Closed Head Injuries in ChildrenWhere are we heading?

Carlos A. Delgado M.D. FAAP

Pediatric Emergency MedicineChildren’s Healthcare of Atlanta

Pediatric Emergency Medicine Associates (PEMA)

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Background

Trauma is a leading cause of death in children older than 1 year in the United States, with head trauma representing 80% or more of the injuries.

5% of head trauma cases, patients die at the site of the accident.

Head trauma has a high emotional, psychosocial, and economic impact • long hospital stays • 5-10% require discharge to a long-term care

facility.

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Anatomical differences with adults

The head is larger in proportion to the body surface area

Stability is dependent on the ligamentous rather than bony structure.

The pediatric brain has a higher water content, 88% versus 77% in adult, which makes the brain softer and more prone to acceleration-deceleration injury.

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The water content is inversely related to the myelinization process.

The unmyelinated brain is more susceptible to shear injuries.

Infants and young children tolerate intracranial pressure (ICP) increases better because of open sutures.

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Frequency

Head injury is estimated to occur in approximately 200 per 100,000 population per year.

The number includes all head injuries that resulted in hospitalization, death, or both in persons aged 0-19 years.

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Mortality/Morbidity

Mortality rate from head trauma is 29% in pediatrics.- death certificate data, -underestimation of actual rate.

Head injury represents 75-97% of pediatric trauma deaths.

Neurologic deficits: 10 - 20% of children with moderate-to-severe head injury (GCS 6-8) • have short-term memory problems • delayed response times, if coma longer than 3

weeks. More 50% with GCS 3-5 have permanent

neurologic deficits

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Age factor

At age 15 years, a dramatic increase occurs, mainly in males, related to their involvement in sports and driving activities.

Infants younger than 1 year have an elevated incidence of head trauma, due to falls and child abuse.

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Basilar skull fracture

In 6-14% of pts with head trauma- hx of a blow to the back of the head.

Loss of consciousness, seizures, and neurologic deficits may or may not be present.

Prolonged nausea, vomiting, and general malaise,• Fracture near the emesis and vestibular

brainstem centers. Battle sign, raccoon eyes, and CSF otorrhea and

rhinorrhea Ocular nerve entrapment - 1-10% of patients.

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Epidural hematoma

Between the skull and the dura and secondary to the laceration of an artery or vein

Epidural hematomas of arterial origin peak in size by 6-8 hours after the injury.

Epidural hematomas of venous origin may grow over 24 or more hours.

Common locations are the temporal, frontal, and occipital lobes.

An overlying skull fracture may be present. Classic lucid interval between the initial loss of

consciousness and subsequent neurologic deterioration- less frequent in the pediatric population.

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Epidural hematoma

Neurologic deterioration: • hemiparesis • unconsciousness• posturing• pupillary changes

Expansion of hematoma and exhaustion of compensatory mechanisms and compression of the temporal lobe and/or brain stem.

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Subdural hematoma

Between the dura and the cortex, subdural hematoma results from tearing of the bridging veins across the dura or laceration of the cortical arteries during acceleration-deceleration forces

Usually associated with severe parenchymal injury, and the presentation is that of profound and progressive neurologic deterioration.

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Subdural hematoma

Subdural hematoma may develop secondary to birth trauma

Shaken baby syndrome: • New-onset seizures • Increased head circumference• Failure to thrive• Tense fontanel. • Focal neurologic deficits usually absent.

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Subarachnoid hemorrhage

Most common form of hemorrhage associated with head trauma

Disruption of the small vessels on the cerebral cortex.

Location: falx cerebri or tentorium and the outer cortical surface.

Nausea, vomiting, headache, restlessness, fever, and nuchal rigidity - blood in the subarachnoid space.

