User:MIDOREDE/sandbox

'''WOUNDS

DEFINITION

A wound or injury can best be defined as ‘’damage to any part of the body (i.e. both externally and internally), by the application of violence’’.

Violence can best be defined as MEDICAL FORCE acting on the body, with transfer of KINETIC ENERGY.

MECHANISM OF WOUNDING

A wound occurs when the INTENSITY OF FORCE exceeds the capability of the tissues to adapt or resist.

The INTENSITY OF FORCE obeys the usual laws of physics in that FORCE = MASS X VELOCITY2/2 i.e. FORCE varies directly as the MASS of the ‘’weapon’’ and directly as the SQUARE of the VELOCITY of impact.

Note: The ‘’weapon’’ can be anything, including the body itself, e.g. violent deceleration of a fall or in a traffic accident. Thus, a 1kg brick pressed to the skull will cause no injury, but the same brick thrown against the skull with a velocity of 10m/sec may smash the skull.

The AREA over which the force acts is another important factor. If a plank of wood is struck against the skin, the tissue damage will be far greater if the narrow edge is used, than if the impact is from the wide surface. This is because the FORCE INTENSITY derived from the same mass and velocity, is applied over a SMALLER AREA, (i.e. ‘’concentrated’’) thus delivering a GREATER IMPACT to any given unit of tissue.

This is very relevant to STAB wounds, as all the kinetic energy  of a moving knife is concentrated into the tiny tip of the blade. The same energy delivered by the large surface area of a cricket bat for example, might not even cause a bruise.

The TRANSFER OF KINETIC ENERGY from the relative movements of a body and a weapon, is the SOURCE OF DAMAGE to the TISSUES. If an ‘’attacking object’’ comes to rest in the tissues, then all its kinetic energy must have been transferred. Thus a bullet passing cleanly through the body fails to exchange all its energy into trauma production, which is the reason for the illegal ‘’DUM-DUM’’ or EXPLOSIVE TIPPED bullets.

If kinetic energy transfer can be: (a) slowed down; or (b) spread over a wider area, the FORCE INTENSITY per unit of time is LESS.

Thus a SEATBELT by the stretching of the belt fabric, will extend the TIME or ENERGY EXCHANGE 	and the large surface area of the seatbelt will spread the kinetic energy transfer over a much larger area than, for example, the few square centimeters of a forehead impacting against a windscreen.

Another way in which KINETIC ENERGY TRANSFER can be modified is in moving the body in the direction of the force e.g. If a boxer ‘’rides the punch’’:

i)	He is decreasing the differential velocity between his head and his opponent’s first; and

ii)	He is increasing the time over which energy transfer occurs (i.e. slowing down kinetic energy transfer time).

Note: With HIGH-SPEED IMPACT such as bullet wounds, stabbings, or sudden violent blows, the INTERTIA of the victim’s body prevents any significant reduction in energy transfer by movement. In TANGENTIAL IMPACT, e.g. glancing blow, only part of the kinetic energy is transferred and the damage will be proportionately less.

CLASSFICATION OF WOUNDS

Wounds may be categorized by the MOTIVATION of their infliction, e.g. suicidal, accidental or homicidal. However it is preferable for the pathologist to classify them by their *APPEARANCE and *METHOD OF CAUSATION.

Classification of Wound Types

1.	Abrasions (colloquially ‘’graze/scratches’’) 2.	Contusions (colloquially ‘’bruiser’’) 3.	Lacerations (colloquially ‘’cuts/tears’’) 4.	Incised wounds (colloquially ‘’cuts/slashes/stabs’’)

N.B. These wounds may present as combinations of the various types, e.g. abrasions with underlying contusions.

1. ABRASIONS

Four types of abrasions occur:

a)	Scratches b)	Grazes/scrapes c)	Friction d)	Imprint/crush/stamp/patterned.

a) Scratches

•	Caused by sharp objects, e.g. pin, thorn, knife-point, finger-nails.


 * Here, only superficial epidermis of skin is removed. Direction of movement may be ascertained by examining the scratch for ‘’heaping up’’ of the surrounding skin.  The epidermal tags tend to pile up at the DISTAL end.

Finger-nail abrasions may be:

i)	Liner scratches (nails dragged down the skin); or ii)	Short, straight/curved marks (skin gripped in static fashion).

These marks and scratches are significant findings in victims of assault especially in:

i)	SEXUAL ATTACKS – Victim resisting sexual/other attack may rake her nails down her assailant’s face causing linear scratches. These may help to identify assailant at a later stage.

ii)	MANUAL/LIGATURE STRANGULATION – Victim’s attempts to tear away the attacking fingers or ligature, result in VERTICAL, (usually) linear scratches on the victim’s neck.

iii)	CHILD ABUSE – The upper arms are a frequent site for GRIPPING AND RESTRAINT, resulting in bruising with superimposed static fingernail abrasions, which may be straight/curved and ±0.5cm long

Thus, fingernail abrasions usually indicate a STRUGGLE, and the identification of these is equally important in the case of the victim and of the assailant. Also, the possibility of ‘’DNA-fingerprinting of the assailant’s should be remembered, and adequate ‘’nail scrape’’ specimens should be collected in such cases.

b) Grazes/Scrape Marks

Caused by contact with rough surfaces, e.g. MVAs- motor vehicle accidents where body is thrown out of car onto ground/tar; glancing kicks or blows.

