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traumatic brain injury.pptx. .
- 1. Traumatic brain injuryand its management
- 2. Definition of TBI “Aninsult 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 Mechanismof Injury: -Blunt Injury a)Motor vehicle collisions b)Assaults c)Falls -Penetrating Injury a)Gunshot wounds b)Stabbing -Explosions
- 4. Head Injury-Pathophysiology Primaryinjury 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 injuryto 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
- 8. Two types ofbrain 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
- 9. Cerebral contusion Most commonFocal brain Injury Sites 🡪 Impact site/ under skull Anteroinferior frontal Anterior Temporal Occipital Regions Petechial hemorrhages 🡪 coalesce 🡪 Intracerebral Hematomas later on.
- 10. Specific Head Injuries SkullFractures- 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
- 12. Specific Head Injuries: TraumaticSubarachnoid 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%
- 13. 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. Specific Head Injuries SubduralHematoma: 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
- 18. Cranial neuropathies occurin 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
- 20. Auditory disturbance- 1. Fractureof petrous temporal bone(longitudinal) 2. Hemotympanum 3. Tympanic membrane perforation Facial nerve palsies - longitudinal or transverse petrous temporal fractures
- 21. Concussion • No structuralinjury 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
- 22. Diffuse axonal injury •Hallmarkof 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
- 23. The shorn Axonsretract and are evident histologically as RETRACTION BALLS. Located predominantly in 1. CORPUS CALLOSUM 2. PERIVENTRICULAR WHITE MATTER 3. BASAL GANGLIA 4. BRAIN STEM
- 24. Grading of DAI Grade I-Hemisphere DAI Grade II-Additional posterior callosal Grade III-Dorsolateral midbrain
- 25. MRI T2 weighted, FLAIR, T2* gradient echo MRI sequences early and late post-injury. Markers of DAI 1. number and volume of lesions resulting from contusions and large deep haemorrhages (T1, T2, FLAIR, and T2*) 2. Residual hemosiderin of microvascular shearing injuries(T2*) 3. Degree of atrophy
- 26. 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
- 27. Level Of Consciousness Glasgow Coma Scale
- 28. 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
- 29. Head Injury-Initial Evaluation andManagement Prevent Secondary 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
- 30. Increased ICP-Management HypertonicSaline Improves CPP and brain tissue O2 levels Decreased ICP by 35% (8-10 mm HG) CPP increased by 14% Repeated doses were not associated with rebound, hypovolemia or HTN
- 31. Treatment of Intracranial Hypertension *Thresholdof 20-25 mmHg may be used. Other values may be substituted in 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
- 32. Cognitive and neuropsychiatricsequelae Personality changes, egocentricity, childishness, irritability, aggressiveness, poor judgement, tactlessness, stubbornness, lethargy, disinterest, reduced drive and initiative, reduced sexual interest Low mood, depression,anxiety disorders
- 33. Epilepsy More commonwith 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)
- 34. 1. Early posttraumaticseizures🡪 within min to hours of injury. 1. No radiological intracranial injury noted in many cases 2. Do not progress 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 epilepsy high- need Rx for 6-12 mo.
- 35. Intravenous phenytoinwithin 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
- 36. 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
- 37. 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
Editor's Notes
- #4 Contact i.e. an object striking the head or the brain striking the inside of the skull Acceleration - Deceleration. Primary injury due to acceleration-deceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains. These forces can cause intran acranial hematoma, diffuse vascular injury, and injury to cranial nerves and the pituitary stalk. A secondary injury is not mechanically induced. It may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury. [5] The secondary damage is caused by casa cade of processes impacting “cerebral blood flow (hyper or hypoperfusion), impaired cerebrovascular autoregulation, cerebral metabolic dysfunction an,d impaired cerebral oxygenation.” [6] The ischemia and oedema are secondary injury types
- #7 Schematic representation of pathophysiology of traumatic brain injury (TBI). BBB dysfunction caused by TBI insult allows transmigration of activated leukocytes into the injured brain parenchyma, which is facilitated by an upregulation of cell adhesion molecules. Activated leukocytes, microglia and astrocytes produce ROS and inflammatory molecules such as cytokines and chemokines that contribute to demyelination and disruption of axonal cytoskeleton, leading to axonal swelling and accumulation of transport proteins at the terminals, hence compromising neuronal activity. Progressive axonal damage results in neurodegeneration. In addition, astrogliosis at the lesion site causes glial scar formation, which creates a non-permissive environment that impedes axonal regeneration. On the other hand, excessive accumulation of glutamate and aspartate neurotransmitters in the synaptic space due to spillage from severed neurons, glutamate-induced aggravated release from pre-synaptic nerve terminals and impaired reuptake mechanisms in traumatic and ischemic brain activate NMDA and AMDA receptors located on post-synaptic membranes, which allow the influx of calcium ions. Together with the release of Ca2+ ions from intracellular store (ER), these events lead to the production of ROS and activation of calpains. As a result of mitochondrial dysfunction, molecules such as apoptosis-inducing factor (AIF) and cytochrome c are released into the cytosol. These cellular and molecular events including the interaction of Fas-Fas ligand ultimately lead to caspase-dependent and -independent neuronal cell death.
- #10 Hemotympanum: Fractures that involve the petrous ridge of the temporal bone will cause blood to pool behind the tympanic membrane causing it to appear purple. This usually appears within hours of injury and may be the earliest clinical finding. Cerebrospinal fluid (CSF) rhinorrhea or otorrhea: “Halo” sign is the double ring pattern described when bloody fluid from the ear or nose containing CSF is dripped onto paper or linen. This sign is based on the principle of chromatography; components of a liquid mixture will separate when traveling through a material. This sign is not specific to the presence of CSF, as saline, tears or other liquids will also produce a ring pattern when mixed with blood. CSF leaks may be delayed hours to days after the initial trauma. Periorbital ecchymosis (raccoon eyes): Pooling of blood surrounding the eyes is most commonly associated with fractures of the anterior cranial fossa. This finding is typically not present during the initial evaluation and is delayed by 1 to 3 days. If bilateral, this finding is highly predictive of a basilar skull fracture. Retroauricular or mastoid ecchymosis (Battle sign): Pooled blood behind the ears in the mastoid region is associated with fractures to the middle cranial fossa. Like Raccoon eyes, this finding is frequently delayed by 1 to 3 days. Middle ear injury is seen in nearly one-third of patients and may present with hemotympanum, disruption of the ossicles, hearing loss, and even CSF leak. Other features include dizziness, tinnitus, and nystagmus
- #32 In 1848, 25-year-old Gage was working as a construction foreman for a railroad company. During the works, explosives were required to blast away rock. This intricate procedure involved explosive powder and a tamping iron rod. In a moment of distraction, Gage detonated the powder and the charge went off, sending the rod through his left cheek. It pierced his skull, and travelled through the front of his brain, exiting the top of his head at high speed. Modern day methods have since revealed that the likely site of damage was to parts of his prefrontal cortex. Gage was thrown to the floor, stunned, but conscious. His body eventually recovered well, but Gage’s behavioural changes were extraordinary. Previously a well-mannered, respectable, smart business man, Gage reportedly became irresponsible, rude and aggressive. He was careless and unable to make good decisions. Women were advised not to stay long in his company, and his friends barely recognised him.