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Diffuse axonal injury

Rapid acceleration-deceleration forces Disruption of the small axonal pathways. Basal ganglia, thalamus, deep hemispheric nuclei,

and corpus callosum. Altered mentation and often prolonged vegetative

state Abnormal neurologic examination findings and the

lack of findings on CT scanning. Small petechial hemorrhages may be present. Prognosis for full recovery often is poor.

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Cushing triad

Bradycardia Hypertension Alteration of respiration

Late manifestation indicative of herniation.

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Hypotension

Should not solely be attributed to intracranial hemorrhage.

Other causes: • internal hemorrhages• spinal cord injury• cardiac contusion• dysrhythmias with secondary impaired cardiac

output. Hypotension with bradycardia in a trauma patient

be suspicious of spinal cord injury.

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Causes

MVA- 27-37% of all pediatric head injuries. Children < 15 years, a pedestrian or a bicyclist

• children aged 5-9 years are the second most frequent cause of death.

15-19yo- passengers and alcohol is often a contributing factor.

Falls are the largest cause of injury in children < 4 years, contributing to 24% of all cases of head trauma.

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Closed head injuries – what’s common knowledge

Kids experiencing low altitude falls, fall from standing and/or weak mechanisms of injury rarely sustain intracranial injuries.

If asymptomatic after the injury and unchanged by the time of exam, the probability of an intracranial injury is low.

If initial Head CT is neg, the chances of unsuspected deterioration is also low.

Long-term outcomes for children with mild head injury, without of significant intracranial bleed, are generally very good, with only a small increase in risk for subtle specific deficits in particular cognitive skills.

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Epidemiology

Nonfatal injuries• 219 per 100,000 per year• 1.5 million head injuries- 20% sports related• 5-10k /100,000 ED visits per year • 1/10th require admission

Fatalities• 75% of trauma deaths involve brain injury• 30-60% fatality if hospitalized in coma

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Epidemiology of Pediatric Head Trauma

Trauma is the leading cause of death among children >1yr.

Traumatic brain injury (TBI) is the leading cause and disability due to trauma.

Annually in the U.S. blunt head trauma (BHT) results in:• 3,000 deaths• 50,000 hospitalizations• 650,000 ED visits (325,000 evaluated with CT

scans)CDC, 2002

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Epidemiology

Hospital admissions for most serious category of head injury increased 38% between 2001 and 2004.

2004 there where 204,000 hospitalizations for TBI • 65 and older – 36% of hospitalizations• 45- 64 yo – 18%• 18- 44 yo – 31%• Adolescents and children - 15%

13% of all admissions with TBI died while hospitalized

Agency for Healthcare Research and Quality (AHRQ) 4/24/2007

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Definitions

Current literature terms:• Head trauma• Traumatic brain injury• Closed head injury• Blunt head trauma• Head injury• Concussion

Traumatic brain injury (TBI): subset of pts with head trauma and an underlying brain injury detected by CT or also someone with trauma to the head without CT evidence of intracranial injury (ICI) but clinically symptomatic.

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Radiological evaluation of the patient with CHI

Skull films Head CT Neurosurgical consultation MRI

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Plain skull films

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What about skull films?

Limited role if no physical findings + skull fracture and no intracranial injury - skull fracture and intracranial injuries

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Skull films

It is still a good test for evaluating CHI’s Skull radiographs are 94-99% sensitive for

detecting linear or depressed skull fractures. CT imaging has a lower sensitivity, ranging from

47-94%

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Skull films

When would it be OK to order one?

Scalp hematoma over course of the middle meningeal artery

Children < 1yr of age with a scalp hematoma Suspected abuse

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Head CT

Use has skyrocketed in the past 10 yrs. Has become the gold standard in evaluation

children with CHI Newer faster scanners have reduced the need for

sedation Available 24/7 in most ED’s

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Controversy over CT for Minor BHT

Arguments for liberal use of CT:

Preventable morbidity/mortality due to unrecognized TBI’s

Preverbal children difficult to evaluate When indicated benefits of CT greatly outweigh risk

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Controversy over CT for Minor BHT

Arguments against liberal use of CT:

Of the 325,000 children evaluated with CT after BHT, ≤ 10 % have TBI

Drawbacks of CT include: transport outside the ED, pharmacological sedation, costs, etc.