These are also called BRUSH ABRASIONS and when they are the result of scraping contact with the ground, the lay term is ‘’gravel rash’’.
 * Here, there is irregular removal of the skin’s epidermis. Direction of movement may once again be shown by situation of DISTAL end epidermal tags (‘’tail-end’’ tags).

c) Friction abrasions

Caused by ropes/cords/clothing which rub against and indent the skin, as a result of tying and pulling: commonly seen in hanging, ligature strangulation, blows from a lash. **All LIGATURE marks are FRICTION abrasions. Drying of the abraided skin results in these marks assuming a DARK BROWN colour with a partment-like texture.

d) Imprint/Stamp/Patterned/Crush abrasions

These result from impact against the skin by objects such as motor tyres, bicycle chains, knotted ropes, plaited lashes. **The epidermis is crushed and the IMPRINT of the impacting object is STAMPED on the surface.

ABRASIONS

ANTE-MORTEM                                               POST-MORTEM

Show slight bleeding and                            No blood flow and

Infiltration blood into the                          No infiltration of blood Superficial tissue. into the tissues.

Assume DARK BROWN                           Dry out rapidly and assume colour (d/t blood from                             PARACHMENT-LIKE ruptured blood vessels                              YELLOW-ORANGE colour. infiltrating the skin).

SMALL BLOOD VESSELS are often seen tracking in                                                                       the PM abraided area. Some PM insect bites also resemble abrasions, especially by ANTS – called ANT-ABRASIONS (shallow,                                                                        superficial lesions with                                                                        scalloped, serpiginous                                                                         margins, usually around                                                                        eyelids and lips).

N.B. PERI-MORTAL ABRASIONS occurring:

a)	Just before death; or b)	At the time of death; or c)	Just after death.

May show characteristics belonging to both types, i.e some blood infiltrated DARK BROWN areas mixed with some YELLOW-ORANGE PARCHMENT-LIKE areas.

OUT COME OF ABRASIONS

Abrasions as such do not cause death. However, they are a possible entry-point for ORGANISMS which may cause fatal septicaemia, gas gangrene, or tetanus. Thus superficial abrasions may be an INDIRECT CAUSE OF DEATH.

2. CONTUSIONS

A contusion is caused by the traumatic rupture of blood vessels, there by liberating free blood into the tissues of the body.

Note: The work BRUISE implies that the lesion is visible through the skin, whilst a CONTUSION can be anywhere in the body. Contusions may involve ANY PART of the body, e.g. Subcutaneous soft tissues, adipose tissues, muscles, connective tissues, deeper vital and non-vital structures and organs, e.g. spleen, heart, lungs, brain, mesentery etc.

A ‘’PURE’’ BRUISE does not involve a breach of skin or tissue continuity, although it may often be complicated by other associated wounds, such as ABRASIONS or 	LACERATIONS.

The Size of a CONTUSION depends on:

a)	The degree of violence used b)	Individual variations c)	The site involved.

Note: a contusion may appear at some distance from the original site of force application, e.g. a ‘’black eye’’ following a head injury.

The SHAPE of a CONTUSION may afford evidence of the TYPE of INSTRUMENT used, e.g. ‘’TRAM-TRACK’’ BRUISES left by sticks or sjamboks. This is caused by the FORCE of the sjambok rupturing vessels in the skin, and forcing the blood at the site of impact into the tissues alongside the sjambok. This results in an impression of 2 elongated areas of bruising, with ± NORMAL SKIN between the bruises. Bruises ± Normal skin The width of the NORMAL SKIN AREA approximates the width of the round object used to inflict the injury.

INDIVIDUAL VARIATIONS

As a general rule WOMEN bruise more easily than MEN; MENSTRUTING Women bruise more easily than other women, the OBESE bruise more easily than the LEAN; the OLD bruise more easily than the YOUNG. In certain medical conditions in which there is a bleeding tendency, e.g. scurvy, liver failure, haemophilia, toxic states, chronic alcoholism or medication:

a)	The fragility of blood vessels may be increase.           And/or b)	The coagulability of blood may be decreased, resulting in EXCESSIVE  contusions AND/Haemorrhage for a given IMPACT.

COLOUR CHANGES in BRUISES also vary with individual. The usual colour changes occur as a result of the chemical degradation of HAEMOGLOBIN, which is released after the red cell envelopes rupture.

RED to PURPLE-BLACK ±  Day  0-1          Haemoglobin

BLUISH-BROWN              ±  Day     2          Haemoglobin

GREENISH-BROWN        ±  Day     3          Haemosiderin + Biliverdin

GREEN                              ±  Day     4-5         Biliverdin YELLOW                           ±  Day     7-10       Bilirubin FADING to DISAPPEARANCE ±  Day     12-15

N.B: These colour changes are a sign of VITAL REACTION i.e. a living body’s inflammatory and repair response to tissue injury. This is a feature which enables the pathologist to give a VERY ROUGH estimate of the AGE of a BRUISE:

1.	By noting the macroscopic colour of a bruise. 2.	By histological examination of a bruise.

Contusions may also be simulated by post-mortem HYPOSTASIS, and these can also be distinguished more accurately histological examination of the relevant tissue. *This is particularly important to remember in cases with PM LIVIDITY/HYPOSTASIS over the anterior and lateral NECK, as these may be mistaken for BRUISES associated with strangulation.

