Traumatic head injury

1. H ead injury management for neurologist Dr. Parag P Moon Senior resident Dept Of Neurology

2. Definition of TBI “An insult to the brain, not of degenerative or congenital nature caused by an external physical force that may produce a diminished or altered state of consciousness, which results in an impairment of cognitive abilities or physical functioning. It can also result in the disturbance of behavioral or emotional functioning.”

3. Pathophysiology of Head 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 vessels results from rotational and translational accelerations . Rotational acceleration causes diffuse shearing/stretch of axonal and vascular cell membranes , increasing their permeability (“ mechanoporation ”)

6. Intracellular calcium influx triggers proteolysis, breakdown of the cytoskeleton, and interruption of axonal transport Accumulation of b amyloid precursor protein, the formation of axonal bulbs (retraction balls), secondary axotomy , 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 Contusion Most common Focal brain Injury Sites  Impact site/ under skull # Anteroinferior frontal Anterior Temporal Occipital Regions Petechial hemorrahges  coalesce  Intracerebral Hematomas later on.

11. Specific Head Injuries Skull Fractures Basilar Fracture Most common-petrous portion of temporal bone, the EAC 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 beneath skull Actively bleeding- Mixed densities Severe anemia- isodense/hypodense Untreated EDH imaging over days Hyperdense Isodense Hypodense w.r.t. brain

16. Treatment Non surgical 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

17. Specific Head Injuries Subdural Hematoma Sudden acceleration-deceleration injury with tearing of bridging veins Common in elderly and alcoholics Associated with DAI Classified as acute, subacute or chronic Acute <2 weeks Chronic >4 weeks

18. Rx- larger- urgent removal 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

19. Cranial neuropathies occur in about 10% of admitted and 30% of severe injuries. Frontal injury, basal skull fracture, and pressure effects account for most Anosmia – frontal injury

20. Visual symptoms result from oculomotor dysfunction, refractive error shifts, damage to the cornea and intraocular structures, visual field loss caused by anterior and posterior visual pathway damage. Traumatic optic neuropathies-at the entry and exit of the optic canal

21. Auditory disturbance- Fracture of petrous temporal bone (longitudinal) Hemotympanum Tympanic membrane perforation Facial nerve palsies -longitudinal or transverse petrous temporal 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 nausea 26 Head Trauma -

23. Diffuse axonal injury 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

24. The shorn Axons retract and are evident histologically as RETRACTION BALLS. Located predominantly in CORPUS CALLOSUM PERIVENTRICULAR WHITE MATTER BASAL GANGLIA 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 MRI sequences early and late post-injury. Markers of DAI number and volume of lesions resulting from contusions and large deep haemorrhages (T1, T2, FLAIR, and T2*) Residual haemosiderin of microvascular shearing injuries(T2*) Degree of atrophy

27. Diffusion tensor imaging (DTI)-reveal evidence of loss of neuronal and glial cells (increased diffusivity) and parallel fibre tracts (reduced anisotropy) Spectroscopy may show a reduction in N-acetyl aspartate , consistent with neuronal loss

28. Post traumatic amnesia Confused and disorientated Lack the capacity to store and retrieve new information Duration of PTA, not of retrograde amnesia, is a useful predictor of outcome Treated with haloperidol and oral resperidone with benzodiazapine

29. Level Of Consciousness Glasgow Coma Scale

30. Children's Coma Scale Ocular response Verbal response Motor 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

31. Levels of TBI Mild TBI Glascow Coma Scale score 13-15 Moderate TBI Glascow Coma Scale score 9-12 Severe TBI Glascow Coma Scale score 8 or less

32. Head Injury-Initial Evaluation and Management Prevent Secondary Brain Injury Hypoxemia Hypotension Anemia Maintainance of MAP above 90mm of Hg Airway control with cervical spine immobilization Orotracheal Rapid Sequence Intubation Hyperglycemia Evacuation of mass

33. Non invasive methods for ICP 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

34. Increased ICP-Management Hypertonic Saline Improves CPP and brain tissue O 2 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 minutes A. 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 cerebral ischemia Used as a last resort measure Maintain PaCO 2 at 30-35 mm Hg Steroids not recommended

37. Increased ICP-Management Barbiturate Coma Not indicated in the ED Lowers ICP, cerebral metabolic O 2 demand Anticonvulsants Reduce occurrence of post-traumatic seizures No improvement in long-term outcome ICP Monitoring Should be performed on TBI with GCS <9 Increased ICP may be managed by drainage

38. Treatment of Intracranial Hypertension *Threshold of 20-25 mmHg may be used. Other values may be substituted in individual conditions. May Repeat Mannitol if Serum Osmolarity < 320 mOsm/L & Pt euvolemic High Dose Barbiturate therapy Hyperventilation to PaCO2 < 30 mmHg Monitoring SjO2, AVDO2, and/orCBF Recommended Other Second Tier Therapies NO YES NO YES NO YES NO Carefully Withdraw ICP Treatment Consider Repeating CT Scan YES Second Tier Therapy Intracranial Hypertension? Hyperventilation to PaCO2 30 - 35 mmHg Intracranial Hypertension? Mannitol (0.25 - 1.0 g/kg IV) Intracranial Hypertension? Ventricular Drainage (if available) Intracranial Hypertension?* Maintain CPP  70 mmHg Insert ICP Monitor

39. Cognitive and neuropsychiatric sequelae Personality changes, egocentricity, childishness, irritability, aggressiveness, poor judgement, tactlessness, stubbornness, lethargy, disinterest, reduced drive and initiative, reduced sexual interest Low mood, depression,anxiety disorders

40. Epilepsy More common with penetrating injury In Blunt trauma predicted by depressed skull fracture, an intracranial clot requiring surgery, and altered awareness for more than 24 hours associated with contusion.

41. Concussive convulsions (occurring seconds after the impact) Immediate epilepsy (occurring up to 12 hours after injury) Early seizures (12 hours to one week post-injury) Late epilepsy (more than one week post-injury)

42. Early posttraumatic seizures within min to hours of injury. No radiological intracranial injury noted in many cases Do not progress later epilepsy Most do not need Rx 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.

43. Intravenous phenytoin within 24 hours of high risk injury 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 within 14 days of the injury, or with recovery of awareness, If it continues for more than eight weeks it is said to have 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 make up(at least one apolipoprotein E e4 allele)

47. Thank you

48. References HEAD INJURY FOR NEUROLOGISTS: Richard Greenwood ; J Neurol Neurosurg Psychiatry 2002 73: i8-i16 Traumatic brain injury; Emily Gilmore and Steven Karceski ; Neurology 2010;74;e28-e31 Guidelines for the Management of Severe Traumatic Brain Injury :A joint initiative of:The Brain Trauma Foundation ,The American Association of Neurological Surgeons ,The Joint Section on Neurotrauma and Critical Care