Most important (theoretical) risk : • lethal malignancy risk from CT may be as high as

1:5000

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CT radiation risks

Helical CT scanners have enhanced diagnostic possibilities and reduced the need for sedation.

Radiation exposure, however, not reduced with helical CT

Radiation exposure with CT 300-600 times of a CXR.

Brenner, 2001,2002,Hall 2002, http:/cancer.gov,2002

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CT Radiation Risks

Estimates (theoretical, not observed) of risks of lethal malignancies extrapolated from survivors of WW II atomic explosions:• 1/2000 head CT scans for children younger

than 1 yr.• 1/5000 for 10 yo

Age and size based radiation reduction efforts are ongoing• 4/5th of CT studies in children are not managed

by pediatric radiologists.

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325,000 CT’s for BHT - 2.7 million total pediatric CT’s annually. CT radiation risks important public-health issue

There are about 600,000 abdominal and head CT examinations annually on children under age of 15.

It is therefore estimated that this could result in 500 deaths from cancer attributable to CT radiation.

Emergency Management

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Emergency Management

Major vs.. minor trauma

Mechanism of injury

Initial manifestations

Glasgow coma scores

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Acute management of CHI

Intervention Goal of Intervention

Supplemental oxygen PaO 2 >60 mm Hg, oxygen saturation >90%

Aggressively treat hypotension

Normal blood pressure

Avoid hyperthermia Normothermia

Minimize pain and stressful stimuli

Limit unnecessary oxygen consumption by brain

Consider rapid sequence intubation, sedation, paralysis

Limit patient stress

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Emergency Management

Low risk injuries• Children who present within 24 hours of the

injury with isolated mild HT and have a normal mental status at presentation, a normal neurologic exam, and no evidence of skull fracture on physical examination.

• Headache• Vomiting• Dizziness

Management• Discharge

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Emergency Management

Moderate risk

• Hx. of LOC• Progressive headache• Vomiting > 6hrs• Seizures• Amnesia• Associate injuries• Drug or alcohol intoxication• Suspected child abuse• Basilar skull fracture

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Emergency Management

Moderate risk injuries

Management• Observation for 4-6 hrs• CT scan• Neurosurgical consultation• Consider admission

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Emergency Management

High risk injuries

• Depressed level of consciousness• Penetrating injury• Depressed skull fracture• Focal neurologic exam

Management• Immediate neurosurgical consultation

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Emergency Management

Airway and c-spine immobilization Breathing Circulation Disability Exposure

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Emergency Management

Indications for intubation• Abnormal respiratory rate• Abnormal respiratory pattern• Loss of protective airway reflexes• Respiratory muscle dysfunction• Chest wall dysfunction• Intracranial hypertension GCS < 8• Prior to EMS transport to another facility in a

potentially unstable patient

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RSI for tracheal intubation of the head-injured patient

1. Preparation• Lidocaine: 1 mg/kg IV (max 50 mg)• Atropine: (i) <10 kg: 0.1 mg IV; (ii) >10 kg: 0.01

mg/kg IV (max 0.3 mg)

2. Induction • Hypnotic: Etomidate: 0.3 mg/kg IV• Paralytic agent: Rocuronium: 1 mg/kg IV

3. Posttracheal intubation sedation• Midazolam: 0.1 mg/kg IV (max 5 mg)

Fentanyl: 1-2 μg/kg IV

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Emergency Management

Circulation Isotonic fluid resuscitation 20cc/kg boluses Control of hemorrhage by direct pressure Maintain MAP > 70 to assure adequate CPP Pressor support when necessary Search for underlying cause of shock

