Traumatic Brain Injury

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Traumatic Brain Injury

• Shantaveer Gangu
• Mentor- Dr.Baldauf MD

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Demographics

• Account for 75 all pediatric trauma
  hospitalizations
• 80 of trauma related deaths in children
• Domestic falls, MVAs, recreational injuries and
  child abuse account for majority of them.
• Gang and drug related assaults are on a rise.
• Firearm injuries to brain account for 12
  pediatric deaths.

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Pathophysiology of Brain Injury
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Primary Brain Injury
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Cerebral Contusion

• Most common Focal brain Injury
• Sites ? Impact site/ under skull
• Anteroinferior frontal
• Anterior Temporal
• Occipital Regions
• Petechial hemorrahges ? coalesce ? Intracerebral
  Hematomas later on.

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DAI

• Hallmark of severe traumatic Brain Injury
• Differential Movement of Adjacent regions of
  Brain during acceleration and Deceleration.
• DAI is major cause of prolonged COMA after TBI,
  probably due to disruption of Ascending Reticular
  connections to Cortex.
• Angular forces gt Oblique/ Sagital Forces

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• The shorn Axons retract and are evident
  histologically as RETRACTION BALLS.
• Located predominantly in
• CORPUS CALLOSUM
• PERIVENTRICULAR WHITE MATTER
• BASAL GANGLIA
• BRAIN STEM

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Secondary Brain Injury

CMRoxy CMRglucose
CBF
OEF/GEF
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Initial Stabilization

• Initial assessment and resuscitative efforts
  proceed concurrently.
• Few things to watch for,
• Airway
• Cervical spine injury
• Hypotension
• Hypothermia
• Neurogenic Hypertension

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• Cervical Spine X-ray Lateral view. 1, Vertebral
  body (TH1). 2, Spinous process of
  C7. 3, Lamina. 4, Inferior articular
  process. 5, Superior articular process. 6,Spinous
  process of C2. 7, Odontoid process. 8, Anterior
  arch of C1 (Atlas). 9,Trachea.

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Neurological Assessment

• Rapid Trauma Neurological Examination
• Level Of Consciousness
• Pupils
• Eom
• Fundi
• Extremity Movement
• Response To Pain
• Deep Tendon Reflexes
• Plantar Responses
• Brainstem Reflexes

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Level Of Consciousness

• Glasgow Coma Scale

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Children's Coma Scale
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Pupillary Exam

• Pupillary size is balance b/n Sympath and
  parasympathetic influences.
• Size, shape and reactivity to light are tested
  parameters.

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Eye Movements

• SO4,LR6, All3

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Brainstem Reflexes
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Deep tendon and superficial reflexes

• DTRs exaggerated after TBI due to cortical
  disinhibition
• Decreased / absent after Spinal cord injury
• Asymmetric DTRs ?unilateral brain/spine injury
• Superficial? lost/decreased in corticospinal
  dysfunction and helpful in localizing lesions
• Plantar response ?

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Neurodiagnostic Evaluation
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Clinical Features In Head Trauma

• Scalp Injuries
• Skull Fractures
• Depressed Skull Fractures
• Basilar Skull Fractures
• Vascular Injuries
• Penetrating Head Injury
• Intracranial Hemorrhage
• Epidural Hematoma
• Subdural Hematoma
• Subarachnoid Hemorrhage
• Intracerebral Hemorrhage

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Scalp Injuries

• Most are laceration
• Simple Linear/ Stellate ? ED Rx
• Extensive, Degloving/Avulsion ? Repair GA
• Overlying Depressed Skull,? Infections ? Repair
  Elevation Of
• Hematomas

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Skull Fractures

• Thin skull? s common place.
• Risk of associated intracranial injuries?
• CT to R/o
• Open
• Closed
• Linear (3/4)
• Comminuted ( multiple branches)
• Diastatic ( edges split apart)?lt3yr?leptomeningeal
  cyst, cephalomalacia,
• Depressed
• Basilar

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Depressed Skull

• From focal blow
• Closed ? 10 FND/15 seizures ? Rx, for cosmetic
  reasons
• lt skull thickness- no elevation
• Open/ frontal sinus intracranial wall ? elevate
  and Sx frontal sinus irrigation
• Free floating remove/replace wrt size and after
  soaking in abx

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Basilar Skull
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Epidural Hematomas (EDH)

• Peak incidence in 2nd decade
• Source ? meningeal vessel, Dural venous sinus,
  diploic vein from skull
• H/o minor head injury Viz fall
• C/f ? wrt size, location, rate of accumulation
• Lucid interval (33), non specific
• Confusion, lethargy, agitation, focal
  neurological deficits.

