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Traumatic Brain Injury

Traumatic Brain Injury. Dayna Ryan, PT, DPT Winter 2012. TRAUMATIC BRAIN INJURY. Lesion: Brain ~ 5 million persons living with TBI ~$60 billion in the United States in 2000. TBI INCIDENCE (March 2010 CDC data). ~ 80% of TBI treated & released.

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Traumatic Brain Injury

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  1. Traumatic Brain Injury Dayna Ryan, PT, DPT Winter 2012

  2. TRAUMATIC BRAIN INJURY • Lesion: Brain • ~ 5 million persons living with TBI • ~$60 billion in the United States in 2000

  3. TBI INCIDENCE (March 2010 CDC data) ~ 80% of TBI treated & released • ~ 1. 7 million TBI occur in the US annually • TBI rates among individuals younger than 65 y. o. • Male : Females = 1.4 : 1

  4. TBI INCIDENCE BY AGE (March 2010 CDC data) • Highest incidence among ages • 0-4 (children), 15-19 (teens), 65+ (elderly) • ~ 90% ER visits by children aged 0-14 y. o. • Highest rates of TBI-related hospitalizations & deaths occur in adults aged > 75 y. o.

  5. CAUSE OF TBI(March 2010 CDC data) • Falls are #1 cause of TBI among all age groups • Highest rates of fall-related TBI in children 0-4 y.o. & adults > 75 y.o. • Highest rates of motor vehicle & assault-related TBI among adults aged 20-24 y.o. • Alcohol involved in >50% of cases

  6. RISK FACTORS • Young (average age of TBI = 29 y. o.) • Male • Risk taking behaviors (age 15-24 y. o.) • Low income inner city dwellers • Substance abuse (50% hospitalizations by TBI due to alcohol intoxication) • Availability of firearm • Previous TBI (e.g. sports-related concussions) • Old age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation, slower reaction time, movements & gait)

  7. CLASSIFICATION OF TBI(BY MECHANISM) Open meninges have been breached, brain is exposed Closed no skull fracture or laceration of the brain coup-contrecoup Primary injury at impact 2nd injury at the opposite side Blast Blast wave from explosion hits the body Air-filled organ or brain surrounded by fluid are particularly at risks of blast injuries

  8. Coup-Countercoup Injury

  9. CLASSIFICATION OF TBI- BY TYPES OF INJURIES • Primary vs. Secondary (Biomolecular response to injury) • Primary = direct injury to the brain • Secondary = damage after the traumatic event, caused by brain hypotension, hypoxia, or herniation • Focal vs. Diffuse or a Combination of the Two • Focal = localized trauma (gun shot) • Diffuse = trauma over a large area (swelling)

  10. CLINICAL CLASSIFICATION OF TBI- BY SEVERITY OF DAMAGE Mild (i.e. concussion): ~ 75% of TBI * Moderate Severe Classification Criteria & Prognosis (* Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; 2003. )

  11. SPECIFIC INJURIES • Concussion (= mild TBI) • Diffuse axonal injury • Contusion • Skull fracture • Intracerebral hematoma • Subdural hematoma • Epidural hematoma • Subarachnoid hemorrhage

  12. headache dizziness irritability decreased memory &concentration depression/anxiety fatigue sleep disturbance pain Patient: MILD T.B.I. (Concussion) COMMON SYMPTOMS THESE SYMPTOMS ARE ALSO COMMON IN THE GENERAL POPULATION AND AMONG CHRONIC PAIN PATIENTS

  13. CONCUSSION (MILD TBI) • Most common head injury • Alteration of consciousness & memory • Non-penetrating (non-opened) injury • CT or MRI usually normal • Good prognosis • Cumulative effects of repeated concussion • can cause chronic dementia • 50-100% mortality rate in second impact syndrome seen in athletes • a 2nd TBI while the 1st is NOT yet resolved

  14. Post-Concussion Syndrome • Characterized by: dizziness, disorientation, nausea, headache, fatigue • Also see decreased control of emotions and personality changes • Attention deficit usually present **If concussion lasts >2 minutes, patient should be kept under observation

  15. DIFFUSE AXON INJURY (DAI) • Severe and fatal head injuries • Widespread axonal damage • As a result of shear and tensile forces within the brain • Coma and decerebrate posturing • Poor prognosis • CT or MRI usually unremarkable

