1) Pediatric head trauma is a leading cause of death and disability in children, with over 650,000 evaluated per year. The causes vary by age, from abuse and falls in infants/toddlers to motor vehicle crashes and assaults in adolescents. 2) Management involves stabilizing the ABCs, preventing secondary brain injury, and obtaining a CT scan if indicated based on decision rules. For severe injuries, intensive care is needed for ICP monitoring, seizure prophylaxis, and treating complications like hypo/hyperglycemia. 3) While outcomes have improved with specialized pediatric trauma care, severe traumatic brain injury continues to carry high mortality rates around 40% and most survivors have long-term impairments.

1. PEDIATRIC HEAD
TRAUMA
Yana Puckett, MD
Cardinal Glennon Children’s Medical Center
Grand Rounds

2. OBJECTIVES
• Epidemiology
• Pathophysiology
• Management
• CT Head Indications
• Abusive Head Trauma

3. EPIDEMIOLOGY
• 650,000 to 1 million children evaluated for head
trauma per year
-80-90% are mild
• Most common cause of death and disability in
childhood in developed countries.
• ½ deaths caused by head injury occur before
patient reaches hospital
• Of all trauma deaths, 25% are caused by head
injury

4. CAUSES OF TBI IN
CHILDREN
Infants: Abuse
Toddlers: Abuse and Falls
School-aged: Injuries (play and sports) and
MVCs
Adolescents: MVCs and assault
Across all age groups, males>females in
minor head injuries

5. BRAIN INJURY
MECHANISMS
Blunt Trauma
Penetrating
Diffuse Axonal Injury
Concussion

6. GRADES OF TBI
• Mild (GCS score 13 to 15)
• Moderate (GCS score 9 to 12)
• Severe (GCS score <9)

7. PATHOPHYSIOLOGY
• Primary Event: direct injury to brain parenchyma.
• Secondary Event:
• Diffuse cerebral swelling following severe
traumatic brain injury is more common among
infants and children as compared with adults

8. MANAGEMENT IN THE ED
• ABCDEs
• Stabilization
• Prevention of secondary brain injury
• Protect the airway & oxygenate
• Correct hypovolemia and hypotension
• CT Scan when appropriate
• Neurosurgery if indicated
• Intensive Care for further monitoring and
management

9. SECONDARY SURVEY
• Head-to-toe examination
• Injuries
• Pneumo- or hemo-thorax
• Intra-abdominal organ injury
• Pelvic fracture
• Actively bleeding wound
• GCS
• Pupillary Size
• Active bleeding scalp wound

10. PHYSICAL EXAM

11. TO CT OR NOT CT?
Lethal malignancies occur between 1 in 500 to 1 in 1000
pediatric head CT scans. Risk increases with decreasing age.
Brenner, David J., et al. "Estimated risks of radiation-induced fatal cancer from pediatric CT." American journal of
roentgenology 176.2 (2001): 289-296.
Cancer risk in 680,000 people exposed to CT scans in childhood
or adolescence: cancer incidence was 24% greater for exposed,
after accounting for age, gender, and year of birth.
Mathews, John D., et al. "Cancer risk in 680 000 people exposed to computed tomography scans in childhood or
adolescence: data linkage study of 11 million Australians." BMJ 346 (2013).
CT of the Brain significantly associated with the risk of
leukemia and brain tumors.
Pearce, Mark S., et al. "Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain
tumours: a retrospective cohort study." The Lancet 380.9840 (2012): 499-505.

12. DECISION RULES ON WHEN
TO ORDER CT IN MILD
HEAD INJURY
1. Canadian Assessment of Tomography for
Childhood Head injury rule (CATCH)
2. Children’s Head Injury Algorithm for the
Prediction of Important Clinical Events (CHALICE)
3. Pediatric Emergency Care Applied Research
Network (PECARN)

15. <2 Y
≥2 Y

16. • 42,412 patients in prospective multicenter
observational study
• If patients were observed before making a
decision on CT, CT rate was lower (31% vs
35%)

17. CONCUSSION
• Imaging normal, but symptoms present
• Ranges from mild to severe
• Amnesia, vomiting, nausea, short periods of
unconsciousness, confusion, headache, speech affected
• Short-lived (hours to days)
• Changes in brain white matter following repetitive head
impacts
• Memory and processing speed affected
• May lead to long-term neurodegenerative diseases
Graham, Robert, et al. "Consequences of Repetitive Head Impacts and Multiple Concussions." (2014).

