3. Intracranial Pressure Flashcards
Factors That Influence ICP
The skull of an adult is in effect a rigid box which contains brain tissue, blood
and CSF. The brain itself has minimal compressibility and so there is very limited
scope for compensation. An increase in the volume of one component invariably
results in an increase in ICP unless the volume of another component decreases
(This is the Monroe–Kellie hypothesis.)
brain tissue (1,400–1,500 g),
blood (100–150 ml),
CSF (110–120 ml) and
extracellular fluid (<100 ml).
The intracranial compliance curve
Normal ICP
Normal ICP is 10–12 mmHg.
Any increase may be significant because of the potential impact on cerebral perfusion.
The CPP is determined by mean arterial pressure (MAP) minus the sum of the central venous pressure (CVP) and the ICP.
CPP = MAP (CVP + ICP).
Mass lesions
: ICP is raised by mass lesions which increase the volume of brain, bone
or meninges. These include tumours of all three structures, as well as infection (with
abscess formation
Volume increases:
Volume increases:
ICP is raised by conditions which increase non-CSF fluid volume.
Intracranial aneurysm, arteriovenous malformation and trauma are all relatively
common causes of subarachnoid or subdural haemorrhage.
ICP is raised by cerebral oedema,
which itself has many causes, including trauma, infection, metabolic dysfunction
(such as hepatic encephalopathy or Reye’s syndrome), hypoxia, venous
obstruction and increased hydrostatic pressure (such as is caused by a steep or
prolonged Trendelenberg position on the operating table).
It may form part of the
symptomatology of altitude sickness (high-altitude cerebral oedema, HACE). It may
also be idiopathic, as in benign intracranial hypertension. (This is a clinical entity defined by an ICP greater than 15 mmHg (but which can reach three times that
figure) in the presence of normal CSF composition, normal conscious level and with
no evident pathological process). Increased ICP may be caused by a rise in intracranial
venous pressure which is offset by intracranial and CSF pressure increases that
restore the required gradient for CSF absorption into the venous system. Some cases
can be managed with corticosteroids, diuretics and acetazolamide, but severe cases
may require the insertion of a lumbothecal–peritoneal shunt
Impaired drainage:
Impaired drainage:
ICP is also raised by conditions which impede drainage of CSF
(which is produced at 0.4 ml min1) and thus increase its intracranial volume.
These include congenital and acquired hydrocephalus, which may also be associated
with trauma, tumour or infection. A blocked ventricular shunt is another
important cause
Pathophysiology
: in the presence of raised ICP, CPP is given by MAP – ICP.
Perfusion will be maintained until CPP starts to fall below 50 mmHg, with the
onset of critical ischaemia at 30–40 mmHg. There may also be focal ischaemia in
the region of a mass lesion. Raised ICP attenuates cerebral autoregulation to the
point at which it is lost completely, after which cerebral blood flow follows MAP
passively.
Measurement of Intracranial Pressure
Subdural pressure transducers.
As the name describes, these devices are placed in
the subdural space and fill with cerebrospinal fluid. After equalization, the pressures
within the closed system can be transduced.
They are less invasive than other
methods, but are less accurate and do not allow sampling or drainage of CSF.
Intraventricular catheters.
These catheters provide the most accurate means of
measuring ICP.
They are usually placed into the lateral ventricle via a burr hole
(most commonly in the right frontal area) and through the parenchyma of the
brain.
In addition to providing pressure measurements, the catheters can also be
used to drain cerebrospinal fluid or to administer drugs such as antibiotics.
The external transducer reference point is the external auditory meatus which
approximates to the intracerebral centre, which is where the foramina of Munro
link the lateral ventricles with the third ventricle. Complications include infection
and blockage.
Intraparenchymal monitors
. These are useful when extreme ventricular compression
makes the insertion of an intraventricular catheter impossible.
They do not use amn column of fluid (i.e. a saline-filled catheter) via which to transduce pressures but
instead use a variety of other technologies.
One example is the use of fibreoptic cables
tipped with miniature mirrors whose displacement by raised ICP reflects light of
varying intensity, which is then transduced into pressure.
Another is the use of
microchip sensors whose resistance alters as ICP changes. These systems cannot be
recalibrated once they are in position, they cannot sample or drain CSF, and because
of their location they may measure only local pressure changes rather than
global ICP.
see also 44 in viva book
Cerebrospinal Fluid (CSF
Formation:
its total volume is around 150 ml, about 80% of which is intracranial.
Most of the extracranial (spinal) CSF is found distal to the conus medullaris. The
choroid arterial plexuses form CSF either by secretion or by the quantitatively much
less significant process of ultrafiltration. It is produced in the lateral, third and fourth
ventricles, at a rate of around 0.4 ml min1 (575 ml 24 h1). The rate of production is
constant and is not related to ICP unless it is sufficiently high to compromise CPP
and reduce blood flow to the choroid plexus.:
Circulation
: CSF passes through the cerebral aqueduct
to the fourth ventricle and thence through the midline
foramen of Magendie and the two lateral foramina of
Luschka to communicate with the subarachnoid space of the brain and spinal cord.
It
is either absorbed directly into cerebral venules (10%) or absorbed by the arachnoid
villi (90%).
Function
Functions: it has a cushioning effect which protects the brain from injury.
Supported by CSF, the effective cerebral weight is only 50g. By translocation from
the intracranial to the extracranial subarachnoid space, CSF can partly buffer
increases in ICP.
Composition:
it has a higher PCO2 than plasma and a lower pH (7.33).
The mean specific gravity is 1.006, with a range of 1.003–1.009.
Its protein content is low (0.2 gl1), so buffering capacity is negligible.
Glucose concentration is lower than in plasma.
Sodium and chloride are higher,
whereas potassium is lower (40%). This is
because the formation of CSF requires the active transport of Na+, Cl and K+ into
the ventricles.
Further Na+ is then added in exchange for K+ (mediated by Na+/K+
ATPase). The influx is maintained by the further exchange of H+ and HCO3
- for Na+ and Cl. H+ and HCO3
- are generated from H2CO3 in
a reaction catalysed by
carbonic anhydrase.
Factors affecting rate of production:
acetazolamide, which is a carbonic anhydrase
inhibitor, may reduce CSF production by as much as 50%. High-dose diuretics also
reduce it by affecting the sodium transport process. (Corticosteroids may increase
production, but not consistently enough to make them a reliable treatment for
postdural puncture headache.)
