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Head Trauma

Outline

• Epidemiology
• Injuries
• Assessment
• Management
  • Cerebral Perfusion Pressure
• Intracranial Pressure
  • Monro-Kellie Doctrine (Manifest Destiny ... not)
• Summary
• Seizure Management
• Review of Secondary Injury Prevention
• Outcome
• Prevention
• References

Epidemiology

• Incidence:
  • 200/100,000 children per year
  • Higher in spring and summer, weekends and afternoons
• Etiologies
  • falls from heights
  • motor vehicle accidents
  • sports and recreational injuries
  • acts of violence
  • 25% of head injuries in children <2 years of age are inflicted
  • interchild violence is becoming more common
• Severity
  • Mild 82% (GCS > 12)
  • Moderate to severe 14% (Moderate: 12 > GCS >8; Severe GCS £ 8)
  • Fatal 5%

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Injuries:

Primary (frequently there are components of both of the following)

• Impact (the head striking a surface)
  • scalp bleeding
  • skull fractures
  • closed
  • open
  • depressed
  • epidural hematomas
    • where the impact disrupts a dural vessel
    • leading to blood accumulation in the epidural space
  • Brain contusions and Lacerations
  • Subgaleal Hematoma
    • potential space outside periosteum, can lead to large hemorrhage and hemodynamic compromise can occur even with minor trauma
• Inertial (violent motion inside the skull)
  • subdurals
  • disruption of blood vessels feeding the arachnoid
  • concussion
  • diffuse axonal injuries
  • most common cause of prolonged coma

Neck Injuries

• sciwra - spinal cord injury without radiological abnormality
• even with normal c-spine films. The flexibility of the neck in childhood, and the large head on a relatively weak neck can result in neck and cervical spine injuries despite normal films. MRI or other cord imaging techniques should be considered when the history is suggestive of severe head and neck trauma.

Secondary Injuries (are due to the following and therefore are potentially limitable)

• hypoxia
• hypotension
• brain swelling/edema
• infarction
• delayed hemorrhage
• pressure necrosis
• herniation

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Assessment

In addition to evaluation of injuries, an important component of management of Head Trauma involves assessment of neurologic status. The Glasgow Coma Scale (GCS) and Modified GCS for Children are the most commonly applied tools for assessment. The score is the sum of scores for the best response in each category, giving a scale from 3-15.

Glasgow Coma Scale		Children's Memorial GCS Modification
Activity/Best Response	Score	Activity/Best Response	Score
Eye Opening		Eye Opening
Spontaneous	4	Spontaneous	4
To Verbal Stimuli	3	To Speech	3
To pain	2	To pain	2
None	1	No response	1
Verbal		Best Motor
Oriented	5	Spontaneous (obeys commands)	6
Confused	4	Localizes Pain	5
Inappropriate Words	3	Withdraws to pain	4
Nonspecific Sounds	2	decorticate posture to pain (flexion)	3
None	1	decerebrate posture to pain (extension)	2
Motor		No response	1
Follows Commands	6	Best Verbal Response
Localizes Pain	5	Oriented (Social Smile, orients, follows)	5
Withdraws to pain	4	Confused/disoriented (consolable)	4
Flexion to pain	3	Inappropriate words/cries	3
Extension to pain	2	Incomprehensible sounds or agitation	2
None	1	None	1

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Management

Goal: to minimize secondary injuries by prevention of the items listed above.

Before we move on to discussion of the individual items above we will review the basics of Head Trauma management

Priorities:

1. Airway
2. Breathing
3. Circulation

Always remember: if your patient is not breathing, and/or does not have a heart beat, it doesn't matter what the extent of other injuries are, they are not going to survive without rapid assessment and intervention.

Issues of ABC's particular to Head Trauma patients:

Airway:

• high association of spinal cord injury with severe head trauma
• maintain head in "sniffing" position for intubation
• SCIWRA - spinal cord injury without radiographic abnormalities is an emerging entity, don't be lulled into complacency by spine films
• frequently have associated facial injuries and or basilar skull fracture
• avoid nasal intubation (including NG placement)
• airway manipulation will commonly cause spikes in ICP
• premedication with Atropine (0.02mg/kg), Pentothal or Versed, Lidocaine (1mg/kg) and muscle relaxants can minimize the ICP spikes

Breathing:

• one of our most powerful tools in emergent ICP management is PCO2
• hyperventilation will be discussed in the next section

Circulation:

• Frequently patients with head trauma will have associated other injuries, often includingsignificant blood loss, leading towards shock. As with any patient in shock aggressive fluid management is necessary.
• Your goal is to achieve euvolemia. As will be discussed in the next section, maintenance of thepatients blood pressure is especially important in managing patients with severe head trauma
• Episodes of Hypotension and Hypoxia are associated with increased morbidity and mortality in patients with severe head trauma. By aggressively addressing the ABC's one can attempt to minimize the occurrence of these events.

