Traumatic Brain Injuries

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Vernon Richard
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1 Traumatic Brain Injuries Scott P. Sherry, MS, PA-C, FCCM Assistant Professor Department of Surgery Division of Trauma, Critical Care and Acute Care Surgery DISCLOSURES Nothing to disclose Discussion of off label medication use Objectives Overview of the cerebral anatomy Description of the epidemiology of TBI Understand and describe different types of TBI Understand and describe management strategies of patients with suspected or known traumatic brain injury including intercranial hypertension Understand prognosis in the TBI patient 1

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3 Meningeal Anatomy Review 3

4 Traumatic Brain Injury 500,000 cases each year in the US 10% die before reaching medical care Severity: 80% mild 10% moderate 10% severe Broad injury pattern Concussion, DAI, SAH, SDH, IPH, IVH, EDH Head Injury Epidemiology Trauma mortality: 40 % secondary to brain injury Overall mortality: 7-36 % (head injury alone) Annual mortality: 100,000 Head Injury Disability Survivors of TBI and permanent disability: 10 % of those with a mild injury 66 % of those with a moderate injury ~100 % of those with a severe injury 90,000 newly disabled per year For those who survive gunshot wounds: 10 % have severe disabilities 20 % have moderate disabilities 4

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6 Traumatic SAH Scattered appearance Has a risk of vasospasm Less incidence than aneurysmal SAH Pedestrian Struck: SDH, SAH Fall from Car: IPH, SDH, SAH 6

7 Epidural Hematoma Usually an arterial injury Has a classic presentation DO NOT MISS THIS Lens shaped appearance to lesion Suture attachments Urgent surgical intervention is warranted Temporal bone fx with middle menigeal artery Generally good recovery with prompt intervention Epidural Hemorrhage Epidural Hemorrhage 7

8 Epidural Hemorrhage Epidural Hemorrhage Epidural Hemorrhage 8

9 Epidural Hemorrhage Epidural Hemorrhage 9

10 Subdural Hematoma Venous injury generally Bridging Veins Crescent shaped lesion Follows subdural tact Has attachment points at the front / back. Some are acute, chronic and acute on chronic bleeds Most common traumatic mass effect lesion Subdural Hematoma Subdural Hematoma 10

11 Subdural Hematoma Subdural Hematoma Subdural Hematoma 11

12 Subdural Hematoma Subdural Hematoma Subdural Hematoma 12

13 Subdural Hematoma Subdural Hematoma Subdural Hematoma 13

14 Subdural Hematoma Subdural Hematoma Subdural Hematoma 14

15 Motor Vehicle Crash: SDH Unwitnessed Fall: SDH Fall from Barstool: IPH, SDH 15

Pedestrian Struck: IPH, SDH Diffuse Axonal Injury Active

Frequently without radiographic abnormality Frequently

this latter finding usually occurs at the grey-white

16 Pedestrian Struck: IPH, SDH Diffuse Axonal Injury Active process triggered by the injury that takes about 24 hours Frequently without radiographic abnormality Frequently seen in areas of radiographically apparent shear injury this latter finding usually occurs at the grey-white junction MRI is diagnostic Major cause of long-term disability 16

17 MVC: IPH, DAI, IVH, SAH Thalamic Bleed Cerebral Edema 17

18 MVC: IPH, DAI, IVH, SAH Assault: IPH PedestrianStruck: IPH 18

19 ATV Crash: Skull Fx, ICH 19

20 Found Down Suspected Fall 20

21 Found Down 21

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29 (BONE) 29

30 (BONE) (BONE) (BONE) 30

31 (BONE) (BONE) (BONE) 31

32 (BONE) (BONE) (BONE) 32

33 (BONE) (BONE) (BONE) 33

34 (BONE) (BONE) Shot Gun Wounds 34

35 Prehospital Care High index of suspicion Trauma Center Transport Immediate Prevention of secondary insults Hypoxia / Hypotension Immediate CT Any LOC Amnesia to event If e/otbi Hospital Care Neurosurgical Consult Prompt transfer if needed Frequent neuro checks 35

PREVENT Secondary Injury Hypoxia and hypotension 2 major causes of secondary CNS injury following head trauma These complications occur frequently Prevention could have the greatest effect of any

