This document provides an overview of acute head injury, including definitions, pathophysiology, classifications, investigations, management, and references. Some key points: - Head injury is defined as blunt and/or penetrating trauma to the head/brain causing temporary or permanent brain dysfunction. Primary injuries occur at impact while secondary injuries are subsequent damage from factors like hypoxia or raised intracranial pressure (ICP). - Raised ICP can lead to herniation syndromes like cerebellar tonsillar herniation, which can compress brainstem centers and cause Cushing's triad of hypertension, bradycardia, and irregular breathing. - Management goals include airway protection, maintaining cerebral perfusion pressure

1. Overview On Acute Head Injury

2. Introduction
• Injury was the 5th (7.86%) commonest cause of hospitalisation in MOH hospital
Malaysia in 2014.(MOH 2015)
• The younger age group between 15-34 years (56.6%) was at the highest risk of
major trauma.
• RTA accounts for the commonest cause of the trauma related hospitalization
• Head injury was the commonest diagnosis leading to intensive care unit (ICU)
admission in 2008 based on The National Audit on Adult Intensive Care Units
(NAICU)
• The incidence is increasing in lower income countries, with the World Health
Organization predicting that TBI and road traffic accidents will be the third greatest
cause of disease and injury worldwide by 2020 (BJA 2013)

3. Definition
• Head injury is also known as traumatic brain injury or acquire brain injury.
• It is defined as blunt and/or penetrating injury to the head (above the neck) and/or
brain due to external force* with temporary or permanent impairment in brain
function which may or may not result in underlying structural changes in the brain
• 3 criteria to be said as a head injury:
I. Presence of external force
II. Physiological disturbance of brain(Neurological deficits)/LOC
III. Anatomical dysfunction (Internal)**
• Aetiology- Any form of trauma or injury

4. • Primary- initial injury to the head; Include NAI
• Secondary-Subsequent damage due to the sequalae of trauma
▪ Hypoxia
▪ Hypotension
▪ Hypoglycaemia
▪ Hypovolemia
▪ Hyperthermia
▪ Raised ICP
▪ Anaemia
▪ Intracranial causes(haematoma, oedema, venous congestion, abscess or infection)

5. Pathophysiology
• Normal cerebral blood flow(CBF) is maintained by cerebral perfusion pressure(CPP)
• CPP is maintained over a range of 60-100mmhg; It is defined as
✓CPP=MAP-(ICP+VP); Under normal circumstances-VP is 0
✓MAP= DBP-1/3(PP);MAP of 70-100mmhg-requirement to maintain organ perfusion
• Immediate after a heard injury-normal CBF falls significantly from 50ml/100g(brain
tissue)/min- 25ml/100g/min. Irreversible neuronal damage occurs as CBF falls below
18ml/100g/min.
• ICP-Normal ICP:5-15mmhg; If above 20mmhg-clinical significance (Transcranial
doppler USG)
• Monro-Kellie hypothesis- Normal cerebral content established a balanced relationship
in maintain ICV as cranium is rigid and fluid cannot be compressed. Raised ICP will
results in the exhaustion of the compensatory mechanism- leading to herniation
syndrome.

6. Herniation Syndrome
• Uncontrolled raised ICP-cerebral herniation
• Normally herniation of the uncus of temporal lobe results in pupil abnormalities-
papilloedema, ipsilateral dilatation of pupil, visual disturbance
• Cerebellar tonsillar herniation- due to any expanding haematoma(Extradural**)
• The herniation through the foramen magnum compress the medullary vasomotor and
respiratory centre – classically producing Cushing’s triads: Hypertension,
Bradycardia and irregular respiration.
• If herniation continue the brain is said to be coning and brain stem death may occur
without rapid intervention.

