Adult Head Injury Flashcards
Factors Contributing to Secondary Injury (6H’s)
- Hypoxia
- Hypotension
- Hypercapnia – causes cerebral vasodilation
- Intercranial haemorrhage
- Hypovolaemia
- Hypertension
Primary and Secondary Head Injuries
Primary: Occurs at time of trauma – cerebral laceration, contusions, haemorrhage
Secondary: Occurs sometime after initial insult and is ongoing process of injury
How to limit effects of secondary brain injury
- Oxygenation
- Good airway management
- Recognising the risk and regular monitoring
- Consistent VSS and intervention on changes
- Keep pt normotensive
Head injury patho
Initial injury (or secondary injury)
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Inflammatory response
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Increased capillary permeability and vasodilation
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Increased cerebral oedema raises ICP
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↓CPP leads to sympathetic response
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Vasoconstriction leads to increased CPP
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Baroreceptors detect high BP and therefore parasympathetic system causes ↓HR
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ICP exceeds MAP resulting neuronal hypoxia and cell death
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Brain herniation and coning = increased brain stem pressure which causes loss of auto regulation
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Decorticate/decerebrate positioning
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Resp/Cardiac Arrest
Cushing’s Triad
- HTN – caused by vasoconstriction secondary to sympathetic response to bradycardia
- Bradycardia – caused by pressure on the Vagus nerve
- Irregular respirations – caused by Cheyne stokes
Fluid Administration with head injury
- Need to overcome raised ICP by maintaining CCP. Need to aim for SBP of >120mmHg
- CPP = MAP – ICP
- If ICP is rising we need to raise MAP in order to achieve CPP
o Need to be cautious of HTN which can increase risk of bleed
5 HEDS
- LOC >5 mins
- Haematoma/bruising/lac to head
- Emesis more than once
- Anticoagulants
- Neurological deficit
- Seizure activity
S+S of rising ICP
- Dyspnoea
- Disorientation
- Acute confusion
- Headache
- Irregular pupils
- Slurred speech
- Seizures
DS4 mgx
R+R
Pos - Supine
MICA C1
Collar