Guideline for the management of Traumatic Brain Injury (TBI)

Where should the patient be managed?

All patients with severe TBI (GCS <9) should be managed in a neurosurgical centre.

40% managed in non neurosurgical centres in UK.
Prospective observational study of 6921 patients. Mortality for those managed in NS centre 35%; 61% if not. Even with adjustment for consideration that those not transferred may have had worse injuries, still 2 fold increase in odds ratio for death.
Patel et al. Lancet 2005

Which patients should have ICP monitoring?

Severe head injury (GCS <9) with an abnormal admission CT scan
Normal CT and 2 or more of:

  • Age >40
  • Hypotension
  • Abnormal posturing
No level 1 evidence for ICPM but considered standard of care.
Cochrane review found no suitable studies to include reviewing whether ICP monitoring improved outcome.
Forsyth et al 2001
Further Cochrane review in 2010 found no suitable studies for inclusion.
Those with ICP >20 do worse.
Marmarou et al 1991. JNS
Monitors do not improve outcome - it is the decisions made based on monitoring that do.

Blood pressure and CPP

Aim for a CPP of 60
Aim for a MAP of 80 (if no ICP monitoring)

Those with CPP
<60 do worse.
Struchen et al 2001 J Neurotrauma
<55 do worse.
Chambers et al . 2001. JNS

Traditional management that CPP should be >70 results from prospective observational data that this leads to better outcomes.
Rosner 1995. JNS.
Theory began by Rosner is that autoregulation curve is shifted to the right so increasing MAP will bring it into the limits of autoregulation. Increasing MAP will cause precapillary vasoconstriction and a reduction in blood volume and thus ICP.
This is unlikely to be true.
Autoregulation is impaired in TBI but no convincing evidence that curve shifted to right.
Animal studies show that increasing MAP increases ICP.
Kongstad J of Trauma 2001
So do human studies. Increased CPP caused further rise in ICP in 30mins.
Oertel J N 2002.

CPP >70 causes x5 incidence respiratory complications.

Controlling brain volume (and ICP) rather than CPP improves outcome (Eker et al 1998 CCM) compared to historical controls.
Vintracran = Vblood + VCSF + Vbrain + Vmass lesion

Regulation of Vblood and Vbrain is medical focus treatment

In health the BBB is impermeable to Na and Cl. Water passing the BBB will be devoid of crystalloids and an opposing osmotic gradient will quickly be established preventing further fluid movement.
Only way to influence water movement in and out of brain tissue is to influence balance between hydrostatic, osmotic and colloidal forces.
In health these are tightly autoregulated.
In TBI pressure autoregulation is lost as is the barrier function of the BBB. Crystalloids and even large molecules can potentially cross the disrupted barrier meaning manipulation of colloidal and osmotic forces may be ineffective or even harmful. This leaves only hydrostatic pressure to manipulate.
Reduction of Ptissue will increase the gradient for flow from vessel to tissue which explains the swelling seen after evacuation of mass lesions, craniectomy or evacuation of CSF.

A decrease in MAP will initially decrease CPP but fluid reabsorption will occur reducing ICP and restoring CPP.

A CPP that is too low for perfusion will worsen outcome. Therefore should aim for the lowest safe CPP and not go above this. Best current evidence is to aim for CPP of 60.

If ICP monitoring is not possible (in a non neurosurgical ICU), assuming an ICP of 20 in TBI means a MAP of 80 would seem appropriate.

Which fluids?

Use CSL or 0.9% saline.
Avoid more hypotonic fluids and colloids.

Albumin increases mortality in TBI (SAFE study).
HES and gelatin worsen 6 month outcome in SAH patients.
As above the BBB is disrupted in TBI which would allow colloids to cross and exacerbate cerebral oedema.
Colloids are therefore absolutely contraindicated in TBI.
Manipulation of osmotic forces is still universally practiced with efforts to keep serum osmolality 300-320 with mannitol or hypertonic saline.
CSL is hypotonic after metabolism of the lactate so is avoided by some but used by others.
0.9% saline has an osmolality of 308 so is considered by some to be ideal.
Which should be used is unclear and there is no evidence either way.