OUTCOME OF CONTUSIONS depends entirely on the SITE, SIZE and EXTENT of the contusions. Sample, superficial bruises usually have non-fatal outcome, whereas contusions of the VITAL ORGANS, e.g. brain, heart, lungs, kidneys may well lead to death. However, even fairly superficial MUSCULAR and SOFT TISSUE HYPOVOLAEMIC SHOCK and RENAL FAILURE due to tubular necrosis (Secondary to shock and myoglobin and haemosiderin deposition in the kidney tubules).

CONTUSION

ANTE-MORTEM                                               POST-MORTEM

Caused before death as discussed. May be caused after death but the amount of FORCE required is                                                                               GREAT.

The size of the bruise is                                    The SIZE of the bruise is also PROPORTIONAL to the amount of               SLIGHT in relation to the amount of FORCE. FORCE.

There is infiltration of blood into the             There is no trace of infiltration of surrounding tissues. blood into the surrounding tissues.

The blood is not easily washed out                The blood can usually be easily out of the tissues. washed out of the tissue.

HISTOLOGICAL examination will                HISTOLOGICAL examination will reveal a VITAL REACTION. show NO VITAL REACTION.

3. LACERATED WOUNDS

The result from a TEARING, CRUSHING or SPLITTING of tissues. They are caused by BLOWS from BLUNT instruments, KICKS, FALLING on EDGED objects etc. Lacerations are commonly found over BONY REACTIONS, e.g. scalp, shins, shoulders, face and thorax because of resistance to the force by the underlying bone. (Skin pinned between BONE and ‘’WEAPON’’ resulting in splitting/tearing/crushing of skin i.e. LACERATIONS).

Appearance

•	The FULL THICKENESS of SKIN is penetrated. •	The EDGES are torn, irregular and often contused. •	Small vessels or strands of tissue stretch across the INTERIOR or the wound. N.B. Lacerated SCALP wounds (and other regions) may sometimes closely resemble INCISED  wounds.

TO DISTINGUISH THEM

1.	EDGES must be examined for IRREGULARITY. 2.	TISSUE BRIDGES in the wound are diagnostic of lacerations. 3.	SCALP HAIRS will survive INTACT across a laceration, whereas an incised wound will divide them. 4.	A knife or axe causing an incised wound is likely to chip or score the underlying SKULL.

Lacerated wounds should always be examined for foreign matter, e.g. bark from a branch or metal from a bar etc.

Puncture wounds

This is a type of LACERATED WOUND where  the DEPTH of the wound is greater than the WIDTH. It is caused by a relatively BLUNT instrument. E.g. poker, ice-pick, dog teeth, blunt bicycle spoke. Note: a puncture wound is not made by a SHARP instrument like a knife.

Depending on the degree of ‘’sharpness’’ of the point, collar of abrasion caused by abrasion and invagination of the skin may be found.

OUTCOME OF LACERATIONS

IN SUPERICIAL lacerations, external bleeding is usually minimal.
 * The danger to life is from INFECTION and SEPSIS.

IN DEEP, EXTENSIVELY LACERATED and PUNCTURE wounds, *the cause of death are from  HAEMORRHAGE and INFECTION with SEPSIS.

Lacerated wounds heal SLOWLY and may produce extensive IRREGULAR scarring.

4. INCISED WOUNDS

There are two types of incised wounds. Both are always made by a SHARP CUTTING EDGE.

1.	Superficially incised (sliced) wounds. 2.	Penetrating incised (stab) wounds. (PI WOUNDS).

Appearance

•	The EDGES of both the above mentioned types are CLEARLY DEFINED and may BLEED PROFUSELY.

In PENETRATING INCISED WOUNDS 	the DEPTH of a PI wound may be GREATER or LESS  than the length of the blade, the latter being dependent on the degree of penetration of the weapon. A GREATER DEPTH than BLADE LENGTH is done to:

1.	Depression of the body surface by the hilt of a knife as it enters the body.

2.	The marked difference in ante-and post-mortem muscle tone, resulting in an inestimable increase or decrease in length of a trace.

ALSO, in PI wounds of the THORAX there is a difference between INSPIRATION and EXPIRATION. In a PI wound of the HEART, the position of the heart during SYSTOLE and DIASTOLE will cause a difference to the length of a track.

The EXTERNAL APPEARANCE of an INCISED WOUND may indicate whether a DOUBLE-EDGED blade (dagger or a SINGLE-EDGED blade (knife) has been used. *In a DOUBLE-EDGED blade wound the extremities of the wound are POINTED and give the appearance of a CANOE.


 * In a SINGLE-EDGED blade wound one of the extremities will be flattened/rounded and the other pointed, and give the appearance of a BOAT.

