Intracranial pressure 2015

SAMIR EL ANSARY
 Global Critical Care
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Normal intracranial pressure in adults
is 8 to 18mm Hg
And in babies the pressure is 10-20
mm.

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.
 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 than 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
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).
 (Cushing response) 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

Cause axial distortion to impair

brainstem perfusion.
 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.

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
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.
Non invasive methods

Invasive 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.
(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
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.

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.
 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.
 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 ineffective after about
24 hrs.

In addition it causes hypotension 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.
 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.
 Mannitol
In small doses 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 withdraws 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.
 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.
 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.
 Global Critical Care
https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY
GOOD LUCK

SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO