1. Care of Acute Head
Injury
Dr Ben Manion
CAPT 2HSB ARES
Neurosurgical registrar
Gold Coast Hospital

2. My background

3. My background

4. Scope
Immediate triage and treatment
Logistics and definitive point of care
Difficulty in accurately predicting the
course of a brain injury

5. Relevance
 Up to 25% of battlefield injuries are head and spine
 115000 traumatic brain injuries US army 2002-2005
 Prevention, diagnosis and treatment of traumatic brain
injury is currently a high profile topic in the US military
 Up to 62% of Iraqi veterans have screened positive for
acquired brain injury
 We may miss up to 40% of brain injuries in the field
 Recent Australian ArmySAFE initiative
 Prompt and rational treatment makes a significant
difference to outcome

6. Trimodal death distribution

7. Primary brain injury
 Events at time of trauma
 Immediate and complete
 Irreversible, prevention is the only intervention
 Begins a cascade of events which can cause
further damage
 Occurs in up to 25% of combat injuries
 Blast effects currently are the predominant
cause

8.  Cascade of blast
effects
 Direct concussive
 Blunt or
penetrating injury
 Contre coup

9. Physiology of brain injury
 Monroe Kellie Doctrine
 Rigid skull with deformable contents
 CPP = MAP – ICP
 Autoregulation fails below 50 or above
160
 Normal ICP 0-15

10. CSF
Arterial Inflow Venous outflow
Capillary blood
Brain Parenchyma
Rigid
Skull
Monroe Kellie Doctrine

11. Physiology of brain injury
 Intracranial pressure
 Monroe Kellie
Doctrine
 Cerebral perfusion
pressure
 Critical point of
herniation
Point of
herniation
60mmHg

12. Secondary Brain Injury
 Hypoxia
 Hypotension
 Ischaemia
 Oedema
 Haemorrhage
 Metabolic derangement – hypercapnia, acidosis,
infection
 Neurotoxic cascades - excitatory amino acids,
endogenous peptides, apoptosis and calcium influx
 Increased ICP – cerebral oedema, hydrocephalus, brain
herniation

13. Assessment
 Patient factors – age, time of injury, GCS, pupils
 Mechanism – Concurrent fatalities, nature of forces involved,
helmet sensors, care with C-spine
 Primary Survey (ABC)
 A: Hypoxia
 C: Hypotension
 Associated injuries
 Must examine prior to sedatives/strong analgesics/paralytics
 Repeat Survey – Changes over time are most important feature of
progression of injury
 Keep accurate records, standard scoring

14. Classification of acute head injury
 Mechanism
 Blunt
 Penetrating
 Mixed
 Morphology
 Skull fracture
 Intracranial lesion
 Severity
 mild (14-15)
 moderate (9-13)
 severe (3-8)

15. Mild head injury
 GCS 14-15
 Awake, amnesic, may be confused
 Vulnerable to C-spine injury
 Remove from field
 CT head if available
 Multiple scanning tools to assess for concussion
being developed (MACE, ANAM)
 May have sequelae

16. Moderate head injury
 GCS 9-13
 Confused, somnolent or aggressive, focal
neurologic deficits
 Protect airway
 Cardiopulmonary stability as priority
 Remove from field with medical support and
airway capabilities
 CT head in all cases
 No role for IV antibiotics in closed head injury

17. Severe head injury
 GCS 3-8
 Follow EMST ABCD primary survey protocol
 Early intubation, 100% oxygen
 C-spine protection with hard collar
 Ventilate to pCO2 35
 Rapid stabilisation of cardiopulmonary axis
 Systolic >100mm Hg
 Minimal volume isotonic resusc fluids, aim for euvolaemia
 Hypotension rarely due to primary head injury
 Early evac with full medical support

18. urther management
Airway secured, supplemental oxygen/CPAP PRN. Ventilator as
needed to maintain pCO2. End tidal CO2, pulse oximetry.
Monitor haemodynamics.
Fluids and pressors. Aim for euvolaemia.
CP assessment
30% head up to facilitate venous drainage
Maintain other parameters
 Glucose, body temp, sodium
 Antiemetics, bowel care, maintain nutrition with feeding tube or PEG.
Minimal sedation to facilitate neurological examination and
assessment of progress.

19. ther Management
Mannitol or hypertonic saline to reduce ICP. Can
aggravate hypovolaemia. Use in signs of herniation. +/-
rusemide (unproven) depending on clinical picture.
Steroids not routinely used
Anticonvulsants if high risk (early seizures, depressed
skull fracture, intracranial haematoma, epilepsy).
Seizures create very high ICP
Monitor sodium
Magnesium currently under investigation, may combat
calcium influx and cellular damage.

20. urgical management
ntracranial pressure monitors
External ventricular drains
Kochers Point
3cm from midline
11cm from nasion

21. xternal ventricular drain
entriculostomy)
nvasive procedure with
moderate risks
Allows CSF sampling, ICP
monitoring and rapid and
ongoing treatment of
hydrocephalus
Commonly inserted at
Kochers point to place
EVD in frontal horn
Less than 5-7cm depth
nsert perpendicular to all
planes

22. urgical management
ntracranial pressure monitors
Decompressive ventricular drains
Scalp wounds
Depressed skull fractures
ntracranial mass lesions
 Most GCS <8 do not have intracranial haematomas
 Burr holes are not often a good solution in an acute
traumatic haematoma, but they may be lifesaving
 Decompressive craniotomy if facilities permit

23. xploratory burr
ole placement
n order of placement
Extend from burrhole
with bone nibblers if
haematoma found
Highly invasive
May cause bleeding
and brain trauma

24. ecompressive craniectomy
Bifrontal
decompressive
craniectomy
performed
day 8 post injury

25. ummary
Rapid assessment
Treat and repeat ABCD
Avoid hypoxia, hypotension
Early retrieval as warranted
Medical and nursing management
Surgical options can aid management

26. eferences
Prevention of secondary brain injury: targeting technology. Littlejohns L,
Bader MK. Department of Clinical Development, Integra NeuroSciences,
Plainsboro, NJ, USA.
ATLS course manual 1997
Prevention of secondary brain injury following Head Trauma; Cowley and da
Silva Trauma.2008; 10: 35-42
Emedicine - Traumatic Brain Injury (TBI) - Definition, Epidemiology,
Pathophysiology; Segun T Dawodu
Calcium in cell injury and death; Zheng Dong,1 Pothana Saikumar,2 Joel M.
Weinberg,3 and Manjeri A. Venkatachalam Annual Review of Pathology:
Mechanisms of Disease
Vol. 1: 405-434
Secondary Brain Injury: Prevention and Intensive Care Management; TVSP
Murthy MD, Parmeet Bhatia MBBS, K Sandhu MD; T Prabhakar MD, R L
Gogna MD; Department of Anesthesia and Intensive care; Army Hospital
R&R), Delhi Cantt; Indian Journal of Neurotrauma (IJNT) 2005, Vol. 2, No.