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Intracranial Pressure

Susunan saraf pusat terdiri dari:

Otak (otak besar dan otak kecil)
Batang otak (terdiri atas
mesensefalon, pons dan medula
Medula spinalis terletak di kanalis

Peredaran darah otak

Otak mendapat darah dari arteri vertebralis dan arteri
karotis interna. Arteri vertebralis adalah cabang dari
arteri subklavia yang masuk rongga tengkorak
melalui foremen oksipitale magnum. Kedua arteri
vertebralis kanan dan kiri berjalan di permukaan
ventral medula oblongata dan pada batas kaudal
pons kedua arteri bersatu membentuk arteri basilaris.
Arteri karotis interna setelah masuk rongga tengkorak
akan memberi cabang yaitu arteri serebri anterior,
arteri serebri media, arteri komunikans posterior,
arteri khoroidea, arteri hipofise superior dan arteri
hipofise inferior.

Peredaran darah vena

Sistim vena sentral terdiri atas:
Aliran vena serebral eksternal atau superfisial
Aliran vena serebral internal atau profunda
Kedua sistim vena ini mengalirkan darah
kedalam sinus venosus. Anastomose banyak
terjadi antara dua kelompok ini melalui
anyaman pembuluh didalam substansi otak.
Dari sinus venosus melalui vena emisries darah
balik ini diteruskan ke vena ekstrakranial.

The contents of the intracranial

1: The brain about 1400 ml.
2: The blood 75-100 ml.
3: The CSF 75-100 ml.
Otak, volume darah dan cairan
serebrospinalis di dalam kranium pada
setiap saat harus relatif konstan (hipotesa


Obstruction to the flow of CSF at any point,

results in dilatation of the venticular system
proximal to the obstruction with profound
effect on intracranial pressure.

Indications for Access

& contraindications
1. CSF analysis: Bacteriological, Immunological , Cytology,
2. Measuring CSF pressure in cases of pseudotumor cerebri, and normal
pressure hydrocephalus.
3. The administration of antimicrobial and antineoplastic agents normally
excluded by the BBB.
4. Therapeutic CSF drainage. in cases of CSF fistula, pseudotumor
cerebri or communicating hydrocephalus.

Methods of access
2. Lumbar puncture
2. Cisternal puncture.
3. Ventricular puncture.

* Local inf.
high ICP. Due to SOL
* Blood dyscrasias.
Anticoaggualnt therapy.

BV= 75 ml
CBF: 50ml/100gm/min

Cerebral Autoregulation

Brain Volume
An increase in brain volume is produced either
by a:
Edema: increase in brain water.

1. Vasogenic edema: extra cellular, disturbance of

BBB. localized around tumors, abscesses,
hemorrhages and localized cerebral contusions. It
may lead to herniation.
2. Cytotoxic edema: intracellular, hypoxia (cardiac
arrest), Intoxication, sever hypothermia. It is usually
3. Osmotic edema: ECF, Abnormal ADH sec. Sever
hemodialysis, or excessive ingestion of water
4. Hydrostatic Edema: ECF due to acute hypertension.

Elastance and Compliance

Compliance: Is that quality of distensibility
available within the intracranial contents, which
enable them to adapt to an expanding IC lesion.
Elastance: Is the resistance offered by the
intracranial contents to the expansion of an
intracranial mass. It is the inverse of compliance
Compliance is decreased by
increased by:
1. Hypercarbia.
2. Hypoxia.
Hyperoxia (PaO2 >1000 mm
3. Sleep.
4. Anesthesia.

Bila terjadi kenaikan yang relatif kecil dari volume otak, keadaan ini
tidak akan cepat menyebabkan tekanan tinggi intrakranial. Sebab
volume yang meninggi ini dapat dikompensasi dengan memindahkan
cairan serebrospinalis dari ronga tengkorak ke kanalis spinalis dan
disamping itu volume darah intrakranial akan menurun oleh karena
Berkurangnya peregangan durameter. Hubungan antara tekanan dan
volume ini dikenal dengan complience. Jika otak, darah dan cairan
serebrospinalis volumenya terus menerus meninggi, maka mekanisme
penyesuaian ini akan gagal dan terjadilah tekanan tinggi intrakranial
(Adams RD, Youmans JR).

Intracranial Compensation

Intracranial pressure
Normal I.C.P. this is 50-200 mm. water (10 mm Hg.) it is
pulsatile owing mainly to I.C. arterial pulsation. It also shows
fluctuations reflecting the respiratory and cardiac cycles.
1. L.P: with the patient on his side, the L.P. needle is connected to
a manometer. This method is not accurate, can not be used
monitoring and can be dangerous.
2. Ventricular cannulation: It is more accurate, can be used for long
periods, but may be complicated by infection.
3. Subdural sensor { These are the safest and most reliable, and
4. Extradural sensor{ and are usually used for monitoring.