36 PREVENT Secondary Injury Hypoxia and hypotension 2 major causes of secondary CNS injury following head trauma These complications occur frequently Prevention could have the greatest effect of any currently available treatment for head trauma Outcome from Severe Brain Injury Univariate predictors of poor outcome: ICP > 25 mm Hg MAP < 70 mm Hg or CPP < 60 mm Hg and fluid balance < -594 ml Clifton et al. Crit Care Med 2002;30:

37 Increased Intracranial Pressure Monroe Kellie Volume of the skull is a constant Brain ~ 85% Blood ~5% CSF ~ 10% An increase in the volume of any of these will raise ICP 37

38 Important Formulas Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure Intercranial Pressure Goal CPP > ~ 60 Guidelines = 50-70mm Hg Increased Intracranial Pressure Management Correct the underlying pathophysiology if possible Airway control and prevention of hypercapnea are crucial Posture and head position ICP monitoring Avoid jugular vein compression Head in neutral position with body Head of bed elevated > 30 deg Cervical collars loose or remove No circumferential ETT Tape Increased Intracranial Pressure Hyperventilation (PaCO2 < 35 mmhg) Works by decreasing blood flow should be reserved for emergency treatment and only for brief periods. Avoid Severe Hyperventilation < 30 38

Increased Intracranial Pressure Pharmacologic options Mannitol 1G / KG Follow up doses 0.

4% Lasix/ Diuretics Increased Intracranial Pressure Sedation and Analgesia Opiods

39 Increased Intracranial Pressure Pharmacologic options Mannitol 1G / KG Follow up doses gm/kg q4h Follow Serum OSM < 320 Hypertonic Saline 3% 7.5% 23.4% Lasix/ Diuretics Increased Intracranial Pressure Sedation and Analgesia Opiods Benzodiazepines Propofol Decrease cerebral metabolic rate, which is coupled to blood flow Prevent hyperthermia 39

40 Increased Intracranial Pressure Neuromuscular junction blockade Titrate with train-of-four stimulator to 1 or 2 twitches High-dose barbiturates E.g., pentobarbital 5 12 mg/kg load followed by infusion to control ICP Risk of infection Slide 118 Increased Intracranial Pressure Surgical options Resect mass lesions if possible Ventriculostomy Drainage Craniectomy Lateral for focal lesions Bifrontal(Kjellberg) for diffuse swelling Slide

CCM April 2013 Recovery - Trajectory Emergence of conscious awareness Recovery of higher processing Return of functional capacity Recovery from

41 CCM April 2013 Recovery - Trajectory Emergence of conscious awareness Recovery of higher processing Return of functional capacity Recovery from COMA Vegetative state Minimally conscious state Emergence from minimally conscious state Functional communication Object use Time course variable 41

Natural History of VS / MCS Not well studied 50% MCS / 3% VS had no or mod disabilities when evaluated after 1 year of injury More rapid improvement in the traumatically injured After recovery of

42 Natural History of VS / MCS Not well studied 50% MCS / 3% VS had no or mod disabilities when evaluated after 1 year of injury More rapid improvement in the traumatically injured After recovery of awareness May have significant neurologic impairments Motor, dystonic, movement disorders, aphasia. Attention, mood, memory, seizure disorders Organ Donation Treat all traumatic brain injuries to the fullest extent Potential for good outcomes is unknown Good prehospital care = good outcomes Good prehospital care with bad outcomes can lead to good outcomes for others Organ donation 42

43 Summary Recognize life threatening neurological problems early and have a high degree of suspicion Intubate for GCS < 8 Treat ICP elevations > 20 aggressively Prevention is KEY You can t get back what you loose 43

PRACTICE GUIDELINE. DEFINITIONS: Mild head injury: Glasgow Coma Scale* (GCS) score Moderate head injury: GCS 9-12 Severe head injury: GCS 3-8

PRACTICE GUIDELINE. DEFINITIONS: Mild head injury: Glasgow Coma Scale* (GCS) score Moderate head injury: GCS 9-12 Severe head injury: GCS 3-8 PRACTICE GUIDELINE Effective Date: 9-1-2012 Manual Reference: Deaconess Trauma Services TITLE: TRAUMATIC BRAIN INJURY GUIDELINE OBJECTIVE: To provide practice management guidelines for traumatic brain