Traumatic Brain Injury

Transcription

1 General Information Traumatic Brain Injury What you need to know Complicated condition with high variability in etiology, severity, distribution of injury, and pattern of functional impairment (Klyce, Graham, Lacey, & Carter, 2018) 75%-90% of traumatic brain injuries are mild traumatic brain injury (DynaMed Plus, 2018) leading causes of traumatic brain injury include falls 28% motor vehicle accidents 20% struck by/against something 19% assaults 11% Suspect head trauma in pt w/: Otorrhea or rhinorrhea Raccoon eyes or battles sign AMS, HA, and/or vomiting Traumatic Brain Injury What happens during the traumatic event? $45 billion yearly in U.S. 1.4 million victims a year 235k rehabilitated 50k die Resultant effects of TBI include Cerebral edema Ischemia/hypoxia Metabolic dysfunction Apoptosis (El Sayed, Zaki, Fayed, Shehata, & Abdelmonem, 2018) irregular interior surface of skull damages fragile brain tissue during acceleration/deceleration/shearing forces direct mechanical trauma can injure cortical tissue traumatic hematomas can damage subcortical structures and lead to vasospasm and ischemia Cellular injury diffuse axonal injury anoxic contusion hemorrhagic perfusion-reperfusion Basilar Skull fracture 1

2 Basilar Skull Fracture Any fracture found at the base of the skull Temporal bone most likely involved 1 in 3 have CSF leak Hemotympanum Halo sign Conductive hearing loss, anosmia, nystagmus, and vomiting Anything else to worry about? Risks associated with TBI Depression Suicide Pituitary dysfunction Chronic Traumatic Encephalopathy Permanent cognitive dysfunction Brain Herniation Death 2

3 Concussion/Mild TBI Concussion/Mild TBI Type of TBI with a short-lived neurologic impairment, with or without loss of consciousness, which resolves without intervention Rapid onset of short-lived neurologic impairment, resolves spontaneously. S/S may evolve over minutes to hours and may be prolonged Initially: immobilize c-spine Activity restriction until sx resolution Hospital admission if: GCS < 15 CSF leak Vomiting Intoxication Athletes should not return to competition until sx resolution both at rest and with activity Post-concussion sx may last for months For patient being discharged- instruct caregiver to monitor closely for hours for: Focal neurologic change Seizure LOC > 30 sec Inability to arouse Consussion For boys and girls in same sports, who do you think has more concussions? Girls! For those playing American football, who has more concussions, high school students or college students? High school! Rate of Concussion/1000 (DynaMed Plus, 2018) American football Girls' soccer 0.36 Boys' lacrosse Boys' soccer 0.22 Girls' basketball 0.21 Wrestling 0.18 Girls' lacrosse Softball 0.07 Boys' basketball 0.07 Boys' and girls' volleyball 0.05 Baseball

4 Concussion Sx (DynaMed Plus, 2018) LOC in < 10%, but HA in most Feel like in a fog Problems with attention/concentration/memory/processing Impaired judgment Emotionally labile Symptom presentation may be delayed for several hours after concussive event Concussion Assessment Sport Concussion Assessment Tool SCAT3, 2013 Moderate/Severe TBI Characterized by any period of observed neurologic dysfunction or confusion, disorientation, change in consciousness, or amnesia (DynaMed Plus, 2018) Best GCS < 13 Abnormal imaging LOC > 30 minutes and/or AMS > 24 hours Post-traumatic amnesia > 1 day May be caused by blunt trauma, acceleration or deceleration forces, or exposure to blast. 4

5 Moderate or Severe Grading Outcome- Glasgow Outcome Score Chronic Traumatic Encephalopathy (CTE) CTE Defined as 1 perivascular phosphorylated tau (ptau) lesion consisting of ptau aggregates in neurons, astrocytes, and cell processes around small blood vessel (DynaMed Plus, 2018) incidence of CTE by highest level of play 0 of 2 pre-high school players 3 of 14 (21%) high school players 48 of 53 (91%) college players 9 of 14 (64%) semiprofessional players 117 of 119 (98%) professional players clinical features in last year of life in 111 men with CTE cognitive symptoms in 93% behavioral or mood symptoms in 91% dementia in 72% motor symptoms in 68% most common cause of death was neurodegenerative among players with severe CTE (62 of 133 players; 47%) and suicide among players with mild CTE (12 of 44 players; 27%) 5