8. Extradural Haematoma
• Lens-shaped haematoma: between skull & dura
• Pathology: result from laceration of middle meningeal artery due to temporal bone #
– can cause rapid neurological deterioration – if > 1cm in width or have
• Positive clinical symptoms-urgent surgical evacuation
• Classically presents with ‘lucid interval’ which precedes rapid deterioration
• 20% of patients with EDH are alert and well; brain is minimally damaged, thus
drainage gives good results

9. Subarachnoid Haematoma
• Crescent shaped haematoma: between dura & arachnoid
• Acute SDH: high-speed acceleration / deceleration trauma which shears small
bridging (emissary) veins
• More severe than EDH (usually due to nature of injury that causes SDH to occur –
associated with higher impact, thus brain has other injuries) – (i.e. shaken baby
syndrome, in which similar shearing forces classically cause intra- and pre-retinal
haemorrhages)
• Pathology: underlying brain damage in addition to expanding SOL
• Removal of blood does not solve brain damage- poorer prognosis
• Chronic SDH: present in elderly and alcoholics days to weeks after initial HI – can
cause focal neurological deficits, AMS, metabolic abnormalities and/or seizures
• If symptomatic = stop anticoagulants / antiplatelets, reverse effect by FPP, PT
complex, factor Vii, platelet transfusion, observe and monitor, once resolve = burr-
hole drainage + subdural drain placement

10. Subarachnoid Haematoma-classical crescent shape
Star shaped appearance (cisterns) see in traumatic
SAH

11. Diffuse axonal injury
• A major cause of unconsciousness and persistent vegetative state after head trauma
• If severe- punctate haemorrhage at the grey-white border
• Arises from injury that causes rotational and shearing forces (high impact injury) –
rapid acceleration and deceleration of brain in the intracranial cavity against relatively
fixed points of attachment at the falx and tentorium (e.g. RTA, falls, assaults, shaken
baby syndrome)
• Maximal effects at corpus callosum and brain stem

12. Signs of a raised ICP
• Ipsilateral pupillary dilatation, unreactive to light may indicates a life-threatening
raised ICP
• Early symptoms and sign of raised ICP include headache, nausea, vomiting,
seizures, papilloedema and focal neurology.
• Late sign: altered consciousness, hypertension, bradycardia and irregular
respiration.
• Pupillary dilatation, decorticate posturing (leg extension, arm flexion) and
decerebrate posturing (leg and arm hyper extension) occurs prior to coning and
brain death.

14. DDx
• Primary anoxic, inflammatory, infectious, toxic or metabolic encephalopathies,
which are not complications of head trauma
• Neoplasm
• Brain infarction (ischaemic stroke) and intracranial haemorrhage (haemorrhagic
stroke) without associated trauma
• Alcohol intoxication(WE,KP), psychotropic drugs or substance abuse
• Seizure
• Sport’s Injuries**

15. Classification according to severity
As per CPG Malaysia 2015 -Early
Management of Head Injury In
Adults.

17. • Post-traumatic amnesia (PTA): The injured person is disoriented and unable to remember events that
occur after the injury.
• Lucid Interval- Temporary regain of consciousness after TBI

18. Initial assessment and Mx
• Patient may present with isolated head injuries or in conjunction with other injuries. Any co-existing
injuries should be actively sought and excluded (As ATLS protocol)
• In any head injuries-cervical spine injury must be assumed till actively excluded. Whenever feasible,
pt should be put on neck collar till neck can be cleared clinically.
• Assess the consciousness with GCS- Pupillary size and response to light should be assess and
recorded (ICP**)
• Ensure airway patency and cervical spine immobilization- airway should be protected by ETT if airway
compromised or obtunded (GCS<8). Life threatening chest injuries(TP,MH,FC,CT) must be promptly
treated.
• Circulatory state should be maintained and assess-site of external haemorrhage should be directly
compress/ damage control surgery if indicated/transfusion; Balanced Crystalloid is used for initial
resuscitation.
• Any life threatening condition can be promptly treated

19. Indication for Brain imaging
• Provided patient is haemodynamically stable; Imaging of choice is NCECT of brain.
Within 1-2 hours
after risk factor being
explored.
Within 6-8hours

20. Anaesthetic Management (AKA Cerebral protection)
The major goals of anaesthetic management of TBI are to
• Maintain CPP (secure the cerebral perfusion)
• Treat increased ICP
• Provide optimal surgical conditions- preoperative optimization
• Avoid secondary insults such as hypoxemia, hyper and hypocarbia, hypo and
hyperglycaemia
• Provide adequate analgesia and amnesia.

