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TBI CME for postgraduate students teaching
- 1. PRESENTER : DRJOANNE QUAY SUPERVISOR : PROF. DATO’ DR MOHD BASRI MAT NOR 1
- 2. OUTLINE • INTRODUCTION • DEFINITIONOF TBI • CLASSIFICATIONS OF TBI • PATHOPHYSIOLOGY • ICU MANAGEMENT 2
- 3. INTRODUCTION • Traumatic braininjury (TBI) is a leading cause of death and disability worldwide • Many survivors live with significant disabilities resulting in major socioeconomic burden and a greater economic toll. • In Malaysia, TBI was deemed as one of the top 3 common admissions reported in ICU • National Trauma Database Malaysia 2009 reported - 80% of traumas were caused by road traffic accidents • 64% of these cases - related to TBI. 3
- 4. DEFINITION • Traumatic braininjury (TBI) is an alteration in brain function, or other evidence of brain pathology, caused by an external force • Outcome of severe TBI ~ 30% risk of death, 5-15% discharged in vegetative state. • Moderate TBI ~ 15% mortality, only 20% back to functioning baseline • Patients in specialized neuro- intensive care units with guideline-driven protocols are associated with better outcomes 4
- 5. CLASSIFICATION OF TBI Theseverity of TBI according to the GCS score (within 48 h): Mild TBI = 14-15 Moderate TBI = 9-13 Severe TBI = <9 *Confounding factors: - Drugs/intoxication - Other Injuries - Hearing impairment - Intubation - Language barrier - Underlying mental impairment 5
- 6. CLASSIFICATION OF TBI FullOutline of UnResponsiveness (FOUR) Score A. EYE RESPONSE 4 eyelids open or opened, tracking, or blinking to command 3 eyelids open but not tracking 2 eyelids closed but open to loud voice 1 eyelids closed but open to pain 0 eyelids remain closed with pain B. MOTOR RESPONSE 4 thumbs-up, fist, or peace sign 3 localizing to pain 2 flexion response to pain 1 extension response to pain 0 no response to pain or generalized myoclonus status 6
- 7. C. BRAINSTEM REFLEXES •4 pupil and corneal reflexes present • 3 one pupil wide and fixed • 2 pupil or corneal reflexes absent • 1 pupil and corneal reflexes absent • 0 absent pupil, corneal, and cough reflex D. RESPIRATION • 4 not intubated, regular breathing pattern • 3 not intubated, Cheyne–Stokes breathing pattern • 2 not intubated, irregular breathing • 1 breathes above ventilator rate • 0 breathes at ventilator rate or apnea 7
- 8. CLASSIFICATION OF TBI NEUROIMAGING TheMarshall scale 8
- 9. CLASSIFICATION OF TBI TheRotterdam scale Prognosis Mortality at 6 months increases with the score : • score 1: 0% • score 2: 7% • score 3: 16% • score 4: 26% • score 5: 53% • score 6: 61% 9
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- 11. PATHOPHYSIOLOGY Primary Injury CT scanshowing DAI. Deep shearing-type injury near the white matter of the left internal capsule CT scan depicting cerebral contusions at basal frontal areas 11
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- 14. Physiological and CellularChanges Associated Secondary Brain Injury • - Primary injury exhausts the compensatory capacity of the brain - Leads to increase in ICP (Monroe - Kelly doctrine) - Results in cerebral ischemia and hypoxia • Inflammation and local tissue damage cause excessive release of excitatory neurotransmitters, resulting in calcium influx to cells, cell edema and death 14
- 15. • Dying cellsrelease mediators (platlet activating factor, leukotrienes, o2 free radicals) --> affecting blood vessel permeability--> vasogenic fluid accumulation --> increasing ICP --> hypoperfusion, cerebral ischemia and neurodegeneration • These can lead to neuronal cell death as well as to cerebral edema and increased ICP that can further exacerbate the brain injury. • Critical aspect of ameliorating secondary brain injury after TBI is the avoidance of secondary brain insults 15
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- 19. Acute Management ofTBI • Prehospital management for moderate and severe TBI is prevention and treatment of hypotension and hypoxia • The injured brain is especially vulnerable to secondary insults in the first 24 hours. • Hypoxia (PaO2 <60 mmHg) and Hypotension (SBP <90 mmHg) were present in 50 and 30 % of patients • Associated with a higher likelihood of a poor outcome 19
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- 21. WHEN TO DOCT BRAIN ? 21
- 22. INDICATION FOR SURGERY •Epidural hematoma – Surgical guidelines recommend evacuation of an epidural hematoma (EDH) larger than 30 mL in volume regardless of a patient's GCS score • Subdural hematoma – Acute subdural hematomas (SDHs) >10 mm in thickness or associated with midline shift >5 mm • Intracerebral hemorrhage – Surgical evacuation of a traumatic intracerebral hemorrhage (ICH) in the posterior fossa when there is evidence of significant mass effect • Depressed skull fracture – Elevation and debridement for open skull fractures depressed greater than the thickness of the cranium or if there is dural penetration, significant intracranial hematoma, frontal sinus involvement 22