Incised wounds often GAPE and have INVERTED edges. Note: Reservation is required in expressing an opinion as to the TYPE of INSTRUMENT which caused a wound, especially in the case of a wound which had been SUTURED or had become SEPTIC.

LACERATED INCISED WOUNDS have features of both LACERATED  wounds and INCISED wounds. These wounds are caused by SHARP, HEAVY and possibly PARTIALLY BLUNT objects e.g. axes or pangas. •	The lacerated portion is found at the extremities of the wound, and is caused by the HEAVINESS and BLUNTNESS of the object, tearing the tissues at the extremities of the wound. •	The incised portion is found in the central part of the wound and is caused by the SHARPNESS of the object, incising the tissues centrally.

OUTCOME OF INCISED WOUNDS

In SUPERFICIALLY INCISED wounds, external bleeding may be profuse but the main danger to life is from INFECTION with SEPSIS.

In PENETRATING INCISED wounds, the cause of death are from: •	SEVERE internal/external HAEMORRHAGE •	Penetration of VITAL ORGANS, e.g. brain, heart, lungs, liver etc. •	INFECTION with SEPSIS. •	In the THORAX --- PNEUMO-and/HAEMOTHORAX. •	In the ABDOMEN --- PERITONITIS.

LACERATED AND INCISED WOUNDS

Ante-morten                                                        Post-morten

1.May have haemorrhage                                   Little if any haemorrhage.

2.Blood infiltrates the surrounding                  Blood does NOT infiltrate the Tissues. Surrounding tissues.

3.Coagulated blood in wound. No coagulation of blood.

4.Retraction, eversion and gaping                    No retraction, eversion or gaping of wounds. of wounds.

5.Evidence of arterial spurting                        No evidence of arterial spurting. Seen on clothing/wall etc. *PM ‘’bleeding’’ always VENOUS.

6.Histological evidence of VITAL RXN. No histological evidence of VITAL RXN.

5. ACCIDENTAL SUICIDAL OR HOMICIDAL WOUNDS may be distinguished from each other by certain features:

1.	NUMBER of wound

In suicide – usually only one fatal wound may be few ‘’tentative’’ or ‘’trial’’ cuts, e.g. over wrists/neck. - rarely >1 serous wound, e.g. repeated hammer blows to head.

2.	POSITION of wounds

Suicides select certain sites where they believe VITAL ORGANS are situated, e.g. heart, throat, wrists, --- known as SITE OF ELECTION.

3.	NATURE of wounds •	Murder of suicide is suggested by INCISED or GUNSHOT wounds of a serious nature. •	Suicidal, mentally-deranged persons more commonly present with CONTUSED and /LACERATED wounds of ‘’self-mutilation’’.

4.	DIRECTION and EXTENT of  wounds

a) Suicidal cut-throat wounds

Since most people are RIGHT-handed, suicidal incised wounds are usually from left to right.

b) Suicidal gunshot wounds- on the R side

Causes of death in cut-throat wound

1.	One or both carotid arteries severed → death due to haemorrhage.

2.	If trachea is incised → blood may be INHALED → MECHANICAL ASPHYXIA.

3.	If trachea is completely divided → it may be drawn into the thorax, with soft tissues falling over the opening → causing MECHANICAL ASPHYXIA. (*ASPHYXIA = ‘’Lack of OXYGEN’’.

5.THE WEAPON

•	In suicide the weapon is most often found beside the body or found loosely clasped in the hand of the deceased.

6.BLOOD STAINS

On clothes or surroundings may give an indication of:

a)	The position of the victim at the time of injury b)	The subsequent movements of the victim.

Note: •	The victim may be dragged/carried to different locations by an assailant, i.e. HOMICIDAL; or

•	The victim may stagger/crawl to a different location himself e.g. after attempting SUICIDE).

7.SIGNS OF STRUGGLE would probably negate suicide, e.g:

8.THE CLOTHES should always be examined before being removed from the body and the relationship between tears in clothing and wounds in the body should be noted, e.g. in firearm deaths, GUNSHOT RESIDUES on clothing may provide vital evidence about:-

a)	Whether wound is an ENTRANCE or EXIT wound: b)	Range of discharge (suicidal vs homicidal) c)	Identity ammunition.

DATING OF WOUNDS

It can be an important matter in forensic medical investigations to determine whether a wound found at autopsy was:

a)	Inflicted BEFORE or AFTER DEATH and b)	If ANTE-MORTEM, HOW LONG before DEATH was it sustained?

This may be achieved by HISTOLOGICAL AND/OR IMMUNO-HISTOCHEMICAL examination of WOUNDS, based on the CHRONOLOGICAL CHANGES of HEALTH and REPAIR mentioned earlier, i.e. wound ---Inflammatory rxn --- Granulation tissue  Scar (VITAL Rxn). However, these changes will vary according to:

a)	size of wound (e.g. LARGE/RAGGED = SLOW) b)	type of wound (bruise/abrasion/incision/laceration c)	type of tissue (epidermal = faster, mesodermal = slower) d)	+/- INFECTION e)	Age and health of victim.

Thus only a RANGE of PROBABILITIES can be determined, but never a definite time interval. Also, the sequence in BRUISES is far less distinct than abrasions or lacerations, and histology is far less helpful.

