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Head injury management for neurologist Dr. Parag P Moon Senior resident Dept Of Neurology

Traumatic head injury

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  • 1. Dr. Parag P MoonSenior residentDept Of Neurology

2. Definition of TBI An insult to the brain, not of degenerative orcongenital nature caused by an external physical forcethat may produce a diminished or altered state ofconsciousness, which results in an impairment ofcognitive abilities or physical functioning. It can alsoresult in the disturbance of behavioral or emotionalfunctioning. 3. Pathophysiology ofHead Injury Mechanism of Injury Blunt Injury Motor vehicle collisions Assaults Falls Penetrating Injury Gunshot wounds Stabbing Explosions 4. Head Injury-Pathophysiology Primary injury Irreversible cellular injury as a direct result of the injury Prevent the event Secondary injury Damage to cells that are not initially injured Occurs hours to weeks after injury Prevent hypoxia and ischemia 5. Primary mechanical injury to axons and blood vesselsresults from rotational and translational accelerations. Rotational acceleration causes diffuse shearing/stretchof axonal and vascular cell membranes, increasingtheir permeability (mechanoporation) 6. Intracellular calcium influx triggers proteolysis,breakdown of the cytoskeleton, and interruption ofaxonal transport Accumulation of b amyloid precursor protein, theformation of axonal bulbs (retraction balls), secondaryaxotomy, and an inflammatory response. 7. Two types of brain injury occur Closed brain injury Open brain injury 8. Closed Head Injury Resulting from falls, motor vehicle crashes, etc. Focal damage and diffuse damage to axons Effects tend to be broad (diffuse) No penetration to the skull 9. Open Head Injury Results from bullet wounds, etc. Largely focal damage Penetration of the skull Effects can be serious 10. Cerebral ContusionMost common Focal brainInjurySites Impact site/ underskull #Anteroinferior frontalAnterior TemporalOccipital RegionsPetechial hemorrahges coalesce IntracerebralHematomas later on. 11. Specific Head Injuries Skull Fractures Basilar Fracture Most common-petrous portion of temporal bone, theEAC and TM Dural tear CSF otorrhea CSF rhinorrhea Battle Sign Raccoon Sign CSF testing Ring sign, glucose or CSF transferrin Should be started on prophylactic antibiotics Ceftriaxone 1-2 gm Hemotympanum Vertigo Hearing loss Seventh nerve palsy 12. Specific Head Injuries Scalp Lacerations May lead to massive blood loss Small galeal lacerations may be left alone Skull Fracture Linear and simple comminuted skull fractures Exploration of wound Prophylactic antibiotics are controversial Occipital fractures have a high incidence of other injury If depressed beyond outer table-requires NS repair 13. Specific Head Injuries Traumatic Subarachnoid Hemorrhage Most common CT finding in moderate to severe TBI If isolated head injury, may present with headache,photophobia and meningismus Early tSAH development triples mortality Size of bleed and outcome Timing of CT Nimodipine reduces death and disability by 55% 14. Specific Head Injuries Epidural Hematoma Occurs in 0.5% of all head injuries Blunt trauma to temporoparietal region middle meningeal artery involved most commonly(66%) Eighty percent with associated skull fracture May occur with venous sinus tears classically associated with a lucid interval Classic presentation only 30% of the time 15. Diagnosis CT is diagnostic Initial Ct Hyperdense Lentiform collection beneathskull Actively bleeding- Mixed densities Severe anemia- isodense/hypodense Untreated EDH imaging over days HyperdenseIsodense Hypodense w.r.t. brain 16. TreatmentNon surgical SurgicalMinimal / no symptomsShould be located outside of Temporal orPost fossaeShould be < 40 ml in volumeShould not be associated with intradurallesionsShould be discovered 6 or more hoursafter the injury 17. Specific Head Injuries Subdural Hematoma Sudden acceleration-deceleration injury with tearing ofbridging veins Common in elderly and alcoholics Associated with DAI Classified as acute, subacute or chronic Acute 4 weeks 18. Rx- larger- urgent removal Small with mass effect/ significant change inconscious/ focal deficits-Removed Small with significant brain injuries + mass effect outof proportion to size of clot-Non operative approach 19. Cranial neuropathies occur in about 10% of admittedand 30% of severe injuries. Frontal injury, basal skull fracture, and pressure effectsaccount for most Anosmia frontal injury 20. Visual symptoms result from oculomotor dysfunction,refractive error shifts, damage to the cornea andintraocular structures, visual field loss caused byanterior and posterior visual pathway damage. Traumatic optic neuropathies-at the entry and exit ofthe optic canal 21. Auditory disturbance-1. Fracture of petrous temporal bone(longitudinal)2. Hemotympanum3. Tympanic membrane perforation Facial nerve palsies -longitudinal or transverse petroustemporal fractures 22. Concussion No structural injury to brain Level of consciousness Variable period of unconsciousness or confusion Followed by return to normal consciousness Retrograde short-term amnesia May repeat questions over and over Associated symptoms Dizziness, headache, ringing in ears, and/or nauseaHead Trauma - 