- Head Injury on ITU
- Pathology
- Cerebral contusion
- DAI
- Traumatic SAH
- Epidural/SDH
- Pathophysiology
- Injury leads to accumulation of lactic acid
- Increased membrane permeability
- Oedema
- Increase release of excitatory neurotransmitters
- Ca²⁺ and Na⁺ influx leads to cell death
- Cell membrane degeneration leads to apoptosis via caspase activity
- Avoid secondary brain injury
- Normotension
- Single episode of SBP <90mmHg is assd with poor outcome. Keep MAP >70mmHg
- Normoxia
- SpO₂ <90% associated with poor outcome
- Normocapnoea
- Aggressive hyperventilation may result in further cerebral ischaemia
- Normothermia
- Normoglycaemia
- Additional monotoring
- ICP monitor
- Cranial doppler
- Jugular bulb oxygen tension
- Management of raised ICP
- Medical
- Ventilate with 100% O₂
- Ventilate to control CO₂. Hypocarbia useful for short term management only
- Ensure adequate MAP. Increasing MAP can lead to a decrease in ICP
- Position check and ensure adequate venous drainage
- Increase sedation
- Consider NMBDs
- Temperature control
- Osmotherapy
- Mannitol
- Hypertonic saline
- Seizure control
- Surgical
- Evacuate haematoma
- Craniectomy
- Lobectomy/removal of contusion
- CSF drainage
- CEACCP
Link:ceaccp.oxfordjournals.org/content/early/2013/02/24/bjaceaccp.mkt010.full.pdf
- CEACCP
Link:ceaccp.oxfordjournals.org/content/4/2/52.full.pdf