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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 [email protected] 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

Head Injury in the ED:Stabilization and Medical Management

AKA “Oh crap, I start Neurosurg next week”

- Amy Gillis, PGY-2

[email protected]

objectives
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
why bother
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)
why bother1
Why Bother?
  • Minor head trauma (GCS 13-15): 80%
  • Moderate head trauma (GCS 9-12): 10% / 20% mortality
  • Severe head trauma (GCS
  • Considerable variations in care remain
  • We have the principle role in preventing *secondary* insults
important physiology
CBF ~ CPP

CPP = MAP – ICP

MAP = [(SBP) + 2(DBP)]/3

Normal ICP = 0-10mmHg

Important Physiology
important physiology1
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

important physiology2
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
types of injury
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
1 traumatic sah
(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
2 acute subdural hematoma
(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
3 epidural hematoma
(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
4 skull fracture
(4) Skull Fracture
  • Significant #:
  • Overlying vaculature  hematoma
  • Depressed #
  • Basal Skull #
  • Open #
  • Intracranial Air
4 skull fracture1
(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”
4 skull fracture2
(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
4 skull fracture3
(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
4 skull fracture4
(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
5 intracerebral hemorrhage
(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
6 contusion
(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
7 diffuse axonal injury
(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
slide21
Stabilization and Management:AirwayBreathing and CirculationTreatment of Elevated ICPMedical Management and Complications
airway
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
  • GCS 9-12 may be more difficult and indications are unclear
  • Must use clinical judgement, weigh risks and benefits
airway1
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)
airway2
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
b is for breathing
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
c is for circulation
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
increased icp
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
treatment of increased icp
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
medical management and complications
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
references
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
references1
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
references2
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

[email protected]

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