26 23. Diffuse axonal injuryHallmark of severe traumatic BrainInjuryDifferential Movement of Adjacentregions of Brain during accelerationand Deceleration.DAI is major cause of prolongedCOMA after TBI, probably due todisruption of Ascending Reticularconnections to Cortex.Angular forces > Oblique/ SagitalForces 24. The shorn Axonsretract and are evidenthistologically asRETRACTION BALLS.Locatedpredominantly in1. CORPUSCALLOSUM2. PERIVENTRICULAR WHITE MATTER3. BASAL GANGLIA4. BRAIN STEM 25. Grading of DAI Grade I-Hemisphere DAI Grade II-Additional posterior callosal Grade III-Dorsolateral midbrain 26. MRI T2 weighted , FLAIR, T2* gradient echo MRIsequences early and late post-injury. Markers of DAI1. number and volume of lesions resulting fromcontusions and large deep haemorrhages (T1, T2,FLAIR, and T2*)2. Residual haemosiderin of microvascular shearinginjuries(T2*)3. Degree of atrophy 27. Diffusion tensor imaging (DTI)-reveal evidence of lossof neuronal and glial cells (increased diffusivity) andparallel fibre tracts (reduced anisotropy) Spectroscopy may show a reduction in N-acetylaspartate, consistent with neuronal loss 28. Post traumatic amnesia Confused and disorientated Lack the capacity to store and retrieve newinformation Duration of PTA, not of retrograde amnesia, is a usefulpredictor of outcome Treated with haloperidol and oral resperidone withbenzodiazapine 29. Level Of Consciousness Glasgow Coma Scale 30. Children's Coma ScaleOcular response Verbal response Motor responseOpens eyes spontaneously4Smiles, orientated tosounds, follows objects,interacts.5Infant moves spontaneously orpurposefully 6EOMI, reactive pupils( opens eyes to speech) 3Cries but consolable,inappropriateinteraction 4Infant withdraws from touch 5EOM impaired, fixed pupils(opens eyes to painful stimuli)2Inconsistentlyinconsolable, moaning3Infant withdraws from pain 4EOM paralyzed, fixed pupils( doesnt open eyes)1Inconsolable, agitated2Abnormal flexion to pain for aninfant (decorticate response) 3No verbal response1Extension to pain (decerebrateresponse) 2No motor response 1 31. Levels of TBI Mild TBI Glascow Coma Scale score13-15 Moderate TBI Glascow Coma Scale score9-12 Severe TBI Glascow Coma Scale score8 or less 32. Head Injury-Initial Evaluationand Management Prevent Secondary Brain Injury Hypoxemia Hypotension Anemia Hyperglycemia Evacuation of mass Maintainance of MAP above 90mm of Hg Airway control with cervical spine immobilization Orotracheal Rapid Sequence Intubation 33. Non invasive methods for ICP Audiological tech- displacement of TM and perilymphaticpressure as a correlate of ICP Infrared light- thickness of CSF from reflected light as acorrelate of ICP Arterial BP wave contours and blood flow velocity mathematical model Changes In optical nerve head with optical coherenttomography IOP as correlate of ICP =With ICP cutoff of 20mmhg it hasSpecificity of 0.7 and sensitivity of 0.97 34. Increased ICP-Management Hypertonic Saline Improves CPP and brain tissue O2 levels Decreased ICP by 35% (8-10 mm HG) CPP increased by 14% MAP remained stable Greatest benefit in those with higher ICP and lower CPP Repeated doses were not associated with rebound,hypovolemia or HTN 30 mL of 23.4% over 15 minutesA. Defillo, Hennepin County Medical Center 35. Increased ICP-Management Mannitol Osmotic agent Effects ICP, CBF, CPP and brain metabolism Free radical scavenger Reduces ICP within 30 minutes, last 6-8 hrs Dosage 0.25-1 gm/kg bolus 36. Increased ICP-Management Hyperventilation Not recommended as prophylactic intervention Never lower than 25 mm Hg Reduces ICP by vasoconstriction, may lead to cerebralischemia Used as a last resort measure Maintain PaCO2 at 30-35 mm Hg Steroids not recommended 37. Increased ICP-Management Barbiturate Coma Not indicated in the ED Lowers ICP, cerebral metabolic O2 demand Anticonvulsants Reduce occurrence of post-traumatic seizures No improvement in long-term outcome ICP Monitoring Should be performed on TBI with GCS 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. 43. Intravenous phenytoin within 24 hours of high riskinjury prevents early seizures, but not late seizures,even in high risk patients Antiepileptics continued for atleast 1 year 44. Post traumatic headache Post-traumatic headache, by definition, starts within14 days of the injury, or with recovery of awareness, If it continues for more than eight weeks it is said tohave become chronic. Can be tension or migraine or combination of two Local soft tissue injury contribute 45. Predictors of outcome Acute predictors admission GCS present/absent pupillary responses Attendant hypoxic/ischaemic injury imaging findings, especially depth of lesion biochemical markers Duration of coma and PTA 46. On long term outcome affected by Increasing age over 50 years, social class, personality,family support, premorbid caseness, and genetic makeup(at least one apolipoprotein E e4 allele) 47. Thank you 48. References HEAD INJURY FOR NEUROLOGISTS: RichardGreenwood ;J Neurol Neurosurg Psychiatry 2002 73: i8-i16 Traumatic brain injury; Emily Gilmore and StevenKarceski ;Neurology 2010;74;e28-e31 Guidelines for the Management of SevereTraumatic Brain Injury:A joint initiative of:The BrainTrauma Foundation ,The American Association ofNeurological Surgeons ,The Joint Section onNeurotrauma and Critical Care