Chapter 5 Head and Spinal Injuries

of microglia, presumably as part of a repair process, with generalized oedema. Swelling of the brain is
congregate at the site of ruptured axons. These are best
extremely common after a substantial head injury,
seen in 20 m thick sections stained with cresyl violet or
especially in children. Though it is an almost inevitable
more specifically using CD68 or Iba1 immunostaining. accompaniment of almost all intracerebral damage as
One problem with the microscopic evidence of both either a local or general phenomenon, it can occur as
microglial clusters as well as DAI (as demonstrated by the sole abnormality and not infrequently prove fatal,
APP expression), is that neither of them is specific as
particularly in young victims. It is the most common
a marker for trauma: retraction globes may also be seencause of raised ICP, being seen more often than
around the periphery of natural lesions such as cerebral
localized space-occupying lesions such as haematomas
infarcts and haemorrhages and microglial clusters have and tumours, though of course these often coexist with
been reported in viral/human immunodeficiency cerebral oedema.
virus (HIV) encephalitis, previous global hypoxia and Uncontrollable swelling and subsequent rise in ICP
fat embolism. Geddes et al. conclude in their excellentis the single most frequent cause of death after severe
review that the demonstration of traumatic axonal traumatic brain injury.42,129 Oedema may be vasogenic,
damage is likely to be of limited use in most forensic hydrostatic, cytotoxic, osmotic or hydrocephalic
situations, except perhaps to confirm that there has (Table 5.1).
been a head injury.128 In vasogenic oedema the permeability of the blood
brain barrier (BBB) increases as the result of an injury
Cerebral oedema to the vasculature due to tumour, trauma, infection,
intracerebral haemorrhage or infarction. Oedema fluid
Swelling of the brain tissue may be a local phenomenon
is primarily in the extracellular space and tends to occur
around almost any lesion, be it contusion, laceration,
in the white matter.
tumour or infarct, but here we are more concerned

Table 5.1 Types of cerebral oedema

Type Oedema location Bloodbrain barrier Mechanism Clinical situations

permeability
Vasogenic Extracellular Increased Increased Tumour, trauma,
White matter permeability of infection, abscess,
vessel walls ICH, infarction
Hydrostatic Extracellular Increased Increased blood Hypertensive
White and grey matter pressure encephalopathy,
epileptic seizure
Cytotoxic Intracellular (mainly) Normal Lack of energy or Hypoxia/ischaemia,
Grey matter (mainly) toxic influence leads Reyes syndrome,
to malfunction of some intoxications
Na/K pump (e.g. cyanide)
Osmotic Intra- and extracellular Normal Hypo-osmolarity of Hyponatraemia,
White and grey matter plasm SIADH, excessive
infusion therapy,
water intoxication,
freshwater drowning
Hydrocephalic Extracellular Normal Leakage of High-pressure
Periventricular white pressurized liquor hydrocephalus,
matter into periventricular pseudotumour

brain tissue cerebri (idiopathic

intracranial
hypertension [IIH])

ICH: intracerebral haemorrhage; SIADH: syndrome of inappropriate antidiuretic hormone hypersecretion.