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7 Initial Management TBI Interventions for high ICP Prioritize and stabilize ABC Cervical spine Severe TBI should always be at facility with neurosurgical service ICP monitoring Reduce in-hospital and 2-week post injury mortality ICP above 22 mm Hg are associated with increased mortality Target CPP attempts to maintain CPP > 70 mm Hg with fluids and pressors risk of adult respiratory failure EEG CSF drainage Hyperventilation Not recommended! Hypothermia No statistical advantage over normothermia Hyperbaric oxygen Showed improved mortality versus standard treatment (p= 0.48, NNT 4) Improved GCS (p = 0.024, NNT 3) Increased brain tissue partial pressure of oxygen (p < ) Decreased ICP (p < ) (DynaMed Plus, 2018) Hypothermia (Ahmed, Bullock, & Dietrich, 2016) Short term cooling (24-48 hours) does not improve outcome in TBI Long term hypothermia may be of benefit Cooling should be done with a well described clinical pathway Rewarming should be gradual rather than abrupt 7

8 Other management Drugs Nutrition Seizure ppx Glucose control Decompressive craniectomy Multi-disciplinary rehab Methylphenidate Succinylcholine Neuromuscular blockers Propofol Mannitol Hypertonic saline 3% or 23.4 % Phenytoin Botox Amantadine Drugs Cerebrolysin- neuro protectant Designed to reverse or prevent cerebral edema, ischemia/hypoxia, metabolic dysfunction, & apoptosis In studies, improved cognition was achieved (p < 0.001) (El Sayed, Zaki, Fayed, Shehata, & Abdelmonem, 2018) Citicoline and Piracetam Mild, moderate, or severe? Image taken from m/ 8

9 Drugs Glyburide Patients assigned to receive 10 mg daily or placebo (w/in 10 hours of injury) Reviewed CT imaging baseline, day 3, and day 7 Those on glyburide showed significantly smaller expansions/rate (Khalili, et al., 2017) ETOH Motor impairment at level of 80 mg/dl Balance and coordination affected at 100 mg/dl Levels > 200 can lead to amnesia or coma Several cognitive impairments ETOH post TBI 9

10 ETOH and TBI ETOH and TBI ETOH has high correlation to TBI Increased risk of injury As high as 51% incidence of ETOH for those with TBI (Klyce, Graham, Lacey, & Carter, 2018) Increased complication during acute treatment (Klyce, Graham, Lacey, & Carter, 2018) Maladjustment in chronic phase of recovery (rehab) Variability of individual response to ETOH make it difficult to predict course of recovery Pt w/ hx of ETOH misuse place them at risk for W/D Common sx include nausea, autonomic arousal, confusion, disoriented, agitated, HA, and sensory disturbances (Klyce, Graham, Lacey, & Carter, 2018) Sx may start within the first 24 hours, and can last up to a week depending on severity and duration of abuse After the TBI, ETOH may: May reduce cerebral blood flow By-products decrease cap membrane stability (Mathias & Osborn, 2018) Increased duration of neuro-inflammatory changes Could ETOH be good? The Evidence Delayed apoptosis Inhibit excitotoxicity Reduce systemic and neuro inflammatory response Lower rate of glucose metabolism at site of contusion Conflicting Meta-analysis by Mathias & Osborn (2018) Cognitive impact Psychological impact ICU LOS Mortality 10

11 ETOH W/D and TBI recovery Often benzodiazepines are administered for safety, including securing airway or protecting spine ETOH level on admission Institute CIWA protocol Study on moderate to severe TBI pts with regards to ETOH w/d and impact on recovery Groups split into TBI + CIWA tx (n=67) or TBI tx alone (n=167) DRS scores not significantly differed on admission 9.6 vs (p=.540), but were significantly different at discharge 6.4 vs. 7 (p = 0.05) (Klyce, Graham, Lacey, & Carter, 2018) 11