1 / 32

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

sofia
Télécharger la présentation

Head Injury in the ED: Stabilization and Medical Management

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related