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Cerebral Perfusion Pressure

CPP = MAP - ICP

Where MAP is the mean arterial pressure

ICP is the intracranial pressure

Cerebral Blood flow is highly dependent on cerebral perfusion pressure. The brain autoregulates to maintain stable CBF at pressures between 50 and 150mmHg. As the perfusion pressure falls below the numbers listed below the blood flow to the brain drops off rapidly and therefore the metabolic demands of the brain go un-met.

Goal CPP's

Mean Arterial Pressure

MAP = COxSVR

Where

• CO is cardiac output
• SVR is systemic vascular resistance
• CO = HR x Stroke Volume
• SV is a function of preload, contractility and afterload (SVR)

To Increase MAP:

• increase CO
  • increase heart rate (chronotropic medications)
  • increase preload (volume)
  • increase contractility (inotropic medications)
• increase SVR
  • vasopressor medications (epinephrine, dopamine, phenylephrine)

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Intracranial Pressure

To understand ICP and it's management there are several concepts that one must first understand.

The head as a closed box

Total volume inside calvarium =

VBrain + Vblood + VCerebrospinal fluid + Vother = constant (in patient with closed fontanel)

Monro-Kellie Doctrine (Manifest Destiny ... not)

a change in one compartment must be balanced by a change in another i.e. if the volume of blood in the brain increases the volume of brain or spinal fluid must decrease to maintain the volume.

VBrain - brain volume increases with swelling and edema

• Edema
  • vasogenic (common around tumors, uncommon in trauma)
  • cytotoxic (secondary to cell injury - common in trauma)
  • interstitial (due to increased CSF hydrostatic pressure)
• Management
  • fluid restriction, but maintain euvolemia (see MAP discussion)
  • hyperosmolar therapy
    • mannitol 0.25-1gm/kg/dose
      • make sure patients have been adequately volume resuscitated first
      • recent evidence suggests using prn for increased ICP, not as scheduled med
    • hypertonic saline (also increases osms)
  • Steroids - ONLY BENEFICIAL IN VASOGENIC EDEMA, they have not been shown to be of any benefit in trauma

Vblood

cerebral blood flow is fairly constant with perfusion pressure in the 50-150 range

Factors that influence CBF

• perfusion pressure (see discussion on CPP)
• pCO2 - cerebral blood vessels are very sensitive to pCO2
  • hyperventilation
    • decreases CBF to both normal and injured brain
    • can be source for further injury by decreasing blood flow
    • current views:
      • hyperventilation is not recommended in the early stages of increased ICP except aggressive hyperventilation (pCO2 <30) for episodes of acute IICP
• cerebral metabolic rate (CMRO2)
  • hypothermia/fever control
    • mild hypothermia and preventing fever is helpful, no evidence of deep hypothermia being of benefit (at or below 32oC is too cold)
  • sedation/analgesia
    • pain, noxious stimuli increase ICP
    • benzodiazepines and narcotics are recommended to prevent spikes
  • seizure control (will be discussed later)
    • seizures increase ICP and metabolic rate, important to gain control
    • pentobarbital coma
    • last resort, decreased metabolic rate but no study to show improvement of outcome causes significant hemodynamic instability
    • versed coma has also been used with fewer side effects
• cerebral oxygen delivery
  • hypoxia causes vasodilation increasing CBF and increasing ICP
  • profound hypoxia causes injury
  • maintain adequate oxygenation

VCerebrospinal fluid

• ventriculostomy - gold standard for ICP monitoring and CSF removal
• other methods include: intraparenchymal monitor, subarachnoid, subdural (bolt) and epidural
• none of which are as reliable as the ventriculostomy
• Controversial as to whether removal of CSF is of benefit, as CSF production can increase to replace losses, increased ICP may act with negative feedback to decrease production

Vother

• in the case of trauma this is usually hematoma
• optimal management would therefore be evacuation
• When to Monitor ICP?
  • When GCS <8, and
  • clinical evidence of elevated ICP
    • from physical exam
    • CT evidence
    • Operating Room observation
  • There is increasing debate as to whether monitoring itself changes outcome, as opposed to aggressive management of presumptive increased ICP

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Summary:

To decrease ICP

• fluid restrict (but not below euvolemia)
• hyperosmolar therapy
• avoid hyperventilation
• save both hyperosmolar and hyperventilation therapy for acute spikes in ICP
• minimize metabolic demands by
  • preventing fever, keep slightly cool
  • pain control/sedation
  • control seizures
• monitor ICP with ventriculostomy if possible, also drain CSF as possible
• evacuate hematomas if compromising pressure

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Seizure Management

As many as 9% of patients have a generalized tonic-clonic seizure after severe head trauma. Seizures increase metabolic demand and can result in hypoxemia and hypercarbia in patients worsening ICP. For this reason aggressive early management is important. Seizures are more common in patients with penetrating injuries or parenchymal bleeds.

