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Head Injury in the ED: Stabilization and Medical Management

Head Injury in the ED: Stabilization and Medical Management. AKA “Oh crap, I start Neurosurg next week” - Amy Gillis, PGY-2. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Objectives. Discuss moderate and severe blunt head injury Adult population (over 18) Epidemiology and importance

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Head Injury in the ED: Stabilization and Medical Management

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  1. Head Injury in the ED:Stabilization and Medical Management AKA “Oh crap, I start Neurosurg next week” - Amy Gillis, PGY-2 www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. Objectives • Discuss moderate and severe blunt head injury • Adult population (over 18) • Epidemiology and importance • Review relevant physiology and anatomy • Review types of injury (1o , 2o, tSAH, SDH, EDH, Skull #, ICH, Contusion, DAI) • No specifics of clinical presentation • Airway management • B and C • Treatment of elevated ICP • Medical management and complications • To survive Neurosurgery

  3. Why Bother? • Most likely to result in long-term disability • 3rd leading cause of injury admission in Canada • In Alberta in 1997/98: • 227 deaths (51 in CHA) • 17% of all injury deaths • 2694 were admitted (324 in CHA) • 11, 981 visited the ED (2024 in CHA)

  4. Why Bother? • Minor head trauma (GCS 13-15): 80% • Moderate head trauma (GCS 9-12): 10% / 20% mortality • Severe head trauma (GCS </= 8): 10% / 40% mortality • Considerable variations in care remain • We have the principle role in preventing *secondary* insults

  5. CBF ~ CPP CPP = MAP – ICP MAP = [(SBP) + 2(DBP)]/3 Normal ICP = 0-10mmHg Important Physiology

  6. Important Physiology Autoregulation (2)“CBF at 100% when MAP/CPP is 50-150 mmHg” • ability to maintain a constant CBF via constriction or dilation in response to MAP, O2, CO2, viscosity (3)head injured patients lose autoregulatory abilities

  7. Important Physiology • Eucapnia allows normal CBF • CO2 causes vasodilation and increased CBF • CO2 causes vasoconstriction, ischemia, decreased • CBF and ICP • O2 causes vasodilation, increased ICP and vasogenic • edema

  8. Primary The initial, “irreversible” mechanical injury: lacerations intracerebral hemorrhage contusions avulsion *Secondary* Further insults that ultimately lead to ischemia: hypotension* hypoxia* anemia* seizures hyperglycemia hyperthermia Types of Injury

  9. Relevant Anatomy

  10. (1) Traumatic SAH • Most common – 30-40% • Blood within the CSF and • subarachnoid (SA) space • Tearing of small SA vessels • Blood is related to GCS and outcome • Blood often seen in the basilar • cisterns, interhemispheric fissures • and sulci • Vasospasm very rare • Surgical: Case to case • Prognosis: Case to case

  11. (2) Acute Subdural Hematoma • 30% of head injuries • Forceful acceleration-deceleration injuries • Blood between the dura and brain • Arterial > venous • Hyperdense, crescent shaped, extend beyond suture lines • Quick clinical course • Surgical: Consider assoc parenchymal injury, thickness (mm, #cuts), ? basal cisterns, ? ventricular effacement, ? shift • Prognosis: 60-80% mortality

  12. (3) Epidural Hematoma • 0.5-1% of head injuries • Rare in kids < 2 and adults > 60 • Blood between the skull and dura • Middle meningeal artery (MMA) > dural sinuses, veins, # line • “Classic” LOC then ‘lucid’ (30%) • Rapid symptomatology • 80% associated with skull # • 40% have other intracranial badness • Surgical: Usually immediate, may observe • Prognosis: Very good

  13. (4) Skull Fracture • Significant #: • Overlying vaculature  hematoma • Depressed # • Basal Skull # • Open # • Intracranial Air

  14. (4) Skull Fracture • Linear Skull Fracture • Entire skull thickness • Temporoparietal, frontal, occiptal • Significant if they cross the middle meningeal groove or major venous dural sinuses and lead to EDH • Usually 3mm wide; widest at midportion, narrowest at ends • Can be comminuted • Surgical: If cosmetic • Prognosis: “Who cares”

