lengthens and must not be taken to indicate so-called ‘asphyxia’.

Hypostasis in other organs

Just as blood settles in dependent skin, so it does in other tissues and organs. The importance in forensic autopsy work is the differentiation of organ hypostasis from ante-mortem lesions. In the intestine, dependent loops of jejunum and ileum may be markedly discoloured and mislead the inexperienced pathologist into suspecting mesenteric infarction or strangulation. This hypostasis is discontinuous, however, revealing interrupted segments when the gut is laid out.

Often loops in the pelvis are worst affected, because of their lower position.

The lungs almost always show a marked difference in colour from front to back, the anterior margins being pale and the posterior edges lying in the paravertebral gutters being dark blue. This is often accompanied by an obvious difference in fluid content, congestion and oedema being more marked posteriorly. The myocardium often shows a dark patch in the posterior wall of the left ventricle that must not be mistaken for early infarction.

One of the most important hypostatic artefacts is haemorrhage behind the oesophagus at the level of the larynx. This has many times been confused with the trauma of strangulation, but the true nature was best investigated by Prinsloo and Gordon (1951). Areas of congestion developing into haemorrhage appear in the loose tissues on the back of the oesophagus lying on the anterior longitudinal ligament of the cervical spine. They may be prominent, sufficient to produce actual haematomas. They arise in the veins and venous plexus on the front of the spine, and can be avoided in cases of strangulation and suspected strangulation by draining the neck of blood before starting the dissection. This can be achieved either by removing the brain first or by opening the chest and incising the great veins in the superior mediastinum.

Differentiation between hypostasis and bruising

This is rarely a problem in fresh bodies, but when decomposition begins the two conditions become blurred. In fresh material the appearance of hypostasis is of a regular, diffuse engorgement of the surface vessels, the colour varying between purple–red and bright pink. The density varies from place to place but there are no sudden changes in colour nor any sharply circumscribed areas as occurs in bruising. As mentioned above, in the early stages of hypostasis there may be mottled blue areas, which later coalesce. This mottling is unlikely to be confused with bruising by any but the most inexperienced pathologist. The position in dependent areas is also characteristic, giving a generally horizontal orienta- tion. Bruises may be anywhere on the body, are often discoid or have an irregular margin, but rarely cover a large area with

uniform density – and do not have a horizontal margin.

Abrasions may be topographically associated with a bruise, but not with hypostasis. When there is difficulty in differen- tiating between the two – usually where there is racial pigmentation or really deep, cyanotic hypostasis that obscures possible bruises – the classic test is to incise the suspect area to see if the underlying blood is intravascular (hypostasis) or infiltrating the tissues outside the vessels (contusion).

Fresh bruises may also be swollen and slightly raised above the surface. If a post-mortem pressure mark (such as from a belt or tight clothing) crosses an area of hypostasis, there will be a pale bloodless zone, but a bruise will not be affected.

Hypostasis is in the most superficial layer of the dermis and any exuded blood can be wiped or washed away from the incised surface. A bruise is often deeper in the skin or underlying tissues and is fixed, being infiltrated through the tissues outside the ruptured vessels. An exception is intradermal bruising, but this is usually patterned or linear and rarely can be confused with hypostasis. Histological examination may be necessary finally to decide the matter.

When post-mortem autolysis has developed, the diffusion of haemolysed blood from vessels makes the differentiation

Hypostasis

FIGURE2.7 White patches within the hypostasis on the face merely indicate pressure against the supporting surface after a face-down position. As in this case, they are usually post-mortem and are not indicators of suffocation.

between hypostasis and bruising difficult and eventually impossible. Even histological examination may be of little help when the tissues become markedly degenerate.

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