Head Injury in the ED: Stabilization and Medical Management - PowerPoint PPT Presentation

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Head Injury in the ED: Stabilization and Medical Management

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... Skull Fracture (4) Skull Fracture (5) Intracerebral Hemorrhage (6) Contusion (7) Diffuse Axonal Injury Stabilization and Management: ... – PowerPoint PPT presentation

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Title: Head Injury in the ED: Stabilization and Medical Management


1
Head Injury in the EDStabilization and Medical
Management
  • AKA Oh crap, I start Neurosurg next week
  • - Amy Gillis, PGY-2

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.co
m
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 lt/ 8) 10 / 40
    mortality
  • Considerable variations in care remain
  • We have the principle role in preventing
    secondary insults

5
Important Physiology
  • CBF CPP
  • CPP MAP ICP
  • MAP (SBP) 2(DBP)/3
  • Normal ICP 0-10mmHg

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
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

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 gt 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 lt 2 and adults gt 60
  • Blood between the skull and dura
  • Middle meningeal artery (MMA) gt 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
  • Battles 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
  • gt 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 gt 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 ManagementAirwayBreathing
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 lt/ 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
  • (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

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

26
C is for Circulation
  • BP lt 90 mmHg led to 150 increase in mortality
  • Recommendations
  • CPP gt 70 mmHg
  • MAP gt/ 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
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

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). Boyds Burr Holes

29
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

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.in anaesthesia.co.in_at_gmail.co
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