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Diagnosis

• CT is diagnostic
• Initial Ct? Hyperdense Lentiform collection
  beneath skull
• Actively bleeding- Mixed densities
• Severe anemia- isodense/hypodense
• Untreated EDH imaging over days? Hyperdense?
  Isodense? Hypodense w.r.t. brain

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Treatment
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Subdural Hematoma

• Common in infants.
• Cause ? high velocity impact/ assault/ child
  abuse/ fall from significant height.
• Associated with cerebral contusions DAI
• Source ? cortical bridging veins/ Dural venous
  sinuses.

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• 50 are unconscious immediately.
• Focal deficits common
• Hemiparesis 50
• Pupillary abnormality- 28-78
• Seizures 6-22
• Rx- larger- urgent removal
• Small -

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• SDHs are High density collections on CT
  conforming to convex surface of brain
• Cant cross falx cerebri/ tentorium cerebelli
  compartmentalized
• Can cross beneath suture lines
• Distorstion of cortical surface/ effacement of
  ipsilateral ventricle/ shift of midline often
  noted.

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SAH

• Trauma is leading cause.
• Acute from disruption of perforating vessels
  around circle of Willis in basal cistern
• Delayed from ruptured pseudo aneurysm.
• Rx maintain intravascular vol to prevent ischemia
  from vasospasm.
• Mortality? 39 national traumatic coma databank

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Intracerebral Bleed

• CT- hyperdense/mixed
• MRI- small petechial bleed DAI
• Rx- small- non operative. Resolve in 2-3 weeks
• Large- Sx drainage.
• Repeat CT in small bleeds after 12-24 hr is
  warranted to r/o coalescence to form large
  hematoma.

• Rare in Peds.
• 60 from small contusions coalesce to form larger
  hematoma.
• Rarely , violent angular acceleration ?bleed in
  deep white matter, basal ganglia, thalamus
• Transtentorial Herniation ? midbrain bleed (
  Duret hemorrhages)
• Common sites?
• Ant Temporal and Inf Frontal lobes impact
  against lateral sphenoid bone/ floor of ant
  fossa

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Penetrating Head Injury

• CT- localizes bullet and bone fragments
• MRI- non advised till magnetic properties of
  bullet known.
• Rx. Surgical
• Debridement of entry and exit wounds
• Remove accessible bullet and bone
• Control hemorrhage
• Repair Dural lacerations closure of wounds.
• NO ATTEMPT TO REMOVE BULLET OR BONE BEYOND ENTRY
  AND EXIT WOUNDS.

• Infants and children? fall on sharp objects with
  thin skull and open foraminae could predispose
  for these injuries.
• R/o child abuse
• Rx Surgical.
• Entry wound debrided and FB removed with in
  driven bone fragments.
• Peri and post op ABX
• Prophylactic anticonvulsants
• Adolescents and children ? Gun Shot Wounds. (
  12) and increasing annually.
• Higher mortality when
• Low GCS on presentation (3-4)
• B/L hemispheric /brainstem injury/
  intraventricular tracking
• Hemodynamic instability/ apnea/both
• Uncontrolled ICP.

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Intracranial Hypertension

• Pathophysiology
• ICP monitoring and control are the cornerstones
  of TBI management
• Normal ICP
• Adults ? lt10mmhg
• Children ? 3-7mmhg
• Infants? 1.5- 6mmhg
• When to treat?
• Adults ? gt 20
• Children ? gt15
• Infants? gt10 Arbitrary numbers most commonly
  used, pending outcome studies

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CBF Autoregulation

• CPP MAP- ICP mmhg
• Normal Brain
• CBF maintained within CPP range of 50-150mmhg as
  vessels can expand / constrict accommodate p
  changes.
• lt50 CPP? maximal Dilation occurs ?CBF falls as
  CPP drops
• gt150CPP? maximal Constriction occurs? CBF raises
  with CPP
• TBI
• CBF falls b/n 50-80 mmhg of CPP? Range of Hypo
  perfusion
• Auto regulation may be ,
• Completely lost? linear relation B/n CBF CPP
• Incompletely lost? Plateau after CPP of 80 mmhg

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Monro-Kellie doctrine Vol of intracranial
compartment must remain constant because of
inelastance of skull

