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    Guidelines for the Management

    of Severe Traumatic Brain Injury

    Dr Deepak Aggarwal, Dr Sanjay GuptaSenior consulatnt Senior consultant

    Deptt of NeurosurgeryRockland Hospitals

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    TBI - Epidemiology

    In 2005, road traffic injuries resulted in the death of anestimated 110 000 persons, 2.5 millionhospitalizations,

    89 million minor injuries and economic losses to thetune of 3% of the gross domestic product (GDP) inIndia.

    Estimated increasing further to 200 000 deaths andmore than 3.5 million hospitalizations annually by 2015.

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    INDICATIONS FOR REFERRAL TO

    HOSPITAL

    Adult patients with any of the following signs and symptomsshould be referred to an appropriate hospital for furtherassessment of potential brain injury:

    GCS

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    loss of consciousness

    severe and persistent headache

    repeated vomiting (two or more occasions) post-traumatic amnesia >5 minutes

    retrograde amnesia >30 minutes

    high risk mechanism of injury (road traffic accident,significant fall)

    coagulopathy, whether drug-induced or otherwise

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    Selection of adults for CT ScanUrgent scan if any of the following (within 1 hr):

    Glasgow Coma Scale (GCS)

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    CT scan within 8 hrs of injury if,

    More than 30 minutes of amnesia of events before impact

    Or any amnesia or loss of consciousness since injury if:

    Aged 65 years

    Coagulopathy or on warfarin

    Dangerous mechanism of injury

    Road traffic accident (RTA) as a pedestrian

    RTA - ejected from car

    Fall >1 m or >5 stair

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    In childrenUrgent scan if any of the following:Witnessed loss of consciousness >5 minutes

    Amnesia (antegrade or retrograde) >5 minutes

    Abnormal drowsiness

    3 Discrete episodes of vomiting

    Clinical suspicion of non accidental injury

    Post-traumatic seizureGCS

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    Suspected open or depressed skull fracture or tensefontanelle

    Signs of base of skull fracture

    Focal neurological deficit

    Aged 5 cm

    Dangerous mechanism of injury (high-speed RTA, fallfrom >3 m, high-speed projectile)

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    Neuro-surgical referral is indicatedAbnormal CT head persisting coma (GCS less than or equal to 8) after initialresuscitation.

    unexplained confusion which persists for more than 4hours; deterioration in GCS score after admission (greaterattention should be paid to motor responsedeterioration);

    progressive focal neurological signs; a seizure without full recovery; definite or suspected penetrating injury; a cerebrospinal f luid leak

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    Secondary Injury

    In the past two decades, medical research hasdemonstrated that all brain damage does not occur atthe moment of impact, but evolves over the ensuinghours and days. This is referred to as secondary injury.

    The injured brain is extremely vulnerable to

    hypotension, hypoxia, and increased intracranialpressure which are causes of secondary injury.

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    Significant Reductions in Mortality

    and Morbidity by:

    Rapid transport to a trauma care facility

    Prompt resuscitation CT scanning

    Prompt evacuation of significant intracranialhematomas

    ICP monitoring and treatment

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    1643 trauma patients treated at seven trauma centerswith differing annual volumes of trauma patients.

    Patients taken to a low volume trauma center hada 30% greater chance of dying

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    Resuscitation of Blood Pressure &

    Oxygenation

    Guideline

    Hypotension (SBP < 90 mm Hg) or hypoxia(apnea of cyanosis in the field or a PaO2< 60 mm Hg)must be scrupulously avoided, if possible, orcorrected immediately.

    Option The mean arterial pressure should be maintained

    above 90 mm Hg throughout the patients course.

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    Prospective prehospital and E.R. study of 717 severehead injury patients in the Traumatic Coma DataBank.

    Hypotension (SBP < 90 mm Hg) occurred in 35% ofpatients and was associated with a two fold increase in

    mortality

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    Initial Management

    Option

    The first priority for the head injured patient is

    complete and rapid physiologic resuscitation.No specific treatment should be directed atintracranial hypertension in the absence of signs oftranstentorial herniation or progressiveneurologic deterioration

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    Indications for ICP Monitoring

    Guideline

    ICP monitoring is appropriate in severe head injury

    patients with an abnormal CT, or a normal CT scan if 2or more of the following are noted on admission:

    SBP < 90 mm Hg

    Age > 40 years

    Uni-/Bilateral motor posturing

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    ICP Monitoring Technology

    Recommendation

    In the current state of technology, the ventricular

    catheter connected to an external strain gauge isthe most accurate, low cost, and reliable methodof monitoring ICP. It also allows therapeuticCSF drainage.

