Minor Head Injury In Children Larry Kleiner Medical Director, Dept of Neurosurgery The Children's Medical Center

Head Trauma

Definition of Mild head injury Glasgow Coma Scale simple reproducible functional valid predicteur Prejudice against children doesn’t account for asymetry prejudice against facial injury/intubation doesn’t account for brainstem reflexes

Eye opening: spontaneous 4 to sound 3 to pain 2 none 1 Modification of the GCS

Modification of the GCS Verbalization Appropriate for age5 –fixes and follows –social smile cries but consolable 4 persistent irritability3 restless,lethargy2 none1

Modification of the GCS Motor Response Spontaneous6 localizes to pain5 withdraws4 decorticate3 decerebrate2 none1

Modification of GCS Glasgow-Liege Scale –includes brainstem reflexes –increases prediction of outcome from 76% to 90% with a.9 confidence level

Modification of the GCS Brainstem reflexes/scoring the GLCS fronto-orbicluar 5 vertical-oculocephalics 4 pupillary reaction to light 3 horizontal-oculocephalics 2 oculo-cardiac 1 none 0

Epidemiology 7-8 million “head injuries”/year million/year with LOC/amnesia - 80% considered minor

Trauma: leading cause of death age 1-19 head injury direct cause in 30-50% major factor in 75% in MVA’s: 75% have head injuries 20% have spinal cord injuries

Epidemiology Head injury overview: 1:10 has loss of consciousness ,00 hospitalizations/year 4,000 deaths/year 15-20,000 prolonged hospitalizations/year

Compared to severe head injuries: generally younger higher frequency of students percentage of males is less alcohol less frequently involved Demographics

Pediatric head Injury higher death rate under the age of two bimodal distribution- bikes/cars 90% are closed, non-penetrating mortality; 1-5% but rises to 17% if coma >12hr. 10% of the deaths are < ten years of age

Demographics Children aren’t little adults Infants aren’t little children

Physiology Unique to Children Skull relation to spine deformability thickness open sutures open fontanel

Physiology Unique to Children Meninges wider subarachnoid space over convexity(shear/tear), over all smaller in proportion to brain (less buoyancy) dura adherently applied to bone

Physiology Unique to Children Brain Increased water content autoregulatory mechanisms pressure/volume compliance shifted left contracoup post traumatic unconsciousness

Pediatric post-concussive Syndrome Characteristics: Stunned/unresponsive pupils dilated,fixed or anisocoric bradycardia pallor perspiration vomiting Mechanism: 1. most likely vasovagal effect 2. some consider post-traumatic seizure effect

Treatment Efficacy of head trauma sheets 66% referred to the document 84% found it answered all questions

Sequellae; at 48 hours headaches 51% dizziness 14% sleepy 14% naus/vomit 12% behavioral changes 7% memory deficits 5% visual changes 3% hearing problems 2% pupillary change 1.5%

Sequellae At one week these signs and symptoms are approximately halved 27% yet to return to normal function at 48hr, 13% at by one week 50% with residual complaints at 3 months recovery from cognitive deficits;1-3months

Sequellae 10-15% have surgical lesions EDH, SDH, ICH, Depressed skull Fx <1% demonstrate talk and die phenomena

sequellae Post Traumatic Seizures In isolation; impact or early sz (<1 week); –not indicative of severe head injury –not indicative of inc. risk for epilepsy –50% occurred in mild group with normal CT –No role for anticonvulsants

Classification of Injury Primary scalp: laceration, avulsion skull Fx: “ping-pong” linear, depressed open/closed, comminuted, basilar neck: soft tissue, bone, vascular brain: focal, diffuse

Primary Head Injuries Skull fractures of concern: open,depressed crosses suture lines crosses known vascular channels –arterial –dural sinuses enters into sinuses basilar

Metabolic hypoxia/hypercarbia hypo/hypernatremia hyperglycemia hormonal dysregulation dysautonomia nutritional Classification of Head Injury Secondary swelling hemorrhage edema vasospasm seizures hypotension ischemia

CT Scans of Intracranial Hemorrhage

Mechanism of Injury Translational linear focal Acceleration- deceleration rotational concussive-shearing forces