21. Investigation
• CBC-Hb, differential count, platelet
• Coagulation profile (PT, aPTT, INR)
• GXM and GSH
• Blood sugar
• Renal function test
• Liver Function
• Thyroid screening
• Effective screening (HIV, Hep B&C,TB)
• Coagulation profile and D-dimer
• ECG and CXR
• Brain CT and Cervical spine imaging.
• Skull X-ray-Basal Skull Fracture
• And related preop investigation**

22. Monitoring
• General: Hydration status
• CVS: ECG, BP(MAP**), pulse oximetry, central venous pressure
• RS: SPO2, ABG, ETCO2
• CNS: Doppler transcranial USG
• Blood sugar profile
• I/O charting hourly-put on CBD

23. • Secure Airway; Modified RSI- Ketamine is not used because significant rise in ICP; If cervical spine not
cleared- Manual in line immobilization
• Propofol is indicated as a sedative agent in the TBI patient with a secure airway. This intravenous
anaesthetic has the advantage of a quick onset and offset of action that facilitates neurologic
assessment. Propofol might be beneficial in this group of patients, because it might decrease neuronal
oxidative stress; Muscle relaxant-Rocuronium is used provided with the availability of Sugammadex
• Hypoxia, hyper/hypocapnia should be avoided as these worsen the outcome; A Recommendation by
the BTF is to avoid a PaO2 less than 60 mmHg and to maintain an oxygen saturation of >90%;
Hyperbaric Oxygen should be given only when signs of Cushing triads and brain herniation- as
temporarily measure of reducing ICP.

24. • Targeted CPP-50-70mmHg; Maintenance of MAP> 80mmHg with vasopressor (NE, Metaraminol);
Fluid-0.9% NS 30-35ml/kg; Hypotonic fluid should be avoided; If massive blood lost-mx according to
massive transfusion protocol.
• Targeted blood glucose of 4-8mmol/l; Any seizures should be treated promptly with appropriate anti-
epileptic.
• Management of raised ICP- >20mmHg requires urgent tx; Non surgical mx- Osmotherapeutic agent:
mannitol(0.25-0.5g/kg) or hypertonic saline 100ml 5% saline; while patient awaiting to transfer-
moderate hyperventilation(PaCO2 abt 30mmhg) avoid hyperventilation-cerebral vasoconstriction
thereby worsen the outcome
• Thiopentone(Rapid onset barbiturates) can be also use to supress cerebral metabolism. Induction
dose of 3-5mg/kg followed by infusion of 3-5mg/kg/hr- with ECG monitoring.
• Therapeutic hypothermia remains controversial**(3) But it is mandatory to maintain normal body
temperature or subnormal (Arnd 37oC) as fever may worsen the cerebral perfusion.(increase CMR)
• Other important considerations in TBI patients include venous thromboembolism and stress ulcer
prophylaxis.
• The BTF recommends pharmacologic DVT prophylaxis if the injury is “stable” and the benefits of
prophylaxis outweighs the risks of haemorrhage progression.
• Consultation with neuro-surgeon/ neurologist for outcome and further mx
• Surgical intervention- evacuation of haematoma, decompressive craniectomy
• Cerebral protection is continued till patient can be safely extubated to avoid secondary insults to the
brain

25. Reference
• CPG Malaysia 2015- Early Mx of Head Injury In Adult
• BJA-Cerebral Protection
https://academic.oup.com/bja/article/99/1/10/269751?login=true
• CMR- Cleveland Clinic(US)-Anesthethic Mx of head injury
• Management of Head Injured Patient in Anaesthesia Point of View
• Perioperative Mx of TBI
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209993/
• Bailey and Love 27ed Chapter 24
Prepared by
LIM LI ZE MBBS BATCH 22