Chapter Regional

injuries

Introduc
Head injuries

9
Neck injuries
Spinal injuries
Chest injuries
Abdomen
Further information sources

ti

■ Introduction
Specific regions of the body may be particularly
susceptible to types of trauma that may not cause
serious or fatal injury elsewhere. A good example
of this may the single stab wound. If this penetrates
the limbs then a serious or fatal outcome is unlikely,
unless a large artery is injured. If a single stab
wound penetrates the heart or the abdominal aorta
on
a fatal outcome is much more likely. Consideration
of patterns of injuries according to the body region,
and the potential complications of those injuries, is
therefore an important component in both the clini-
cal and pathological evaluation of trauma.
■ Head injuries
Any trauma to the head or face that has the potential
for damaging the brain can have devastating conse-
quences. Normally the brain is protected within the
bony skull, but it is not well restrained within this
compartment and injuries to the brain result from
dif- ferences between the motion of the solid skull
and the relatively ‘fluid’ brain. There are three main
com- ponents of the head: the scalp, the skull and the
brain.
Scalp
The scalp is vascular, hair-bearing skin; at its
base is a thick fibrous membrane called the galea
aponeurotica. Lying between the galea and the
skull is a very thin sheet of connective tissue that
is penetrated by blood vessels (emissary veins)
emerging through the skull, and beneath this con-
nective tissue is the periosteum of the outer table
of the skull. Injury to the vascular scalp can lead
to profuse bleeding which, although can usually
be stopped by local application of pressure, in
some circumstances (e.g. acute alcohol intoxica-
tion) can lead to physiological shock and death.
Bleeding scalp injuries can continue to ooze after
death, particularly when the head is in a depend-
ent position.
The scalp is easily injured by blunt trauma as
it can be crushed between the weapon and the
underlying skull. Bruises of the scalp are associated
with prominent oedema because this normal tissue
response cannot spread and dissipate as easily as in
other areas of the body. The easiest way to detect
scalp injuries is by finger palpation, but shaving is
often required for optimal evaluation, documenta-
tion and photography of injury in the deceased, and
98
Figure 9.1 Scalp laceration caused by a heavy torch. Following
shaving of hair from around the injury, the crushed and abraded
wound edges can clearly be seen.
sometimes in the living. In the living a good history
from the individual, and lighting, can localize any
injury. It is surprisingly difficult to identify the site
of profuse bleeding from the scalp in an individual
with abundant head hair. In the living if there is
evidence of stamping or implement assault it may
also be necessary to shave the hair so that potential
‘patterned injury’ can be identified and recorded for
overlay comparison.
Lacerations of the scalp can usually be distin-
guished from incised wounds; careful examination
often reveals crushed, abraded or macerated wound
edges and tissue bridges in the wound depths
(Figure 9.1). Occasionally such a distinction is more
difficult, and it may be that the nature and properties
of the scalp, its relative ‘thinness’ and tethering to
the skull, contributes to the appearance of an incised
wound following blunt impact.
Tangential forces or glancing blows, either from
an implement or from a rotating wheel (e.g. in a
road traffic accident), may tear large flaps of tis-
sue, exposing the underlying skull. If hair becomes
entangled in rotating machinery, portions of the
scalp may be avulsed. These are referred to as
‘scalping‘ injuries.
Skull fractures
The skeleton of the human head is divided into
three main parts: the mandible, the facial skeleton
and the closed container that contains the brain,
the calvaria. The calvaria is made up of eight plates
of bone, each of varying thickness, with buttresses
may also cause bilateral periorbital bruising, as may
impacts to the central forehead, even though no
passing through and across the bony margins. The
skull is designed in part to protect the brain and in
part to provide a mobile but secure platform for the He
receptor organs of the special senses. ad
The complexity of the skull structure means inj
that mechanisms of skull fracture can be extremely uri
complex as a result of both direct force (e.g. direct
impact to the parietal bone causing a linear frac-
es
ture) and indirect force (e.g. an orbital blowout
fracture caused by impact to the eyeball). These
mechanisms have been studied extensively and
much is known about the way the skull behaves
when forces are applied to the head. The skull,
although rigid, is capable of some distortion and if
the forces applied exceed the ability of the skull
to distort, fractures will occur. The site of fracture
therefore represents that point at which the
delivered energy has exceeded the capability of
the skull to distort, which is not necessarily at the
site of impact, unless that applied force has resulted
