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Traumatic Brain Injury Shantaveer Gangu Mentor- Dr.Baldauf MD.

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Presentation on theme: "Traumatic Brain Injury Shantaveer Gangu Mentor- Dr.Baldauf MD."— Presentation transcript:

1 Traumatic Brain Injury Shantaveer Gangu Mentor- Dr.Baldauf MD

2 Demographics Account for 75% all pediatric trauma hospitalizations 80% of trauma related deaths in children Domestic falls, MVA’s, 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.

3 Pathophysiology of Brain Injury Brain Injury PrimarySecondary 1.Delayed cell death 2.Intracranial hypertension and mass lesion 3.Ischemia  systemic hypoxia,hypercarbia and hypotension

4 Primary Brain Injury Contra- coup DiffuseDAI

5 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.

6 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

7 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

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

9 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

10 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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12 Neurological Assessment Rapid Trauma Neurological Examination 1.Level Of Consciousness 2.Pupils 3.Eom 4.Fundi 5.Extremity Movement 6.Response To Pain 7.Deep Tendon Reflexes 8.Plantar Responses 9.Brainstem Reflexes

13 Level Of Consciousness Glasgow Coma Scale Eye OpeningBest VerbalBest Motor Spontaneous 4Oriented 5Obeys Command 6 To Voice 3Confused 4Localizes 5 To Pain 2Inappropriate 3Withdraws 4 None 1Incomprehensible 2Flexion 3 None 1Extension 2 None 1

14 Children's Coma Scale Ocular responseVerbal responseMotor response Opens eyes spontaneously 4 Smiles, orientated to sounds, follows objects, interacts. 5 Infant moves spontaneously or purposefully 6 EOMI, reactive pupils ( opens eyes to speech) 3 Cries but consolable, inappropriate interaction 4 Infant withdraws from touch 5 EOM impaired, fixed pupils (opens eyes to painful stimuli) 2 Inconsistently inconsolable, moaning 3 Infant withdraws from pain 4 EOM paralyzed, fixed pupils ( doesn’t open eyes) 1 Inconsolable, agitated 2 Abnormal flexion to pain for an infant (decorticate response) 3 No verbal response 1 Extension to pain (decerebrate response) 2 No motor response 1

15 Pupillary Exam Pupillary size is balance b/n Sympath and parasympathetic influences. Size, shape and reactivity to light are tested parameters. MydriasisMiosis 3 Cr.N. damage- Mydriasis Carotid A. injury in neck or skull base Unilateral mydriasis – Transtentorial ( Uncal) Herniation Horner’s syndrome- Miosis with Ipsilateral ptosis and anhydrosis. Traumatic iridoplegia Hypothalamic, cervicothoracic or direct orbital injury. Seizure/ postictal state Atropine / Sympathomimetics

16 Eye Movements SO4,LR6, All3 Injury locationAbnormality Cavernous sinus/Sup Orbital fissureAll 3 Cr.N’s ( 3,4,6) are affected + V1 division Transtentorial ( Uncal ) herniation3 Cr.N Raised ICP ( false localizing sign)Isolated Abducens(6) palsy Frontal eyes field ( brodman’s area 8)Ipsilateral tonic conjugate deviation Seizure involving frontal eyes fieldConjugate deviation to contralateral side Occipital lobe injury ( unilateral)Hemianopsia + ipsilateral conjugate gaze preference

17 Brainstem Reflexes Facial palsy unilateral7 N injury- Basilar skull # Corneal reflex ( V1+V2)Rostral Pontine function Dolls eye maneuverVestibuloocular function Ice water caloric test ( never in awake child) COWS normal response Coma – same side deviation Stuporous/obtunded – nystagmus to contralateral rapid component Gag and cough reflex9,10 th N + brainstem swallowing centers Periodic( Cheyne-stokes)b/l hemispheric/diencephalic injury to as caudal as upper pons Apneustic ( prolonged ispiratory plateau)Mid- caudal pons injury Ataxic breathing( irregular stuttering resp) Medullary respiratory generator center.

