It is the
term applied to the pressure of CSF with in the cranium.
intracranial pressure in adults is 8 to 18mm Hg and in babies the pressure
is 10-20mm less when measured through a lumbar puncture. ICP is not a
static state, but one that is influenced by several factors. The recording
of ICP shows 2 forms of pressure fluctuations. There is a rise with
cardiac systole (due to distention of intracranial arteriolar tree which
follows ) and a slower change in pressure with respiration, falling with
each inspiration and rising with expiration. Straining, compression of
neck veins can also cause sudden, considerable rise in pressure. The
conception of the cranium acting as a near rigid container of virtually
incompressible substances in the form of brain, blood & CSF in known as
the Monro Kellie doctrine. CSF can be displaced through the
foramen magnum into spinal theca.
dural sheath can accept a quantity of CSF as it does not fit the canal
closely, being surrounded by a layer of loose areolar tissue & plexus of
epidural veins. In addition, in states of increased ICP there is increase
in passage of blood through venous emissaries.
pressure is a result of at least 2 factors, the volume of the brain (about
1400ml in an adult) being constant.
(a) CSF which
is constantly secreted & after circulating absorbed at an equal rate. CSF
circulation is slow (500 to 700 ml/day). At a given time the cranium
contains 75 ml of CSF.
Intracranial circulation of blood which is about 1000 litres per day
delivered at a pressure of 100 mmHg and at a given time, the cranium
contains 75 ml. Any obstruction to venous outflow will entail an increase
in the volume of intracranial blood and ICP. As the ICP increases, the
cerebral venous pressure increases in parallel so as to remain 2 to 5 mm
higher or else the venous system would collapse. Because of this
relationship CPP (mean art pressure - venous pressure or mean ICP)
can be satisfactorily estimated from mean art pressure - ICP.
has described 3 wave patterns ICP waves (A, B, and C waves). A
waves are pathological. There is a rapid rise in ICP up to 50-100 mm
Hg followed by a variable period during which the ICP remains elevated
followed by a rapid fall to the baseline and when they persist for longer
periods, they are called 'plateau' waves which are pathological.
'Truncated' or atypical ones, that do not exceed an elevation of 50 mm Hg,
are early indicators of neurological deterioration. B & C
waves are related to respiration and 'Traube-Hering-Mayer' waves
respectively and are of little clinical significance.
Cerebral blood flow (CBF):
accounts for only 2% of total body weight, yet its blood flow represents
15% of resting cardiac output and uses 20% total amount of oxygen
consumed. Each 24 hours brain requires 1000 liters in order to obtain 71
lit of oxygen and 100 gm of glucose. The CBF remains constant over a wide
range of arterial pressures (between 60 to 150 mm hg) when the mean
arterial pressure is increased beyond 150 mm hg there is increased blood
flow. CBF ceases when art. mean pressure drops to 20mm Hg. In chronically
hypertensive this auto regulation limits appear to be reset.
nature of this auto regulation is not known.
theory suggests direct reaction of the cerebral arterial smooth muscles to
humoral theory involves regulations by the direct effect of by- products
Neurogenic theory rests on perivascular nerves.
The auto regulation is
influenced by various factors.
cerebrovascular system and BP, even moderate alterations of pCO2
are capable of markedly altering CBF. Within the range of 30 to 60 mm Hg
there is a 2.5% change in CBF as the pCO2 changes by 1 mmHg. With less
then 20 and more than 80 mmHg there is no further change. In old age and
arteriosclerosis, there is marked decrease in pCO2 influence.
effects of pO2
are not as marked as CO2
Changes. Moderate variation of O2 above and below the normal level do not
affect CBF. pO2 causes constriction of a non ischemic brain along with
reduction in CBF. In ischemic hemisphere, increasing the pO2 has no
effect. Cerebral vaso dilatation begins with pO2 of 50 mm Hg & CBF
increases. When pO2 falls to 30 mmHg, CBF may have tripled.
influences the CBF through the cerebral perfusion pressure (CPP) which
is the difference between mean arterial pressure (MAP) and ICP. Raise in
ICP would lead to a fall in CPP and every effort should be taken to
maintain the CPP to 50 mm Hg or more during treatment of raised ICP.
