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It is the term applied to the pressure of CSF with in the
cranium.
Physiology:
Normal 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.
The spinal 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.
Intracranial 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.
(b) 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.
Lundberg 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):
The brain 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.
The exact nature of this auto regulation is not known.
(a) myogenic theory suggests direct reaction of the cerebral
arterial smooth muscles to the stretch.
(b) The humoral theory involves regulations by the direct
effect of by- products of metabolism
(c) Neurogenic theory rests on perivascular nerves.
The auto regulation is influenced by various factors.
With normal 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.
The 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.
The ICP 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:
Increased ICP is defined as a sustained elevation in
pressure above 20mm of Hg/cm of H20.
The 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 occurs.
The cause of raise in ICP and the rate at which it occurs
are also important.
Many patients 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 probably intact.
In patients 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.
In acute hydrocephalus, there is rapid deterioration
as there is no time for compensation.
The raise in ICP disturbs brain function by
(1) Reduction in CBF
(2) 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.
Clinical features if raised ICP:
Raised ICP causes arterial hypertension, bradycardia (Cushing's
response) and respiratory changes.
It is 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.
The 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.
Pulmonary 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 cord.
ICP monitoring:
ICP monitoring is most often used in head trauma in the
following situations:
1) GCS less than 8
2) Drowsy with CT findings (operative or non operative)
3) Post op hematoma evacuation
4) High risk patients (a) Above 40 yrs. (b) Low BP (c)
Those who require ventilation.
There is nothing to achieve in monitoring ICP in the
patients with GCS of less than 3.
Methods:
Non invasive methods:
(1) Clinical 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.
(2) 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.
(3) Manual feeling the craniotomy flap or skull defect, if
any, give a clue.
Invasive methods:
(1) 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%).
(2) Other 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 adequately.
(3) Ladd 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.
(4) A mechanically coupled surface monitoring device is the
'cardio search pneumatic sensor' used subdurally or extradurally. These
systems are not widely used.
(5) 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.
(6) Fully 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.
(7) Lumbar puncture and measurement of CSF pressure for
obvious reasons is not recommended.
Benefits 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.
3) Cerebral 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.
The problems of ICP monitoring are cost, infection, and
hemorrhage. The effective maintenance requires a dedicated team effort.
Treatment of increased ICP:
There is no doubt the best treatment for increased ICP is
the removal of the causative lesion such as tumors, hydrocephalus, and
hematomas.
Post 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.
There is 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.
Treatment is aimed at preventing the secondary events.
Clinical and ICP monitoring will help.
The following therapeutic measures are available.
1) I line of management:
General measures 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 instituted promptly.
Adequate analgesia is often forgotten; it is a
must even in unconscious patients.
2) II line of management
Induced cerebral vasoconstriction -
Hyperventilation, hyper baric O2, hypothermia
Osmotherapy - Mannitol, glycerol ,urea
Anesthetic agents - Barbiturates,
gamma hydroxybutyrate, Etomidate,
Surgical 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.
Debate 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.
a) Hyperventilation 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 same.
The present 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.
Hyper baric O2, hypothermia are still in experimental stage,
especially in Japan . They basically induce cerebral vasoconstriction and
reduce the cerebral blood volume and the ICP.
b) 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 scavenger.
Mannitol is 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.
1) 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 erythrocyte flexibility.
2) The 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 axial lesions.
3) Another theory is, mannitol with draws
water across the ependyma of the ventricles in a manner analogous to that
produced by ventricular drainage.
The 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.
c) 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 ICP.
Phenobarbital 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.
Surgical
decompression:
Decompressive 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.
There are occasional reports from few centers
recommending such procedures.
Medicine is 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.
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