• Intracranial bleed• Spinal shock• Thoracic or abdominal injury

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Emergency Management

Symptoms of increased ICP:• Headache • Vomiting• Meningismus• Irritability• Visual loss• Gait disturbance

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Emergency Management

Symptoms of increased ICP:• Altered level of consciousness• Papilledema• Cranial nerve palsy• Progressive hemiparesis• Head tilt• Posturing

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Hyperosmolar Therapy in TBI

Hypertonic saline (3%) at 0.1-1.0 ml/kg continuous infusion effective for controlling ICP

Mannitol also effective (0.25-1.0 g/kg) Dose-related reduction in

ICP Maintain euvolemia

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Treatment of elevated ICPnew alternatives

Hypertonic saline (7.45%) 255 mOsm single continuous infusion

Mannitol 20%

Both equally effective in decreasing ICP Mannitol may improve brain circulation by

improving blood rheology

Critical Care Med 2008 Mar;36(3):795-800

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Mannitol ↓ICP ↓Blood viscosity →↓Blood vessel diameter Maintain CBF at lower CBV Requires intact autoregulation Osmotic effect promotes shift of water from

parenchyma to circulation May accumulate in injured brain with reverse shifts May be benefit of intermittent boluses Children tolerate higher osm(365 mOsm) than

adults (320 mOsm)

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Hyperosmolar Therapy in TBIHypertonic saline

Low penetration across blood-brain barrier Similar rheologic, osmotic effects as mannitol

Restoration of cellular resting membrane potential Stimulation of ANP release Anti-inflammatory effects

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Studies needed:

Compare mannitol and hypertonic saline Long term neuro outcome Continuous vs bolus for ICP spikes Optimal dosing Safe thresholds Nephrotoxicity Rebound ICP Central pontine myelinolysis

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Treatment of elevated ICP

There is no evidence that barbiturate therapy in patients with acute severe head injury improves outcome.

Prophylactic anti-epileptics are effective in reducing early seizures, but there is no evidence that treatment with prophylactic anti-epileptics reduces the occurrence of late seizures, or has any effect on death and neurological disability.

Cochrane Database Syst Rev 2000, 2007

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Concussion(closed head injury without structural head injury)

Grade I - transient confusion, no LOC, symptoms last < than 15 mins.

Grade II - transient confusion, no LOC, symptoms last > 15 mins

Grade III - LOC

* I & II – mild traumatic brain injury (TBI)

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Return to Play Guidelines according to  Grade and Number of Concussions

(keep in mind asymptomatic means no headache, dizziness,  or impaired orientation, concentration, or memory during rest or exertion)

Grade I

1st Concussion:  May return to play if asymptomatic for 1 week

2nd Concussion:  Return to play in 2 weeks if asymptomatic at the time for 1 week

3rd Concussion:  Terminate season but may return to play next season if asymptomatic

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II

1st Concussion:  May return to after asymptomatic for 1 week

2nd Concussion:  Minimum of 1 month; may return to play then if asymptomatic for 1 week; however, consider terminating the season

3rd Concussion:  Terminate season but may return to play next season if asymptomatic

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III

1st Concussion:  Minimum of 1 month; may return to play if asymptomatic for 1 week

2nd Concussion:  Terminate Season; may return to play next season if asymptomatic

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Concussion

Grade I- return to play after 20 minutes Grade II- return to play after 1 week Grade III – return after 1 mo.

Cantu et al An overview of concussion consensus statements since 2000 Neurosurg focus 2006: 21(4): E10

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Post concussive syndrome

The most common significant sequelae to concussions.

Physical, emotional, cognitive symptoms that may persist more than a year.

Common signs include: decreased mental processing speed, decreased short term memory and attention span, irritability, fatigue, sleep disturbance, persistent headaches.

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Second impact syndrome

Most feared and potentially catastrophic consequence of concussions.

It is a second concussive injury that occurs before the initial concussion has completely resolved.

Caused by increased intracranial pressure due to loss of vascular auto regulation; may lead to herniation and death with even mild second injury to a symptomatic child.

