Traumatic Brain Injury (TBI) Management Flashcards
(31 cards)
Primary brain injury
- Occurs at the moment of impact
- Pattern & extent of damage depends in nature of impact
- Nottreatable
- Targetprevention (public health issue)
Secondary brain injury
Focus of medical intervention is to minimise secondary brain injury • Optimise oxygenation • Optimise cerebral perfusion • Blood glucose • Hypo / hypercapnia • Body temperature?
Secondary processes which occur at the cell & molecular level to exacerbate neurological damage.
• Neurotransmitter release (glutamate) • Free radical generation • Calcium mediated damage • Inflammatory response • Mitochondrial dysfunction • Early gene activation 8
Monro-kellie Doctrine
That there is a solid box which is the cranium and there is intracranial compensation for expanding mass, as one thing grows the others must leak to somewhere causing an increase in cranial pressure
Early Management of Head Injury
- Assessment and identification of the patient at risk of secondary brain injury
- Pre-emptive investigation (CT scan)
Glasgow Coma Scale
EYES 1-4
VERBAL 1-5
MOTOR RESPONSE 1-6
severe head injury GCS
8 OR LESS
moderate head injury
9-12
mild head injury
13-15
Request CT scan immediately in adult patients if:
- GCS <13 on initial assessment in A & E
- GCS <15 2 hours after injury
- Suspected open or depressed skull #
- Any sign of basal skull #
- Post traumatic seizure
- 1 or more episode of vomiting (3 in kids)
- Amnesia for events more than 30 mins before impact
• Red flags:
– Loss of consciousness, drowsiness, confusion, fits
– Painful headache which doesn’t settle, vomiting or visual disturbance
– Clear fluid from ear or nose, bleeding from ears, new deafness (CSF rhinorrhoea test for glucose or beta 2 transferrin)
– Problems understanding or speaking, loss of balance, difficulty walking or weakness in arms or legs
Breathing
- Administer oxygen
- Monitor SpO2
- Monitor ABGs
- GCS < 8 intubate
• Minimise demand for oxygen
the need for O2 results in the dilation of blood vessels, allowing more blood to the brain, thus increasing intracranial pressure which = bad
– Convulsions occur in 15% of severe head injuries • Treat with phenytoin in early head injury
– Brain metabolic rate increases 6-9% for every degree rise in temperature
• Treat pyrexia
what kind of sedation would be used
(propofol / midazolam)
Carbon dioxide management
• Cerebralvessel diameter (and CBF) changes over a wide range of PaCO2
• Target directed therapy:
PaCO2 4.5 -5.0kPa
circulation
CPP = MAP - ICP
cerebral perfusion pressure = mean arterial pressure (diastolic pressure + 1/3 pulse pressure) - intracranial pressure
Cerebral Autoregulation
- Cerebral arterioles react to local changes in the environment (pressure & chemical)
- Normally autoregulation maintains a constant blood flow between MAP 50 mmHg and 150 mmHg.
- Traumatised or ischaemic brain, CBF may become blood pressure dependent.
After severe head injury what are the ideal maintenance targets
• Maintain CPP above 60 - 70mmHg
• Maintain systolic blood pressure higher than
90mmHg (preferably higher than 120mmHg)
• ICP less than 20mmHg (invasive pressure monitor)
Hypotension
• Not due to head injury • Look for other causes – Chest trauma – Pelvic fracture Stop bleeding Intravenous fluids (n. saline)
Encourage venous drainage
- Nurse head up tilt (150 - 300 )
* Check straps and ties are not obstructing venous flow
Identify features suggesting at
risk of intracranial mass in a patients history
high impact injury
significant retrograde amnesia
History of coagulopathy post traumatic seizure
panda eyes
peri-orbital bruising
Battles sign
petrous temporal bone fracture
Extradural Haematoma
very uncommon but has good outcome if treated • Strongly associated with skull fracture • Middle meningeal artery • 1/3 due to venous bleeding • Classically a lucid interval