  16. CONTUSION • Coup-countercoup injuries • Can involve a small (mild) or large (severe) area • Most common in the frontal & temporal lobes • Lesion often enlarge during the first week after injuries

  17. HEMORRHAGE • Intracerebral hematoma • Subdural hematoma • Subarachnoid hemorrhage • Epidural hematoma

  18. Intracerebral hematoma • In brain parenchyma • hematoma may enlarge during the first few days after injury • Subdural hematoma • Beneath the dura • Acute or chronic (>2 wk) • Laceration of bridging • cortical veins during sudden head deceleration • A feature of shaken baby syndrome

  19. Subarachnoid hemorrhage • Poor prognosis if bleeding into ventricular system • Need to r/o aneurysm

  20. Epidural hematoma • In epidural space • Between dura mater & skull • Acute bleeding • Common in temporal bone fracture

  21. Severe TBI • Assess severity of brain injury • Acute surgical care: expanding mass lesion from increasing ICP • Address life-threatening injuries (ABC – airway, breathing, circulation) • Prevent complications • Preventative Rehab interventions

  22. GENERAL SYMPTOMS & SIGNS • Altered Level of Consciousness • Cognitive & Behavioral Deficits • Cranial Nerve Damages • Motor Deficits • Sensory Deficits

  23. Altered Level of Consciousness • Reduction in response to stimuli • Due to diffuse bilateral cerebral hemispheric damage or a lesion in the brainstem • Arousal is associated with wakefulness and depends on an intact reticular formation and upper brainstem • Coma rarely last > 4 wks • Coma is used to determine current status and prognosis

  24. Altered Level of Consciousness • Coma: state of unresponsiveness; not opening eyes • Persistent vegetative state or stupor: no evident cerebral cortical function; eye opening with sleep-wake cycles • Obtundity: decreased interest in the environment; slowed responses to stimulation; sleep more than normal; drowsiness between sleep states • Lethargy: severe drowsiness; aroused by moderate stimuli & then drift back to sleep • Confusion: disorientation, bewilderment, and difficulty following commands • Clouding: inattention & reduced wakefulness

  25. COGNITIVE IMPAIRMENT • Difficulties in: • Attention, concentration • Learning, memory • Abstract thinking, information processing • Problem solving • Initiation, executive functions • Inaccurate perception (leaning) • Deficits often remain despite a full return of consciousness

  26. MEMORY DEFICITS IN TBI Retrograde amnesia Loss of memory of events immediately preceding the injury Post-traumatic amnesia (PTA) (impaired anterograde memory) (50 first dates) Unable to recall events that occur after the injury Inability to form new memory No carryover or tasks requiring memory / learning Duration of PTA indicates the severity of injury

  27. BEHAVIORAL IMPAIRMENT • Mood disturbances including depression and anxiety • Symptoms depending on brain area involved • Inappropriate, excessive social behaviors • Inappropriate sexual behaviors • Irritability; rage; refuse to cooperate • Euphoria; involuntary laughing or crying • Apathy; indifference • Motor, sensory, verbal perserveration

  28. CRANIAL NERVE DAMAGE • Usually occur following focal damage in the brainstem or herniation • Disturbances in CN function • e.g. gaze and tracking deficits, diplopia, ptosis, facial sensory deficits, absent corneal reflex, hearing & vestibular dysfunction, cardiac irregularities, dysphagia, loss of gag reflex • CN dysfunction reflects level of lesion • Normal pupillary reflex (to light) indicates a lesion rostral to the midbrain

  29. MOTOR DEFICITS • Usually flaccidat onset • Increased tone, spasticity and rigidity developgradually • Decortical posturing • Hyperactive UE flexors • Hyperactive LE extensors • Decerebrate posturing • Hyperactive UE & LE extensors

  30. A. Decerebrate posturing • seen in cerebral hemisphere/white matter, internal capsule and thalamic lesions • B. Decortical posturing • seen with midbrain lesions/compression; also with cerebellar and posteria fossa lesions

  31. MOTOR DEFICITS • Monoplegia, hemiplegia • Abnormal reflexes (e.g. palmar grasp & Babinski reflex) • Abnormal balance reactions • Cerebellar and BG dysfunction: e.g. ataxia, dysmetria, tremor, bradykinesia SENSORY DEFICITS • Somatosensory dysfunction is determined by the brain area involved

