INTRACRANIAL PRESSURE

By
Iskandar

INTRODUCTION
The

cranium-vertebrae is a rigid structure.

The major intracranial content :
- Brain (include neuroglial &
interstitial fluid).
- Blood (arterial & venous).
- Cerebrospinal fluid.
Intracranial volume is constant.
Normal ICP : 10-15 mmhg (136-204 mmH2O).

INTRACRANIAL CONTENTS
CONTENT

VOLUME

PERCENTAGE

- Brain

1400 ml

80%
(Brain 70%, Interstitial
fluid 10%)

- Blood

150 ml

10%

- CSF

150 ml

10%

TOTAL

1700 ml

100%

MONRO-KELLIE-BURROWS DOCTRINE
Physiologic state with normal ICP.
B.
Intracranial mass with compensation
(normal ICP) :
- Small-moderate SOL.
- Increasing volume is compensated by
decrease intracranial content. Venous
volume decreases through egress of
venous blood from the intracranial
cavity into the jugular vein and CSF
volume decreases through egress of
CSF into the spinal canal.
- Below pressure-buffer capacity of
venous blood and CSF.
C.
Large Intracranial mass with
decompensation and elevated ICP
(beyond the pressure-buffer capacity
of venous blood and CSF.
A.

PRESSURE-VOLUME CURVE
Compliance (dV/dP) :
Change in volume observed for a
given change in pressure.
Represent the accomodative
potensial of intracranial space.
High when cranial cavity will permit
the accomodation of a large mass
with very little change in pressure.
Elastance (dP/dV) :
Inverse the compliance.
Change in pressure observed for a
given change in volume.
Represent the resistence to outward
expansion of an intracranial mass.

BLOOD BRAIN BARRIER

Not all substances that are carrier in the blood reach neural tissue, a barrier
blocks entry of many substances into the brain.
Function : to regulate the flow of biologically active substances into the brain
and protect the sensitive neural tissue from toxic materials.
Two mechanism by which material may be transported across the
endothelial cells :
- Lipid soluble : in a passive manner.
- Amino acid and sugar : by specific carriermediated mechanism.
BBB : important in certain clinical setting :
- Disruption by any cause, plasma components easily cross the barrier into
neural tissue, causing vasogenic edema.
- Tight junction can be transiently opened artificially by intraarterial injection
of a bolus an osmotic agent, such as manitol, which dehydrates the
endothelial cells. During this interval, whuch lasts for a few hours, certain
chemoterapeutic or other agent can be administered that would not
otherwisw cross the barrier.
- When manitol is given intravenously, the consentration in the cerebral
capillary is quite low;however, it is sufficient to create an osmotic gradient
between the cerebral tissue and the capillary, allowing withdrawal of
interstitial fluid into the capillary lumen. An intact tight junction is necessary
for this to occur. If the tight junction are not intact, manitol will permeate the
neural tissue, preventing the formation of an osmotic gradient.

BLOOD BRAIN BARRIER

Differences between somatic and brain capillaries
:
Somatic cap :
- Fenestration between endothelial cells allow
free flow of plasma component into the
tissue.
- There is bulk flow of plasma component
across endethelial cells via pinocytotic
vesicles.
Brain capillary :
- The endotelial cells are attached to each
other by tight junctions. This junctions act as
barrier to the passive movement of many
substances across the endothelium.
- There are no intervening fenestrae.
- Certain selected plasma component cross
the endothelial membrane if they are lipid
soluble;others, such as amino acid and
sugars, are transported across the
endothelial cells through carrier mediated
mechanism.
- The larger of mitichondria in the brain
endothelial cells generate energy for active
transport.