in a localized depressed fracture. The skull’s capa-
bility to distort before fracturing varies with age,
and an infant skull may permit significant distortion
following impact without fracturing.
Apart from depressed fractures underlying major,
localized areas of trauma, skull fractures alone are
not necessarily life threatening. The presence of a
skull fracture indicates the application of blunt force
to the head, and it is the transmission of such force to
the intracranial contents – including the brain –
that has the potential to cause life-threatening
injury. Fatal brain injury can occur in the absence
of exter- nally visible scalp injury, or skull fracture
and, con- versely, scalp injury overlying skull
fracture may be associated with minimal (or no
recognizable) brain injury or neurological deficit. In
clinical practice, however, intracranial injury
should always be sus- pected in the presence of
skull fracture.
A pathologist can only make broad comments
about the possible effect upon an individual of a
blow to the head. As with all injuries, a wide spec-
trum of effects is to be expected in a population sus-
taining the same injury in exactly the same way.
Scalp abrasions, bruises or lacerations represent
contact injuries, and their presence will assist in the
identification of the point of contact/impact. Bruises,
however, may evolve, and ‘move’ in tissues planes,
and may not precisely represent the site of contact/
impact by the time the scalp is examined. Abrasions
do identify sites of impact. A direct blow to the nose
can cause blunt force injuries to the nose itself, but
99
impact was applied to the eyes or orbital region.
Blows to the top of the head commonly result in
 long, linear fractures that pass down the pari- etal
bones and may, if the force applied was severe, pass
inwards across the floor of the skull, usually just
anterior to the petrous temporal bone in the middle
cranial fossa. If the vault fractures extend through
the skull base from both sides, they may meet in the
midline, at the pituitary fossa, and pro- duce a
complete fracture across the skull base: this is
known as a hinge fracture (Figure 9.2). This type of
fracture indicates the application of severe force and
may be seen, for example, in traffic accidents or falls
from high buildings.
Falls from a height onto the top of the skull or
onto the feet, where the force is transmitted to the
base of the skull through the spine, may result in
ring fracture of the base of the skull around the
foramen magnum, whereas significant ‘broad sur-
face’ blows to the skull vault, particularly the pari-
etal bones, may result in a ‘spider’s web’ type of
fracture composed of radiating lines transected by
concentric circles.
Depressed fractures will force fragments of skull
inwards and, because of the bilayer construction of
Figure 9.2 A ‘hinge fracture’ of the skull base caused by impact
to the left side of the head after the victim was thrown to the
9 Regional injuries
ground, having been hit by a car.
100
Emissary vein Scalp Cortical vein
Figure 9.3 Depressed skull fracture, with rounded contours,
closely replicating the dimensions of a round-headed hammer.
the skull, the degree of inner table fragmentation
may be much greater than that of the outer table and
fragments of bone can be driven into the underly-
ing meninges, blood vessels and brain tissue. Blows
to the head by implements, such as round-headed
hammers may cause depressed vault fractures that
have a curved outline with dimensions and a profile
similar to that of the impacting surface of the imple-
ment (Figure 9.3).
The orbital plates, the upper surfaces of the orbits
within the skull, are composed of extremely thin
sheets of bone which are easily fractured, and these
‘blow-out’ fractures may be the only indication of
the application of significant force to the skull. They
are frequently seen as a consequence of a fall onto
the back of the head.
Special mention must be made of skull fractures
in children and infants. These fractures are
extremely important forensically but their
interpretation can be extremely difficult. It is self-
evident that skull fractures may be the result of
either deliberate or accidental acts and
differentiation will depend on the consideration of
as much relevant information as possible (see also
Chapter 7, p. 71).
Intracranial haemorrhage
The clinical significance of any space-occupying
lesion within the cranial cavity is the effect that the
raised intracranial pressure caused has on brain
structure and function.
Intracranial bleeding, resulting in a space-
occupying lesion, is the cause of many deaths and
disability following head injury, often as a result of
delayed or missed diagnosis. Bleeding can compress
the brain and, if it continues for sufficient time, and
D
u
ra Cerebral artery Skull
Pericranium Fracture line
Thicker outer table
Diplöe Dura He
Thinner inner table
Meningeal artery
ad
Venous sinus inj
Pia mater
Arachnoid mater Haematoma uri
es
Subarachnoid space Brain
Arachnoid
granulation Meningeal artery
Falx (a)
Figure 9.4 Forensic anatomy of the skull and meninges.

