MANAGEMENT OF TRAUMATIC HEAD INJURY

MODES OF HEAD INJURY

Contusion injury: Results from a direct force over the brain. It is histopathologically
defined by areas of micro-haemorrhages often aligned at right angles to the cortical
surface or as a confluent haemorrhage. Typically affecting gyral crests and
progressing to areas of necrosis involving subjacent white matter.

Axonal injury: Results from acceleration-deceleration mechanism of injury. It is

histopathologically defined by an initial axonal deformation with interruption of
axoplasmic transport and subsequent accumulation of cytoskeletal components,
leading to axonal swelling. After 12h, there is distal axonal Wallerian degeneration.
Deep punctate haemorrhages occur in areas of cleavage planes, where the variation
of the angular momentum is more pronounced.

Fig 1: Mechanism of axonal injury

Initial Management
Resuscitation
This should be according to ATLS guidelines. Specific points:
AVOID prophylactic hyperventilation (aim ETCO2 35-40mmHg)
AVOID arterial oxygen desaturation (aim Sat O2>96%)
ENSURE stabilisation of the cervical spine
AVOID hypotension (BPs > 90mmHg) - Level II BTF

ICU admission
Standard monitoring and line insertion.
Basic Management Principles

The basic principles in the ICU management of patients with severe brain injury are
to identify any treatable surgical pathologies, and to prevent secondary brain injury
by monitoring and control of intracranial pressure and cerebral perfusion pressure.
Consideration must also be given to identification and management of any other non
cerebral injuries sustained

a. Decrease Risk of SECONDARY INJURY (the golden hour)

Maintenance of normothermia specifically avoid hyperthermia
Maintenance of normocapnia - aim ETCO2 35-40mmHg
Avoid arterial oxygen desaturation (goal: O2Sat > 96% or PaO2 >60mmHg)
Avoid hypotension (aim BPs > 90mmHg, lesser data regarding Mean Arterial
Pressure)
Avoid sustained hyperglycemia as well as ANY episode of hypoglycemia
(shown to increase lactate production and brain injury
Phenytoin load (15mg/kg) with maintenance (5mg/kg/day) to decrease risk of
early seizures (<7 days). Does not prevent delayed seizures.
The rationale for these measures is based in experimental models showing:
More than 40% of all head injuries develop swelling and raised ICP.
CBF is reduced in more than 50% of baseline during the first 24h after head
injury, with studies showing mismatch perfusion and histological evidence of
ischemia.
Cerebral autoregulation and cerebral vasoreactivity are impaired within the
72h after a brain injury, being cerebral blood flow directly dependant on
cerebral perfusion pressure and therefore to mean systemic blood pressure.
Prophylactic hyperventilation has been correlated with worse neurological
outcome.
There is a trend towards cerebral hypoperfusion in early phases after brain
injury, so an adjusted balance of oxygen delivery and consumption is
necessary.
b. Treat Underlying Process
Neurosurgical intervention for evacuation of hematoma, repair of depressed
skull fractures etc, if indicated.
ICP monitoring indications - BTF:
1).GCS <9 on scene post-resuscitation AND
Abnormal CT head
2) GCS <9 on scene post-resuscitation AND
Normal CT head with age>40yo and either:
Abnormal motor posturing
or hypotension (MAP<50mmhg).

 ICP monitoring has not been shown to improve outcome but allows titration of
therapy. Raised ICPs (>20) are associated with worse outcome.
Type of ICP monitoring: determined by local protocols:
Type of
Catheter
Position
Advantages

EVD

Camino

Richmond-Bold

Intraventricular
Intraparenchymal Subdural
Monitoring and therapeutic Inserted through
Minimally
purpose, as drains CSF.
a sheath that
invasive, it is
Allows administration of
allows
extraparenchymal
intraventricular drugs.
monitoring of
Minimal risk of
Recognised Gold Standard
PTi02, tissue
bleeding during
No drift
temperature and
insertion.
Recalibration in vivo
microdialysis.
Can be
calibrated under
sterile conditions
Disadvantages
Leads to ventriculitis if
Shows a phase
Low reliability
prolonged insertion (>10%
shift related to
risk infection beyond day
the days of
6 insertion)
insertion
Insertion can lead to bleed
Insertion can
Can block or show poor
lead to bleed
transduction
Graphic representation of types of ICP Monitors:

c. Ensure Cerebral Perfusion Pressure (CPP)

Aim for CPP > 60mmHg - 70 mmHg < -BTF (3,4)
Optimal fluid resuscitation (crystalloids, colloids. 4% Albumin not
recommended in this population for trend towards increased mortality [SAFE
study]).
Use of vasopressors Noradrenaline is the agent of choice in the unit,

The rationale for these measures is:

CPP target therapy has shown to lead to better neurological outcomes than
an ICP target therapy.
A CPP >60mmHg ensures brain perfusion without the systemic complications
related to pursuing higher levels of pressure Ref Claudia Robertson 1999
Whilst the classical vasodilator cascade of Rosner approach advocated
maintaining CPP>70 mmHg, the Lund approach advocated a CPP>50 mmHg
Ref Nordstrom 2003. The bottom-line is that the state of the cerebral autoregulation
will determine whereas there is higher risk of vasogenic edema or tissue
ischemia respectively.