  15. (4) Skull Fracture • Depressed Skull Fracture • Predispose to significant IC injury • Predispose to complications (sz, inf) • Direct impact (hammer, bat) • Parietal, temporal regions • Caution on palpation • Depression may be distal to laceration • Swelling may mask • 25% report LOC • CT scan for history or exam findings • Admit for observation • Surgical: Elevation if cosmetic, significantly below skull table • Prognosis: Very good

  16. (4) Skull Fracture • Basal Skull Fracture • 20% of head injuries • 50% associated with IC injury • Clinical Signs (50% of cases): • Hemotympanum – # temporal bone; bleed into middle ear • Rhinorrhea/Otorrhea - # causes a dural tear; communication with SA space, paranasal sinuses and middle ear • Battle’s sign – disrupt bones of auricular area • Racoon eyes – orbital roof #, blood stains periorbital fat, no swelling, well demarcated • CN palsies – compression/entrapment of CN of basal foramina, direct nerve damage • Treatment: No abx • Surgical: “If gaping holes exist” • Prognosis: Death if damage to internal carotid, sphenoid bone; otherwise good

  17. (4) Skull Fracture • Open # Intracranial Air • Scalp laceration overlies a # • If dura disrupted, communication exists to the brain • Also includes # through paranasal sinuses and middle ear • Surgical: Careful irrigation and • debridement, otherwise nothing • Prognosis: Good

  18. (5) Intracerebral Hemorrhage • Formed deep within the brain • Caused by tensile and shearing forces; brain vs. cranium • Subsequent stretch and tear of deep arterioles • Most often frontal and temporal • > 50% sustain LOC at impact • Often causes increased ICP • Surgical: Usually none, evacuation if significant hematoma • Prognosis: 45% mortality if unconscious in ED

  19. (6) Contusion • From parenchymal vessel damage • Scattered petechial hemorrhage + edema  widespread  further • hemorrhage and swelling • Problematic mass, compression, ischemia, necrosis, cavitation • Often delayed in clinical presentation • Surgical: Usually none, evacuation if significant hematoma • Prognosis: Good to poor

  20. (7) Diffuse Axonal Injury • 44% of primary lesions in severe head injury • Cause of traumatic coma not caused by mass lesions or ischemic foci • Shear and tensile forces with additional disruption of cortical physiology and microanatomy • Severity determined by clinical course: • (1) Mild DAI – Coma for 6-24 hours; initial posturing; mortality 15% • (2) Moderate DAI – Most common; coma > 24 hours; initial posturing; amnesia; cognitive deficits; 25% mortality • (3) Severe DAI – Prolonged coma; demonstrate persistent brainstem and autonomic dysfxn; vegetative state or death

  21. Stabilization and Management:AirwayBreathing and CirculationTreatment of Elevated ICPMedical Management and Complications

  22. Airway • Specific Indications for Intubation • Optimize oxygenation and ventilation • Declining LOC • Unable to protect airway • Risk to ICP from agitation, lack of cooperation • To control the situation • GCS </= 8 • GCS 9-12 may be more difficult and indications are unclear • Must use clinical judgement, weigh risks and benefits

  23. Airway • Rapid sequence intubation (RSI) is always required • Your patient may have altered mental status, but they are not anesthetised • Drugs chosen to optimize cerebral and cardiac hemodynamic parameters • There is significant in ICP with airway stimulation (laryngoscopy and intubation)

  24. Airway *blunt SNS/airway response *attenuate SNS/maintain BP *defasciculate *decreases ICP/maintains MAP* * “/ “/minimal cardiac effects *decreases ICP/caution with BP *clinically insignificant effects on ICP • (A) Pretreat • Lidocaine 1.5-2 mg/kg IV • Fentanyl 3-5 µ/kg IV • Rocuronium 0.1mg/kg • (B) Induction • Thiopental 3-5 mg/kg IV* • Etomidate 0.3 mg/kg IV • Propofol 0.5-1 mg/kg IV • (C) Paralysis • Succinylcholine 1.5 mg/kg

