RAISED ICP
Atandrila Das
Monro-Kellie Doctrine
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Cranial cavity is a rigid sphere
Filled to capacity with non compressible
contents
Increase in the volume of one of the
constituents will lead to a rise in pressure
Intracranial pressure-volume
relationship
Cerebral blood flow
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CBF = (CAP – JVP) / CVR
CBF is normally maintained at a relatively constant level by
autoregulation of CVR over a wide range of BP
In the setting of raised ICP, CBF can be reduced
CPP is a clinical surrogate for the adequacy of cerebral
perfusion.
CPP = MAP – ICP
CPP becomes dependent on MAP when autoregulation
compromised
To maintain CPP in the setting of raised ICP, systemic BP
needs to be elevated.
Contents
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Brain – 80%
Blood – 10%
CSF – 10%
Causes of raised ICP
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Increased volume of normal contents
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Brain: oedema, benign intracranial HTN
CSF: hydrocephalus
Blood: vasodilatation, venous thrombosis
Space occupying lesions
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Tumour
Abscess
Intracranial heamorrhage
Symptoms/signs
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DROWSINESS
Headache
Nausea/vomiting
Papilloedema
Cushing’s triad
Normal fundus
Papilloedema
Cerebral herniation
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Can occur depending on cause of raised ICP
3 major types:
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Transtentotial
Foramen magnum
subfalcine
Transtentorial
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Displacement of brain and herniation of
uncus of temporal lobe through the tentorial
hiatus
Causes compression of:
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midbrain : contralateral hemiparesis (usually),
Cushing response, , respiratory failure (cheynestokes)
CN III: dilatation of ipsilateral pupil initially
Posterior cerebral artery: hemianopia
Foramen magnum (coning)
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Progressively increasing ICP causes further
downward herniation of the brainstem into foramen
magnum or coning.
This results in shearing of the perforators supplying
the brainstem and haemorrhage within (Duret
heamorrhage).
Traction damage to pituitary stalk resulting in DI.
With progressive herniation pupils change from
dilated and fixed to midsize and unreactive.
Signifying irreversible events leading to brainstem
death.
Subfalcine
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Cingulate gyrus herniates under falx.
Usually asymptomatic unless ACA kinks and
occludes causing bifrontal infarction.
ICP monitoring
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Indications:
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Head injury
Following major intracranial surgery
Assessment of benign intracranial HTN
Normal ICP: 10-15mmHg
Can be recorded from ventricle, brain substance,
subdural or extradural space
Risks: CNS infection and intracranial haemorrhage
A waves
Management
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Definitive treatment: treat underlying patholgy
To control raised ICP:
1.
2.
3.
4.
5.
6.
7.
Head elevation
Controlled ventilation: maintain PaCO2 at 30-35 mmHg. Reduction
of CO2 will reduce cerebral vasodilatation
Sedation/paralysis: decrease metabolic demand
If ventricular catheter in situ, drain CSF
Diuretic therapy: mannitol – osmotic diuretic, increases serum osm
and draws water out of the brain. Usual dose: 0.5-1.0g/kg. monitor
serum osm
Hypertonic saline
Barbiturate therapy: thiopentone when given as a bolus dose can
be helpful in temporarily reducing ICP.
Bibliography
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Essential Neurosurgery. Prof. A Kaye. Third edition
Handbook of neurosurgery. M. Greenberg. Sixth
edition
Uptodate: Evaluation and management of elevated
intracranial pressure in adults. E.Smith
http://www.millerneurosurgery.com/index.php/proced
ures