• Normal State- ICV is a balance b/n Blood, brain
  CSF.
• With ICSOL? ICP remains normal till compensation
  can occur
• At the Point of decompensation The ICP starts to
  increase.
• The brains compensatory reserve is called
  Compliance
• Measure of compliance ?
• Volume pressure response
• Pressure Volume Index ( PVI)
• V/ LOG P1P2

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Transient elevation in ICPLundberg Waves

• A wave?
• Duration 2-15 min
• Amplitude 50-80mmhg
• Results from
• Transient occlusion of venous outflow as bridging
  veins occlude against compressed dura. Or
  transient vasodialtion and hence increase CBF as
  a response to ischemia
• Sustained A waves may indicate sustained
  elevation in ICP and hence low brain compliance
• 2. B waves ? changes in ICP w.r.t. Ventilation
• 3. C waves ? short lived waves w.r.t. arterial
  Traube-Herring waves

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Shape of ICP wave form as an indicator of
Compliance

• Normal ICP has 3 wave forms.
• Percussion wave- first and highest amplitude wave
• Dicrotic wave second wave
• Tidal wave- third and lowest amplitude
• In reduced brain compliance the Dicrotic and
  Tidal waves augment exceeding the percussion
  waves.

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ICP measurement

• Intraventricular Cath coupled to ICP transducer
  is Gold standard.
• Which patients need ICP monitoring??
• TBI abnormal CT scan who are not following
  commands ( 50-63)
• Comatose Normal CT had lower risk ( 13)
  unless associated with
• Older age
• Systemic Hypotension , lt90mmhg
• Motor posturing, with these risk is upto 60
• Most clinicians use abnormal CT scan result low
  GCS scores ( lt 8) as candidates for ICP
  monitoring

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Non invasive ICP measurement
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Mangement of ICP

• Goal ? to maintain CPP by
• Reducing ICP, and/or
• Increasing MAP hyper/normo volumia preffered as
  opposed old school Hypovol
• Brief periods of hypotension can double the
  mortality rates
• CPP should be match with cerebral metabolic
  demand to avoid hypoperfusion / hypeeperfusion.
• Cerebral OEF is helpful as,
• Decrease in CBF? increase OEF? increase AvDo2
  fraction
• AvDo2 diff b/n O2 content of Arterial jugular
  mixed venous blood.
• Considering Ao2 as constant, venous O2 alone can
  solely be assessed.
• Normal svJo2 is 65, a drop to 50-55 ? global
  cerebral ischemia

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Hyperdynamic therapy

• To maintain CPP of about gt70, by increasing MAP
• CPP MAP-ICP
• IVF- crystalloid/colloid
• PRBC if low HCT(lt30)
• Pressors as needed ( Dopa, Dobu,Phenylephri)
• if autoregulation is intact?? incres CPP?
  vasoconstriction? constant CBF?less volume?
  reduction in ICP.
• Systemic Hypo ? Vice versa

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Increasing CPP by reducing ICP
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Specific measures to reduce ICP
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• CSF drainage- effective and safe.
• Provides gradient for bulk flow of edema fluid
  from parenchyma of brain to ventricles.
• Continous 5-10 torr gradient
• Intermittent for 1-5 min when needed.

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Diuretics
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• Steroids No role currently in TBI
• Barbiturates- usually last resort med.

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• ALGORITH for treatment of elevated ICP with
  severe head injury.
• ( Brain trauma Foundation, American Association
  of neurological Surgeons, Joint section of
  Neurotrauma and critical care)

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Bispectral Index

• Bispectral index (BIS) is one of several recently
  developed technologies which purport to monitor
  depth of anesthesia.
• Uses ,
• Monitor depth of anesthesia
• Reduce incidence of intraoperative awareness
• Monitor recovery from brain injury
• With ICP to monitor during therapeutic burst
  suppression.
• 0-100 scale.
• 40-60? good depth of Anesthesia.

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POST TRAUMATIC SEIZURES

• Complicate 10 pediatric head injuries
• Impact seizures ? follow minor injury , occur on
  impact
• Early posttraumatic seizures? within min to hours
  of injury.
• No radiological intracranial injury noted in many
  cases
• Do not portend later epilepsy
• Most do not need Rx
• Outcome good.
• Late seizure ? gt24 hrs after injury
• Visible intracranial injury.
• Penetrating injuries/ depressed / SDH/ Lower GCS
  score
• Long term risk of epilespy high- need Rx for 6-12
  mo.

• Seizure prophylaxis
• Only during first week Or till intracranial
  hypertension phase is passed.
• Prolonged usage has cognitive deficits on long
  term follow ups.
• Phenytoin commonly used

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Thank You