For patients with seizures:

• immediate control with rapid acting benzodiazepine
• diazepam (Valium) 0.1mg/kg IV, or
• lorazepam (Ativan) 0.1mg/kg IV
• Then load with Dilantin (20mg/kg total dose)

For patients without seizures:

• because of risk associated with seizures, prophylaxis is recommended for all patients with severe head trauma who are comatose, after hemodynamic stability is achieved.
• Dilantin 20mg/kg load recommended
• this is preferred over phenobarb because it has less respiratory depression and less effect on the patient's level of consciousness

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Review of Secondary Injury Prevention

We stated earlier that the following list is responsible for a majority of the preventable injury following severe head trauma. Now we can look at them with regard to cerebral perfusion pressure management principles

Secondary Injuries

Hypoxia:

• effect: causes local vasodilation which increases Vblood and therefore increases ICP,decreasing CPP
• management goals:
  • maintain O2 delivery
  • adequate Hgb, goal usually 9-10gm/dl if needing to transfuse. getting above 12 may
  • cause viscosity problems
  • supplemental O2

Hypotension

• effect: decreases CPP, therefore decreases cerebral blood flow
• management goals:
  • euvolemia
  • fluid resuscitate as needed, goal to not overly hydrate
  • inotropes other mechanisms to increase BP, Dopamine, epinephrine, dobutamine

Brain Swelling/Edema (Vbrain)

• effect: increases Vbrain, increasing ICP and decreasing CPP
• management goals:
  • minimize edema as outlined earlier

Infarction

• effect: tissue damages causes inflammation, cytotoxin release, can increase metabolic demand, alter blood flow, changing CPP
• management goals:
  • maintain CPP

Delayed Hemorrhage

• effect: increases Vother by formation of epidural, subdural hematomas. This increases ICP, causing decreased CPP
• management goals:
  • monitor neuro status for acute changes
  • monitor coagulation status, try to normalize coags to avoid bleed
  • early recognition and intervention are key

Pressure Necrosis

• effect: causes loss of brain parenchyma due to increased ICP and decreased CPP, especially in local areas
• management goals:
  • decrease ICP as outlined earlier

Herniation

• effect: death due to compression of brain stem and loss of autonomic function
• management goals:
  • close neurologic monitoring and intervention
  • monitoring pupils
  • acute changes in neurologic status (pupil change, posturing, etc.) must be met by
  • hyperventilation (now keep pCO < 30)
  • hyperosmolar therapy - stat dose of Mannitol 1gm/kg
  • other intervention to decrease ICP

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Outcome

neurological sequelae

• motor deficits
  • spasticity, incoordination and ataxia are most common
  • feeding difficulties
  • dysphagia, GER
• sensory deficits
  • vary depending on injury, any cranial nerve can be involved
  • hearing and vision should be formally tested
  • communication
  • both speech (motor) and language (cognitive) deficits are common
• cognitive
  • directly related to severity of trauma
  • don't sustain as complete recovery as from motor deficits
• behavioral
  • personality changes related to lack of control are common

Predictors of neurologic deficits:

• 20% of mild brain injury have some deficit
• 90-100% of moderate to severe will have deficit
• related to:
  • duration of coma (longer is worse)
  • focal injuries are worse
  • secondary brain injuries (diffuse swelling has high incidence of deficits)
  • epidurals evacuated early have good recovery
  • insidious subdurals that are not recognized early have high incidence of deficits

Seizures

• 2-9% of children will have seizures following trauma
• risk factors:
  • brain contusion/hematoma (particularly subdural)
  • diffuse cerebral edema
  • GCS < or = 12
• may not have seizures in initial period after trauma
• most (95%) will develop them within 3 years of injury

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Prevention

All head trauma is potentially preventable

• Falls from heights
  • protective environment
  • child safe playgrounds
  • use of gates by stairs
  • minimize use of walkers
• Motor vehicle accidents
  • use of helmets by bicyclists
  • (88% reduction in head injury in Seattle)
  • use of car seats
  • pedestrian education
  • driver education
  • better car design
• Assault
  • limitation of gun availability
  • education about shaken babies

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References:

See the excellent on-line chapter in the All-Net PICU Text Book

Noah ZL, et al "Management of the Child with Severe Brain Injury." Critical Care Clinics 8(1): 59-77. January 1992

• Reviews the basics of initial and ICU management of patients with severe brain injury.

Michaud LJ, et al. "Traumatic Brain Injury in Children." Pediatric Clinics of North America 40 (3): 553-565. June 1993.

• Written from a rehabilitation standpoint, has nice summary of the types of injuries and prognosis. a large amount of the epidemiology in this handout was taken from this paper.

Temkin NR, Dikmen SS and Winn HR. "Post-Traumatic Seizures." Neurosurgery Clinics of NorthAmerica 2(2): 425-435. April 1991.

• An excellent review of the literature of post-traumatic seizures. Looks more at efforts to prevent long term seizures, which unfortunately seems unfruitful.

Levin HS. "Head Trauma." Current Opinion in Neurology 1993 6: 841-6.

• A concise review of the gamut of head injury both in pediatrics and adults. Has an excellent summary of the literature in the resource section.

Chestnut RM, Prough DS eds. Critical Care of Severe Head Injury. New Horizons 3 (3): 365-593.

• A very comprehensive review of the most recent research on almost every aspect of head trauma from bench work to clinical practice.

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This page is meant for educational purposes only, questions or comments regarding the contents should be directed to the author at: tegtm001@gold.tc.umn.edu

This page last updated 7/21/98 for format, 3/97 for content