The management of intracranial pressure (ICP) is a key part of neurocritical care, particularly in patients with traumatic brain injury (TBI). As such, a good understanding of it is very important.
An essential starting point in the Monro-Kellie doctrine (from well back in 1783):
The cranium is a fixed box
An increase in the volume of the cranial contents will result in an increase in pressure
An increase in the volume of one of the cranial contents must be offset by a decrease in the other contents to avoid this increase in pressure.
There are 3 contents of the cranium:
Brain - approx 1.4kg
Cerebrospinal fluid (CSF) - 50-120ml
Blood - 50-70ml
As such, it is clear that there isn’t much room for compensation in the event of an increase in intracranial volume. This can be seen graphically. Initially there is compensation, through change in volume of other contents, followed by a decompensation phase, with a rapid rise in pressure.
The normal ICP is 7-17 mmHg Above an ICP of 20 mmHg, areas of focal ischaemia will start to develop. Above an ICP of 50 mmHg, global ischaemia will develop. As ICP rises they will be an increased pressure gradient driving movement of brain structures. If this progresses to movement of the brain through the foramen magnum, then there will be compression of the brain stem and death (a.k.a. coning).
Cerebral Blood Flow
Cerebral Blood Flow (CBF) Given the relationship between pressure and flow, and the fact that the blood volume of the cranium is one of the ‘modifiable’ volumes, an understanding of the factors that affect CBF is really important.
Normal CBF is approx. 50ml/100g/min, which is about 700ml/min (about 15% of cardiac output). This does vary from 20ml/100g/min for grey matter, and 70ml/100g/min for white matter.
Cerebral Perfusion Pressure
As with other tissues, the concept of a perfusion pressure is important in some regards. The CPP is this concept for the brain and is particularly important in TBI when some of the autoregulatory mechanisms are impaired. It is defined as:
Cerebral perfusion pressure = Mean arterial pressure - intracranial pressure (or central venous pressure - whichever is highest).
In essence, it is simply a representation of the pressure gradient which flow will occur over.
As noted however, there are normally autoregulatory mechanisms which maintain CBF over a wide range of conditions. The important ones are:
Autoregulation to pO2
Autoregulation to pCO2
Metabolic autoregulation As with other tissues, metabolic activity of the brain tissue cause local mediators to be produced which generally have a vasodilatory effect. As such, an increase in metabolic activity results in an increase in CBF.
Pressure autoregulation Systemic blood pressure varies fairly significantly through daily activity, but a constant maintenance of CBF is essential. As such, mechanisms have developed to allow a constant CBF across a wide range of systemic blood pressures.
This can be seen graphically. In general, the limits of autoregulation are quoted as a MAP of 50 mmHg and 150 mmHg. Beyond these limits, compensatory changes in the blood vessels can no longer compensate for the pressure changes, and the relationship between CBF and blood pressure becomes linear. As noted, in injured brain this autoregulation may be lost and CBF may become linearly dependent on the CPP.
Autoregulation to pO2 The partial pressure of oxygen (pO2) in the blood generally has a minimal impact on CBF. However, there is a significant reflex response when the pO2 drops below 6.7 kPa, with a dramatic rise in CBF. This reflex is to ensure oxygen delivery to the brain is protected.
Autoregulation to pCO2 Conversely, CBF is fairly sensitive to changes in the pCO2. Increases in the pCO2 causes cerebral vasodilation and a corresponding increase in CBF. Conversely, a decrease in pCO2 causes vasoconstriction and a decrease in CBF. The limit of this vasoconstriction occurs at about 3.3 kPa, below which there is no real further change to CBF.
Much of the management of raised ICP draws on the principles of the pathophysiology discussed above, and in particular the manipulation of these. This description focuses mainly on the management of ICP in patients with traumatic brain injury, but much of it is applicable in other aetiologies. They draw on the tiered approach protocol used by SRFT, available at: http://www.neuroicu.guru/ Whenever there is a deterioration in the patient’s clinical conditions, the question should be asked as to whether this might be due to an intracranial cause? If this is possible, repeat imaging of their head may be needed to assess if there is a lesion that is amenable to neurosurgical intervention.