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- 25. Treatments Decompressive Craniectomy Prophylactic Hypothermia HyperosmolarTheraphy Cebebrospinal Fluid Drainage Ventilation Theraphies Anaesthetics, Analgesics and Sedatives Steroids Nutrition Infection Prophylaxis Deep Vein Thrombosis Prophylaxis Seizure Prophylaxis Monitoring Intracranial Presue Cerebral Perfusion Pressure Advanced Cerebral Monitoring Thresholds Blood Pressure Intracranial Pressure Cerebral Perfusion Pressure Advanced Cerebral Monitoring 25
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- 31. WHEN IS ICPMONITORING INDICATED? 31
- 32. ICP MONITORING 4 mainanatomic sites used in the clinical measurement of ICP: • Intraventricular • Intraparenchymal • Subarachnoid • Epidural 32
- 33. METHODS ADVANTAGES DISADVANTAGES ExternalVentricular Drainage Gold standard Accurate Simple measurement Allow treatment of some cause of elevated ICP Infection – 20% of patient Hemorrhage during placement Intraparenchymal Ease of placement Lower risk of infection and hemorrhage - <1% Inability to drain CSF Greater risk of mechanical failure due to complexity Subarachnoid Less invasive Lower risk of infection and hemorrhage Clog with debris cause unreliable measurement Less accurate Epidural Used in management of coagulopathic patients with hepatic encephalopathy complicated with cerebral edema Low risk of intracerebral Hemorrhage Inaccurate 33
- 34. ICP MONITORING ANDWAVE INTERPRETATION 34
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- 36. ADMISSION AND INITIALMANAGEMENT 36
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- 39. Background: Current guidelinesfor the treatment of adult severe traumatic brain injury (sTBI) consist of high-quality evidence reports, but not accompanied by management protocols Results: established three distinct treatment protocols, each with three tiers whereby higher tiers involve therapies with higher risk 39
- 40. MANAGEMENT OF SEVERETBI GUIDED BY INTRACRANIAL PRESSURE AND BRAIN TISSUE OXYGEN A combination of the two parameters creates a matrix of four potential clinical conditions No Level I evidence that supports the use of brain tissue oxygen monitoring, the phase II BOOST2 trial demonstrated that a protocol guided by ICP and PbtO2 could reduce brain hypoxia 40
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- 42. SUMMARY Recommendation Justification Blood pressureSBP ≥100 mmHg- patients 50 to 69 years old ≥110 mmHg for patients 15 to 49 or >70 years old Cerebral perfusion pressure CPP of 60 to 70 mmHg ICP < 22 mmHg Ventilation PaO2 >60 mmHg Avoid PaCO2 <30 mmHg Temperature management Avoid temperature > 38 °C Antiseizure medication Prophylactic AEDs for 1 week 42
- 43. SUMMARY Recommendation Justification Glucose managementBlood sugar 6-10.0 mmol/L Nutritional support Establish early enteral feeding within 5-7 days Sedation and analgesia RASS of -4 to -5 , when ICP elevated RASS of 0 to -2 when ICP controlled Glucocorticoids Harmful according to CRASH trial ICP and CPP monitoring ICP should be monitored in all salvageable patients with a severe TBI and abnormal CT scan 43
- 44. • CRASH 3trial - the use of tranexamic acid in TBI patients with GCS <13 or with any intracranial bleeding on CT within 3 hours of injury. • Reduction in the risk of head injury-related death in patients treated with tranexamic acid, which almost reached statistical significance. • Administration of 1 gram of tranexamic acid as a bolus, followed by 1 gram of tranexamic acid infused over 8 hours 44
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- 46. PROPHYLACTIC HYPOTHERMIA POLAR andEurotherm3235 Study 46
- 47. DECOMPRESSIVE CRANIECTOMY Conclusion fromDECRA and RESCUEicp : Decompressive craniectomy for patients with traumatic brain injury improved survival, while increasing the likelihood of poor neurological outcomes. RESCUEicp DECRA 47
- 48. REFERENCES • Hawryluk, GregoryW J et al. “A management algorithm for patients with intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury ConsensusConference (SIBICC).” Intensive care medicine vol. 45,12 (2019): 1783- 1794.doi:10.1007/s00134-019-05805-9 • Chesnut, Randall et al. “A management algorithm for adult patients with both brain oxygen and intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC) • UpToDate - Traumatic brain injury: Epidemiology, classification, and pathophysiology • UpToDate - Management of acute moderate and severe traumatic brain injury • UpToDate – Anesthesia for patients with acute traumatic brain injury • UpToDate – Evaluation and management of elevated intracranial pressure in adults • BTF. Guidelines for the Management of Severe Traumatic Brain Injury.4th Ed. 2016 48