Vasodilatory cascade of Rosner

d. Specific Treatment of High Intracranial Pressure

1. Step One
Ensure head up 30 degrees, if C--Spine stable
Head in central position to avoid compression of jugular venous return and
minimize cerebral vascular congestion.
CSF drainage through EVD monitor: height to be determined by neurosurgical
criteria.
Daily quantity of CSF drainage as an marker of EVD dependency.

Maximise analgesia + sedation

Ensure PaCO 2 within acceptable limits are usually 35 + / 2mm Hg
Use of sedation scales BIS monitoring to avoid over sedation
Follow up CT brain to exclude new neurosurgical indications and progress of
initial injuries.
Exclude other pathological processes such as: traumatic dissection of carotids
or vertebral arteries; venous thrombosis; brainstem injury; posterior fossa
compression.

2. Step Two
Osmotic therapy
No level I evidence supporting the use of Mannitol versus hypertonic saline.
Mannitol Level II BTF.
- Dose of 0.25-1 gr /K as bolus
- Avoid continuous infusions of Mannitol
- Avoid hypovolemia secondary to induced osmotic polyuria.
- Still controversial mechanism of action

Hypertonic saline
- 3% saline versus 7.5% saline, versus 10% boluses.
- Active provided blood brain barrier (BBB) is intact, by: Inducing
intracellular dehydration; Increasing cerebral vessel diameter and cerebral
blood flow (CBF); improving blood rheology by increase cell deformability;
decreasing neutrophil priming; decreasing glutamate reuptake.
- Avoid Na >160mmol and/or serum Osmolarity >320mOsm, to minimise
risk of acute renal failure.
- No robust data supporting different types of hypertonic solutions.
Induced hypothermia
- Achieved with: convective measures (cooling packs, cooling blankets) or
intravascular devices.
- Muscle relaxants may be needed to avoid shivering, alternatively induced
hypermagnesemia has shown to reduce shivering (5).
- Prophylactic hypothermia does not increase mortality and effectively
reduces ICP, if managed correctly.
- Greater effect when sustained for > 48h and instituted early.
- Associated with better Glasgow Outcome Scale (GOS) with targeted
temperatures 33-35 degrees C.
- Unclear total length of treatment, degree of hypothermia and rate of
rewarming
3. Step Three
Decompressive craniectomy
Current studies have failed to demonstrate an improvement in neurological
outcome or in mortality but consensus inclusion criteria and a definition of
the optimal timing are required (6).
2 international RCT: DECRA trial (7) and lately RESCUE trial (8) -currently
in progress.
4. Step Four

Decrease metabolic rate and oxygen consumption with barbiturate or

propofol induced burst-suppression (9)
Level II evidence for the use of barbiturates if refractory ICP BTF
Requires continuous EEG monitoring to ensure goal
Propofol infusion < 4mg/k/h in adults (to avoid propofol syndrome) until
burst suppression.
Thiopentone versus pentobarbital, only small randomised studies
suggesting benefit of Thiopentone at high doses (10).
Risks involved with barbiturate coma: increased incidence of HAP/VAP,
drug interactions; critical illness polyneuro-myopathy enteral feed
intolerance, rebound hyperkalaemia prolonged ICU stay.

Fig 2: Example of head injury management according to multi-monitoring:

Role of additional monitoring techniques

Neurological multi-monitoring: there is currently no data that shows a

change in outcome by applying multi-monitoring strategies; however its
usefulness relates to the specific therapy instituted (1,2). Multi-monitoring is
applied depending on use of resources and local policies:
Oximetry monitoring includes:
NIRS spectroscopy: Near-Infrared wavelength of light penetrate the
scalp and brain to few centimetres of death. These light waves are
differently absorbed by oxygenated and de-oxygenated hemoglobin
and cytocrome aa3. Based on the modified Beer-Lambert law, optical
attenuation is quantified using reflectance spectroscopy.

PTi02: Through the insertion of intraparenchimal multi-channel

pressure sensors, peri-contusional tissue oxygenation can be
monitored to titrate perfusion pressure. (Values of <15mmHg during
30 minutes, increases mortality Stiefel 2005).

SJ02: Retrograde jugular bulb oximetry catheters widely used in the

past are currently more experimental due to the global rather than
local information that provide. However, in difuse head injury has good
correlation with tissue oxygenation and NIRS. It has been shown that
values < 50% are associated with worse neurological outcomes
Robertson 1993.

Cerebral blood flow (CBF) monitoring: Transcranial Doppler for the assessment
of cerebral autoregulation; diastolic perfusion pressures; differentiation between

hyperemia and post-traumatic vasospasm; intracranial hypertension or trend

towards cerebral tamponade.

