TRAUMATIC BRAIN INJURY:

AN EVIDENCE-BASED
REVIEW OF MANAGEMENT
 EPIDEMIOLOGY

Traumatic Brain Injury (TBI) is the leading cause of

death and disability in young adults in the developed
world.
In the UK, 1,4 million patient/year
10.9% are classified as moderate or severe
Many patients are left significant disability
Road traffic accident will be the third greates cause
of disease and injury worldwide in 2020 (WHO)
The most useful classification of severity based on the
level of conscioussenes as assessed by GCS
Patient should be rescucitated and reversible causes
corrected before GCS assessment.
 TBI can be divided into primary and secondary injury
The primary occurs as a consequence of the initial
physical insult
Neurological injury progresses over hours and days,
resulting in a secondary injury
Much of this secondary injury may be amenable to
intervention
Secondary injury also occurs as a result of further
physiological insults.
Hypoxia, hypotension, hyper/hypocapnea,
hyper/hypoglycemia have all been shown to increase
the risk of secondary brain injury
 ACUTE MANAGEMENT

Crucial period
Mortality and morbidity can be influenced by
intervention to prevent secondary brain injury
Targeted rescucitation and early specialistic
management have resulte in a decline in mortality
over the last few decade
 PRE HOSPITAL CARE

Simultaneous assessment, stabilization , and

therapeutic interventions
Priority are to prevent hypoxia and hypotension
Patient with moderate of severe TBI should be
transferre to a designated trauma centre
 MANAGEMENT IN THE EMERGENCY
DEPARTMENT
In hospital rescucitation begins with ATLS priorities
using an ABCDE approach
Assessment on neurological status based on GCS,
papillary response and localizing signs.
Tracheal intubation remains the goal standard for
airway management in patien with GCS of <8
Adequate sedation and muscle ralaxation will
reduce cerebral metabolic oxygent requirement,
optimize ventilation and prevent coughing and
straining
 As the most common cause of hypotension after
trauma is haemorrhage, the initial treatment is fluid
rescucitation
For most patients an isotonic fluid such as normal
saline is suitable.
There is some evidence that hypertonic saline may be
useful as a rescucitation fluid
Hypotomic fluid must be avoided
Colloid confer no benefit
SAFE (Saline or Albumine for Fluid Rescucitation in
Patients with Traumatic Brain Injury) study found an
increased risk of death in patient who received
albumin rather than saline
 After TBI there is a profound cathecolamine response
making hyperglycaemia common
Glucose containing fluids should be avoided and blood
sugar monitored
Many patient are taking anticoagulants or antiplatelet
drugs often for cardiac arrhytmias, cardiac stent, or
prosthetic heart valves
Patient on warfarin with strong suspicious for an
intracranial bleed afgter TBI shoud have reversed
immediately with prothrombin complex before wating
for an INR result or CT Scan
Dose range PCC between 15 and 50 U/kg dependent
on INR
Platelet infusion or desmopressin may be useful in those
patients on aspirin and clopidogrel who require urgent
neurosurgical intervention
 IMAGING

The investigating of choice is CT Scanning

Early imaging reduce time to detection of life
threatening complication and is associated with
better outcomes
those recommended by the National Institute of
Clinical Excellence, have been developed to
determine who requires CT scan.
Skull x rays are useful only as part of skeletal survey in
children with non accidental injury.
As brain injury evolves over time, repeat imaging is
commonly indicated and always necessary if there is
clinical deterioration or an increase in ICP
 TRANSFER