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Future trends in concussion management

Interactive computerized assessment tools to evaluate concussion will evaluate most areas of the brain in a shorter period of time but will functionally test the athlete in a game-like situation without the risk of re-injury

Cost effective streamlined neuropsychological assessment.

Screen test to identify those populations w/ high susceptibility to concussion may protect those at increased risk.

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What to look for after a head injury

Normal signs in the first 2 days:• Fatigue and desire for extra sleep• Headache (mild)• Nausea and vomiting (occasional)• Problems thinking, concentrating, attention span

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Findings that need immediate medical attention

Marked change in personality- confusion, irritability Worsening headache associated with nausea and

vomiting Numbness, tingling or weakness of arms , legs,

changes in breathing patterns or seizure Eye and vision changes - double vision, blurred

vision unequal pupils

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New science-Evidence Based Medicine

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PECARN FINDINGS

The sequence of variables defining very low risk for clinically important outcome

Incorporating CT results into final rule.

The final rule/algorithm is on the way……

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PECARN Findings

PECARN, the Pediatric Emergency Applied Research Network, presented several important results from a head injury surveillance study with more than 43,000 patients.

Holmes et al. presented information on subsequent problems or deteriorations of 12,000 children <18 years with blunt head trauma and negative CTs.

Negative predictive value was 100% for ultimate need for neurosurgical intervention, with 6 subsequent positive findings on repeat scan which did not require intervention.11

PAS 2008 Hawaii

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TBI & Isolated headache or vomiting

P. Dayan reviewed the association of isolated headache (i-H) or isolated vomiting (i-V) with need for neurosurgical intervention in children who present with a GCS of 15.

42,995/43,490 patients were enrolled (77% ) Of 1228 patients with isolated vomiting, 3 patients

(0.2%) required intervention, one after one episode of vomiting, one after four episodes, and one for whom the number of episodes was not recorded. One 7 month old with isolated vomiting required neurosurgery, but he “had not been acting like himself” before presenting; the other fell 6-10 feet, had multiple episodes

PAS 2008 Hawaii

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Neither number of emesis episodes nor time duration were associated with positive findings.

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Isolated headache

2,796 patients had isolated headache, none of whom required neurosurgical intervention.

In the 22% with a head CT, 4 had signs of TBI. One 17 year old with a football injury from a helmet to helmet collision required hospitalization for two days, but no surgery.

Two of the patients with TBI had diffuse headache, and none had headache only at the site of injury.

Conclusion: Children with i-V and i-HA after BHT, the risk of TBI on CT is low, and the risk of TBI requiring intervention is very low.

 PAS 2008 Hawaii

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Blunt Head Trauma in ChildrenHistorical factors

History of LOC (+/- amnesia)

Most controversial historical finding

Common (30-50% of pediatric BHT)• Reliability of history? • Accuracy of report of

duration? • Amnesia in pre-verbal

children?

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Isolated LOC

Risks with isolated loss of consciousness (LOC) Of 790 pts with a history of i-LOC, only 4 had TBI on CT and 1 (0.1%, 95% CI: 0, 0.7%) required acute intervention ( evacuation of an epidural hematoma). This patient, complained of headache not documented on the case report form, vomiting in the ED, and a scalp hematoma on CT.

For patients with any LOC (N=6847) versus those with no LOC (N=34,746), TBI requiring acute intervention was required for 438 (6.4%) versus 195 (0.6%).

The authors concluded that TBI occurs more often in children with a history of LOC, but in the absence of other signs or symptoms the risk of TBI is very small.13

PAS 2008 Hawaii

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PECARN variables for predicting low risk for clinically important outcome

Age ≥ 2 No altered MS ( GCS 15) No headache except for mild headache at site of

injury No emesis No LOC No basilar skull fracture No severe mechanism of injury- ejection, rollover,

high impact, projectiles etc

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PECARN variables for predicting low risk for clinically important outcome

Age < 2 No altered MS ( GCS 15) No or just frontal scalp hematoma No LOC >5 secs No severe mechanism of injury- ejection, rollover,

high impact, projectiles No palpable skull fracture No seizure No emesis No signs of scalp trauma if younger than 3 mo.