Other than INJURIES TO THE BRAIN (in particular the brainstem) or to A LARGE BLOOD VESSEL (in particular the Aorta) most of injuries can RARELY be declared to have caused SUDDEN DEATH or RAPID LOSS of FUNCTION. In, for example homicidal cases, the ADRENALIN response of ‘’FRIGHT, FLIGHT or FIGHT’’, may greatly suppress PAIN, and injured victims may be able to perform astonishing physical feats, before collapsing and dying. •	(Bernard Knight tells of a victim of a STABBED HEART, who ran more than a quarter of a mile before collapsing). •	Thus the old forensic aphorism – ‘’Seldom say never – seldom say always’’ is extremely applicable in these situations.

COMPLICATIONS FOLLOWING WOUNDS

The ‘’PRIMARY’’ cause of death is described as the DISEASE or INJURY which INITIATED  the train of morbid events leading to death. The ‘’TERMINAL’’ cause of death is usually a COMPLICATION which occurs as a result of the INITIAL INJURY, e.g. a person with a head injury (the PRIMARY cause) often develops bronchopneumonia (the TERMINAL cause).

N.B: While  (primary) wound may appear to be relatively minor or may not be rapidly fatal, it may be complicated by further events which may lead to death. Thus, in wounds with COMPLICATIONS which result in death, it must be remembered that the INITIAL INJURY remains the ‘’PRIMARY’’ cause of death, i.e. subsequent fatal complications would not have arisen in the absence of the primary (1o) wound (s).

EXAMPLE OF COMPLICATIONS

c)	INFECTION --- septicaemia --- septic shock --- DIC. d)	HAEMORRHAGE --- hypovolaemic shock. e)	RENAL FAILURE following e.g. shock or severe crush injuries. f)	HAEMO-/PNEUMOTHORAX following chest wounds. g)	BRONCHOPNEUMONIA following coma or immobility. h)	PULMONARY THROMBO-EMBOLISM following deep venous thrombosis due to, e.g. prolonged immobility. i)	AIR EMBOLISM following penetrating chest wounds. j)	FAT-EMBOLISM following long bone fractures or extensive soft tissue trauma. k)	METABOLIC DISTURBANCES usually associated with shock.

Thus a person may die WEEKS or even MONTHS after an ACCIDENT or ASSULT as a result of one or more COMPLICATIONS. Nevertheless, regardless of the TIME PERIOD which elapses between the INITIAL INJURIES and DEATH, such a death remains a DEATH resulting from UNNATURAL CAUSES.

PELVIC-ABDOMINAL AND CHEST TRAUMA

GENERAL

Injuries may be distinguished as OPEN or CLOSED injuries.

OPEN INJURIES are injuries with a *SKIN WOUND +/- injury to the *UNDERLYING ORGANS, e.g. •	Stab wounds  →   (penetrating) incised wounds •	Gunshot wounds →  penetrating/perforating wounds.

CLOSED INJURIES/(NON-PENETRATING) are injuries to the *UNDERLYING STRUCTURES +/- bruising +/-abrasions of the *OVERLYING SKIN. They are caused by BLUNT FORCE, e.g. •	Kicks with a boot •	Falling objects etc.

1. CHEST TRAUMA

Damage can be sustained to either the CHEST WALL and/or its CONTENTS.

A. CHEST-WALL INJURIES

These are most commonly RIB FRACTURES, usually due to BLUNT FORCE. RIB FRACTURES do not greatly embarrass respiration UNLESS:

a)	they are so NUMEROUS that they prevent expansion of the thorax, e.g. ‘’flail chest’’ with paradoxical respiration. b)	BROKEN rib ends PENETRATE the pleura, lungs or heart →  haemo-/pneumothorax. c)	PAIN limits the respiratory effort → bronchopneumonia.

B. CHEST-CONTENTS INJURIES

The major structures at risk are:

1.	the lungs and main bronchi 2.	the heart 3.	the great vessels (AORTA and PULMONARY ARTERY).

1. LUNG INJURIES

Blunt and penetrating injuries may result in: •	PULMONARY contusions, lacerations or incised wound.

Complications

a)	Haemorrhage into the chest cavity from damaged hilar vessels or large parenchymal vessels → haemothorax → respiratory compromise +/- → hypovolaemic shock.

b)	Free air in the pleural cavity i.e. pneumothorax - → +/- tension pneumothorax   →     collapsed lungs    →  respiratory compromise.

c)	Infections, e.g. lung abscess, empyema, bronchopneumonia.

2. HEART INJURIES

Blunt and penetrating injuries may result in: CARDIAC contusions, lacerations, incised wounds, avulsion from its root vessels (e.g. in aircraft crashes), infarction e.g. if coronary arteries injured).

Complications

a)	Haemorrhage (particularly with PENETRATING INCISED (P.I.) wounds of the thin-walled RIGHT VENTRICLE, due to absence of the ‘’self-sealing’’ effect of the thick MUSCULAR LEFT VENTRICLE). b)	Myocardial infarction following P.I. wound of a major coronary artery. c)	Haemopericardium →CARDIAC TAMPONADE i.e. blood accumulates in the pericardial sac →  raised intrapericardial pressure  → prevents atria from filling during diastole →     CARDIAC FAILURE.

