Applied physiology: head injury Flashcards
What is primary brain injury?
- Occurs at the moment of impact
- Pattern and extent of injury depend on the nature of the impact
- Not treatable - neurones are poor at regenerating
- Public health issue- target prevention
What is secondary brain injury?
- Focus of medical intervention is to minimise the secondary brain injury
- Damage that occurs as a result of secondary processes which occur at the cell and molecular level to exacerbate neurological damage
Describe what happens in secondary brain injury
- Neurones get damaged and become hypoxic and under-refused leading to lactic acid build up due to anaerobic respiration
- ATP depletes so ion pumps begin to fail and then:
- (glutamate) neurotransmitter release
- Free radical generation
- Calcium mediated damage
- Inflammatory response
- Mitochondrial dysfunction
- Early gene activation
What is the Monroe-kellie doctrine?
the sum of the volumes in the brain is consistent (up until the point of compensation ICP is normal)
Describe the physiological processes that occur in primary brain injury to then cause secondary brain injury
Pathway 1:
• Activation of bimolecular mediators of injury
• Neuronal damage
• Cytotoxic oedema
Pathway 2:
• Cerebral vessel damage - opening of the BBB
• Increased interstitial fluid and tissue pressure
• Vasogenic oedema
Both feed into and back from: (this goes in a loop) • Decreased cerebral perfusion pressure • Vasodilation • Increased Cerebral blood volume • Increased intracranial pressure
What happens to intracranial pressure after compensation has been reached?
There is an exponential rise in pressure (when looking at its increase with volume)
Describe early management of traumatic brain injury
- Assessment and identification of patient at risk of secondary brain injury - history taking and GCS
- Pre-emptive investigation (CT scan)
Who should be sent to hospital following a traumatic Brian injury?
- Extremes of age (<5 years (incase non-accidental) and >65 years (drug complications e.g. blood thinners)
- Amnesia for events before or after injury
- High energy injury
- Vomiting
- Seizure
- Bleeding/clotting disorder (check platelets)
When is Glasgow coma scale used in the treatment of head injury?
- Initial management
- Ongoing assessment
- Best GCS post resuscitation is of prognostic value only
What are the 3 components of GCS?
- Eyes
- Motor
- Verbal
Describe the scoring for eyes for GCS
- 4 - eyes open spontaneously
- 3- eyes open to speech
- 2- eyes open in response to pain
- 1- eyes do not open
- NT is patient is unable to open their eyes e.g. due to swelling
Describe the scoring for verbal response for GCS
- 5- Orientated
- 4- Confused
- 3- Inappropriate words
- 2- Incomprehensible sounds
- 1- No response despite verbal and physical stimuli
- NT - dysphasic, T- intubated
Describe the scoring for motor response for GCS
- 6- obeys commands
- 5- localises to central pain
- 4- normal flexion towards the source of pain
- 3- Abnormal flexion
- 2- Extension to pain
- 1- response to painful stimuli
What is the maximum GCS score?
15 : E4V5M6
What GCS score classes as a minimal head injury?
15
What GCS score classes as a mild head injury?
13-15
What GCS score classes as a moderate head injury?
9-12
What GCS score classes as a severe head injury?
8 or less: COMA
When should a CT scan be requested immediately?
- GCS>13 on initial assessment in A&E
- GCS>15 2 hours after injury
- Suspected open or depressed skull fracture
- Post traumatic seizure
- 1 or more episodes of vomiting
- Amnesia for events more than 30 minutes before impact
What are the red flags?
- Loss of consciousness, drowsiness, confusion, fits
- Painful headache that doesn’t settle, vomiting or visual disturbance
- Clear fluid from ear or nose, bleeding from the ears, new deafness
- Problems understanding or speaking, loss of balance, difficulty walking or weakness in arms or legs
Oxygenation and head injury
• If they are hypoxic, their head injury is not causing it:
- may be intoxicated, interfering with respiration
- airway may be closed
• Open their airway but remember the cervical spine: if suspected fracture, immobilise and until immobilised: jaw thrust
Breathing and head injury
- Administer oxygen
- Monitor spO2
- Monitor ABGs
- If GCS<8, intubate
- You want to avoid hypoxia as the cerebral arteries will dilate, increasing blood flow and therefore intracranial pressure
How can you minimise oxygen demand?
- Convusions occur in 15% of head injuries, treat with phenytoin
- Treat pyrexia: brain metabolic rate increases 6-9% for every degree rise in temperature
- Think about sedation (propofol/midazolam) - surpasses the metabolic rate but means you can’t assess GCS
Carbon dioxide and head injury
- Cerebral vessel diameter and CBF changes over a wide range of PaCO2
- Target directed therapy: PaCO2: 4.5-5.0kPa
BP and head injury
- When assessed 25% are hypotensive
* Low blood pressure is not caused by head injury
How can you calculate cerebral perfusion pressure?
Mean arterial pressure - intracranial pressure
How can you calculate mean arterial pressure?
Diastolic + 1/3 pulse pressure
Describe auto regulation in the brain
- Cerebral arterioles react to local changes in the environment (pressure and chemical)
- Normally auto regulation maintains MAP of 50mmHg and 150mmHg
- Traumatised or ischaemic brain, CBF may become blood pressure dependent
Pressure target goals after severe head injury
- Maintain Cerebral perfusion pressure above 60-70mmHg
- Maintain the systolic blood pressure higher than 90mmHg (preferably higher than 120mmHg)
- ICP is less than 20mmHg (invasive pressure monitor)
What is a normal intracranial pressure?
10mmHg
What should you do if a patient is hypotensive?
- Look for other causes: not due to head injury: chest trauma, pelvic fracture
- Stop bleeding
- Intravenous fluids (n. saline)
How can you encourage venous drainage?
- Nurse tilts head up 15-30 degrees
* Check straps and ties are not obstructing venous flow
What are the features suggesting an intracranial mass?
From their history: • High impact injury • Significant retrograde amnesia • History of coagulopathy • post traumatic seizure
Examination:
• GCS 12/15 or less, 13-14/15 and failing to improve after 2 hours
• Clinical signs of skull fracture
Peri orbital bleeding
Possible anterior cranial fossa fracture
Battle’s sign
- Possible petrous temporal bone fracture
- Bruising may take time to develop
- Bruising behind the ear
Extradural haematoma
- Relatively uncommon
- Strongly associated with skull fracture
- Middle meningeal artery
- 1/3 due to venous drainage
- Classically a lucid interval
- Good outcome if it is treated
- Biconvex
Subdural haematoma
- Common
- Complicates 20-30% of head injuries
- Rupture of veins travelling from the brain surface to the saggital sinus
- Prognosis is worse
- Crescenteric shape
Subarachnoid haemorrhage
- Associated with a ruptured berry aneurysm
* More commonly caused by head injury
Intercerebral haemorrhage
- Stretching and shearing skull injury
- Impact on the side of the skull
- Often contra coup injury (high impact, brain strike other side of the skull)
Clinical herniation
- Dilated or unreactive pupils
- Extensor posturing
- Decrease in GCS of 2 or more points
Physiological Principe - CO2
Temporary hyperventilation can decrease ICP and buy time, it brings the CO2 levels down
Drugs used in head injury treatment
- 20% mannitol to decrease blood viscosity, osmotic diuretic
- Hypertonc saline
- Tranexamic acid
Control of Glucose
• Dangers of unrecognised hypoglycaemia
When contacting neurosurgeons, what information should you give?
- Mechanism of injury
- Age of patient
- Respiratory and cardiovascular status of patient
- GCS score and pupil response
- Alcohol and drugs
- Associated injuries
- Result of CT scan