in sufficient quantity, can raise the pressure within

the cranial cavity. As the intracranial pressure
increases, blood flow to the brain decreases and,
if the intracranial pressure reaches a point where it
equals or exceeds arterial blood pressure, the blood
flow to the brain will cease.
The anatomy of the blood vessels within the skull
has a major influence on the type of bleeding that
will occur following trauma (Figure 9.4). The menin-
geal arteries run in grooves in the inner table of the
skull and lie outside the dura. They are generally
protected from the shearing effect of sudden move-
ment but are damaged by fracture lines that cross
their course. The venous sinuses lie within the dura
and the connecting veins pass between the sinuses
and the cortical veins; these vessels are at particular (b)
risk of ‘shearing’ injury when there is differential
movement between the brain and the skull. The true Figure 9.5 Extradural haemorrhage. Schematic representation
(a) of the formation of an extradural haemorrhage and autopsy
blood supply to the brain, the cerebral arteries and
appearance (b) of a large right-sided, temporoparietal, extradural
veins, lies beneath the arachnoid membrane and is haemorrhage associated with deep scalp bruising at the site of impact.
generally protected from all but penetrating injuries. There was a linear skull fracture on the right passing through the
Two main types of haemorrhage within the skull middle meningeal artery.
cavity, each resulting in haemorrhage in different
planes, are extradural and subdural haemorrhage.
damaged perforating veins or dural sinuses, in which
Extradural haemorrhage is associated with dam-
case the development of symptoms will be slower.
age to the meningeal artery, particularly the middle
The second most important cause of traumatic
meningeal artery, in its course in the temporal bone
intracranial haemorrhage is damage to the commu-
(Figure 9.5). Damage to this vessel leads to arterial nicating veins, as they cross the (potential) ‘subdural
bleeding into the extradural space. As the blood space’, causing subdural haemorrhage (Figure 9.6).
accu- mulates, it separates the dura from the This venous damage is not necessarily associated
overlying skull and forms a haematoma. Arterial with fractures of the skull. In many instances, par-
bleeding is likely to be fast, and the development of ticularly in the very young and the very old, there
the haematoma will result in a rapid displacement may be no apparent history or evidence of any
of the brain and the rapid onset of symptoms. trauma to the head. These venous injuries are asso-
Extradural haemorrhages are ones that in the clinical ciated with rotational or shearing forces that cause
setting may present with head trauma and then a the brain to move relative to the inner surface of
‘lucid period’ of half an hour or more, before rapid the skull; this motion is thought to stretch the thin-
deterioration. Rarely, extradural haemor- rhage can walled veins, causing them to rupture. The venous
develop as a result of venous bleeding from

101
 Dural sinus
Skull subdural haematoma) may be enclosed in gelatinous
Dura ‘membranes’, which can harden into a firm rub-
Arachnoid bery capsule in extreme cases. Such old collections
of subdural blood are most commonly seen in the
Pia and
brain surface elderly, whose cerebral atrophy allows space for the
formation of the haematoma without apparent sig-
nificant clinical effect. Chronic subdural haematomas
are also seen in those prone to frequent falls, such
Ruptured bridging vein as those with alcohol dependencies. Occasionally,
Haematoma subdural haemorrhages may be present for many
(a) months or even years before diagnosis, which
can be difficult because of the often non-specific
neurological changes. Spontaneous subdural haem-
orrhages car occur.
The effects of both extradural and subdural
haemorrhages are essentially the same: they can
act as space-occupying lesions compressing the
brain and, as discussed below, at their most
severe, causing internal herniation (e.g. through
the tento- rium cerebelli). However, there may also
be result- ant brain contusion and swelling because
of trauma, which accelerates the clinical
deterioration and can hasten a fatal outcome.
(b)
Figure 9.6 Subdural haemorrhage. Schematic representation of the
formation of a subdural haematoma (a) and autopsy appearance of
an acute right-sided subdural haemorrhage (b).
Traumatic subarachnoid
haemorrhage
bleeding lies in the subdural space. Recent subdural Small areas of subarachnoid haemorrhage are
haemorrhages are dark red in colour and shiny, but common where there has been direct trauma to
begin to turn brown after several days; microscopi- the brain, either from an intrusive injury, such as
cally, haemosiderin can be identified with Perl’s a depressed fracture, or from movement of the
stain (Figure 9.7). Older subdural collections brain against the inner surface of the skull as
(chronic a result of acceleration or deceleration injuries.
These small injuries are usually associated with
areas of underlying cortical contusion and some-
times laceration.
Large basal subarachnoid haemorrhages can
be of traumatic origin and follow blows or kicks to
the neck, particularly to the upper neck adjacent to
the ear, but any blow, or even perhaps avoidance
of a blow, which results in rapid rotation and flex-
ion of the head on the neck can cause this damage.
The vertebral arteries are confined within forami-
nae in the lateral margins of the upper six cervi-
cal vertebrae and are susceptible to trauma either
9 Regional injuries