- 49. SBA A 27-year-old manis admitted with a severe traumatic brain injury following a road-traffic collision. He has sustained a large subdural haematoma and undergoes prompt surgical evacuation. Post-operatively, he is transferred, intubated and sedated to the intensive care unit, with an intracranial pressure monitor inserted. Which of the following is most likely to be associated with an improved clinical outcome from traumatic brain injury? A. A cerebral perfusion pressure of greater than 75 mmHg B. Induced hypothermia C. High-dose steroids D. Prophylactic thiopentone infusion E. Normoglycaemia 49
- 50. SBA A 27-year-old manis admitted with a severe traumatic brain injury following a road-traffic collision. He has sustained a large subdural haematoma and undergoes prompt surgical evacuation. Post-operatively, he is transferred, intubated and sedated to the intensive care unit, with an intracranial pressure monitor inserted. Which of the following is most likely to be associated with an improved clinical outcome from traumatic brain injury? A. A cerebral perfusion pressure of greater than 75 mmHg B. Induced hypothermia C. High-dose steroids D. Prophylactic thiopentone infusion E. Normoglycaemia 50
- 51. SBA 5 days agoa 25-year-old woman suffered a traumatic brain injury. Despite a normal CT, she demonstrated bilateral motor posturing. She therefore had an intracranial pressure (ICP) bolt inserted shortly after admission in order to monitor her ICP. You begin your morning review by analysing her ICP waveform. Which of the following would concern you most acutely? A Lundberg A waves B A flat trace C A baseline value of 20mmHg D Lundberg B waves E The most prominent upstroke being the P2 (tidal) wave 51
- 52. SBA 5 days agoa 25-year-old woman su!ered a traumatic brain injury. Despite a normal CT, she demonstrated bilateral motor posturing. She therefore had an intracranial pressure (ICP) bolt inserted shortly after admission in order to monitor her ICP. You begin your morning review by analysing her ICP waveform. Which of the following would concern you most acutely? A Lundberg A waves B A flat trace C A baseline value of 20mmHg D Lundberg B waves E The most prominent upstroke being the P2 (tidal) wave 52
- 53. SBA A 26-year-old gentlemanis admitted to the emergency department with a closed traumatic brain injury following a road traffic collision. On application of a painful central stimulus, his eyes remain closed, he extends his left arm and he makes incomprehensible sounds. Computed tomography (CT) of the head reveals a large left-sided fronto-parietal contusion with obvious midline shift. Which of the following would be the most appropriate initial interventions, after intubation and ventilation? A. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg, and active cooling to a core temperature of 34 °C B. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), insertion of an intracranial pressure monitor and maintenance of a cerebral perfusion pressure of 60 mmHg C. Aim for a PaCO2 of 4.5 kPa (33.7mmHg) and maintenance of a mean arterial pressure of 100 mmHg D. Aim for a PaCO2 of 4.0 kPa (30mmHg) and maintenance of a mean arterial pressure of 80 mmHg E. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg and administration of high-dose intravenous methylprednisolone 53
- 54. SBA A 26-year-old gentlemanis admitted to the emergency department with a closed traumatic brain injury following a road traffic collision. On application of a painful central stimulus, his eyes remain closed, he extends his left arm and he makes incomprehensible sounds. Computed tomography (CT) of the head reveals a large left-sided fronto-parietal contusion with obvious midline shift. Which of the following would be the most appropriate initial interventions, after intubation and ventilation? A. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg, and active cooling to a core temperature of 34 °C B. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), insertion of an intracranial pressure monitor and maintenance of a cerebral perfusion pressure of 60 mmHg C. Aim for a PaCO2 of 4.5 kPa (33.7mmHg) and maintenance of a mean arterial pressure of 100 mmHg D. Aim for a PaCO2 of 4.0 kPa (30mmHg) and maintenance of a mean arterial pressure of 80 mmHg E. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg and administration of high-dose intravenous methylprednisolone 54
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