Adapted from Paetau A, hman J, Kalimo H. Aivoedeema. In: Mkinen M, Carpn O, Kosma V-M, Lehto V-P, Paavonen T,
Stenbck F (eds). Patologia, Kustannus Oy Duodecim, 2012 with permission.
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In hydrostatic oedema BBB fails because of increased
blood pressure, as in hypertensive encephalopathy
or in epileptic seizure. The excess water is mainly
extracellular both in white and grey matter.
Cytotoxic oedema results from disturbance of the
energy-dependent transmembrane ionic pumps, most
commonly due to ischaemia as a result of vascular
occlusion or other causes, such as traumatic brain
injury, metabolic disorders or certain intoxications.130
This leads to intracellular accumulation of fluid, mainly
in the grey matter, due to its high metabolic activity
and greater astrocyte density.
Osmotic oedema results from hypo-osmolality of
blood plasma in conditions where the BBB is intact but
blood becomes too diluted, e.g. because of freshwater
drowning, water intoxication or excessive administration
of intravenous fluids or the syndrome of inappropriate
antidiuretic hormone hypersecretion (SIADH).
Hydrocephalic or interstitial oedema is caused by
leakage of pressurized CSF through the ependyma
into periventricular brain tissue because of obstruction
within the ventricular system or the obstruction is distal
to the ventricles, e.g. decreased transfer of CSF into the
subarachnoid space, impaired flow of CSF in constricted
subarachnoid space or hindered reabsorption of CSF via
arachnoid granulations into venous blood.
The autopsy features of cerebral oedema are readily
recognized. On removing the calvarium, the dura
is stretched and tense, the brain bulging through the
first incision in the membrane. The gyri are pale and
Normal
Normal weight
(<1500g)
Palpable sulci
Rounded gyri
Normal hippocampal
gyrus and uncus
Normal cerebellar
tonsil
Figure 5.48 Signs of cerebral oedema.
Cerebral injuries
flattened, and the sulci filled, giving the normally
corrugated cerebral surface a smoothness that can
easily be felt at autopsy. The cut surface is pale and,
especially in children, the ventricles may be reduced to
slits by the swelling of the adjacent white matter.
Severe cerebral oedema causes the larger volume
cerebral hemispheres to press down upon the tentorium
and herniate through the tentorial opening. The
hippocampal gyrus may impact in the opening, lesser
degrees causing grooving of the hippocampal unci.
Both these effects may lead to haemorrhage and necrosis
at the sites of pressure, especially where the sharp edge
of the tentorium cuts into the cerebral tissue. The tonsils
of the cerebellum may be impacted or coned into the
foramen magnum, and sometimes are forced down into
the upper part of the spinal canal. The pathologist must be
careful not to mistake the normal anatomical grooving
that often exists around the cerebellar tonsils for coning.
There should be other signs of brain swelling and true
tonsillar herniation will show discolouration or even
necrosis of the ischaemic, trapped tissue (Figs 5.485.50).
Cerebral oedema may be the only intracranial
abnormality found at autopsy after a substantial head
injury has occurred. This seems to be more commonly
found in children and, in the absence of any other
demonstrable lesions, the cause of death has to be
attributed to this swelling of the brain, compressing the
vital centres in the brainstem.
Obviously, many other cases of cerebral oedema
resolve either spontaneously or with treatment, so
Oedematous
Increased weight
(>1500g)
Flattened gyriIn
Filled sulci
Grooved uncus
Swollen hipocampal
gyrus
Herniated cerebellar
tonsil
Midline shift if
oedema is unilateral
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Chapter 5 Head and Spinal Injuries
Figure 5.49 Tonsillar herniation as a consequence of
lumbar puncture in a patient with increased intracranial
pressure. The pressure gradient has forced the cerebellar
tonsils into foramen magnum and caused compression of
the brainstem and patients death. (Reproduced by kind
permission of Professor H. Kalimo.)
Figure 5.50 Transtentorial herniation in brain trauma.
Compression of medial temporal lobes against the
tentorium edges has caused bilateral haemorrhagic
necroses (white arrows). In addition, the compression of
left posterior cerebral artery has resulted in haemorrhagic
infarcts in the left temporal lobe (black asterisk). There
is also a slight shift of the midline to the right (white line).
(Reproduced by kind permission of Professor H. Kalimo.)
206
that fortunately no opportunity arises to prove its
existence by post-mortem examination. Such oedema
is, however, not infrequently found during surgical
exploration for a meningeal haemorrhage, the latter
sometimes being presented though often only brain
swelling is demonstrated.
Cerebral oedema may be self-potentiating, in
that once it begins as a result of direct brain trauma,
the consequent rise in ICP then impairs the venous
return from the intracranial sinuses. The pressure is
insufficient to restrict the arterial inflow, so further
congestion and swelling occur. This may lead to
worsening cerebral hypoxia and oedema to the stage
of actual cerebral infarction and brain death again, a
distressing common syndrome seen especially in child
victims of head injuries, usually from road accidents.
Cerebral oedema, either traumatic or hypoxic, can
develop with surprising rapidity, especially in children.
Macroscopic evidence of brain swelling can be seen at
autopsy in cases where the interval between trauma or
onset of hypoxia and death was less than 1 hour.
Several methods are available to reverse oedema,
including hyperventilation, which acts by providing
full oxygenation and reducing the peripheral carbon
dioxide tension, thus causing constriction of arterioles
resulting in a reduction of the amount of intracranial
blood and therefore also the brain volume and
transudation.
Diagnosis of early cerebral
hypoxiaischaemia
Unfortunately for the pathologist, most of the hypoxic
ischaemic conditions seen in forensic practice cause
death too quickly for any recognizable histological
changes to develop. Acute deaths from strangulation,
suffocation and choking occur within minutes or less,
even excepting the sudden vasovagal type of cardiac
arrest.
There are, however, occasions when a longer period
of survival occurs after an acute ischaemic episode and
in some of these there may be the opportunity to detect
histological changes in the central nervous system
(CNS). Probably a minimum of 24 hours of survival
is necessary for unequivocal changes to be observed,
though some neuropathologists claim to detect signs
after as little as 1 hour. More cautious investigators
prefer 4 hours as the minimum. A short post-mortem
interval is a considerable advantage in searching for
these changes, as they are subtle and can be overlaid by
post-mortem autolysis, even if the latter is slight.