traumatic brain injury.pptx. .

Neurology

1. Traumatic brain injury and its management

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 a) Motor vehicle collisions b) Assaults c) Falls - Penetrating Injury a) Gunshot wounds b) 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. -P rimary 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”) - Intracellular calcium influx triggers proteolysis, breakdown of the cytoskeleton, and interruption of axonal transport

6. Two types of brain injury Closed brain 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 Open brain injury: Results from bullet wounds, etc. Largely focal damage Penetration of the skull Effects can be serious

7. Cerebral c ontusion Most common Focal brain Injury Sites 🡪 Impact site/ under skull Anteroinferior frontal Anterior Temporal Occipital Regions Petechial hemorrhages 🡪 coalesce 🡪 Intracerebral Hematomas later on.

8. Specific Head Injuries Skull Fractures- Basilar Fracture Most common-petrous portion of temporal bone, the external auditory canal and temporomandibular region. 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

9. 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%

10. 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

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

12. 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 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 optic canal

13. Auditory disturbance- Fracture of petrous temporal bone(longitudinal) Hemotympanum Tympanic membrane perforation Facial nerve palsies -longitudinal or transverse petrous temporal fractures

14. 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 Head Trauma - 26

15. 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

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

17. Grading of DAI Grade I-Hemisphere DAI Grade II-Additional posterior callosal Grade III-Dorsolateral midbrain

18. 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 hemosiderin of microvascular shearing injuries(T2*) Degree of atrophy

19. 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

20. Level Of Consciousness  Glasgow Coma Scale

21. 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

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

23. 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% Repeated doses were not associated with rebound, hypovolemia or HTN

24. Treatment of Intracranial Hypertension *Threshold of 20-25 mmHg may be used. Other values may be substituted in individual conditions. May Repeat Mannito if Serum Osmolarity < 320 mOsm/L & Pt euvolemic High Dose Barbiturate therapy Hyperventilation to PaCO2 < 30 mmHg Monitoring SjO2, AVDO2, and/orCBF Recommended NO YES NO YES NO YES NO Carefully Withdraw ICP Treatment Consider Repeating CT Scan YES Other Second Tier Therapies 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?* Insert ICP Monitor Maintain CPP ≈ 70 mmHg

25. 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

26. Epilepsy More common with penetrating injury 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)

27. 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 epilepsy high- need Rx for 6-12 mo.

28. Intravenous phenytoin within 24 hours of high risk injury prevents early seizures, but not late seizures, even in high risk patients Antiepileptics continued for at least 1 year

29. 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

30. 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