Neuro - TBI

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

There are a number of mechanisms by which the injured brain may suffer
a secondary insult. These are divided into three categories:
1 Reduced cerebral oxygen delivery
i Anaemia, e.g. due to bleeding from associated injuries
ii Hypoxaemia, e.g. hypoventilation, V/Q mismatch due to aspiration, pulmonary contusions, haemo/pneumothorax
iii Hypotension, e.g. hypovolaemia, neurogenic shock, myocardial contusions
iv Increased ICP, e.g. DAI, intracranial bleeding, obstructive hydrocephalus
2 Increased cerebral oxygen requirement (CMRO2)
i Seizures
ii Pyrexia
3 Cellular mechanisms
i Excitotoxicity due to neurotransmitter release
ii Inflammation
iii Hyperglycaemia
iv Free radical damage
Hypotension (SBP <90 mmHg) and hypoxaemia (SpO2 <90%) are independent
risk factors for mortality following severe head injury and should be treated
aggressively

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 haemorrhageA: 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 4.5-5.0C: 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

What are the indicators of a poor prognosis in TBI?

Answer 8

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

Question 9

Describe the tiered approach to raised ICP?

Answer 9

Tier 1

• Increase analgesia and/or sedation
• Maintain PaCO2 at the lower end of normal (4.5-5.0 kPa)
• Blood pressure support to maintain CPP 60-70mmHg

Tier 2

• Achieve normothermia (pharmacologically or external device)
• If not done already, placement of EVD for CSF drainage
• A further increase in sedation e.g. midazolam
• Give a further bolus of osmotic therapy as above
• Consider neuromuscular blockade
• Consider repeating a CT scan

Tier 3

• Escalate osmotic therapy within limits of Na+ < 155 mmol/L and serum Osmolarity <320 mOsm/L
• Brain oximetry: increase PEEP and FiO2. Aim Hb >100g/L.
• Optimise CPP (if hyperaemia is evident, aim for a lower CPP)
• Consider EEG and the treatment of seizures
• Consider the possibility of both systemic and CNS infections

As/before aggressive treatment measures are discussed it is important to evaluate the patient’s prognosis, their functional baseline, previous wishes and the neurological outcome which is felt achievable. Is this a Devastating Brain Injury (DBI)?

Tier 4

• Activate cooling to 35 degrees
• Barbiturate coma

Suggested method: Ensure CO monitoring. Give a test dose 500mg thiopentone. If an ICP response is seen and sustained, start a thiopentone infusion with continuous EEG to burst suppression

• Decompressive craniectomy