Raised intracranial pressure

Raised intracranial pressure

Physiology of intracranial pressure

Pathophysiology The adult skull may be regarded as a rigid unyielding box con­taining brain, cerebrospinal fluid (CSF) and blood. At normal supine pressures of 0.67-2 kPa (5-15 mmHg, 6-18 cm H20). measured from the level of the foramen of Monro these three components maintain volumetric equilibrium. An increase in the volume of any of the components will result in an increase in intracranial pressure (ICP) unless there is a

proportionate decrease in the volume of one of the other components owing to compensat dry volumetric changes having physical and physiological limits the ability to maintain a constant ICP can be exceed by a change in volume that is too fast or too great
shifting CSF and displacing blood from venous structures. A crit­ical point is reached however when small changes in volume cause exponential increases in ICP during this phase the brain adapts by shifting CSF and displacing blood from venous structures a critical piont is reached however when small changes in volume cause exponential increase in ICP

The relationship of volume to pressure is described in terms of compliance or elastance of the intracranial space. Compliance is expressed as dV/dP and is the amount of give available within the intracranial compartment. Elastance is the inverse and is resistance offered to the expansion of a mass or the brain itself When patients initially present with symptoms of raised ICP, brain compliance has already been reduced and small volume changes have the potential to cause precipitous increases in ICP and a reduced level of consciousness

Between physiological ranges of blood pressure, the brain is able to maintain a constant cerebral blood flow.This is achieved by a process called autoregulation , where by the brain adjusts the intracranial vascular resistance by altering the vessel diameter and tone. With hypovolaemic shock, malignant hyper­tension, subarachnoid haemorrhage or diffuse severe head injuries, this ability is compromised and the cerebral perfusion pressure becomes virtually dependent on the mean arterial pres­sure Normal cerebral blood flow (CBF) is about 800 ml min or20% of the total cardiac output. The blood flow is a function of the cerebral perfusion pressure (CPP) and the cerebral vascular resistance (CVR
The cerebral perfusion pressure is a function of the systemic mean arterial pressure (MAP) and the ICP.
As intracranial pressure increases, in order to maintain a con­stant CPP, there has to be a compensatory rise in the MAP. A hypertensive response is therefore elicited which classically is associated with a bradycardia. This is termed the Cushing reflex after the eminent neurosurgeon who first described it

Conditions that may compromise autoregulation of ICP

• Hypovolaemic shock
• Malignant hypertension
Subarachnoid haemorrhage

  • Diffuse head injuries

Summary of physiology of intracranial pressure

• The adult skull is on unyielding box
It contains brain, blood and cerebrospinal fluid CSF
• If one of these contents increases in volume intracranial pressure ICP may go up
• The brain's ability to compensate for raised ICP is rapidly exhausted
• Raised ICP is dangerous to the brain

Clinical features

These are largely determined by the underlying cause. However, some of the clinical symptoms and signs will be the same as headache• nausea and vomiting;drowsiness;• papilloedema

These headaches are usually worse in the morning owing to vasodilatation caused by hypoventilation and consequent CO2 retention during sleep.They are typically progressive but relieved by an upright position and are frequently associated with nausea and vomiting. As the brain has no sensation, they are caused by traction and distortion of the pain-sensitive blood vessels and dura. Compression of the reticular activating system in the brain­ stem results in drowsiness. In an infant, raised ICP will cause a tense bulging fontanelle.
As the eyes are extensions of the forebrain, the optic nerves
carry with them the meningeal coverings. The raised ICP is thus transmitted directly to the optic nerve head via the CSE This results in obstruction to axoplasmic flow in the retinal neurones that cause swelling of the optic disc. This is seen on funduscopy as blurring of the disc margins eventually retinal haem­orrhages and, if prolonged, optic atrophy. Traction on the abducens (sixth) nerves by caudal displacement of the brain stem may cause nerve palsies (the 'false localizing sign

Continuous monitoring of ICP reveals stereotyped variations superimposed upon baseline fluctuations. 'A' waves are transient plateaux of increased pressure to greater than 50 mmHg, which last for 5-10 min. They are abnormal and indicate low compli­ance within the intracranial cavity. Skull radiographs may demon­strate sutural separation in children, pronounced 'copper-beating' marking of the cranial vault, and thinning of the dorsum sellae with erosion of the posterior clinoid processes


This should primarily be directed at removing the cause for the increased ICP Intracranial volume can be mechanically decreased by removing an intracranial mass or haematoma, reducing intracranial venous blood volume by facilitating venous outflow via the jugular' veins, ventilation to reduce the carbon dioxide  level to 4-4.53 kPa (3~34 mmHg) (avoiding vasoconstriction­.in patients with ischaemic disease) or by draining  CSF through ventriculostom. steroids seem most effective in decreasing ICP resulting from vasogenic oedema associated with brain tumours, infection or surgical   manipulation(dexamethasone, 4 mg, 6-hourly). They work  by stabilising the blood-brain barrier and reducing oxygen radical injury mannitol
an osmotic dehydrating agent (1 g kg-I, 4- to 6-  hourly by drawing water from parts of the brain with an intact brain barrier. If this is disrupted, as in a cerebral contusion mannitol can leach out into the brain and potentiate the mass effect

In head injuries it should therefore only be administered after consultation with a neurosurgeon.­
It becomes ineffect­ive when brain osmolarity becomes iso-osmolar with that of the serum
barbiturates given as a bolus (thiopentone, 3-5 mg kg-) can although the exact mechanism remains obscure. dosed are titrated to give a level of 2.5-3.5 mg%.lnfusions to control,brust suppression on electroencephalogram have been postulated to diminish ICP by reducing cerebral metabolism. The initial response is due to vasoconstriction, but it is possible to also reduce CPP by causing hypotension Fursemide.
reduces lCP by reducing cerebral oedema and CSF production It may act synergistically with mannitol. hypothermia down to 34°C is currently undergoing assessment as brain protection agent.
there is a clear relationship between raised pressure and morbidity and mortality. The vital physiological  parameter in severely head-injured patients is the CPP this is a function of the mean arterial blood pressure and the CIP and to optimise outcome, should be maintained above 65-79 mmHg This requires a close working relationship between the intensivist and the neurosurgeon 



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