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Blunt Head Trauma in ChildrenPhysical Examination

Decreased level of consciousness• GCS

Definition varies GCS ≥13? ≥14? 15?

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Activity Best response Score

Eye opening Spontaneous 4

To speech 3

To pain 2

None 1

Verbal Oriented* (coos,babbles)

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Confused* (irritable cries)

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Inappropriate words* (cries to pain)

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Nonspecific sounds* (moans to pain)

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None 1

Motor Normal spontaneous movements 6

Localizes pain* (withdraws to touch)

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Withdraws to pain 4

Abnormal flexion-decorticate rigidity 3

Abnormal extension-decerebrate rigidity 2

None 1

Glasgow Coma Scale Score*modified for infants

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Infant Face Scale.

Eye opening

Spontaneously 4

To verbal stimulation or to touch 3

To pain 2

No response 1

Verbal/facial response

Cries (grimaces with crying sounds and/or tears) spontaneously, with handling, or to minor pain; alternating with periods of quiet wakefulness when not asleep

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Cries (grimaces with crying sounds and/or tears) spontaneously, with handling, or to minor pain; alternating with sleep only (no quiet wakefulness maintained)

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Cries to deep pain only 3

Grimaces only to pain (facial movement without sounds or tears) 2

No facial expression to pain 1

Motor

Spontaneous normal movements 6

Spontaneous normal movements reduced in frequency or excursion; hypoactive 5

Nonspecific movement to deep pain only 4

Abnormal rhythmic spontaneous movements; seizure-like activity 3

Extension, either spontaneous or to painful stimuli 2

Flaccid 1

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Blunt Head trauma in ChildrenPhysical Examination

Decreased level of consciousness:

Risk of TBI if GCS is = 15 is 2-3% Risk of TBI if GCS is =14 is 7-8% Risk of TBI if GCS is = 13 is 25% !!!

GCS is an important predictor in multivariate analyses

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Blunt Head trauma in ChildrenPhysical Examination

Clinical evidence of skull fracture :

~ 20 % of children with basilar skull fracture and GCS =15 have TBI

Signs of depressed skull fracture is highly associated with TBI

In multivariate analyses, signs of basilar skull fx and also signs/presence of any skull fx is highly associated with TBI.

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Prevention

Follow return to play guidelines• Child with symptoms should never return to play• Follow a step-wise return to play

Insist in protective gear usage• Helmets, face shields• Equipment should be worn properly and

replaced when damaged. Adhere to rules of the sport, play fair and smart. Follow safe sport techniques Follow up with PCP after any head injury

• Neuropsychological testing

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Future trends in concussion management

Interactive computerized assessment tools to evaluate concussion will evaluate most areas of the brain in a shorter period of time but will functionally test the athlete in a game-like situation without the risk of re-injury

Cost effective streamlined neuropsychological assessment.

Screen test to identify those populations w/ high susceptibility to concussion may protect those at increased risk.

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So what is the current research leading us to?

We must be cautious and aware of radiation exposure in children

We need to make sure our institutions are using pediatric appropriate doses of radiation

Headache, vomiting, GCS <13, and skull fracture may be better predictors of TBI than LOC without other findings.

Continued multicenter research in this subject may bring new light in decision making for children that present with blunt head trauma.

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Summary

Pediatric head trauma is an important public health issue associated with significant morbidity and mortality,

Higher rate of occult ICI in infants requires a lower threshold for obtaining head CT in this age group.

24-48 hrs of close observation is essential for all children with head trauma either at home or inpatient.

Remember to consider child abuse as possible mechanism of head injury in children < 2 yrs of age.

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