Pathophysiology of increased intracranial pressure:
is defined as a sustained elevation in pressure above 20mm of Hg/cm of
craniospinal cavity may be considered as a balloon. During slow increase
in volume in a continuous mode, the ICP raises to a plateau level at which
the increase level of CSF absorption keeps pace with the increase in
volume. Intermittent expansion causes only a transient rise in ICP at
first. When sufficient CSF has been absorbed to accommodate the volume the
ICP returns to normal. Expansion to a critical volume does however cause
persistent raise in ICP which thereafter increases logarithmically with
increasing volume (Volume - pressure relationship). The ICP finally
raises to the level of arterial pressure which it self begins to increase,
accompanied by bradycardia or other disturbances of heart rhythm (Cushing
response). This is accompanied by dilatation of small pial arteries and
some slowing of venous flow which is followed by pulsatile venous flow.
The rise in
ICP to the level of systemic arterial pressure extinguishes cerebral
circulation which will restart only if arterial pressure raises
sufficiently beyond the ICP to restore CBF. If it fails, brain death
The cause of
raise in ICP and the rate at which it occurs are also important.
with benign ICT or obstructive hydrocephalus show little or no ill effect,
the reason being the brain it self is normal and auto regulation is
with parenchymal lesion (tumor, hematoma and contusion), because of the
shift of brain and disturbed auto regulation, CBF may by compromised with
relatively low levels of ICP.
hydrocephalus, there is rapid deterioration as there is no time for
The raise in
ICP disturbs brain function by
Transtentorial or foramen magnum herniation resulting in selective
compression and ischaemia in the brain stem.
Transtentorial herniation with brainstem compression can lead to clinical
deterioration even with adequate CBF. A temporal mass may cause uncal
herniation without raised ICP. Similarly a frontal mass can cause axial
distortion to impair brainstem perfusion.
features if raised ICP:
causes arterial hypertension, bradycardia (Cushing's
response) and respiratory changes.
traditionally accepted that hypertension and bradycardia are due to
ischaemia or pressure on the brainstem. There is also a suggestion that
they could be due to removal of supratentorial inhibition of brainstem
vasopressor centers due to cerebral ischaemia and that bradycardia is
independent of the rise in blood pressure.
respiratory changes depend on the level of brainstem involved. The
midbrain involvement result in Chyne-Stokes respiration. When
midbrain and pons are involved, there is sustained hyperventilation. There
is rapid and shallow respiration when upper medulla involvement with
ataxic breathing in the final stages.
edema seems to be due to increased sympathetic activity as a result of the
effects of raised ICP on the hypothalamus, medulla or cervical spinal
monitoring is most often used in head trauma in the following situations:
1) GCS less
with CT findings (operative or non operative)
3) Post op
4) High risk
patients (a) Above 40 yrs. (b) Low BP (c) Those who require ventilation.
nothing to achieve in monitoring ICP in the patients with GCS of less than
deterioration in neurological status is widely considered as sign of
increased ICP. Bradycardia, increased pulse pressure, pupillary dilation
are normally accepted as signs of increased ICP. The clinical monitoring
is age old and time tested.
Transcranial doppler, tympanic membrane displacement, and ultrasound 'time
of flight' techniques have been advocated. Several devices have been
described for measuring ICP through open fontanel. Ladd fiber optic system
has been used extra cutaneously.
feeling the craniotomy flap or skull defect, if any, give a clue.
Intraventricular monitoring remains one of the popular techniques,
especially in patients with ventriculomegaly. Additional advantage is the
potential for draining CSF therapeutically. Insertion of ventricular
catheter is not always simple and can cause hemorrhage and infection (5%).
most commonly used devices are the hollow screw and bolt devices, and the
sub dural catheter. Richmond screw and Becker bolt are used extra durally.
