Intracranial disorders
Pathophysiology
of raised intracranial pressure
Introduction
The adult skull may be regarded as a rigid
unyielding box containing brain, cerebrospinal fluid (CSF) and blood. At normal
supine pressures of 5—15 mmHg (6—18 cmH2O), measured from the
level of the foramen of Munroe, these three components maintain volumetric
equilibrium. An increase in the volume of any one of the components will result
in an increase in intracranial pressure (ICP) unless there is a proportionate
decrease in the volume of one of the other components. These observations were
first reported by Alexander Munro (Professor of Anatomy, Edinburgh, 1783) and 40
years later confirmed by Kellie — becoming known as the Munro—Kellie
doctrine.
Owing
to compensatory volumetric changes having physical and physiological limits, the
ability to maintain a constant ICP can be exceeded by a change in volume that is
too fast or too great. This intracranial pressure—volume relationship is
illustrated in the curve (Fig. 35.8).
Initially
quite large increases in volume produce only small changes in pressure. During
this phase the brain adapts by shifting CSF and moving blood from venous
structures. A critical point is reached however when small changes in volume
cause exponential increases in ICP.
The
relationship of volume to pressure is described in terms of compliance or
elastance of the intracranial space. Compliance is expressed as ( dV/dP) and is the amount of ‘give’ available within the
intracranial compartment. Elastance is the inverse and is the resistance offered
to the expansion of a mass or the brain itself. When patients initially present
with symptoms of raised ICP it is invariably when brain compliance has been
reduced and small volume changes have the potential to cause precipitous
increases in ICP and a reduced level of consciousness.
Between
physiological ranges of blood pressure, the brain is able to maintain a constant
cerebral blood flow. This is achieved by a process called autoregulation (Fig. 35.9),
whereby the brain adjusts the intracranial vascular resistance. With
hypovolaemic shock, malignant hypertension, subarachnoid haemorrhage or
diffuse severe head injuries, this ability is compromised and the cerebral
perfusion pressure becomes virtually dependent on the mean arterial pressure.
Normal
cerebral blood flow (CBF) is about 800 ml/min or 20% of the total cardiac
output. The blood flow is a function of the cerebral perfusion pressure (CPP)
and the cerebral vascular resistance (CVR).
The
cerebral perfusion pressure is a function of the systemic mean arterial pressure
(MAP) and the ICP.
CPP = MAP - ICP
As
intracranial pressure increases, in order to maintain a constant CPP, there has
to be a compensatory rise in the MAP. A hypertensive response is therefore
elicited which classically is associated with a bradycardia. This is termed the
Cushing reflex after the eminent American neurosurgeon.
Clinical features
These are largely determined by the underlying
cause. However, some of the clinical symptoms and signs will be the same:
•
headache;
•
nausea and vomiting;
•
drowsiness;
•
papilloedema.
These
headaches are usually worse in the morning owing to vasodilatation caused by
hypoventilation and consequent CO2 retention during sleep. They are
typically progressive but relieved by an upright position and are frequently
associated with nausea and vomiting. As the brain has no sensation they are
caused by traction and distortion of the pain-sensitive blood vessels and dura.
Compression of the reticular activating system in the brainstem results in
drowsiness. In an infant, raised ICP will cause a tense bulging fontanelle.
As
the eyes are extensions of the forebrain, the optic nerves carry with them the
meningeal coverings. The ICP is thus transmitted directly to the optic nerve
head via the CSF. This results in obstruction to axoplasmic flow in the retinal
neurons causing swelling. This is seen on fundoscopy as blurring of the disc
margins (Fig. 35.10),
eventually
retinal haemorrhages and if prolonged, optic atrophy. Traction on the abducent
(sixth) nerves by caudal displacement of the brainstem may cause nerve palsies
— the false localising sign.
Continuous monitoring of ICP reveals
stereotyped variations superimposed upon baseline fluctuations. ‘A’ waves
are transient plateaux of increased pressure to greater than 50 mmHg which last
for 5—10 minutes. They are abnormal and indicate low compliance within the
intracranial cavity. Skull X-rays may demonstrate sutural separation in
children, pronounced ‘copper-beating’ marking of the cranial vault and
thinning of the dorsum sellae with erosion of the posterior clinoid processes.
Treatment
This should primarily be directed at removing
the cause for the increased ICR Intracranial volume can be mechanically
decreased by removing an intracranial mass or haematoma, reducing intracranial
venous blood volume by facilitating venous outflow via the jugular veins,
ventilated to bring the carbon dioxide toxin (PCO2) down to 4—4.5
(avoiding vasoconstriction in patients with ischaemic disease) or by
draining CSF through a ventriculostomy.
Steroids
seem most effective in decreasing ICP resulting from vasogenic oedema associated
with brain turnouts or surgical manipulation (dexamethasone 4 mg 6 hourly). They
work by stabilising the blood—brain barrier and reducing oxygen radical
injury.
Mannitol,
an osmotic dehydrating agent (1 g/kg 4—6 hourly), works by drawing water from
parts of the brain with an intact blood—brain barrier. If this is disrupted as
in a cerebral contusion, Mannitol can leach out into the brain and potentiate
the mass effect. In head injuries it should therefore only be administered after
consultation with a neurosurgeon. It becomes ineffective when brain osmolarity
becomes iso-osmolar with that of the serum.
Barbiturates
given as a bolos (thiopentone 3—5 mg/kg)
can reduce ICP, although the exact mechanism remains obscure. Subsequent doses
are titrated to give a level of 2.5—3.5 mg
per cent. Infusions to control burst suppression on electroencephalogram (EEG)
have been postulated to diminish ICP by reducing cerebral metabolism. The
initial response is due to vasoconstriction but it is possible to reduce CPP by
causing hypotension.
Frusemide
reduces ICP by reducing cerebral oedema and CSF production. It may act
synergistically with mannitol. Hypothermia down to 340C is currently
undergoing assessment as a brain protection agent.