with or without fracture of the foramina. It was

Figure 9.7 Microscopy of a ‘healing’ acute subdural
haemorrhage, of approximately 4 days’ duration, with iron-
pigment-laden macrophages demonstrated by Perls’ staining.
traditionally thought that traumatic damage to the
arteries occurred at the site at which they penetrate
the spinal dura to enter the posterior fossa of the
skull, although it is becoming increasingly evident
that arterial injury leading to basal subarachnoid

102

(a)
(b)
Figure 9.8 Traumatic basal subarachnoid haemorrhage.
(a) Autopsy appearance of basal subarachnoid haemorrhage,
covering the brain-stem, visualized following removal of the cerebral
hemispheres and tentorium cerebelli. The basilar artery has been
ligated. (b) The source of the bleeding is a tear in a vertebral artery,
confirmed following visualization of fluid leakage from the
cannulated injured vessel.
haemorrhage occurs in the intracranial portions of
the vertebral arteries (Figure 9.8).
Most basal subarachnoid haemorrhages are,
however, non-traumatic in origin and arise from the
spontaneous rupture of a berry aneurysm of one of
the arteries in the circle of Willis (see Chapter 6,
p. 59). In the deceased, particular care must be taken
to exclude this natural cause, and special autopsy
dissection techniques are required to evaluate the
integrity of the vertebral arteries.
Brain injury
Injuries that have resulted in skull fractures or
intracranial haemorrhage are clear macroscopic
markers of significant force having been applied
to the head and therefore to the brain. Sometimes,
however, these markers are absent but, as a result
of acceleration or deceleration forces, the brain has
been significantly traumatized. Whatever the pre-
cise cause of the trauma, the effects on the brain,
as a whole, are the same and, as a consequence
of the body’s response to primary traumatic brain He
injury, cerebral oedema develops (i.e. secondary ad
brain injury). The mechanism of cerebral oedema is inj
complex, but is in part caused by transudation of uri
fluid into the extracellular space.
es
As oedema develops, the brain swells and, as
the skull cannot expand beyond the confines of the
cranial cavity to compensate for this swelling, the
intracranial pressure rises and the brain is
‘squeezed’ around meningeal folds (downwards
through the tentorium cerebelli, causing injury to the
temporal lobe unci and exerting pressure on the
brain-stem, for example), and downwards through
the foramen magnum (i.e. coning, causing injury to
the cerebellar tonsils and exerting pressure on the
brain-stem) in a process called internal herniation
(Figure 9.9).
The weight of the oedematous brain is increased
and the surface of the brain is markedly flattened,
often with haemorrhage and necrosis of the unci
and the cerebellar tonsils; sectioning reveals com-
pression of the ventricles, sometimes into thin
slits.
Direct injuries to the brain from depressed
or comminuted skull fractures result in areas of
bruising and laceration of the cortex, often asso-
ciated with larger sites of haemorrhage. These
injuries can occur at any site, above or below
the tentorium. Penetrating injuries from gunshots
or from stab wounds can cause injuries deep
within the white matter, and the tissue adjacent
to the wound tracks will often be contused and
lacerated.
Normal Oedematous
Normal weight Increased weight
(<1500 g) (>1500 g)
Palpable sulci Flattened gyri
Rounded gyri
Filled sulci
Normal Grooved uncus,
hippocampal swollen hipocampal
gyrus and
uncus
gyrus
Herniated cerebellar
Normal cerebellar tonsil
tonsil Midline shift if oedema
is unilateral
Figure 9.9 Schematic representation of the effects of brain
swelling and ‘internal herniation’ caused by raised intracranial
pressure.
103