Traumatic Brain Injury

1. Traumatic Brain Injury ShantaveerGangu 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

4. Primary Brain Injury

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 CORPUS CALLOSUM PERIVENTRICULAR WHITE MATTER BASAL GANGLIA BRAIN STEM

8. Secondary Brain Injury CBF OEF/GEF CMRoxy CMRglucose

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

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

13. Level Of Consciousness • Glasgow Coma Scale

14. Children's Coma Scale

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

16. Eye Movements • SO4,LR6, All3

17. Brainstem Reflexes

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 

19. Neurodiagnostic Evaluation

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

22. 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)<3yrleptomeningeal cyst, cephalomalacia, • Depressed • 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 #

25. 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.

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

28. Treatment

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.

30. 50% are unconscious immediately. Focal deficits common Hemiparesis – 50% Pupillary abnormality- 28-78% Seizures – 6-22% Rx- larger- urgent removal Small -

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 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}

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

35. 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}

36. 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 , Completely lost linear relation B/n CBF & CPP 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  Volume pressure response Pressure Volume Index ( PVI) = V/ LOG P1P2

38. 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

39. 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.

40. 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 , <90mmhg Motor posturing, with these risk is upto 60% Most clinicians use abnormal CT scan result + low GCS scores ( < 8) as candidates for ICP monitoring

42. Non invasive ICP measurement

43. Mangement of ICP • Goal  to maintain CPP by • Reducing ICP, and/or • Increasing MAP { hyper/normovolumiapreffered 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

46. Specific measures to reduce ICP

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

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

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)