Traumatic Brain Injury

Shantaveer Gangu Mentor- Dr.Baldauf MD

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.

Pathophysiology of Brain Injury

Brain Injury

Primary

Secondary

2.Intracranial hypertension and mass lesion

1.Delayed cell death

3.Ischemia systemic hypoxia,hypercarbia and hypotension

Primary Brain Injury

@SITE Focal Primary Diffuse Contracoup DAI

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.

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 > Oblique/ Sagital Forces

The shorn Axons retract and are evident histologically as RETRACTION BALLS. Located predominantly in 1. CORPUS CALLOSUM 2. PERIVENTRICULAR WHITE MATTER 3. BASAL GANGLIA 4. BRAIN STEM

Secondary Brain Injury

Biochemical Cascade AA/Neurotransmitter release CBF Intracellular Ca++ accumulation and cytoskeletal/ enzymatic breakdown Extracellular Cytokines and GF Blood Flow changes(Global/regional) Uncoupling of Substrate delivery and extraction CMRoxy CMRglucose External Compression Intraparenchymal Extraxial (subdural/epidural) OEF/GEF Pneumocephalus Depressed skull fracture

Generation of free radicals

Initial Stabilization
Initial assessment and resuscitative efforts proceed concurrently. Few things to watch for, 1.Airway 2.Cervical spine injury 3.Hypotension 4.Hypothermia 5.Neurogenic Hypertension

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.

Neurological Assessment
Rapid Trauma Neurological Examination
1. 2. 3. 4. 5. 6. 7. 8. 9. Level Of Consciousness Pupils Eom Fundi Extremity Movement Response To Pain Deep Tendon Reflexes Plantar Responses Brainstem Reflexes

Level Of Consciousness
Glasgow Coma Scale
Eye Opening Best Verbal Best Motor

Spontaneous
To Voice To Pain None

4
3 2 1

Oriented
Confused Inappropriate

5
4 3

Obeys Command 6
Localizes 5

Withdraws 4 Flexion 3

Incomprehensible 2

None

Extension
None

2
1

Children's Coma Scale

Ocular response Opens eyes spontaneously 4 Verbal response Smiles, orientated to sounds, follows objects, interacts. 5 3 Cries but consolable, inappropriate interaction 4 Inconsistently inconsolable, moaning 3 Motor response Infant moves spontaneously or purposefully 6

EOMI, reactive pupils ( opens eyes to speech)

Infant withdraws from touch 5

EOM impaired, fixed pupils (opens eyes to painful stimuli) 2

Infant withdraws from pain 4

EOM paralyzed, fixed pupils ( doesnt open eyes) 1

Inconsolable, agitated 2
No verbal response 1

Abnormal flexion to pain for an infant (decorticate response) 3

Extension to pain (decerebrate response) 2

No motor response

Mydriasis

Miosis
Carotid A. injury in neck or skull base Horners syndrome- Miosis with Ipsilateral ptosis and anhydrosis. Hypothalamic, cervicothoracic or direct orbital injury.

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

3 Cr.N. damageMydriasis Unilateral mydriasis Transtentorial ( Uncal) Herniation Traumatic iridoplegia

Seizure/ postictal state

Atropine / Sympathomimetics

Eye Movements
SO4,LR6, All3
Injury location Cavernous sinus/Sup Orbital fissure Transtentorial ( Uncal ) herniation Raised ICP ( false localizing sign) Frontal eyes field ( brodmans area 8) Abnormality All 3 Cr.Ns ( 3,4,6) are affected + V1 division 3 Cr.N Isolated Abducens(6) palsy Ipsilateral tonic conjugate deviation

Seizure involving frontal eyes field

Occipital lobe injury ( unilateral)

Conjugate deviation to contralateral side

Hemianopsia + ipsilateral conjugate gaze preference

Brainstem Reflexes
Facial palsy unilateral Corneal reflex ( V1+V2) Dolls eye maneuver Ice water caloric test ( never in awake child) 7 N injury- Basilar skull # Rostral Pontine function Vestibuloocular function COWS normal response Coma same side deviation Stuporous/obtunded nystagmus to contralateral rapid component 9,10th N + brainstem swallowing centers b/l hemispheric/diencephalic injury to as caudal as upper pons

Gag and cough reflex Periodic( Cheyne-stokes)

Apneustic ( prolonged ispiratory plateau) Ataxic breathing( irregular stuttering resp)

Mid- caudal pons injury Medullary respiratory generator center.