Mechanisms of injury Age Related birth injury; skull fx via canal vs forceps, CN posterior fossa SDH infant/toddler; falls, abuse children falls, bikes, pedestrian-MVA, bike-MVA teens; falls, MVA, assaults

Triage Approach/attitude apparent stability DOES NOT= insignificant injury stay directed, utilize protocols- avoid inertia repeat neurologic exam looking for change consider the mechanism of injury-think broadly alcohol level <.2 doesn’t alter neurologic much, but consider drug effect

Triage History mechanism of injury (should “fit” what you see) neurologic- recent, remote; baseline, SZ, HI general-medical, drugs psychological/educational

Triage Physical Exam CGLCS pupils respiratory pattern sensory modalities SEARCH FOR FOCALITY! reflexes – –DTR – –cutaneous mental status

Signs of Rostro-caudal deterioration decreased LOC headache vomiting visual changes pupilary change Cushing Triad loss of function – –motor/sensory respiratory pattern change

Triage As A Rule Any pupillary inequality> 1 mm in a head injured child must be attributed to an intracranial injury until proven otherwise

Pathophysiology Monroe-Kellie doctrine three compartments blood brain CSF change in one requires reciprocal change in the others

Clinical Findings in 4500 pediatric head injuries Initial LOC % normal56.0 confused30.2 major impairment13.8 Vomiting30.3 Skull Fx 26.6 linear 72.8 depressed 27.2 compound 19.7 Seizures7.4 paralysis3.8 pupil abn3.6 retinal hem2.6 subdural hem5.2 epidural hem0.9 major sequellae5.9 mortality5.4

Clinical Profile from 937 Pediatric Head Injuries 84% CGCS Mean age 5.5 Males>females 2:1 Falls>pedestrian/MVA 75% “alert” on admission 13% had surgical lesions 0.3% with CGCS died avg. length of stay ; 2.8 days

Clinical profile Presence of Mass lesions Glasgow Coma Scale 15: 7.1 % Glasgow Coma Scale 14: 9.7 % Glasgow Coma Scale 13: 13.6 %

Identifying Risk Facteurs LOC >16 minutes =>45X>risk of poor outcome small punctate hem/ contusion on CT did not adversely effect outcome compared to normal CT. Linear,basilar,depressed skull Fxs did Not effect outcome Diastatic and compound depressed skull Fxs had poor outcomes respectively 50% vs 14%

Identifying Risk Facteurs GCGS and the patient’s MENTAL STATUS were the best predicteurs of potential deterioration or the presence of a mass lesion

Identifying risk facteurs Skull X-ray; what role if any?? Not essential for decision making process HOWEVER –presence=>inc risk of lesion\deterioration – useful in penetrating injuries – useful in Non-accidental trauma – useful in following growing Fx of childhood

Etiologies of delayed detoriation Mass lesions: EDH/SDH/ICH electrolyte imbalance cerebral edema seizures

Recommendations Glasgow Coma Scale 13-14: CT scan and admit for observation Glasgow Coma Scale 15 with normal neurologic exam/mental status, and normal CT; discharge with home observation. CT optional? Relevance of duration/presence of LOC- varied opinion.

Recommendations;Concussion and Sports Confusion w/o amnesia/LOC asymptomatic; observation 1/2 hr confusion with amnesia, no LOC observe 24 hr, asymptomatic return to activity after one week LOC; formal medical evaluation asymptomatic return to activity in 2-4 wks

Fail-Safe vs the Doomsday EDH Small percentage(<1%) will develop a delayed lesion with Normal original CT –In patients with abnormal CT scans: 30% of patients: develop a delayed lesion not present on first CT or worsening of original lesion Most will occur within the first hrs

Bicycle Facts 400,000 Rx/yr 1/3 HI 300deaths/yr 80% HI annual cost:$8 billion 2200/yr sustain permanent disability, helmets would prevent 1700 helmets reduce risk of injury85% Helmet laws have reduced mortality 80% Bikes are assoc with more childhood injury than any other consumer product operated by children Universal use of helmets would prevent one HI every 4 min and save a life DAILY

Is it a crap shoot? KNOWLEDGE IS POWER