18 Deep tendon and superficial reflexes DTR’s exaggerated after TBI due to cortical disinhibition Decreased / absent after Spinal cord injury Asymmetric DTR’s  unilateral brain/spine injury Superficial  lost/decreased in corticospinal dysfunction and helpful in localizing lesions Plantar response  Normal reflexIntact descending corticospinal inhibition Positive BabinskiInterrupted inhibition pathways

19 Neurodiagnostic Evaluation Skull RadiographControversial usage, costs> benefits 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. 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 MRIBetter than CT in subacute and chronic phases of injury to detect contusions/shearing in white matter/c.callosum Invaluable in spinal cord injury Cerebral angiographyCarotid/vertebrobasilar dissections/occlusions Pesudoaneurysms

20 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

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

22 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)  <3yr  leptomeningeal cyst, cephalomalacia, 6.Depressed 7.Basilar

23 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

24 Basilar Skull # Basilar Petrous Bone LongitudinalTransverse Cribriform Plate Rhinorrhea

25 Epidural Hematomas (EDH) Peak incidence in 2 nd 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.

26 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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28 Treatment Non surgicalSurgical 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

29 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. AdultsChild/infants Cerebral convexities over frontal/ temporal regions Occipital + Parietal cortex Parafalcine ( post falx cerebri), supratentorial { abuse}

30 50% are unconscious immediately. Focal deficits common Hemiparesis – 50% Pupillary abnormality % Seizures – 6-22% Rx- larger- urgent removal Small - Small with mass effect/ significant change in conscious/ focal deficits Removed Small with significant brain injuries + mass effect out of proportion to size of clot Non operative approach

31 SDH’s 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.

32 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}

33 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 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}

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

35 Intracranial Hypertension Pathophysiology – ICP monitoring and control are the cornerstones of TBI management – Normal ICP Adults  <10mmhg Children  3-7mmhg Infants  mmhg – When to treat? Adults  > 20 Children  >15 Infants  >10 { Arbitrary numbers most commonly used, pending outcome studies}

36 CBF Autoregulation CPP = MAP- ICP { mmhg} Normal Brain CBF maintained within CPP range of mmhg 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 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

37 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

38 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

39 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.

40 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 ( %) 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

41 Device / methodRisk / benefit 1. Intraventricular catheterAdv- drainage of CSF to reduce ICP DisAdv- infection/ ventricular compression leads to inaccuracy 2. subdural/ subarachnoid bolts ( Philadelphia, Leeds, Richmond bolts) Occlusion of port in device leads to inaccuracy 3. Fiberoptic cath ( Camino labs)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

42 Non invasive ICP measurement Ultrasonographic techPediatr Crit Care Med 2010 Vol. 11, No. 5 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 ICPWith ICP cutoff of 20mmhg it has Specificity of 0.7 and sensitivity of 0.97

43 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

44 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 CBF  less volume  reduction in ICP. Systemic Hypo ? Vice versa

45 Increasing CPP by reducing ICP Sedation and pain controlFentanyl/ midazolam drip Etomidate in initial phase Quiet envir + min extern stimuli Pharmacological paralysis if neededIncrease in Pneumonia+ sepsis IV/ ET lidocaine ( ET > IV)During intubation, before ET suctioning,ET manipulation Elevation of head end by 20-30degRed venous press  ICP Can cause orthostatic changes  fall CPP  rebound ICP rise Excessive PEEP, tight cervical collar, neck flexion/ rotation Can rise ICP Bladder distention  riseContin drainage Occult seizures  unexplained riseProphylactic Anticonvulsants Fever  riseRx + hypothermia.

46 Specific measures to reduce ICP HyperventilationRapid & effective response. Red Paco2/incr pH  vasoconstricton  Red CBF Disadvantages 1.paco2 < 30 torr  red CBF to ischemic level 2.Regional variation in autoreg  hyperventilation induced reverse vascular steal 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

47 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.

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

49 Steroids – No role currently in TBI Barbiturates- usually last resort med. ProsCons Reduce ICP, CBF, CMRO2 Inhibit free lipid peroxidation  reduce cellular damage Close ICU monitoring Hypotension Hyponatremia Myocardial depression

50 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)

51 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 scale  good depth of Anesthesia.

52 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

53 Thank You


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