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
Normal reflex
Positive Babinski

Intact descending corticospinal inhibition

Interrupted inhibition pathways

Neurodiagnostic Evaluation
Skull Radiograph CT Contiguous slices from vertex to foramen Magnum. Extend to C3 if upper spine # suspected Brain, Blood and Bone windows May miss # that run parallel to CT slice and located at vertex. Controversial usage, costs> benefits Indications controversial, a must in 1.Penetrating head trauma 2.basilar/ depressed skull # 3.Posttraumatic seizure 4.Severe head injury In addition anyone with, 1.Altered level of consiousness 2.Focal deficits 3.Persistent headaches/ repeated emesis Better than CT in subacute and chronic phases of injury to detect contusions/shearing in white matter/c.callosum Invaluable in spinal cord injury Carotid/vertebrobasilar dissections/occlusions Pesudoaneurysms

MRI

Cerebral angiography

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

Scalp Injuries
Most are laceration
Simple Linear/ Stellate ED Rx Extensive, Degloving/Avulsion Repair GA Overlying Depressed Skull#, Infections Repair+ Elevation Of # Hematomas
Subgaleal Galeal Apo & Periost Cross Suture Lines Hypotension & Anemia(bp,hct) Cephalohematomas Periost & Skull Limited By S.Lines Calcify And Disfiguring Sx

Skull Fractures
Thin skull #s common place. Risk of # associated intracranial injuries? CT to R/o 1. Open 2. Closed 3. Linear (3/4) 4. Comminuted ( multiple branches) 5. Diastatic ( edges split apart)<3yrleptomeningeal cyst, cephalomalacia, 6. Depressed 7. Basilar

Depressed Skull #
From focal blow Closed 10% FND/15% seizures Rx, for cosmetic reasons < 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

Basilar Skull #
Basilar

Petrous Bone

Cribriform Plate

Longitudinal

Transverse

Rhinorrhea

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.

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

Treatment
Non surgical Minimal / no symptoms Should be located outside of Temporal or Post fossae Should be < 40 ml in volume Should not be associated with intradural lesions Should be discovered 6 or more hours after the injury Surgical

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.
Adults
Cerebral convexities over frontal/ temporal regions

Child/infants
Occipital + Parietal cortex Parafalcine ( post falx cerebri), supratentorial { abuse}

50% are unconscious immediately. Focal deficits common Hemiparesis 50% Pupillary abnormality- 28-78% Seizures 6-22%
Rx- larger- urgent removal Small Small with mass effect/ significant change in conscious/ focal deficits Small with significant brain injuries + mass effect out of proportion to size of clot Removed

Non operative approach

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.

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}

Intracerebral CT- hyperdense/mixed Bleed MRI- small petechial bleed+

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}

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.

Penetrating Head Injury

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 1.Low GCS on presentation (3-4) 2.B/L hemispheric /brainstem injury/ intraventricular tracking 3.Hemodynamic instability/ apnea/both 4.Uncontrolled ICP.

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.

Intracranial Hypertension
Pathophysiology
ICP monitoring and control are the cornerstones of TBI management Normal ICP
Adults <10mmhg Children 3-7mmhg Infants 1.5- 6mmhg

When to treat?
Adults > 20 Children >15 Infants >10 { Arbitrary numbers most commonly used, pending outcome studies}

CBF Autoregulation
CPP = MAP- ICP { mmhg} Normal Brain CBF maintained within CPP range of 50-150mmhg as vessels can expand / constrict accommodate p changes. <50 CPP maximal Dilation occurs CBF falls as CPP drops >150CPP 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 , 1. Completely lost linear relation B/n CBF & CPP 2. Incompletely lost Plateau after CPP of 80 mmhg

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 1.Volume pressure response 2.Pressure Volume Index ( PVI) = V/ LOG P1P2

Transient elevation in ICP Lundberg Waves

1. 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

Shape of ICP wave form as an indicator of Compliance

Normal ICP has 3 wave forms. 1.Percussion wave- first and highest amplitude wave 2.Dicrotic wave second wave 3.Tidal wave- third and lowest amplitude
In reduced brain compliance the Dicrotic and Tidal waves augment exceeding the percussion waves.

