Intracranial disorders

Pathophysiology of raised intracranial pressure

Introduction

The adult skull may be regarded as a rigid unyielding box containing brain, cerebrospinal fluid (CSF) and blood. At normal supine pressures of 5—15 mmHg (6—18 cmH2O), measured from the level of the foramen of Munroe, these three components maintain volumetric equilibrium. An increase in the volume of any one 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. These observations were first reported by Alexander Munro (Professor of Anatomy, Edinburgh, 1783) and 40 years later confirmed by Kellie — becoming known as the Munro—Kellie doctrine.

Owing to compensatory volumetric changes having physical and physiological limits, the ability to maintain a constant ICP can be exceeded by a change in volume that is too fast or too great. This intracranial pressure—volume relationship is illustrated in the curve (Fig. 35.8). Initially quite large increases in volume produce only small changes in pressure. During this phase the brain adapts by shifting CSF and moving blood from venous structures. A critical point is reached however when small changes in volume cause exponential increases 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 the resistance offered to the expansion of a mass or the brain itself. When patients initially present with symptoms of raised ICP it is invariably when brain com­pliance has 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 (Fig. 35.9), whereby the brain adjusts the intracranial vascular resistance. 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 or 20% of the total cardiac output. The blood flow is a function of the cerebral perfusion pressure (CPP) and the cerebral vascular resistance (CVR).

                 CBF = CPP/CVR

The cerebral perfusion pressure is a function of the systemic mean arterial pressure (MAP) and the ICP.

                   CPP = MAP - 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 American neurosurgeon.

Clinical features

These are largely determined by the underlying cause. How­ever, some of the clinical symptoms and signs will be the same:

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 brainstem 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 ICP is thus transmitted directly to the optic nerve head via the CSF. This results in obstruction to axoplasmic flow in the retinal neurons causing swelling. This is seen on fundoscopy as blurring of the disc margins (Fig. 35.10), eventually retinal haemorrhages and if prolonged, optic atrophy. Traction on the abducent (sixth) nerves by caudal displacement of the brainstem may cause nerve palsies — the false localising 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 minutes. They are abnormal and indicate low compliance within the intracranial cavity. Skull X-rays 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.

Treatment

This should primarily be directed at removing the cause for the increased ICR 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, ventilated to bring the carbon dioxide toxin (PCO2) down to 4—4.5 (avoiding vasoconstriction in patients with ischaemic disease) or by draining CSF through a ventriculostomy.

Steroids seem most effective in decreasing ICP resulting from vasogenic oedema associated with brain turnouts 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 4—6 hourly), works by drawing water from parts of the brain with an intact blood—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 bolos (thiopentone 3—5 mg/kg) can reduce ICP, although the exact mechanism remains obscure. Subsequent doses are titrated to give a level of 2.5—3.5 mg per cent. Infusions to control burst suppression on electro­encephalogram (EEG) have been postulated to diminish ICP by reducing cerebral metabolism. The initial response is due to vasoconstriction but it is possible to reduce CPP by causing hypotension.

Frusemide reduces ICP by reducing cerebral oedema and CSF production. It may act synergistically with mannitol. Hypothermia down to 340C is currently undergoing assessment as a brain protection agent.

Although no randomised clinical study has ever been per­formed conclusively proving the value of ICP monitoring in reducing morbidity following brain injury, 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 ICP and, to optimise out­come, should be maintained above 65 mmHg. This requires a close working relationship between the intensivist and the neurosurgeon.