A fluid filled catheter in the subdural space, connected to arterial
pressure monitoring system is cost effective and serves the purpose
device is currently in wide use. It employs a fibre optic system to detect
the distortion of a tiny mirror within with balloon system. It can be used
in the subdural , extradural and even extra cutaneously.
mechanically coupled surface monitoring device is the 'cardio search
pneumatic sensor' used subdurally or extradurally. These systems are not
Electronic devices (Camino & Galtesh design) are getting popular world
over. Intraparenchymal probes, the measured pressure may be
compartmentalized and not necessarily representative of real ICP. In
addition to ICP monitoring, modern intraparenchymal sensors help study the
chemical environment of the site of pathology.
implantable devices are valuable in a small group who requires long term
ICP monitoring for brain tumors, hydrocephalus or other chronic brain
diseases. Cosmon intrcranial pressure telesensor can be implanted as a
part of shunt system. Ommaya reservoir is an alternative which can be
punctured & CSF pressure readings are obtained.
puncture and measurement of CSF pressure for obvious reasons is not
of ICP monitoring:
There is no
doubt that ICP monitoring helps in management of conditions where one
expects prolonged intracranial hypertension. Monitoring is the only means
by which therapy can be selectively employed and the effectiveness of
therapy can be accurately studied.
1) Where ever
clinical monitoring is not possible, such as during hyper ventilation
therapy and high dose barbiturate therapy, ICP monitoring helps.
2) Pre op
monitoring helps in assessment of NPH before a shunting procedure.
perfusion pressure (CPP), regulation of cerebral blood flow, and volume,
CSF absorption capacity, brain compensatory reserve, and content of
vasogenic events can be studied with ICP monitoring. Some of these
parameters help in prediction of prognosis of survival following head
injury and optimization of' 'CPP guided therapy'.
4) It can
provide additional assessment of brain death. Brain perfusion effectively
ceases in nearly all, once ICP exceeds diastolic blood pressure.
of ICP monitoring are cost, infection, and hemorrhage. The effective
maintenance requires a dedicated team effort.
Treatment of increased
There is no
doubt the best treatment for increased ICP is the removal of the causative
lesion such as tumors, hydrocephalus, and hematomas.
operative increased ICP should be uncommon these days with increased use
of microscope and special techniques to avoid brain retraction. As we so
often see, a basal meningioma once completely removed, has a smooth post
op period, whereas a convexity or even falx meningioma may be easily
removed but post operative period may be stormy, mainly due to impairment
of venous drainage, either due to intraoperative injury to veins and post
operative diuretic therapy as practiced in some centers.
still a debate whether increased ICP is the cause or result of the brain
damage. Many feel both compliment each other. There is one school which
questions the very existence of increased ICP. Not all the midline shift
seen in CTs indicate increased ICP. It just means ICP was high during the
shift. The shift takes longer to reverse even after ICP returns to normal
. It is widely accepted the increased ICP is a temporary phenomenon
lasting for a short time unless there is a fresh secondary injury due to a
clot, hypoxia or electrolyte disturbance.
aimed at preventing the secondary events. Clinical and ICP monitoring will
therapeutic measures are available.
line of management:
form the I line of treatment essentially
making the patient comfortable and ABC of trauma management are
effectively instituted. Careful attention to nutrition and electrolytes,
bladder and bowel functions and appropriate treatment of infections are
analgesia is often forgotten; it is a must even in unconscious
line of management
cerebral vasoconstriction - Hyperventilation, hyper baric O2,
Osmotherapy - Mannitol, glycerol ,urea
agents - Barbiturates, gamma hydroxybutyrate, Etomidate,
decompression -Many do not recommend decompressive surgery.
This aims at
combating increased ICP which is assumed when there is neurological
deterioration or if ICP monitoring is available and the ICP goes above 25
cm of H2O.
