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Traumatic Brain Injury: Resuscitation and management of intracranial hypertension

Created: 22/5/2007
Updated: 22/5/2007


Traumatic Brain Injury: Initial Resuscitation and Principles of Management of Intracranial Hypertension

Clemens Pahl FRCA DICM
Advanced Trainee in Intensive Care Medicine and Anaesthetics 

Focus on initial resuscitation

Initial resuscitation of patients with traumatic brain injury (TBI) should follow Advanced Trauma Life Support guidelines (with the ABCDE approach). It is important to emphasise that the quality of the initial resuscitation has a direct impact on the quality of the long-term outcome from severe brain injury.

Figure 1

Important aspects of initial management include:

• Consider the possibility of concomitant cervical spine injury in an unconscious patient with TBI (estimated to be about 5 to 10%). Adequate cervical spine immobilisation needs to be maintained until the cervical spine is formally cleared
• Patients with severe TBI should be intubated and mechanically ventilated
• Opiates (e.g. fentanyl and alfentanil) can be used to obtund the stress response to intubation and prevent a surge in intracranial pressure (ICP)
• Continuous end-tidal carbon dioxide monitoring and invasive arterial monitoring are mandatory. Cerebral vessel diameter and ultimately cerebral blood flow (CBF) change proportionally over a wide range of PaCO2 values (Figure 1). Both hypercapnia and hyperventilation should be avoided. The aim is to maintain normocapnia (PaCO2 of 4.5 to 5.0 kPa). Cerebral microdialysis techniques in patients with severe TBI demonstrate that even brief episodes of hyperventilation cause cerebral ischaemia. Hyperventilation should be reserved for cases of cerebral herniation (manifested by a sudden fall in consciousness, sudden pupillary dilatation, decorticate or decerebrate posturing or a massive peak in ICP)
• PaO2 should be kept >11 kPa. In healthy individuals. CBF is traditionally thought to be unchanged until PaO2 falls below about 6.5 kPa, but rises sharply with further reductions (Figure 1). However, more recent work on healthy volunteers challenges this value and suggests that the PaO2 threshold is actually 8.0 to 8.5 kPa
• Following haemorrhage control and correction of hypovolaemia, an adequate cerebral perfusion pressure (CPP) needs to be ensured. ICP can be assumed to be greater than 20 to 30 mmHg. Thus, the target mean arterial pressure (MAP) should be 90 to 95 mmHg to ensure a cerebral perfusion pressure of greater than 60 mmHg:


• Close cooperation between the neurosurgeons and intensive care practitioners is essential to plan both appropriate neurocritical care and possible neurosurgical investigations and interventions
• CT imaging of the head should be considered to exclude the presence of any pathological lesion amenable to surgically intervention
• CT imaging of the cervical spine, thorax, abdomen and pelvis should also be considered if not already done
• The head should be elevated by 30 degrees to improve jugular venous return and reduce ICP.
• Important points in the neurological assessment include:

o documentation of sequential GCSs
o pupillary size and reaction (particularly important after intubation)
o limb movements
o focal neurological signs before intubation.

• An infusion of mannitol (0.5 to 1g/kg) may be indicated on neurosurgical device (especially in the presence of a dilated and non-reactive pupil)
• If the patient does not require surgery to evacuate an intracranial mass lesion or other life- or limb-saving operations, transfer to the ICU can be initiated. Alternatively, an out-of-hospital transfer to a specialist neurosurgical centre can be organised

Focus on the principles of managing intracranial hypertension

Figure 2

Two main principles underlie the management of intracranial hypertension.

The first is the Monroe-Kelly doctrine (Figure 2). Under normal conditions, the volume of the rigid skull has three components: brain tissue (almost 90% of the total), blood and CSF. Pathologically, a fourth component can be added (e.g. tumour or haematoma). None of these components are appreciably compressible. Therefore, if one component increases in volume, the other components must accommodate.

It follows that intracranial hypertension can in theory be treated by reducing the volume of one of the four components of the cranium:

1. Brain tissue
• Reduction of brain oedema by mannitol or hypertonic saline
• Volume reduction of brain parenchyma by surgical resection (e.g. lobectomy)

2. Blood volume
• Reduction of brain blood volume by hyperventilation or vasopressor therapy to induce arterial vasoconstriction
• Prevention and therapy of seizures to avoid vasodilatation induced by increased metabolism and oxygen demand

3. CSF
• Reduction in CSF volume by external drainage

4. Pathological lesions
• Surgical removal of pathological lesions (e.g. haematoma evacuation, tumour excision)

In addition, part of the skull may be removed surgically (a “decompressive craniectomy”) to create room for brain swelling and protect against the detrimental effects of an increased ICP.

The second principle is to protect against secondary brain damage following the primary insult (Rosner’s conjecture).
It embraces all the factors responsible for causing secondary insult via cerebral ischaemia:

• systemic factors
o arterial hypotension
o hypoxaemia
o pyrexia
o hyperglycaemia

• brain factors
o intracranial hypertension
o seizures
o inflammatory and cytotoxic

Key references

Brain Trauma Foundation.
Guidelines for the management of severe traumatic brain injury: Cerebral perfusion pressure.

Dutton RP, McCunn M. 
Traumatic Brain Injury. 
Curr Opin Crit Care 2003

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