Traumatic brain injury

Question 1

How can traumatic brain injury be classified?

Answer 1

ATLS classification:
Based on GCS after initial resuscitation:

Mild: 13-15
Moderate: 9-12
Severe: <9

Question 2

What is the pathophysiology of primary traumatic brain injury?

Answer 2

Multifactorial
Primary injury leads to:
1. Cerebral vascular injury -> bleeding -> vasospasm, space occupying haematoma and vasogenic oedema
2. Diffuse axonal injury and contusions -> neurotransmitter release-> neuronal apoptosis and cytotoxic oedema

Vasospasm leads to decreased CPP
All other effects lead to raised ICP

Question 3

What is the pathophysiology of secondary brain injury?

Answer 3

Variety of mechanisms:

1. Decreased cerebral oxygen delivery
   - haemorrhage and hypotension from initial trauma
   - hypotension from anaesthetic agents
   - hypoxia/hypoventilation from compromised GCS or trauma associated lung injury/aspiration.
   - decreased cerebral blood flow from raised ICP
2. Increased cerebral metabolic/oxygen demand
   - seizures
   - pyrexia
3. Cellular damage
   - neurotransmitter release
   - inflammation
   - hyperglycaemia
   - free radical damage

Question 4

How is diffuse axonal injury graded?

Answer 4

The DAI associated with traumatic neuronal shearing from deceleration or rotational forces can be devastating, but initially radiological underwhelming compared to extensive haemorrhage.
The Marshall grading system uses CT imaging to grade I-IV:
I - no visible intracranial injury
II - basal cisterns patent, midline shift <5mm
III - cisterns compressed
IV - midline shift >5mm

Question 5

What monitoring should you use in severe brain injury?

Answer 5

All patients:

• invasive arterial BP monitoring
• ECG
• ETCO2
• ICP monitoring (severe TBI and abnormal CT) OR (severe TBI and normal CT if: age >40, poor motor score, SBP <90)

Additional useful tests:

• Jugular bulb O2 sats - catheter at level of C1 verterbral body. Value <50% necessitates intervention (hyperventilation or osmotherapy).
• EEG
• transcranial doppler
• cerebral microdialysis

Question 6

What is the immediate management of TBI?

Answer 6

Manage according to ATLS C-ABCDE approach, with primary survey to focus on stabilisation and presenting GCS followed by early prevention of secondary brain injury:
C:- manage any catastrophic haemorrhage
A: Based on initial GCS (<9) or decreasing motor score (worsening by 2 or more) ->intubate and ventilate. MILS and bougie.
B: Ventilate to achieve pO2 >12 or sats >94% and pCO2 initially 4.5-5.0
C: Achieve a balance with BP between worsening any traumatic bleeding with adequate CPP. Target CPP 60-70 for neuroprotection. In absence of ICP monitoring, assume ICP of 20 and aim MAP of 80-90.
Avoid impairments to cerebral venous drainage and head up 30 degrees.
Avoid colloid and albumin Resus - blood products if necessary and vasopressors.
D: Document GCS and pupils regularly, manage any seizures with levetiracetam or phenytoin, aim for normoglycemia. Avoid coughing.
E: Avoid pyrexia, continue to manage associated trauma. Expedite CT trauma imaging and discuss with Neurosurgical team.

Question 7

How should we care for brain injured patients?

Answer 7

1. Prevention of secondary brain injury with neuroprotective measures:
   - normothermia
   - normoglycemia
   - normocapnia (4.5-5.0)
   - normoxia (pO2 >10)
   - normotension (aim MAP 80 assuming ICP 20 to achieve CPP 60)
   - 30 degrees head up to prevent venous drainage.
2. Prevention of non-neurological complications:
   - VAP care bundles
   - VTE prophylaxis
   - physiotherapy
   - early enteral feeding
   - stress ulcer prophylaxis
   - bowel care

Question 8

How is raised ICP managed?

Answer 8

A sustained ICP >21 need escalation of treatment.
Baseline should always be well implemented standard neuroprotection measures.
Escalation options include:
- hyperventilation aiming for pCO2 4.0-4.5
- deepening sedation and ensuring adequate NMB - consider barbiturate coma.
- osmotherapy - hypertonic saline 1-2ml/kg 5%, mannitol 0.5g/kg 20% ~ 200ml
- trial of increased MAP

If above not working, re-scan and assess for neurosurgical intervention e.g. craniotomy, EVD

DECRA and RESCUEicp showed decompressive craniotomy can improve survival but does so at the cost of increased survival with significant morbidity and neurological dysfunction.

Question 9

What are the indicators of a poor prognosis in TBI?

Answer 9

• advanced age
• cardiac arrest
• poor motor score on presentation
• low GCS on presentation
• bilateral unreactive pupils
• untreatable raised ICP with DAI
• extra cranial complications