There is a
small group of surgeons who start the II line in conditions where ICP is
expected to raise without waiting for a rise. Many feel that institution
of measures to reduce ICP invariably compromises CBF and wait for the
raise in ICP before starting the II line of management.
continues in the II line of management as well. Some prefer osmotherapy
alone as the II line. Some prefer measures to induce cerebral
vasoconstriction, thereby reducing CBF and reduce ICP. Some go for both.
aims at keeping the pCO2 down to
30-25 mm Hg so that CBF falls and cerebral blood volume is reduced and
thereby reducing the ICP. Prolonged hyperventilation should be avoided and
becomes in- effective after about 24 hrs. In addition it causes hypo
tension due to decreased venous return . It is claimed a pCO2 under 20
results in ischemia, although there is no experimental proof for the
trend is to maintain normal ventilation with pCO2 in the range of 30 - 35
mmHg and pO2 of 120 - 140 mmHg. When there is clinical deterioration such
as pupillary dilatation or widened pulse pressure, hyperventilation may be
instituted (preferably with an Ambu bag) until the ICP comes down.
O2, hypothermia are still in experimental stage, especially in Japan .
They basically induce cerebral vasoconstriction and reduce the cerebral
blood volume and the ICP.
Osmotherapy is useful in the cytotoxic edema stage, when capillary
permeability is intact, by increasing the serum osmolality. Mannitol is
still the magic drug to reduce to ICP, but only if used properly: it is
the most common osmotic diuretic used. It may also act as a free radical
not inert and harmless. Glycerol and urea are hardly used these
days. Several theories have been advanced concerning the mechanism by
which it reduces ICP.
It increases the erythrocyte flexibility, which decreases blood viscosity
and causes a reflex vasoconstriction that reduces cerebral blood volume
and decreases ICP and may reduce CSF production by the choroids plexus. In
small doses it protects the brain from ischemic insults due to increased
diuretic effect is mainly around the lesion, where blood brain barrier
integrity is impaired and there is no significant effect on normal brain.
As one would have observed, intraaxial lesions respond better than extra
Another theory is, mannitol with draws water across the ependyma of the
ventricles in a manner analogous to that produced by ventricular drainage.
traditional dose is 1 gm/kg/24 hr of 20% to 25% i.v. either as a bolus or
more commonly intermittently.
There is no
role for dehydration. Mannitol effect on ICP is maximal 1/2 hr after
infusion and lasts for 3 or 4 hrs as a rule. The correct dose is the
smallest dose which will have sufficient effect on ICP. When repeated
doses are required, the base line serum osmolality gradually increases and
when this exceeds 330 mosm/1 mannitol therapy should cease. Further use is
ineffective and likely to induce renal failure. Diuretics such as
frusemide, either alone or in conjunction with mannitol help to hasten its
excretion and reduce the baseline serum osmolality prior to next dose.
Some claim, that frusemide compliments mannitol and increases the output.
Some give frusemide before mannitol, so that it reduces circulatory
overload. The so called rebound phenomenon is due to reversal of osmotic
gradient as a result of progressive leak of the osmotic agent across
defective blood brain barrier, or is due to recurrence of increased ICP.
Barbiturates can lower the ICP when other measures fail; but have no
prophylactic value. They inhibit free radical mediated lipid peroxidation
and suppress cerebral metabolism; cerebral metabolic requirements and
thereby cerebral blood volume are reduced resulting in the reduction of
is most widely used. A loading dose of 10mg/kg over 30 minutes and
1-3mg/kg every hour is widely employed. Facilities for close monitoring of
ICP and hemodynamic instability should accompany any barbiturate therapy.
d) High dose
steroid therapy was popular some years ago and still used by some.
It restores cell wall integrity and helps in recovery and reduce edema.
Barbiturates and other anesthetic agents reduce CBF and arterial pressure
thereby reducing ICP. In addition it reduces brain metabolism and energy
demand which facilitate better healing.
craniotomies such as sub temporal decompression are recommended only in
highly selected patients these days. Herniation of brain thro' defect,
cause further injury, further edema and further increased ICP. But in
occasional cases, when every other measure has failed, such decompression
craniotomy may be justified.
occasional reports from few centers recommending such procedures.
an ever changing field. Standard and safety precautions must be followed.
But as new research and clinical experience broaden our knowledge, changes
in treatment and drugs therapy become necessary or appropriate. Ultimately
it is the responsibility of treating surgeon relying on his experience and
knowledge of the patient to decide the best for the patient.