CEREBRAL EDEMA
Vasogenic Edema
(extracellular)

Cytotoxic Edema
(Intracellular)

Interstitial Edema
(Extracellular)

Pathogenesis

Increased capillary
permeability

Cellular swelling (neuronal,

glial & endothalial cells)

Increased brain water due

to impairment of absorption
of CSF

Location

Mainly white Matter

Gray and white matter

Transependymal flow of
CSF and interstitial edema
in the periventricular white
matter in HCP

Composition

Plasma filtrate containing

plasma protein

Increased intracellular
water and sodium due to
failure of membrane
transport

CSF

Extracellular Fluid Volume

Increased

Decreased

Increased

Cause of Edema

Primary or metastatic
tumor, abscess,trauma, late
stage of infarction

Early stage of infarction,

water intoxication, hypoxia
of neural tissue

Obstructive or
communicating HCP

Effect of Steroid

Effective

Not effective

Not effective

Effect of Mannitol

Effective

Effective

Questionable

CEREBRAL EDEMA

Normal : the intercellular

tight junction are intact.
Vasogenic edema : The
tight junction are not
competent, allowing
leakage of plasma into the
interstitial space.
Cytotoxic edema : There is
a primary failure of ATPdependent sodium pump
mechanism resulting in
intracelular accumulation
of sodium and secondarily
water.

CEREBRAL BLOOD FLOW

Normal

: 55-60 ml/100 gr brain tissue/mnt.

In Gray matter : 75 ml/100 gr/mnt.
In White matter : 45 ml/100 gr.mnt.
The most significant factor that determines CBF
at any given time is CPP.
CPP = MABP-ICP.
MABP = SBP+2DBP or DBP+1/3PP
3
The ability to maintain blood flow to the brain at
a constant level over a wide range of mean
arterial pressure (50-160 mmhg) is called
autoregulation.

EFFECTS OF ARTERIAL BP, PaCO2

AND PaO2 ON CBF
Three major factor regulate
CBF under physiologic
conditions :
Systemic blood
pressure.
PaCO2.
PaO2.

PATHOLOGIC EFFECT OF INCREASED ICP

Increased ICP can cause deleterious effect
on the brain in two ways :
Brain ischemia, may occur when the CPP
is reduced to critical level.
Focal masses, can cause distortion and
herniation of the brain, resulting in
compression of critical brainsteam
structures.

BRAIN HERNIATION

Supratentorial Herniation :
- Cingulate Herniation
(Subfalxin Herniation).
- Uncal Transtentorial
Herniation.
- Central Transtentorial
Herniation.
Infratentorial Herniation :
- Tonsilar Herniation.
- Upward Cerebellar
Herniation.

CINGULATE HERNIATION

A focal mass lesion in the supratentorial compartment

exerts progressive pressure locally on the ipsilateral
hemisphere.
A supratentorial mass lesion may displace the cingulate
gyrus, which is next to the free edge of the falx cerebri,
and cause it to herniate under the falx to the opposite
side.
The anterior cerebral artery may be compromised by the
tight, sharp edge of the falx cerebri.
There are no clinical sign and symptom specific to a
cingulate herniation unless ACA kinks and occludes
causing bifontral infarction.
Usually warns of impending transtentorial herniation.

UNCAL TRANSTENTORIAL HERNIATION

Most

commonly herniation syndrome observed

clinically.
Often seen with lesions of the middle cranial
fossa.
Uncus, the most inferomedial structure of the
temporal lobe, herniate between the rostral brain
steam and the tentorial edge into the posterior
fossa.
Clinical syndromas : Progressively impaired
consciousness, dilated ipsilateral pupil,
contralateral hemiparesis.
The PCA may be compromised, causing
secondary infarction of the occipital lobe on one
or both side.

