3. Intracranial Pressure

The skull of an adult is in effect a rigid box which contains brain tissue, blood and CSF. The brain itself has minimal compressibility and so there is very limited scope for compensation. An increase in the volume of one component invariably results in an increase in ICP unless the volume of another component decreases (This is the Monroe–Kellie hypothesis.) brain tissue (1,400–1,500 g), blood (100–150 ml), CSF (110–120 ml) and extracellular fluid (<100 ml). The intracranial compliance curve

Normal ICP is 10–12 mmHg. Any increase may be significant because of the potential impact on cerebral perfusion. The CPP is determined by mean arterial pressure (MAP) minus the sum of the central venous pressure (CVP) and the ICP. CPP = MAP  (CVP + ICP).

: ICP is raised by mass lesions which increase the volume of brain, bone or meninges. These include tumours of all three structures, as well as infection (with abscess formation

Volume increases: ICP is raised by conditions which increase non-CSF fluid volume. Intracranial aneurysm, arteriovenous malformation and trauma are all relatively common causes of subarachnoid or subdural haemorrhage. ICP is raised by cerebral oedema, which itself has many causes, including trauma, infection, metabolic dysfunction (such as hepatic encephalopathy or Reye’s syndrome), hypoxia, venous obstruction and increased hydrostatic pressure (such as is caused by a steep or prolonged Trendelenberg position on the operating table). It may form part of the symptomatology of altitude sickness (high-altitude cerebral oedema, HACE). It may also be idiopathic, as in benign intracranial hypertension. (This is a clinical entity defined by an ICP greater than 15 mmHg (but which can reach three times that figure) in the presence of normal CSF composition, normal conscious level and with no evident pathological process). Increased ICP may be caused by a rise in intracranial venous pressure which is offset by intracranial and CSF pressure increases that restore the required gradient for CSF absorption into the venous system. Some cases can be managed with corticosteroids, diuretics and acetazolamide, but severe cases may require the insertion of a lumbothecal–peritoneal shunt

Impaired drainage: ICP is also raised by conditions which impede drainage of CSF (which is produced at 0.4 ml min1) and thus increase its intracranial volume. These include congenital and acquired hydrocephalus, which may also be associated with trauma, tumour or infection. A blocked ventricular shunt is another important cause

: in the presence of raised ICP, CPP is given by MAP – ICP. Perfusion will be maintained until CPP starts to fall below 50 mmHg, with the onset of critical ischaemia at 30–40 mmHg. There may also be focal ischaemia in the region of a mass lesion. Raised ICP attenuates cerebral autoregulation to the point at which it is lost completely, after which cerebral blood flow follows MAP passively.

Subdural pressure transducers. As the name describes, these devices are placed in the subdural space and fill with cerebrospinal fluid. After equalization, the pressures within the closed system can be transduced. They are less invasive than other methods, but are less accurate and do not allow sampling or drainage of CSF.

These catheters provide the most accurate means of measuring ICP. They are usually placed into the lateral ventricle via a burr hole (most commonly in the right frontal area) and through the parenchyma of the brain. In addition to providing pressure measurements, the catheters can also be used to drain cerebrospinal fluid or to administer drugs such as antibiotics. The external transducer reference point is the external auditory meatus which approximates to the intracerebral centre, which is where the foramina of Munro link the lateral ventricles with the third ventricle. Complications include infection and blockage.

. These are useful when extreme ventricular compression makes the insertion of an intraventricular catheter impossible. They do not use amn column of fluid (i.e. a saline-filled catheter) via which to transduce pressures but instead use a variety of other technologies. One example is the use of fibreoptic cables tipped with miniature mirrors whose displacement by raised ICP reflects light of varying intensity, which is then transduced into pressure. Another is the use of microchip sensors whose resistance alters as ICP changes. These systems cannot be recalibrated once they are in position, they cannot sample or drain CSF, and because of their location they may measure only local pressure changes rather than global ICP.

its total volume is around 150 ml, about 80% of which is intracranial. Most of the extracranial (spinal) CSF is found distal to the conus medullaris. The choroid arterial plexuses form CSF either by secretion or by the quantitatively much less significant process of ultrafiltration. It is produced in the lateral, third and fourth ventricles, at a rate of around 0.4 ml min1 (575 ml 24 h1). The rate of production is constant and is not related to ICP unless it is sufficiently high to compromise CPP and reduce blood flow to the choroid plexus.:

: CSF passes through the cerebral aqueduct to the fourth ventricle and thence through the midline foramen of Magendie and the two lateral foramina of Luschka to communicate with the subarachnoid space of the brain and spinal cord. It is either absorbed directly into cerebral venules (10%) or absorbed by the arachnoid villi (90%).

