TRAUMATIC BRAIN INJURY:

AN EVIDENCE-BASED
REVIEW OF MANAGEMENT
DR. FARHAD, SPBS
 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 .20–25 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