Head injury in the ed stabilization and medical management
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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

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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


Relevant anatomy

Relevant Anatomy


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


Head injury in the ed stabilization and medical management

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

  • 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

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