8/13/2019 Pathophysiology EDH
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Pathophysiology
The underlying cause of death in patients with EDHs is the
volume of blood that constitutes them aswell as the rapidity in
which this blood accumulates. In most fatal cases the volume of
blood isbetween 75 to 120 ml, with some showing greater volumes.
When epidurals reach this volumerapidly, as occurs in arterial
bleeds, they exert what is referred to as mass effect, which in
turnincreases intracranial pressure (ICP).
Within the skull there is a normal ICP, which is usually between
0-10 mm Hg, which is found in thebrain itself and cerebrospinal
fluid (CSF). This ICP in turn exerts pressure on the blood vessels
withinthe cranium. Any change in ICP is due to a change in volume
of one of these components, the brain,CSF or the blood in the
vessels. This pressure –volume relationship within the cranial
vault isreferred to as the Monro-Kellie hypothesis. In essence what
it says is that in order to maintain normal
ICP any increase in volume of one of these components, such as
an EDH, must be compensated for bya decrease in the volume of the
other components. Thus, the mass effect induced by the expandingEDH
must give rise to a decrease in volume within the brain, the
ventricles with its contained CSF andthe volume of blood within the
vessels in order to try and maintain normal ICP. These
compensatorymechanisms can maintain an ICP up to 20-25 mm Hg, which
is considered the upper range of normal,for any change in volume of
less than 75 to 120 ml. However, once the volume of EDH exceeds
therange of 75 to 120 ml, these compensatory mechanisms can no
longer maintain even the upper limitsof a normal ICP. Once a
pressure of 25 mm Hg is reached any continued expansion of the EDH
willlead to marked life threatening increases in ICP. At this point
the continued expansion of the EDH willcause the underlying
cerebral hemisphere to shift toward the opposite side. This
shifting of thecerebral hemisphere is referred to as a midline
shift and or subfalcine herniation. Since subfalcineherniation is
the most common type and believed to be the precursor of all other
types of herniation Iwill give a brief description of this form of
herniation.
Subfalcine herniation is also referred to as cingulated
herniation. It is due to displacement of thefrontal lobe of the
shifting cerebral hemisphere toward the opposite side. This results
in its mostmedial part, that which is adjacent to the flax cerebri,
the cingulated gyrus, to pass beneath theinferior border of the
falx. In the process this can cause compression of the anterior
cerebral artery,which in turn decreases blood supply to the frontal
lobe. Such shifting is also associated with collapseof the shifting
cerebral hemispheres ventricles with displacement of its contained
CSF into the spinalcanal. The compromise of blood supply of the
anterior cerebral artery can lead to edema of theparenchyma
supplied by that artery, which in turn causes an increase in volume
of that portion of thebrain due to the accumulation of edema fluid,
and in turn is followed by further increase in ICP. Thus,a vicious
cycle is created, which if not addressed quickly and adequately
will lead to other severeforms of herniation leading to pressure on
the brainstem through its downward displacement into theforamen
magnum and its consequent compression by the cerebellar tonsils.
Such pressure willultimately lead to hemorrhages within the
midbrain (Duret hemorrhages) with compromise of thereticular
activating system and subsequent coma and compromise of the cardiac
and respiratorycontrol centers within the medulla, which leads to
death.