    ICP transduction via fiber-optic or strain gauge devicesplaced in ventricular catheters provide similar benefitsbut at a higher cost.

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    ICP Treatment Threshold

    Guideline

    ICP treatment should be initiated at an upperthreshold of 20 - 25 mm Hg.

    The ICP threshold that was most predictive of 6month outcome was analyzed in 428 severely headinjured patients.

    The proportion of hourly ICP reading greater than 20mm Hg was a significant independent determinantof outcome.

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    Cerebral Perfusion Pressure

    Option

    Cerebral Perfusion Pressure should bemaintained at a minimum of 70 mm Hg.

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    158 patients with GCS < 7 managed according to aCPP protocol:

    Maintain euvolemia (CVP 8-10 mm Hg)

    Ventriculostomy CSF drainage at 15 mm Hg

    Systemic vasopressors to maintain CPP at least 70 mm Hg

    Hyperventilation, barbiturates, hypothermia not used.

    Mortality 29% and 2% vegetative for entire group. Favorableoutcome in GCS 3 of 35% ranging up to 75% for GCS 7.

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    HyperventilationStandard

    In the absence of increased intracranial pressure (ICP),chronic prolonged hyperventilation therapy (PaCO2of 25 mmHg or less) should be avoided after severe traumatic braininjury

    Guideline The use of prophylactic hyperventilation (PaCO2< 35 mm Hg)

    therapy during the first 24 hours after severe TBI should beavoided because it can compromise cerebral perfusion duringa time when cerebral blood flow (CBF) is reduced.

    Option Hyperventilation therapy may be necessary for brief periods

    when there is acute neurologic deterioration, or for longerperiods if there is intracranial hypertension refractory tosedation, paralysis, cerebrospinal f luid (CSF) drainage, and

    osmotic diuretics.

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    A randomized prospective clinical trial in 113 patientsto study the effect of hyperventilation (PaCo225 mmHg) compared to normal ventilation (PaCo235 mm

    Hg) in patients with similar severe head injury.

    Significantly fewer patients made a good recovery at3 and 6 months post injury who had a GCS 6 or 7onadmission.

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    Mannitol

    Guideline

    Mannitol is effective for control of raised ICP aftersevere head injury.

    Option

    Effective doses range from 0.25 - 1.0 gm/kg

    body weight.

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    Option

    The indications for the use of mannitol prior to ICPmonitoring are signs of transtentorial herniation orprogressive neurological deterioration not attributableto systemic pathology.

    However, hypovolemia should be avoided by

    fluid replacement

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    Barbiturates

    Guideline

    High-dose barbiturate therapy may be considered inhemodynamically stable salvagable severe head injurypatients with intracranial hypertension refractory tomaximal medical and surgical ICP lowering therapy.

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    Steroids

    Standard

    The use of steroids is not recommended for improvingoutcome or reducing intracranial pressure in patients

    with severe head injury. CRASH trial- 10,008 adults with head injury and a

    Glasgow Coma Scale score of 14 or less, within 8 h ofinjury, to a 48-h infusion of corticosteroid (methyl-

    prednisolone) or placebo There was no evidence that the effect of corticosteroids

    differed by injury severity or time since injury

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    Anti seizure Prophylaxis

    Standard

    Prophylactic use of phenytoin, carbamazepine,phenobarbital or valproate is not recommended forpreventing latepost-traumatic seizures.

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    404 post traumatic head injury patients (GCS 3-10and abnormal head CT) randomized to treatmentwith phenytoin or placebo for one year with a two

    year follow up. In the first week after injury 4% of the patients

    receiving phenytoin had seizures compared to 14%taking placebo.

    After the first week there was no significantdifference between the rate of seizures in the twogroups.

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    Nutrition

    Guideline

    Replacement of 140% of Resting MetabolicExpenditure in non-paralyzed patients and100% Resting Metabolic Expenditure inparalyzed patients using enteral or parenteral formulascontaining at least 15% of calories as protein by theseventh day after injury.

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    Prospective trial in 38 patients randomly assigned toreceive total parenteral nutrition (TPN) or standard

    enteral nutrition (SEN). There were significantly more deaths in the group

    that did not receive full caloric replacement by the7th day after injury.

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    Conclusion Best outcome in high volume centre

    Timely referral, investigation and interventionimproves outcome

    Secondary injury is preventable, if cared

    Steroid has no role in head injury

    Nutrition supplement is an essential part in patients

    with severe head injury

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    THANK YOU