Functions: it has a cushioning effect which protects the brain from injury. Supported by CSF, the effective cerebral weight is only 50g. By translocation from the intracranial to the extracranial subarachnoid space, CSF can partly buffer increases in ICP.

it has a higher PCO2 than plasma and a lower pH (7.33). The mean specific gravity is 1.006, with a range of 1.003–1.009. Its protein content is low (0.2 gl1), so buffering capacity is negligible. Glucose concentration is lower than in plasma. Sodium and chloride are higher, whereas potassium is lower (40%). This is because the formation of CSF requires the active transport of Na+, Cl and K+ into the ventricles. Further Na+ is then added in exchange for K+ (mediated by Na+/K+ ATPase). The influx is maintained by the further exchange of H+ and HCO3 - for Na+ and Cl. H+ and HCO3 - are generated from H2CO3 in a reaction catalysed by carbonic anhydrase.

acetazolamide, which is a carbonic anhydrase inhibitor, may reduce CSF production by as much as 50%. High-dose diuretics also reduce it by affecting the sodium transport process. (Corticosteroids may increase production, but not consistently enough to make them a reliable treatment for postdural puncture headache.)

Increasing age Low admission GCS Pupillary signs Systolic blood pressure <90 mmHg Low arterial O2 tension High arterial CO2 tension ICP >20 mmHg High blood glucose

This is the damage that occurs at the time of the initial insult and may be the result of: Trauma Haemorrhage Tumour

This is additional ischaemic neurological damage that occurs after the initial injury as a result of: Hypoxaemia Hypercapnia Hypotension Raised ICP Cerebral arterial spasm Hyperglycaemia. Possible mechanisms: Glutamate and aspartate act on NMDA receptors causing increased intracellular calcium, activation of phospholipases, breakdown of arachidonic acid and generation of free radicals.

Treatment of raised ICP should be initiated if >20–25 mmHg and is aimed at reducing the volume of the three components making up the intracranial contents: namely brain, blood and CSF. Firstly, maintenance of an adequate cerebral perfusion pressure should be ensured. Arterial blood gases should be corrected. The patient should be sedated to a satisfactory level. Attention can then be paid to the following

Mannitol (0.25–1.0 g/kg) is frequently used to reduce cerebral oedema. Loop diuretics, e.g. frusemide (0.5 mg/kg) given within 10–15 min of mannitol produce a synergistic effect. They encourage a more hypotonic diuresis that prolongs the duration of intravascular osmotic load produced by mannitol. Cerebral oedema may be worsened with inattention to the serum osmolarity, which should be kept between 300 and 310 mosmol. Hypotonic solutions should be avoided. Treat diabetes insipidus with DDAVP. Surgical removal of brain tissue. Hypertonic saline administration in patients with head injury or brain tumour have demonstrated a reduction in ICP, however the overall results of studies are inconclusive and require further trials to define its role.

Surgical removal of blood (i.e. clot). Avoid impeding venous drainage by tight tube ties, high ventilation pressures or excessive neck rotation. Venous drainage can be aided by a 30◦ head-up position. Hyperventilation can be effective in the short term but should not be used in the long term because of the potential for causing ischaemia (can be monitored by jugular bulb venous oxygen saturation and cerebral oximetry). Reducing cerebral metabolic requirements with thiopentone will decrease cerebral blood volume by decreasing cerebral blood flow, but has the disadvantage of prolonged sedation. Hyperglycaemia has deleterious effects on metabolism and cerebral perfusion. Blood glucose should be maintained between 4.5 and 8 mmol/l. Control of fitting (fitting increases CMRO2 and therefore cerebral blood flow). Avoidance of pyrexia will help to prevent increases in the CMRO2 and associated increases in CBF and ICP. Induced hypothermia has been used in an attempt to improve outcome. However, a recent multicentre study does not support its routine use.

A study published in the New England Journal of Medicine (Feb 2001) looked at the effect of induced hypothermia (to 33 ◦C) on outcome at 6 months after closed head injury. The trial was stopped after 392 patients (500 planned) because there was no improvement in outcome and, in fact, patients in the over-45 years group did worse. The authors recommended not deliberately cooling patients who were normothermic on admission. However, if they were hypothermic on admission, then they should not be aggressively warmed. Studies of head-injured patients with severe intracranial hypertension have demonstrated a beneficial effect in mild hypothermia.

CSF can be drained via an external ventricular drain (EVD). Production is reduced by mannitol and frusemide.

Osmotic diuretic Rheological effects ↓ red cell rigidity (rbc membrane) ↓ haematocrit (haemodilution) Free-radical scavenger Dose is usually 0.5 g/kg rapid infusion Giving frusemide 0.5 mg/kg 10–15 minutes after mannitol prolongs its effect (see above) Efficacy depends on intact BBB