In order to understand the management of raised intra-cranial pressure it is vital to understand some basic physiological principles.
The normal intra-cranial pressure is 5-15mmHg, but >20mmHg is where potential pathological effects may occurr.
The first important one is the Munro-Kellie Doctrine Phenomenon
This states that the skull is a rigid and fixed structure (not in children) and that within the skull lies the components of brain matter, csf, blood and a potential mass. It suggests that any increase in one of the components will lead to a rise in intra-cranial pressure. There are initial compensatory mechanisms of a total 150mls either via diverting CSF to lumbar theca or via increasing venous outflow, however once past the point at which the compensatory mechanism have occurred a rapid rise in ICP will occurr.
Here is the key message and formula to learn
VICP= Vblood+Vbrain+Vcsf+Vmass (e.g tumour, haematoma, abscess)
- Examples of increasing volume of blood- e.g cerebral vasodilation or venous obstruction e.g in Idiopathic Intracranial Hypertension
- Examples of increasing volume of the brain e.g cerebral oedema
- Examples of increasing CSF: Hydrocephalus
- Examples of increasing mass lesions: include the tumour etc
It is therefore possible to tailor your management to reduce the ICP using these basic principles
This is a beautiful illustration of the Phenomenon and how it makes total sense! It is very good to be able to real this off in an exam OSCE.
A large ICP will impair the ability to perfuse the brain leading to ischaemia; conversley a large MAP will lead to a significantly increased blood flow leading to worse haemorrhage.
Mean Arterial Pressure= SBP+(2XDB)/3. Calculating the MAP is a common question they ask in exams including in the recent MRCS Part A.
As mentioned above the inital compensatory mechanisms via csf diversion and increasing venous outflow can improve the ICP however post a ‘critical volume’ 150mls- a dangerous rise in ICP can occurr.
Certain factors affecting flow include metabolites, CO2, Oxygen will affect the vessel diameter
Alternatively in patients with cerebral vasospasm following a SAH, will have reduced vessel diameter and increased resistance, therefore reducing blood flow leading to cerebral ischaemia. In these patients increasing the pressure will lead to increased cerebral blood flow reducing the risk of cerebral ischaemia, a feared complication post SAH.
Factors Affecting Cerebral Vasculature
Chemoregulatory factors and Autoregulatory factors both play a vital role in managing the volume of blood to the brain.
Chemoregulatory factors increasing cerebral blood flow:
- PaCO2-hypercapnia leads to cerebral vasodilation
- PaO2- hypoxia leads to cerebral vasodilation
- Metabolites and metabolic acidosis leads to cerebral vasodilation
Chemoregularatory factors decreasing cerebral blood flow:
- PaCO2- hypocapnia leads to cererbal vasoconstriction
- Alkalosis leads to cerebral vasoconstriction
- Reduction in metabolic by products
The brain receives 15% of the cardiac output and this equates to roughly as 750ml/minute.
The flow rate differs dependent upon grey and white matter. The white matter flow rate is roughly 20mls/100g/minute and the grey matter 100mls/100g/min.
Autoregulation is defined as the ability to maintain perfusion to an organ despite changes in blood pressure. Between 50-150mmHg the brain has the ability to maintain perfusion. During head injury or sub-arachnoid haemorrhage auto-regulation is impaired altering cerebral blood flow
Learning these key principles is essential to understanding raised ICP, as tailoring management is underpinned to the above material.