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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 </= 8): 10% / 40% mortality

  • 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


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 </= 8

  • 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 nausea, vomiting, focal weakness or paresthesias or other focal neuro signs

  • 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 nausea, vomiting, focal weakness or paresthesias or other focal neuro signs

“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 nausea, vomiting, focal weakness or paresthesias or other focal neuro signs

  • 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 nausea, vomiting, focal weakness or paresthesias or other focal neuro signs

  • 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 nausea, vomiting, focal weakness or paresthesias or other focal neuro signs

  • 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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