Mechanisms of formation of haemopericardium

i)	In penetrating wounds of the pericardium and heart, blood accumulates in the pericardial sac faster than it can escape.

Or

ii)	In blunt cardiac contusions/lacerations, pericardium is INTACT and there is no escape route for blood. N.B:** 300-500ml of rapidly accumulating blood is sufficient to cause CARDIAC ARREST.

3. GREAT VESSEL INJURIES – mainly involving the thoracic AORTA and Pulmonary artery:

a)	DECELERATION injuries of the AORTA commonly cause PARTIAL/TOTAL TRANSECTION of the AORTA in the descending part of its arch (± 1.5cm distal to the attachment of the ligamentum arteriosum), +/- associated parallel INTIMAL TEARS near it, called ‘’LADDER RUNG TEARS’’.  N.B:  These tears/transactions are at RIGHT ANGLES to the aortic axis.

b)	PENETRATING INJURIES, notably, STAB and GUNSHOT wounds also often involve the GREAT VESSELS.

Complications

a) Massive Haemorrhage →  shock. b) Haemopericardium → cardiac tamponade if the wound is INTRAPERICARDIAL i.e. in/near the origins of the great vessels.

INTRA-ABDOMINAL and PELVIC structure at risk are:

a)	SOLID ORGANS – liver, spleen, pancreas, kidneys, adrenal glands. b)	HOLLOW ORGANS – bowel, bladder (especially when filled with fluid or food in BLUNT TRAUMA) c)	MAJOR BLOOD VESSELS – mesenteric vessels, abdominal aorta,inferior vena cava, ileac vessels, renal and adrenal vessels. d)	PERVIC BONES.

BLUNT TRAUMA:

Commonly due to MVAs (steering wheel impacts and d/t deceleration accidents etc; ASSAULT 	(kicks, punches, stamps) FALLING OBJECTS (rocks etc).

PENETRATING TRAUMA:

Commonly due to STABS and GUNSHOT wounds

The following features may be present:

A. IN PENETRATING WOUNDS

i)	incised wounds of structures due to STABS ii)	perforating, lacerated wounds of structures due to GUNSHOTS.

B. IN BLUNT TRAUMA

i)	bruising/abrasions of the overlying SKIN. ii)	Bruising of the abdominal wall muscles and fat. iii)	Extensive bleeding into the peritoneal cavity, (if rupture of solid organ/laceration of vessels). iv)	Bowel (especially full stomach/small bowel) contusions/lacerations. v)	Mesenteric lacerations with damage to mesenteric vessels: a)	vessel lacerations --- haemorrhage b)	vessel endothelial damage --- mesenteric thrombosis --- bowel infarction --- perforation --- peritonitis. vi)	Ruptured spleen --- haemorrhage. (pathologically enlarged spleen d/t e.g. MALARIA is more vulnerable). vii)	Rupture liver --- haemorrhage. viii)	Kidney injuries – pericapsular haemorrhage (more common, contusions, rupture (rare).

Note: Kidneys are rarely damaged by frontal blunt trauma due to their deep location posteriorly in the abdomen, in the paravertebral gutters. However, they may be damaged, for example, kicks to the LOIN.

ix)	Pelvic fractures with contusion or pelvic organs x)	Ruptured bladder (if full). xi)	Genitalia – urethral, scrotal or vulvo-vaginal injuries, d/t – sexual assaults, groin kicks, stracidle injuries.

COMPLICATIONS

1.	Haemorrhage from injured spleen, liver, mesenteric vessels/aorta/vena cava/iliac vessels. 2.	infarction of bowel following mesenteric thrombosis. 3.	perforation of bowel: a)	chemical peritonitis (may cause severe SHOCK and rapid death). b)	Infection – general peritonitis.

4.	Bowel trauma – severe intractable paralytic ileus. 5.	Pancreatic trauma – widespread FAT NECROSIS (from leaked pancreatic enzyme)

Note: Certain underlying individual pathological conditions may aggravate tissue responses to injury: e.g.

a)	blood clotting dyscrasias – excessive b)	enlarged spleen – ruptures more easily with NO or minimal trauma. c)	Osteoporosis – ‘’pathological’’ fractures, .i.e. with NO or minimal trauma. d)	Complicated atheroma of the aorta – friability, therefore ruptures more easily. e)	Aortic aneurysms – rupture more easily with minimal or NO trauma. f)	Myocardial infarction scars = weaker ---rupture spontaneously or with minimal trauma. g)	Emphysematous pleural bullae --- rupture spontaneously or with minimal trauma.