ICP measurement
Intraventricular Cath coupled to ICP transducer is Gold standard.
Which patients need ICP monitoring?? 1.TBI + abnormal CT scan who are not following commands ( 5063%) 2.Comatose + Normal CT had lower risk ( 13%) unless associated with 1. Older age 2. Systemic Hypotension , <90mmhg 3. Motor posturing, with these risk is upto 60% 3.Most clinicians use abnormal CT scan result + low GCS scores ( < 8) as candidates for ICP monitoring

Device / method 1. Intraventricular catheter

Risk / benefit Adv- drainage of CSF to reduce ICP DisAdv- infection/ ventricular compression leads to inaccuracy
Occlusion of port in device leads to inaccuracy Improved fidelity & longevity Can be placed Intraparenchymal/ intraventricular/ subdural Used to drain CSF Accuracy maintained even with fully collapsed ventricles Single cath can be used as long as needed

2. subdural/ subarachnoid bolts ( Philadelphia, Leeds, Richmond bolts) 3. Fiberoptic cath ( Camino labs)

Non invasive ICP measurement

Ultrasonographic tech Audiological tech- displacement of TM and perilymphatic pressure as a correlate of ICP Infrared light- thickness of CSF from reflected light as a correlate of ICP Arterial BP wave contours and blood flow velocity mathematical model Changes In optical nerve head with optical coherent tomography IOP as correlate of ICP With ICP cutoff of 20mmhg it has Specificity of 0.7 and sensitivity of 0.97 Pediatr Crit Care Med 2010 Vol. 11, No. 5

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

Hyperdynamic therapy
To maintain CPP of about >70, by increasing MAP { CPP= MAP-ICP} IVF- crystalloid/colloid PRBC if low HCT(<30%) Pressors as needed ( Dopa, Dobu,Phenylephri) if autoregulation is intact? incres CPP vasoconstriction constant CBFless volume reduction in ICP. Systemic Hypo ? Vice versa

Increasing CPP by reducing ICP

Sedation and pain control Quiet envir + min extern stimuli Pharmacological paralysis if needed IV/ ET lidocaine ( ET > IV) Elevation of head end by 20-30deg Increase in Pneumonia+ sepsis During intubation, before ET suctioning,ET manipulation Red venous press ICP Can cause orthostatic changesfall CPP rebound ICP rise Can rise ICP Contin drainage Prophylactic Anticonvulsants Rx + hypothermia. Fentanyl/ midazolam drip Etomidate in initial phase

Excessive PEEP, tight cervical collar, neck flexion/ rotation Bladder distention rise Occult seizures unexplained rise Fever rise

Specific measures to reduce ICP

Hyperventilation Rapid & effective response. Red Paco2/incr pH vasoconstricton Red CBF Current recommendations 1. routine hypervent ( 35 ) not be used in first 24 hrs 2.Chronic hypervent be avoided in absence of documented ICP rise 3.Reserved for deterioration not responding to other measures. 4.When needed with caution, PaCo2 never <30 torr. 5.svJo2 can be used as indicator of extreme ischemia( CBF fall) 6.If used, withdrawn slowly to avoid rebound rise

Disadvantages 1.paco2 < 30 torr red CBF to ischemic level 2.Regional variation in autoreg hyperventilation induced reverse vascular steal

 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.

Diuretics
Mannitol works as osmotic diuretic extract extra and intra cellular edema fluid from brain Additional mech reduces blood viscocity ( by hemodilution) and improves Rheology Increas CBF vasocons decreas volume red ICP. Risks 1. Repeated dose reduced osmotic gradient 2. Hyperosmolar state ( serum osm>320 mOsm) renal failure, rhabdomyolysis, hemolysis Disadv- may preferentially affect normal areas ( intact BBB) vs affected zones ( disrupted BBB) 3 dosing methods intermittant boluses when ICP 15-20 Intermittant Q6 hrly Continous infusion

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

Pros Reduce ICP , CBF, CMRO2 Inhibit free lipid peroxidation reduce cellular damage Cons Close ICU monitoring Hypotension Hyponatremia Myocardial depression

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)

Bispectral Index

Bispectral index (BIS) is one of several recently developed technologies which purport to monitor depth of anesthesia. Uses ,
1. Monitor depth of anesthesia 2. Reduce incidence of intraoperative awareness 3. Monitor recovery from brain injury 4. With ICP to monitor during therapeutic burst suppression. 5. 0-100 scale. 6. 40-60 good depth of Anesthesia.

POST TRAUMATIC SEIZURES

Complicate 10% pediatric head injuries 1. Impact seizures follow minor injury , occur on impact 2. Early posttraumatic seizures within min to hours of injury. 1. No radiological intracranial injury noted in many cases 2. Do not portend later epilepsy 3. Most do not need Rx 4. Outcome good. Late seizure >24 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

Thank You