RAISED ICP Atandrila Das

Monro-Kellie Doctrine 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 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 Brain – 80% Blood – 10% CSF – 10%

Causes of raised ICP Increased volume of normal contents – Brain: oedema, benign intracranial HTN – CSF: hydrocephalus – Blood: vasodilatation, venous thrombosis Space occupying lesions – Tumour – Abscess – Intracranial heamorrhage

Symptoms/signs DROWSINESS Headache Nausea/vomiting Papilloedema Cushing’s triad

Normal fundus

Papilloedema

Cerebral herniation Can occur depending on cause of raised ICP 3 major types: – Transtentotial – Foramen magnum – subfalcine

Transtentorial Displacement of brain and herniation of uncus of temporal lobe through the tentorial hiatus Causes compression of: – midbrain : contralateral hemiparesis (usually), Cushing response,, respiratory failure (cheyne- stokes) – CN III: dilatation of ipsilateral pupil initially – Posterior cerebral artery: hemianopia

Foramen magnum (coning) 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 Cingulate gyrus herniates under falx. Usually asymptomatic unless ACA kinks and occludes causing bifrontal infarction.

ICP monitoring Indications: – 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 Definitive treatment: treat underlying patholgy To control raised ICP: 1. Head elevation 2. Controlled ventilation: maintain PaCO2 at mmHg. Reduction of CO2 will reduce cerebral vasodilatation 3. Sedation/paralysis: decrease metabolic demand 4. If ventricular catheter in situ, drain CSF 5. Diuretic therapy: mannitol – osmotic diuretic, increases serum osm and draws water out of the brain. Usual dose: g/kg. monitor serum osm 6. Hypertonic saline 7. Barbiturate therapy: thiopentone when given as a bolus dose can be helpful in temporarily reducing ICP.

Bibliography 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 ures