What is intracranial pressure? How is it measured?

The intracranial pressure (ICP) is simply the hydrostatic pressure within the skull, reflecting the pressure of the cerebrospinal fluid (CSF) and brain parenchyma. At rest in a normal supine adult, ICP is 5–15 mmHg; ICP varies throughout the cardiac and respiratory cycles. Even in a normal brain, coughing, straining and sneezing can transiently increase ICP to as high as 50 mmHg.

Unfortunately, ICP cannot be estimated, only invasively measured. ICP may be measured by a variety of devices, each with their advantages and disadvantages:

• 
  

  External ventricular drain (EVD): a catheter inserted into the lateral ventricle, which is considered the ‘gold standard’ for measuring ICP. In addition to ICP measurement, an EVD can be used to remove CSF for diagnostic and therapeutic purposes (to reduce ICP – see later) and for the administration of intrathecal medication. However, to measure ICP, the EVD must be ‘clamped’; that is, CSF cannot be simultaneously drained. An EVD may be surgically challenging to insert, especially if the ventricles are small or displaced. Also, EVDs are frequently complicated by blockage and are associated with an infection risk of up to 5%.

  
  
• 
  

  Intraparenchymal probe: a fibre-optic-tipped catheter placed within the brain parenchyma through a small burr hole. An intraparenchymal probe is much easier to insert than an EVD and can be used in situations where the ventricles are compressed or displaced. Measurement of ICP using an intraparenchymal probe is almost as accurate as an EVD, and infection rates are substantially lower. However, there are concerns about the accuracy of intraparenchymal catheters used for prolonged periods: the catheter is zeroed at the time of insertion and cannot be recalibrated in situ.¹ An intraparenchymal probe only measures the pressure of the brain parenchyma in which it is located, which may not represent global ICP.

  
  
• 
  

  Subarachnoid and subdural probes: now considered relatively obsolete. Although associated with a low rate of infection, these probes are less accurate, prone to blockage and require regular flushing.

What is the Monro–Kellie hypothesis?

The Monro–Kellie hypothesis states that the cranium is a rigid box of fixed volume, which contains:

• 
  

  Brain tissue, 1400 g or approximately 80% of the intracranial volume;

  
  
• 
  

  CSF, 150 mL or approximately 10% of intracranial volume;

  
  
• 
  

  Arterial and venous blood, 150 mL or approximately 10% of intracranial volume.

An increase in the volume of any of these intracranial contents will increase ICP, unless there is also a corresponding reduction in the volume of one or both of the other contents. For example:

• 
  

  An increase in the volume of brain tissue may be localised (e.g. a brain tumour or abscess) or generalised (as occurs with cerebral oedema).

  
  
• 
  

  The volume of CSF may be increased in hydrocephalus (see Chapter 46).

  
  
• 
  

  The volume of intracranial blood may be increased following haemorrhage (extradural, subdural or intraparenchymal) or venous sinus thrombosis.

When one of the intracranial contents increases in volume, there is a limited capacity for displacement of the other contents:

• 
  

  Some CSF is displaced from the cranium into the spinal subarachnoid space. Whilst the rate of CSF production remains approximately the same, CSF absorption by the arachnoid villi is increased.

  
  
• 
  

  Dural venous sinuses are compressed, displacing venous blood into the internal jugular vein, thus reducing the volume of intracranial blood.

After these small compensatory changes have occurred, ICP will rise. The only options left are then potentially disastrous: a reduction in arterial blood volume or displacement of brain parenchyma through the foramen magnum (Figure 49.1).

• 
  

  Symptoms suggesting raised ICP include:

  
  
  
  
  1. 
     

     – A headache that is worse in the morning and is exacerbated by straining and lying flat;

     
     
  2. 
     

     – Nausea and vomiting.

  
  
  
  
• 
  

  Signs of raised ICP include:

  
  
  
  
  1. 
     

     – A bulging, tense fontanelle in infants and neonates;

     
     
  2. 
     

     – Papilloedema;

     
     
  3. 
     

     – Altered consciousness.

  
  
  
  
• 
  

  Severe intracranial hypertension may result in additional signs as a result of brain displacement:

  
  
  
  
  1. 
     

     – Cranial nerve palsies: most commonly the abducens (cranial nerve VI) due to its lengthy course through the skull.

     
     
  2. 
     

     – Pupillary dilatation: caused by compression of the oculomotor nerve (cranial nerve III).

     
     
  3. 
     

     – Cushing’s triad:

     
     
     
     
     1. 
        

        ▪ Systemic hypertension;

        
        
     2. 
        

        ▪ Bradycardia;

        
        
     3. 
        

        ▪ Abnormal respiratory pattern.

     
     

  
  

Figure 49.1 Change in intracranial pressure with increasing intracranial volume.

Can you explain Cushing’s triad?

As discussed in Chapter 48, cerebral perfusion pressure (CPP) is related to mean arterial pressure (MAP) and ICP:

According to this equation, an increase in ICP results in a decrease in CPP, unless MAP also increases.

The Cushing response is a late physiological response to increasing ICP. When CPP falls below 50 mmHg, the cerebral arterioles are maximally vasodilated and cerebral autoregulation fails. Cerebral blood flow (CBF) falls below the ‘normal’ value of 50 mL/100 g/min, resulting in cellular ischaemia (Chapter 48, Figure 48.1).

In the event of brainstem ischaemia, the brain has an ‘emergency’ hypertensive mechanism: the vasomotor area dramatically increases sympathetic nervous system outflow, triggering an intense systemic arteriolar vasoconstriction that results in systemic hypertension. The rise in MAP restores perfusion, and hence CBF, to the brainstem. In response to systemic hypertension, the arterial baroreceptors induce a reflex bradycardia.

If ICP continues to rise, the brain parenchyma starts to be displaced downwards. The cerebellar tonsils are pushed through the foramen magnum, a process referred to as ‘tonsillar herniation’ or ‘coning’. The cerebellar tonsils compress the brainstem, causing the failure of brainstem functions:

• 
  

  Irregular breathing and apnoea through compression of the respiratory centre;

  
  
• 
  

  Decreased consciousness: Glasgow Coma Scale (GCS) of 3–5 is usual;

  
  
• 
  

  Hypotension, as the vasomotor centre is compressed.

The Cushing reflex is a desperate attempt to maintain CPP (and therefore CBF) in the face of substantially increased ICP. Unless swift action is taken (and often despite this being done), brainstem death is inevitable.