SUBENDOCARDIAL HAEMORRHAGE

In victims of SEVERE TRAUMA, these may be found in the HEART:

•	On the posterior wall of the left ventricle •	The left side of the interventricular septum •	The papillary muscles •	And the trabeculae carnae. These haemorrhages are FLAME-SHAPED and CONFLUENT, and tend to occur in ONE CONTINUOUS SHEET. They are commonly seen in the following circumstance:

1.	after sudden, severe HYPOTENSION due to SHOCK (hypovolaemic). 2.	HEAD INJURIES. 3.	HYPERTHERMIA. 4.	HEAVY-METAL POINSONING e.g. arsenic 5.	HANGING 6.	OBSTETRIC CATASTROPHES, e.g. ante-/post-partum haemorrhage Ruptured ectopic) Abortions            ) →  haemorrhage Ruptured uterus )

The can appear EXTREMELY RAPIDLY – within a few heartbeats. They are NOT necessarily associated with DIRECT TRAUMA TO THE HEART!!

MECHANISM of production is obscure, but the common factor seems to be SUDDEN HYPOTENSION: Two theories: 1. Sudden reduction in intraventricular pressure with normal pressure in coronary arteries → unsupported by equal pressure in the ventricular lumen  →  RUPTURE of SUBENDOCARDIAL VESSELS.

2. Phenomenon mediated by the AUTONOMIC NERVOUS SYSTEM:- Increased catecholamines → vasospasm → subendocardial  ISCHAEMIA + NECROSIS + HAEMORRHAGE.

HEAD INJURIES

CONTENTS OF LECTURE

I  Classification II Mechanisms of Head Injuries III Scalp injuries IV Skull injuries V Membrane Haemorrhages/Extracerebral, Intracranial Haemorrhages. a)	Extra (Epi-) dural Haemorrhage b)	Subdural Haemorrhage c)	Subarachnoid Haemorrhage

VI Focal Brain Damage a)	Pontomedullary Rent b)	Cortical contusions c)	Intracerebral Haematoma

VII Diffuse Brain Damage a)	Multiple Petechial Haemorrhages b)	Diffuse Axonal Injury (DAI) c)	Hypoxic/Ischaemic Damage d)	Cerebral Swelling

VIII Raised Intracranial Pressure IX   Intracranial Infection X     Associated Extracranial Autopsy Findings XI    Special Cases: Head Injuries XII   Mechanisms of Death in Head Injuries XIII  Reconstruction of Events XIV  References

HEAD INJURIES

I Classification

1.	Scalp and Skull Injuries.

2.	Extracerebral Intracranial Haematomas (membrane haemorrhages). a)	Extradural haematoma b)	Subdural haematoma c)	Subarachnoid haemorrhage

3.	Brain Damage

a)	Focal Brain Damage

i)	Pontomedullary Rent ii)	Cortical Contusions iii)	Intracerebral haematomas

b)	Diffuse Brain

i)	Multiple Petechiae ii)	Diffuse Axonal Injury iii)	Hypoxic/ischaemic iv)	Swelling (oedema/congestion)

4.	Complications

a)	Raised intracranial pressure b)	Infection

II Mechanisms of Head Injuries

1.	Anatomical considerations

a)	The adult head weight ± 4.5kg This is pivoted on the cervical spine. b)	The scalp: various layers. c)	The skull/cranial cavity: hard – barely deformable with bony prominence. d)	Dural folds: falx and tentorium. e)	Brain: virtually incompressible, but can be deformed. f)	CSF, blood, ventricles.

2.	Principal phenomena

There are two important categories regarding the mechanisms of head injuries:

Contact and movement phenomena (non-contact).

Contact phenomena result from an object striking the head and consist of (a) local effects, e.g. laceration of the scalp, fracture of the skull, extra-dural haematomas or intracerebral haemorrhages. Contact phenomena also generate (b) shock waves at the site of impact, that travel through the brain resulting in e.g. fracture of the base of the skull, cortical contusions remote from the impact (contre coup contusions), or intracerebral haemorrhages.

Movement phenomena

The normal position and shape of the brain is affected by sudden changes in the movement of the head. The brain will be deformed and changes in the distribution of CSF will occur.

The movement of the brain can either be due to:

a)	acceleration/deceleration; or b)	Brain lag

In the past particular emphasis has been placed on their acceleration or deceleration of the head in the pathogenesis of brain damage; both, however, produce similar effects.

Acceleration or deceleration results from head movement in the instant after or prior to an injury. Angular (rotational) acceleration/deceleration causes the most serious cerebral injuries. Loss of consciousness is also associated with angular or rotational acceleration/deceleration.

In experiments on squirrel monkeys Ommaya and Gennarelli (1974) established that translational acceleration (i.e. moving the head from posterior to anterior along a straight line) did not produce concussion whereas angular acceleration (rotational) with a centre of rotation in the lower cervical spine readily did so.

When the head is suddenly set in motion the brain may lag towards the trailing cranial surface. This is termed brain lag. The principle can be demonstrated with a piece of cotton wool in a bottle filled with water. If the bottle is moved very slowly, the cotton wool does not change its position. When the bottle is moved quickly, especially in rotation, the cotton wool lags behind, i.e. it moves more slowly than the bottle.

3. The stresses/strains/forces

The contact and movement phenomena lead to various strains:

a)	Compressive strains: The tissue are compressed or forced together, e.g. scalp being split (lacerated) against the underlying skull.

b)	Tensile strains: The tissues are being pulled apart or rarified, e.g. tearing or avulsion of scalp; skull fractures on bending of the bone.

c)	Shearing strains: The tissues are deformed or distorted (like a pack of cards being displaced and each card moves or slides upon the adjacent card). **This is the most important force or strain in the pathogenesis of brain injury.