  25. Cerebral O2 delivery is threatened by loss of autoregulation Hypoxemia* causes a significant increase in mortality PO2 < 60 mmHg causes ICP Want 100% O2 Prophylactic hyperventilation is bad Ventilate to CO2 of 35-45 mmHg B is for Breathing

  26. C is for Circulation • BP < 90 mmHg* led to 150% increase in mortality • Recommendations: • CPP > 70 mmHg • MAP >/= 90 mmHg • SBP ~ 120 – 140 mmHg • Assumes ICP threshold of 20 mmHg • Crystalloid to restore intravascular volume • Prevent anemia*; transfuse to a HCT of 30-33% • Consider pressors only as a temporizing measure • Art line, CVP, foley

  27. General signs of ICP include H/A, dizziness, LOC, nausea, vomiting, focal weakness or paresthesias or other focal neuro signs In this population, more significant, ominous signs include: Acute change in mental status Cushing Reflex Asymmetrical pupils Contralateral paralysis ICP is well above 20 mmHg Increased ICP

  28. Treatment of Increased ICP • 1). Elevated HOB to 30o • 2). Align neck (allows maximum jugular venous outflow) • 3). Hyperventilation to CO2 of 28-35 mmHg; brief • intervention • 4). Mannitol (0.75-1g/kg IV) reduces cerebral volume • “Use in active herniation” • Contraindicated in shock • 5). Lasix • 6). Boyd’s Burr Holes

  29. Seizure Prophylaxis “Only for those with a witnessed seizure (on scene or in the ED)” Phenytoin loaded at 18mg/kg Hyperglycemia Worsens outcomes Hyperthermia Increases O2 demand; hypothermia considered an effective means of managing ICP Medical complications 1) DIC – present in 90% of severe head injury 2) Neurogenic pulmonary edema  ARDS 3) ECG changes – present in 50% of patients; SVT, ST depression, large upright or deeply inverted t waves, prolonged QT and U waves Medical Management and Complications

  30. References • Bulger EM et al: Management of severe head injury: Institutional variations in care and effect on outcome. Critical Care Medicine 30(8): 1870-1876, 2002 • Chesnut R: The management of severe traumatic brain injury. Emergency Medicine Clinics of North America 15(3): 581-605, 1997 • Craen RA, Gelb AW: The anesthetic management of neurosurgical emergencies. 39(5): R29-R34, 1992 • Garner AA, Schoettker P: Efficacy of pre-hospital interventions for the management of severe blunt head injury. 33(4): 329-337, 2002 • Goh KYC, Ahuja A, Walkden SB, Poon WS: Is routine computed tomographic (CT) scanning necessary in suspected basal skull fractures? 28(5): 353-357, 1997

  31. References • Kramer DA, Richman M, Schnieder SM: Traumatic brain injury: State-of-the-art protocols for evaluation, management, and resuscitation. Emergency Medicine Reports: www.emronline.com, 1998 • Kraus JJ, Metzler MD, Coplin WM: Critical care issues in stroke and subarachnoid hemorrhage. Neurological Research 24(S1): S47-S57, 2002 • Marik P, Chen K, Varon J, Fromm R, Sternbach GL: Management of increased intracranial pressure: A review for clinicians. The Journal of Emergency Medicine 17(4): 711-719, 1999 • Paterakis K et al: Outcome of patients with diffuse axonal injury: The significance and prognostic value of MRI in the acute phase. The Journal of Trauma 49(6): 1071-1075, 2000

  32. References • Rosen: Section II – System Injuries – Head: 287-314 • Samii M, Tatagiba M: Skull base trauma: Diagnosis and management. Neurological Research 24: 147-156, 2002 • Stieg PE, Kase CS: Intracranial hemorrhage: Diagnosis and emergency management. Neurologic Clinics 16(2): 373-390, 1998 • Tintinalli: Chapter 247 – Head Injury www.anaesthesia.co.inanaesthesia.co.in@gmail.com

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