An ICP of > 20 mmHg for over 5 minutes needs an urgent medical review, with an intervention to gain control of the ICP again. This may involve escalation within the tier, or up to a high tier of management.
Tier 1 This aims to optimise the simple factors of raised ICP.
Minimise obstruction to cerebral venous flow - check ETT ties aren’t too tight, removed cervical collars if appropriate (e.g. sedated), neutral head position.
Head up at 30 degrees - optimises venous drainage
Ensure normoxia (SpO2 94-98%, pO2 10-12 kPa) - this maintains adequate oxygen delivery to the brain and prevents the vasodilation and rise if cerebral blood volume at low pO2 levels.
Ventilate to low normocapnia (pCO2 4.5-5 kPa) - the avoids the excessive vasodilation and high blood volumes of higher pCO2 levels, but also minimises the degree of vasoconstriction that might impair CBF.
Deeply sedate - target a Richmond Agitation and Sedation Score (RASS) of -5. Escalate sedative agents as needed, including adding a benzodiazepine. This reduces cerebral metabolic activity.
Avoid coughing - this causes significant rises in ICP and so must be avoided, even on deeply stimulating procedures such as suctioning. Neuromuscular blockade may be considered if this isn’t managed with sedation alone.
Other neuroprotective measures are also employed at this tier:
Maintain a CPP of 60-70 mmHg - optimise fluid volume status first, but may also need vasopressor therapy in the form of noradrenaline.
Ensure liberal normoglycaemia - target a glucose of 5-10 mmol/L. This minimises the harm of elevated blood glucose levels and the risks of hypoglycaemic episodes.
Consider the role for an external ventricular drain (EVD) - this may aid drainage of CSF, thus reducing intracranial volume.
Tier 2 If tier 1 measures are failing to control the ICP, there is escalation to tier 2. At this point, there should again be a stop to assess what the problem might be:
Are all tier 1 measures being successfully implemented?
Is the problem due to an intracranial or systemic issue?
Is a repeat CT scan needed?
Hyperventilation - increase minute ventilation to achieve a pCO2 of 4-4.5 kPa. The response to this needs assessing through ABGs.
Normothermia - treat any elevated temperature with active cooling, either externally or through an intravascular device. The prevents excess cerebral metabolic activity, with theoretical benefits in blood flow.
Osmotherapy - this is discussed in more detail in the notes on TBI.
Diuretics - consideration may be given to the use of furosemide if the patient is over 3 litres positive since admission. This has a theoretical benefit on oedema.
Review CPP - a higher CPP target may be indicated in some scenarios. This will generally be a consultant decision. If there is failing autoregulation (more common for instance in diffuse axonal injury) a target CPP of 70 mmHg may be beneficial, and thus a trial could be considered. Assessment of cardiovascular status is important again at this point to ensure adequate volume status e.g. cardiac output monitoring. A higher CPP has been associated with increased rates of acute lung injury, therefore not without risk.
Tier 3 At this stage a review is again appropriate to ensure optimal care has been given so far:
Are all tier 1 and 2 measures being delivered effectively?
Is the CPP at an adequate value?
Is a repeat CT scan indicated to assess for an acute lesional change?
At this stage there are limited good options, but they include:
Decompressive craniectomy - this increases the volume of the cranium, thus reducing the pressure. The pathology is still the same and there are still significant risks.
Barbiturate coma - Barbiturates cause profound suppression of cerebral metabolic activity, thus reducing O2 demand and blood flow.
Therapeutic hypothermia - cooling causes a similar suppression in cerebral metabolic activity, though with a different set of complications.
Recent trials have provided challenging data on the implementation of these measures (see RescueICP and Eurotherm) which will be discussed in more detail in the TBI notes (Available here)