CENTRAL TRANSTENTORIAL HERNIATION

AKA :

Transtentorial herniation.
Cause : Mass lesions far from the tentorial
incisura, such as in frontal, parietal or occipital,
ex : Bilateral SDH, acute hydrocephalus, etc.
There is a downward displacement of the
diencephalon and midbrain centally through the
tentorial incisura.
Clinical syndromas : Tend to have bilaterally
small reactive pupils, exhibits cheyne-stokes
respiration, is quite obtunded, and may show
loss of vertical gaze

TONSILAR HERNIATION

Cause : acute expansion of posterior fossa lesions, or

result from an ill-advesed lumbar puncture in a patient
with a mass lesion within thr cranial cavity.
The tonsil of cerebellum herniates through the foramen
magnum into tha upper spinal canal, compressing the
medulla.
Manifestations of acute medullary compression :
cardiorespiratory impairment, hypertension, high pulse
pressure, cheyne-stokes respiration, neurogenic
hiperventilation and impaired consciousness.
Cerebellar tonsil cone through the for. Megnum,
compressing the medulla
respiratory arrest.

UPWARD CEREBELLAR HERNIATION

Occasionally

seen with posterior fossa

masses, may be exacerbated by
ventriculostomy.
Cerebellar vermis ascends above
tentorium, compressing the midbrain.
Posisibly occluding SCA
cerebellar
infaction.
May compress sylvian aqueduct
obstructive hydrocephalus.

SIGNS AND SYMPTOMS

Cardinal signs :
- Headache.
- Vomiting.
- Papiledema.
Symmtoms increased ICP vary depending on whether the increased
ICP :
- Chronic (Slowly progressive).
- Acute (rapidly evolving lesion).
Cushings triad :
- Hypertension.
- Bradycardia.
- Respiratory irregularity.
The full triad is only seen in about 33% of cases Increased ICP.

TREATMENT OF INCREASED ICP

The

most direct way

to normalize raised
ICP to the physiologic
range is eliminate the
cause.
The algorithm for
treating intracranial
hypertension

The Algorithm for Treating Intracranial Hypertension

TREATMENT OF INCREASED ICP

Patient Position :
Head up 30 and neck straight.
Reducing ICP (by enhancing venous
outflow and by promoting displacement of
CSF from the intracranial compartment to
the spinal compartment), and CBF is
unaffected by elevating the head to 30.
The onset of action : Immediate.

TREATMENT OF INCREASED ICP

Hyperventilation :
Reducing ICP by reducing CBF and blood
volume through vasocontriction.
Generally initiated for acute management
of increased ICP.
Should be moderate, bringing the PCO2
down to 28-32 mmhg.
Reducing the PCO2 much further will
decrease blood flow to critically low level.

TREATMENT OF INCREASED ICP

Manitol :
It has many pharmacologic effects, but the most significant one is osmotic
effect, increase serum osmolality, helps to draw fluid from the brain
parenchyma into the vascular space.The others effect : Decrease CSF
production, increase CBF and cerebral oxygen consumption, decrease
blood viscosity, thereby improving perfusion.
Normal serum osmolality : 275-290 mOs/kg.
Not metabolized.
Not cross the BBB.
Usual doses : 0,25-1 gr/kg at 4-6 hour interval, given in repeated bolus.
An increase in serum osmolality of as littleis enough to have a
significant effect on cerebral edema.
Generally effective for 48-72 hours, beyond 72 hours is ineffective because
manitol slowly leaks out of the blood vessel, especially in areas of BBB
breakdown, with loss of osmotic gradient.
Should be carefully monitored during therapy : serum osmolality and
electrolytes.

TREATMENT OF INCREASED ICP

Ventricular Drainage :
Simplest, most effective and quickest method of
decreasing ICP.
Advantages : Reducing ICP and ICP monitor.
This modalityis particularly effective in patients with
cerebral edema.
Experimental : The vasogenic edema fluid that has
extravasated into the interstitial space is cleared by
diffusion into either the ventricular system or
subarachnoid space.
Draining the ventricular fluid and decreasing the
intraventricular pressure promotes rapid diffusion of
edema fluid from the side of pathology.

TREATMENT OF INCREASED ICP

Dexametahsone :

TREATMENT OF INCREASED ICP

Barbiturat Coma :