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Minor Head Injury In Children Larry Kleiner Medical Director, Dept of Neurosurgery The Children's Medical Center
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Head Trauma
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Definition of Mild head injury Glasgow Coma Scale 13-15 simple reproducible functional valid predicteur Prejudice against children doesn’t account for asymetry prejudice against facial injury/intubation doesn’t account for brainstem reflexes
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Eye opening: spontaneous 4 to sound 3 to pain 2 none 1 Modification of the GCS
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Modification of the GCS Verbalization Appropriate for age5 –fixes and follows –social smile cries but consolable 4 persistent irritability3 restless,lethargy2 none1
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Modification of the GCS Motor Response Spontaneous6 localizes to pain5 withdraws4 decorticate3 decerebrate2 none1
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Modification of GCS Glasgow-Liege Scale –includes brainstem reflexes –increases prediction of outcome from 76% to 90% with a.9 confidence level
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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
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Epidemiology 7-8 million “head injuries”/year 1.5-2.0 million/year with LOC/amnesia - 80% considered minor
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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
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Epidemiology Head injury overview: 1:10 has loss of consciousness 250-500,00 hospitalizations/year 4,000 deaths/year 15-20,000 prolonged hospitalizations/year
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Compared to severe head injuries: generally younger higher frequency of students percentage of males is less alcohol less frequently involved Demographics
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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
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Demographics Children aren’t little adults Infants aren’t little children
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Physiology Unique to Children Skull relation to spine deformability thickness open sutures open fontanel
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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
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Physiology Unique to Children Brain Increased water content autoregulatory mechanisms pressure/volume compliance shifted left contracoup post traumatic unconsciousness
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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
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Treatment Efficacy of head trauma sheets 66% referred to the document 84% found it answered all questions
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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%
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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
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Sequellae 10-15% have surgical lesions EDH, SDH, ICH, Depressed skull Fx <1% demonstrate talk and die phenomena
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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
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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
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Primary Head Injuries Skull fractures of concern: open,depressed crosses suture lines crosses known vascular channels –arterial –dural sinuses enters into sinuses basilar
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Metabolic hypoxia/hypercarbia hypo/hypernatremia hyperglycemia hormonal dysregulation dysautonomia nutritional Classification of Head Injury Secondary swelling hemorrhage edema vasospasm seizures hypotension ischemia
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CT Scans of Intracranial Hemorrhage
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Mechanism of Injury Translational linear focal Acceleration- deceleration rotational concussive-shearing forces
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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
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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
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Triage History mechanism of injury (should “fit” what you see) neurologic- recent, remote; baseline, SZ, HI general-medical, drugs psychological/educational
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Triage Physical Exam CGLCS pupils respiratory pattern sensory modalities SEARCH FOR FOCALITY! reflexes – –DTR – –cutaneous mental status
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Signs of Rostro-caudal deterioration decreased LOC headache vomiting visual changes pupilary change Cushing Triad loss of function – –motor/sensory respiratory pattern change
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Triage As A Rule Any pupillary inequality> 1 mm in a head injured child must be attributed to an intracranial injury until proven otherwise
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Pathophysiology Monroe-Kellie doctrine three compartments blood brain CSF change in one requires reciprocal change in the others
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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
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Clinical Profile from 937 Pediatric Head Injuries 84% CGCS 13-15 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
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Clinical profile Presence of Mass lesions Glasgow Coma Scale 15: 7.1 % Glasgow Coma Scale 14: 9.7 % Glasgow Coma Scale 13: 13.6 %
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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%
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Identifying Risk Facteurs GCGS and the patient’s MENTAL STATUS were the best predicteurs of potential deterioration or the presence of a mass lesion
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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
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Etiologies of delayed detoriation Mass lesions: EDH/SDH/ICH electrolyte imbalance cerebral edema seizures
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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.
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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
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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 24-36 hrs
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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
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Is it a crap shoot? KNOWLEDGE IS POWER
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