Initial rescutitation and stabilization of the patient

should be completed before trasfer.
The risks of delayed transfer must be balanced against
that of an unstable patient or ill-prepared transfer
team
Management priorities remain maintenance of who
are persistenoxygenation and ABP and minimizing
increase in ICP.
Patient who are persistently hypotention despite
resucitation should not be transferred until the cause
established and the patient stabilized
Patient with GCS of <8 should be intubated and
ventilated aiming for PaO2 >kPa and a PaCO2 value
of 4.5-5.0 kPa with adequate sedation, analgesia and
muscle relaxation
 ANESTESI UNTUK KRANIOTOMI
TRAUMA
About one third of patient with severe TBI need
neurosurgical intervention
Rapid treatment is crucial
Acute SDH in patien with severe TBI have 90% mortality
if surgical evacuation occurs > 4 h after injury
compared with 30% for those evacuated earlier
Perioperative management should be a seamless
continuation of the rescucitation process already
begun and an opportunity to correct pre existing
secondary insult
Surgery and anathesia predispose the patient to
additional risks such as hyypotension because of blood
loss or effect of anaesthetic agents
 The goals of anaesthesia are
optimization of cerebral perfusion pressure (CPP) and the
prevention of intracranial hypertension;
adequate anaesthesia and analgesia;
prevention of secondary insults by adequate oxygenation,
normocapnia, and avoidance of hyper- or hypoglycaemia
and ll hyperthermia.
Ventilation should be controlled to maintain
oxygenation and normocapnia as confirmed by ABG
analysis
Intraoperative hypotension is associated with a three-
fold increase in mortality
Several studies have shown an association between
hyperglycaemia and poor neurological outcome in
patients with TBI.
 MANAGEMENT OF ICP

Consensus guidelines recommend treatment of an

ICP .2025 mm Hg
Measurement of ICP allows early detection of
evolving mass lesions and enables the calculation of
CPP from the relationship CPP = MAP - ICP
The primary goal of an adequate CPP is to maintain
CBF and tissue oxygenation and its manipulation has
become central to the management of TBI
Current consensus is a target of >60 mm Hg.
ICP can be controlled by variety of methods:
Hyperventilation, Hyperosmolar therapy,
hypothermia, barbiturate, neurosurgical intervention
 Hyperventilation
Reduction of PaCO2 causes cerebral vasoconstriction, reducing
CBV and ICP
Moderate hyperventilation to PaCO2 value of 4,0-4,5 kPa, guided
by jugular venous oxygen saturation
Hyperosmolar therapy
Mannitol dose 0,25-1 g/kg, intermittent boluses appear to be more
effective than continuous infusion
Care must be taken to prevent serum osmolarity increase above
320 mOsm, associated with neurological and renal complication
Other potentential comlication: hypotension, intravascular volume
depletion, hyperkalemia, and rebound intracranial hypertension
The use of hypertonic saline is increasing, has fewer side effects
and may control ICP refractory to mannitol
Dose of hypertonic sanline, 2ml/kg of 5% solution is typical
 Hypothermia
Hypothermia has been shown to be neuroprotective in animal
study and has many theoretical benefits
Moderate hypothermia effectively reduces ICP
The effect of hypothermia, 32-35 C, titrated to re4duce ICP <20
mmHg
Barbiturates
IV barbiturates lower ICP
Associated with significant cardiovascular instability and so are
reserved for refractory intracranial hypertension
Neurosurgical intervention
Drainage of cerebrospinal fluid via an external ventricular
drainage is an effective method of reducing ICP
Decompressive craniectomy is currently reserved for when
other method of ICP control have failed
 CONTINUING MANAGEMENT

The purpose of continuing care is to provide optimum

opportunity for brain recovery
aintenance of oxygenation, normocapnia, and
haemodynamic stability is essential
Advanced monitoring may include cerebral
oxygenation, measurement of CBF, microdialysis, and
electrophysiological monitoring
Early nutritional support is associated with better
outcomes and enteral administration is preferable
Hypoglycaemia must be avoided.
Although there is little evidence for prophylactic
anticonvulsants, some advocate their use in high-risk
groups such as those with depressed skull fractures.
 SUMMARY

TBI is common and a major public health problem

no single treatment has been shown to improve
outcome
Management continues to be focused on
prevention of secondary injuries and maintenance
of CPP
National guidelines and management algorithms
seem to be associated with better survival but
ignore individual patient variability and injury-
specific factors