  32. COMPLICATIONS • Increased intracranial pressure (ICP) • Heterotoptic ossification: • osteoclast destroy bone, so increase od Ca in blood, form boney spurs at joint. • DVT • Spasticity / Contracture • Decubitus ulcer (tuberosity) • Seizure

  33. INCREASED INTRACRANIAL PRESSURE (ICP) • Secondary complications develop over hours or days after the primary injury • Cause: swelling, fluid build-up in the brain & hematomas • Increased ICP compresses the brain within the rigid skull • Serious, life-threatening • ICP monitoring: • Medications • Fluid management • Decompressive craniectomy Lynda Yang http://www-personal.umich.edu/~chronis/ICP.html

  34. Cycle of Primary and Secondary Injury Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure

  35. HETEROTOPIC OSSIFICATION • Abnormal bone growth around a joint • Most commonly in hips, elbows, shoulders and knees • Onset 4-12 wk after injury • Diagnostic test • X-ray • Bone scan with increased uptake • Elevation of alkaline phospatase • Symptoms and signs • loss of ROM, tenderness, palpable mass, redness, swelling, pain with movement

  36. DIAGNOSIS OF TBI • History • Clinical exam • Imaging • Functional capacity

  37. HISTORY • Magnitude of injury • Altered consciousness and memory • witnessed • self-report • Duration of coma correlates with severity of injury

  38. CLINICAL EXAM • Evidence of trauma • Glasgow Coma Scale • Ranchos Los Amigos Cognitive Scale • Post-traumatic amnesia

  39. GLASGOW COMA SCALE • EYE OPENING SCORE • spontaneous E4 • to speech E3 • to pain E2 • none E1

  40. GLASGOW COMA SCALE • VERBAL RESPONSE SCORE • appropriate V5 • confused, disoriented V4 • inappropriate words V3 • unintelligible V2 • none V1

  41. GLASGOW COMA SCALE • MOTOR RESPONSE SCORE • Follows commands M6 • Localized (to pain) M5 • Generalized (to pain) M4 • Decorticate posturing (flexion) M3 • Decerebrate posturing (extension) M2 • None M1

  42. GLASGOW COMA SCALE • Most accurate early in course • >12 = Mild • 9-12 = Moderate • <8 for longer than 6 hours = severe • 3 = Dead

  43. RANCHO LOS AMIGOS COGNITIVE SCALE I. no response II. generalized response III. localized response IV. confused, agitated V. confused, inappropriate VI. confused, appropriate VII. automatic, appropriate VIII. purposeful, appropriate

  44. Diagnostic Imaging • CT • MRI • DTI • SPECT • PET

  45. Computed Tomography • Anatomic • Bone & brain tissue • Can see damage to gray matter • 1st line of imaging studies • Rapid (< 1 min for whole brain) • Less costly • Accessible (even with monitor, life-support equipment, or combative patient) • Best for skull fx, hemorrhage vs. edema, & intracerebral hemorrhage

  46. Computed Tomography • Abnormal findings in ~ 18% of patients without neurologic deficits • Severity of findings correlates with outcome • Not sensitive enough in detecting mild TBI (concussion) • May underestimate non-hemorrhagic lesion • May not show non-hemorrhagic parenchymal (neurons and glial cell) injuries

  47. M.R.I. • Anatomic • Most sensitive 24-48 hours after injury • Higher resolution than CT • Better for hemorrhagic contusions (after first 24 hours) • More sensitive than CT to diffuse axon injury • Scans > 6 months post-injury correlate with outcome • Disadvantage compared to CT • Duration of scan time, more costly • Not for combative patients

  48. Diffusion Tensor Imaging Neuroimaging that builds on MRI technology Study movement of fluid in the brain Detect damage in the white matter (axons) Axons are colored according to orientation

  49. Single Photon Emission Computed Tomography (S.P.E.C.T.) • Injection of a small amount of short-lived radioactive particles into the blood • Image of regional blood flow • More sensitive than MRI • Limited value in acute stage • Abnormal in many patients with normal neurologic exam, CT, and MRI • Poor image resolution • Not readily available

  50. Positron Emission Tomography Study metabolic activity and function Used in mild TBI

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