Normal CBF (diastolic flow preserved and normal PI index)

Cerebral tamponade: reversed diastolic flow

Metabolic: Microdialysis monitoring after the consensus conference in 2004,

microdialysis in association with other brain monitoring techniches may assist in
delivery of targeted therapy for prevention of secondary injury; therefore instituted
in patients with subarachnoid hemorhage and head injury allows monitor the
following markers:
* Energy-related metabolites: glucose, lactate, piruvate
(Lactate/piruvate ratio is batter marker of tissue ischemia
than lactate alone) Persson 1996
* Neurotransmiters: glutamate, aspartate, gammaAminobutiric.
* Exogenous substances: drugs levels.

Physiological monitoring: EEG or Compressed Spectra Array (CSA) for burst

suppression and BIS for depth of sedation.

Fast Fourier Transformation of multiple frequencies over time

Other trials in TBI:

-Progesterone as neuroprotective agent. Primary endpoint is mortality at 30 days
after trauma.

Key points:
CPP target therapy aiming for CPP>60 minimises systemic complications
related to fluid overload and cardiovascular complications when compared
with higher targets (CPP>70) and minimises episodes of hypoperfusion
pressure when compared with CPP>50
Hyperventilation should not be applied in the absence of acute signs of
herniation and/or without Microdyalisis monitoring
If required, early decompresive craniectomy needs to be considered in cases
of refractory ICP.
Thiopentone coma is an effective measure to control ICP, and its use is
supported by the BTF guidelines
Avoiding hyperthermia is a fundamental measure in the treatment of head
injury

Questions:
1. With regards to hyperventilation in the acute phase of TBI:
a)- It is safe and necessary when ICP is raised
b)- Should never be applied
c)-Hyperventilation may be necessary when signs of herniation
d)-Hyperventilation is recommended for refractory ICP when metabolic
monitoring such as Microdyalisis or cerebral blood flow monitoring is
applied.
e)-c and d are correct
2. With regards to ICP monitoring
a)- It is necessary in all head injuries to allow early treatment
b)- The Intraparenchimal monitors are the gold standard
c)- Intraventricular drains have lesser risk of infections than
intraparenchimal monitors

d)- Intraparenchimal monitors are routinely calibrated and show

minimal phase drift
e) none of above is correct

3. With regards to cerebral blood flow after head injury

a)- Cerebral autoregulation is normally impaired in acute phase of
head injury
b)-Cerebral microcirculation can show heterogeneous distribution
c)- CPP target therapy has shown to be more physiological than ICP
targeted therapy.
d)- The classical CPP > 70 target has shown to lead to vasogenic
edema and more systemic complications.
e)- all of above are true

4. With regards to hypothermia

a)- A 2001 Randomised control trial (Clifton et al) suggested that
hypothermia did not change outcome and was associated with
adverse effects, however the methodology of this trial was
later on criticized, leading to the need of further studies.
b)- Hypothermia is effective in reducing ICP and it is supported by the
BTF guidelines.
c)- The rate of hypothermia and rewarming as well as the length of
hypothermia are still controversial
d)- Active rewarming is contraindicated when hypothermia is applied
e)- all of above are true.

5. In the treatment of refractory ICP

a)-The use of Mannitol is supported by the BTF guidelines
b)- The use of hypertonic saline is effective but there is no strong data
showing advantage among different types of solutions.
c)- Early decompresive craniectomy is currently being assessed on the
RESCUE trial
d) the DECRA trial included patients having a delayed decompresive
craniectomy
e)-all of above are true
Answers:
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Reference List

(1) Andrews PJ, Citerio G. Intracranial pressure. Part one: historical overview and basic
concepts 7. Intensive Care Med 2004; 30(9):1730-1733.
(2) Hlatky R, Robertson CS. Multimodality monitoring in severe head injury
3. Curr Opin Anaesthesiol 2002; 15(5):489-493.
(3) Hlatky R, Furuya Y, Valadka AB, Robertson CS. Management of cerebral perfusion
pressure 11. Semin Respir Crit Care Med 2001;22(1):3-12.
(4) Robertson CS. Management of cerebral perfusion pressure after traumatic brain injury.
Anesthesiology 2001 December;95(6):1513-7.
(5) Wadhwa A, Sengupta P, Durrani J et al. Magnesium sulphate only slightly reduces the
shivering threshold in humans. Br J Anaesth 2005; 94(6):756-762.
(6) Munch E, Horn P, Schurer L, Piepgras A, Paul T, Schmiedek P. Management of severe
traumatic brain injury by decompressive craniectomy. Neurosurgery 2000; 47(2):315322.
(7) The DECRA trial
(8) The RESCUE Trial
(9) Angelini G, Ketzler JT, Coursin DB. Use of propofol and other nonbenzodiazepine
sedatives in the intensive care unit
1. Crit Care Clin 2001; 17(4):863-880.
(10) Perez-Barcena J, Llompart-Pou JA, Homar J et al. Pentobarbital versus thiopental in the
treatment of refractory intracranial hypertension in patients with traumatic brain injury:
a randomized controlled trial