III Scalp Injuries

1. Basic Anatomy (5 layers)

1.1	S – Skin 1.2	C – Dense Connective Tissue 1.3	A – Epicranial aponeurosis (flattened tendon uniting the bellies                 of  the occipito-frontalis muscle) 1.4	L – Loose Connective Tissue (Subaponeurotic layer) 1.5	P – Periosteum (pericranium)

2. Wounds of the scalp are similar to those found elsewhere on the body (.e.g. incised and bullet wounds), but can be obscured or modified by hair, hats, helmets etc. Abrasions of the scalp are, for example, less common due to protective effect of the hair.

3. Lacerations

a)	May simulate incised wounds (the scalp splits when compressed against skull). b)	May bleed profusely (very vascular: also heals rapidly). c)	Shape and character may indicate weapons e.g:

i) Stellate laceration    – rounded object         ii) Y-shaped laceration – rod (linear object) iii) Crescent shape         - hammer

4. Bruises of the Scalp

Haemorrhages between the various layers of the scalp. Very often in the subaponeurotic layer (subaponeurotic haemorrhage): Due to lack of anterior attachments of the epicranial aponeurosis, a bruise to the frontal region may gravitate into the upper and lower eyelids (peri-orbital haematoma) or a temporal bruise may gravitate down behind the ear.

Note: Other causes of a peri-orbital haematoma (‘’black eye’’): i) direct trauma ii) percolation of blood from a fractured orbital plate (anterior cranial fossa).

5. Site of Injury

With injuries to the vertex, one should be very suspicious of an assault rather than a fall.

6. Emissary Veins

Traverse the layers of scalp and penetrate skull to communicate with the intracranial venous circulation. This provides an easy pathway for the passage of infection from the scalp to the intracranial contents.

IV. THE SKULL

1. Anatomy

The adult cranium consists of two parallel tables of compact bone separated by a central zone of cancellous bone (Diploe). The outer table is about twice the thickness of the inner table. It varies in thickness in adults and from place to place in the same skull.

2. Skull Fractures

2.1 Fractures due to direct application of force

a) Focal damage

When a blunt instrument strikes the skull or the skull hits a hard object, damage to the skull may be:

i) Limited to the site to which the force was applied or ii) remote from the point of impact, (‘’shockwave’’) or iii) both local and remote from the site of impact.

The effects of any force striking the head will vary in degree according to the elasticity and tensile strength of the area struck, the shape, speed and weight of the injuring agent, and the position and degree of fixation of the head at the moment of impact.

Under impact of the striking force the outer table of the skull is compressed and the inner table stretched (tensile). **The break in the bone therefore usually begins in the inner surface extending to involve the outer surface. Sometimes only the outer table is depressed. If the force is bullet passing through the bone, the fracture may be entirely local The bony defect in the outer table is cleanly cut and the inner table is beveled (entrance wound.)  There may be fissure fractures radiating from the bony defect.

b) General deformation of the skull

With considerable force applied to one point there may be distortion of the shape of the skull with fissured fractures at sites distant from the point of impact to the base. The run in the direction of, and may link up with, bone damage at the site of impact.

The vault, because of its convexity and elasticity, is admirably constructed to withstand sudden distortion without breaking. The base, on the other hand, because of its rigidity and the many foramina passing through it, is peculiarly susceptible to fracture when the shape of the skull as a whole is suddenly changed.

Of considerable importance in determining the course pursued by fracture lines from the point of impact to the base are the six reinforcing buttresses that project from the base. These bony thickenings are: mid-frontal, mid-occipital, anterior and posterior temporal. They tend to direct the line of fracture toward the floor of their respective fossae.

2.2 Fractures of the skull due to Indirect force

When the force is transmitted to the skull through the mandible or the spine, a more-or-less annular fracture may occur at the base and surrounding the foramen magnum (ring fracture). This may occur if the force drives:

i) the mandible against the base of the skull, or ii) the skull against the spine; or iii) the spine against the skull, e.g. in heavy falls on buttocks or feet; or v)	If the blow tends to tear the skull away from the spine, e.g. in upward and forward blows against the spine, e.g. in upward and forward blows against the occipital. The skull to the spine.

3. Medico-legal aspects of skull fractures

a)	The exact amount of force causing a fracture cannot be determined with certainty. b)	Death is not caused by a skull fracture per se but by accompanying lesions e.g. brain injury, haemorrhages, infection etc. c)	A skull can fracture without brain damage and brain damage can occur without a fracture. d)	Skull fractures can indicate the type of weapon used, e.g. axe.

V. MEMBRANE HAEMORRHAGE EXTRACEREBRAL/INTRACRANIAL HAEMORRHAGES

A. Extra- (Epi-) dural haemorrhage is situated between the skull and the dura mater. This is classically caused by a rupture of the middle mengineal artery (the anterior branch in 90% of cases) in the region of the squamous part of the temporal bone. This type of haemorrhage is usually associated with fractures of the skull in this area. 'Bold text'Bold textBold text'Bold text''