Effects of increased ICP

A: Effects on vital signs:
These appear to be due to compression and distortion
of the brain stem. These effects are noticed in patients
with critically raised intracranial pressure, and in
experimental animals.
1. Decrease in respiratory rate.
2. Bradycardia.
3. Cardiac arrhythmias.
4. Pupillary constriction, followed by unilateral pupillary
5. Increase in pulse pressure.
6. Increase in arterial blood pressure.

B: Effect on cerebral blood flow:

CBF = -------------------CVR
When ICP increases, cerebral blood flow remains
constant by auto regulation. the efficiency of this
compensation depends on the rate of expansion of the
lesion, it's nature and site. And also on the compliance
of the intracranial contents.
CBF is increased in response to raised ICP, by cerebral
vasodilatation, However this causes increase in cerebral
blood volume and produces further brain swelling.
When maximal vasodilatation occurs, further increase
in ICP causes reduction in cerebral BF.

C: Clinical effects (symptoms and signs):

Significant raised intracranial pressure can be
present with out symptoms or signs.

Global symptoms of elevated ICP

Probably mediated via the pain fibers of cranial
nerve (CN) V in the dura and blood vessels

Depressed global consciousness

Due to either the local effect of mass lesions or
pressure on the midbrain reticular formation


Focal symptoms
May be caused by local effects in patients
with mass lesions or herniation syndromes

Additional features of traumatic head


Decreased level of consciousness

Pain coming in waves
Visual changes
Alterations in vital signs

Infants may present with less specific


Bulging fontanel
Flat affect
Poor feeding


Nocturnal awakening
Worsening by cough, micturition, or defecation
Recurrent and localized
Progressive increase in frequency or severity

Growth abnormalities
Nuchal rigidity
Focal neurologic deficit
Persistent vomiting
Known risk factor for intracranial pathology

(eg, neurocutaneous syndrome, macrocephaly, hormonal


Personality change

If present can
confirm the
Papilledema may
be absent in acute
ICP elevations
because it takes
several days to
become apparent
Is not invariably
present in patients
with intracranial

may be present in
patients with
pressure, and
should raise the
suspicion of
head trauma

Infants may
Split sutures
Bulging fontanel

Sun setting"
appearance of the
eyes may appear

Dilated pupil
Usually on the side of
the lesion

Cranial nerve palsies

of the third, fourth,
and sixth cranial
nerves can occur
3rd nerve palsy most
May cause double
vision or abnormal
head posture

Level of consciousness
Can range from irritability to obtundation or

Hemiparesis, hyperreflexia, and hypertonia

Are late signs

Cushing triad
Systemic hypertension, bradycardia, and
respiratory depression
Another late sign, and may be a preterminal event

D :Internal Brain
herniation: resulting in
strangulation, compression
of vital structures and
blood vessels.

1.Cingulate herniation
2.Central transtentorial
3.Uncal herniation
4.Tonsilar herniation

1. Cingulate herniation: compress the internal cerebral vein

and the anterior
cerebral artery Unilateral or bilateral weakness, loss of
bladder control, and coma
2. Central transtentorial herniation:
* Compression of the 3rd. nerve -------------> Dilated pupils .
* Compression of the post. cerebral art. ----> Hemianopia.
Total blindness.
* Compression or ischemia of the brain stem.->
Decerebration. Coma.
* Distortion of the brain stem --------------> Hemorrhages.
3. Uncal herniation. compression of the mid-brain, 3rd nerve
and the post.
cerebral art.
4. Tonsilar herniation: Occurs when the cerebellar tonsils,
herniate through the foramen magnum, resulting in
compression of
medulla, Decerebration, coma, cardiovascular and

Medical Treatment of
raised intra cranial pressure.
1. Sedation, and positioning:
2. Hypertonic solutions:
* Manitol: 0.5- 1gm/ Kg body wt. over 30 min. bolus
* Furosemide: is effective in reducing brain edema, and
reducing CSF
40-120 mg daily.
* Glycerol: can be given orally as well as I.V. 0.5-2 gm/
Kg. every 4 hrs.
3. Steroids: Dexamethasone 4mg four times a day.
4. Hyperventilation:
5. Hyperbaric oxygen: (rarely used).
6. Hypothermia:
7. Induced barbiturate coma: Has been used to reduce
intracranial pressure in head injuries, and to increase