Aim for a PO2 of > 10
If FiO2 > 0.5 then aim for PO2 of > 8

Hypoxia worsens outcomes by secondary brain injury.
DO2 is dependent mostly on saturation which will ordinarily be normal if PO2 is > 8. Aiming for higher targets than this may cause lung injury if high concentrations of oxygen are needed.


Aim for a CO2 of 4.5 - 5

Effects of lowering CO2 are only transient with cerebral arterioles returning to original calibre in 4-6h. Carmona-Suazo 2000 CCM
Hypocapnia causes hypoperfusion via vasoconstriction. Blood flows of <20ml/100g/min have been shown on PET scanning.
Worse outcome in randomised controlled trial of CO2 of 3.2.
Muizelaar. 1991. JNS
Keep above 4 - EBIC guideline (European brain injury consortium).
Hyperventilation is only a temporising measure, for example to control dangerously high ICP before surgical intervention. This does not apply in a DGH.


Deep sedation with 4mg/kg/h propofol with midazolam added if required.
If ICP monitoring is in situ then deep sedation will only be required if ICP is high

Reduction of cerebral energy requirements will reduce blood volume safely and reduce ICP.
This is achieved with deep sedation. More than 4mg/kg/h propofol may cause high triglycerides and propofol infusion syndrome.
Without ICP monitoring it is essential that CMRO2 is minimised to keep ICP as low as possible.
Paralysis will be unnecessary with deep sedation - any signs of arousal should prompt deeper sedation rather than paralysis.
Barbiturate coma reduces O2 requirement to 25% reducing blood volume and ICP.
Reduces MAP which reduces ICP (oedema re-absorption).
Cochrane review found no evidence for improved outcome.
Roberts 2000
Deep sedation with propofol and midazolam will achieve the same effects and also allow monitoring by sedation holds.

Temperature control

Aim for temp 35-37.
If cold do not actively rewarm but allow it to occur slowly.

Hyperthermia cerebral blood flow, cerebral metabolic oxygen requirement and oxygen utilization ICP brain ischaemia
Cochrane review (Alderson 2004) found no evidence for benefit of hypothermia. Increased pneumonia if cold.
Rapid rewarming harmful.
NABIS:H trial Clifton 2001 NEJM
Patients under 45
may benefit from hypothermia but further trails awaited.

Seizure prophylaxis

Give phenytoin for 7 days

BTF guidelines recommend that prophylactic anticonvulsants to prevent late epilepsy should not be given. However, seizures are a potentially devastating cause of secondary brain injury in the acute phase so are used in most centres.


Start enteral feed early

Cochrane review found feeding in TBI within 72h improves outcome. Yanagawa 2002

Glucose control

Maintain blood glucose at 5-10

The brain uses glucose for energy so hypoglycaemia will cause neuronal death. Tight glucose control has been shown to increase the incidence of hypoglycaemia and increases morbidity in general ICU patients. VISEP
Glycaemic control improves survival and neurological outcome in TBI.
Clayton BJA 2004.
Hyperglycaemia increases cerebral metabolism, blood volume and ICP.

Positioning and other

Maintain 30-45 degree head up tilt.
Make sure the ETT tie is not too tight
Avoid coughing (deep sedation)

This will improve brain venous drainage and minimise ICP.
Aim of positioning is to minimise SVC pressure which should be zero with modest head up tilt.
Head up tilt reduces VAP.

Faliure of medical management

Sustained ICP of >25 with the above medical management should prompt surgical intervention.
This will involve either CSF drainage via an EVD or a decompressive craniectomy +/- contusion removal.

There is little evidence to support this but there is no other option.

Decompressive craniectomy in TBI
NEJM 2011;364:1493-1502
Decompression as rescue (compared to medical management with refractory raised ICP) reduced ICP and reduced LOV and LOS but resulted in worse outcomes.
Decompressive group had twice as many with non-reactive pupils which when accounted for made the outcomes non significantly worse.
Could be due to axonal stretch or reperfusion injury or upward herniation.
May be of benefit if applied early but no data to support it as yet.

Complications of TBI

sodium for DI, SIADH and Cerebral Salt Wasting.