18. EPIDURAL HEMATOMA
• 50% skull fractures
• Rapid deterioration of
neurologic status
• Between skull and dura,
no direct injury to brain
• Better outcome than
subdural hematoma

19. SUBDURAL HEMATOMA
• Between dura and
brain surface – DIRECT
injury to brain
• Chronic SDH usually
abuse, usually require
surgical intervention
• 60% associated skull
fracture

20. DIFFUSE AXONAL INJURY
• 15-20% associated
mortality
• CT scan does not
show well
• Poor GCS with
normal CT scan
• Important to repeat
CT after 24-48 hours
–edema, delayed
hematoma

21. ABUSIVE HEAD TRAUMA
• Common cause of death, particularly
among children younger than 12 months of
age
• Retinal hemorrhages are common (though
not pathognomonic) and correlate with the
severity of injury.
• Mortality rates as high as 23% reported
• Majority of surviving children have
permanent neurologic impairment.

22. RISK FACTORS ABUSIVE HEAD
TRAUMA
Risk Factors: perinatal illness, birth defects, incessant crying,
male gender
Family: drug and ETOH use in parents, young maternal age,
family disruption/separation, history of abuse in family
members

23. NAT WORK-UP
• Physical Exam
• Retinal hemorrhages 60-85% of abusive
head injury
• Rule out coagulopathy, labs, skeletal
survey, head CT, ophthalmology exam

24. SEVERE TRAUMATIC BRAIN INJURY
• Mortality approximately 40%
• Moderate recovery: <10%
• 75% of children with multiple trauma
injuries have severe TBI
• 80% of all trauma deaths associated
with severe TBI

25. AIRWAY/BREATHING
• Intubation (GCS<8 or deteriorating)
• Analgesia: attenuates effects of pain
and stress on ICP, decreases metabolic
rate.

26. HYPERVENTILATION
• Reduces ICP by producing hypocapnia-induced cerebral
vasoconstriction
• Reduces cerebral blood flow and cerebral volume
• Studies in both adult and pediatric populations have
demonstrated that hyperventilation results in decreased
cerebral oxygenation and may induce brain ischemia.
• Avoid prophylactic severe hyperventilation to PaCO2<30
mmHg in initial 48 hours after injury
• Keep PaCO2 between 30 – 35 mmHg
Kiening, Karl L., et al. "Brain tissue pO2-monitoring in comatose patients: implications for
therapy." Neurological research 19.3 (1997): 233-240.

27. CIRCULATION
• In severe TBI, hypotensive episodes double
mortality.
• Fluid resuscitation (isotonic solution)
• Maintain MAP >80 mmHg
• Fix sources of bleeding on the external head
• Vasopressors to keep MAP >80 mmHg
• Cushing’s Reflex: Hypertension and Bradycardia!
• Head positioning: 30 degrees

28. ICP MONITORING
• ICP >20 mmHg associated with increased
morbidity and mortality
• Clinical signs: headache, nausea, vomiting,
seizure, lethargy, Cushing’s triad, agonal
respirations
• Herniation: unilateral or bilateral pupillary
dilation, hemiparesis, motor posturing, and
/or progressive neurological deterioration.

29. SEIZURE PROPHYLAXIS
• Risk Factors: intraparenchymal
hemorrhage, retained bone and metal
fragments, depressed skull fracture, focal
neurological deficits, LOC, GCS <10,
severity of injury, subdural or epidural
hematoma, penetrating injury.
Ateş, Özkan, et al. "Post-traumatic early epilepsy in pediatric age group with emphasis on influential factors." Child's
Nervous System 22.3 (2006): 279-284.
• Infants and children have lower seizure
threshold than adults (Holmes GL et al. Pediatric
Neurol 2005; 33:1-11)

30. SEIZURE PROPHYLAXIS
• Seizure prophylaxis for first 7 days after
TBI recommended.
Hunt, Elizabeth A. "Phenytoin in traumatic brain injury." Archives of disease in childhood 86.1 (2002): 62-63.

31. HYPERGLYCEMIA
• Associated with poor outcomes in children with
TBI
• In 1 study, for children <14 years old going for
emergent craniotomy for TBI
• Perioperative hyperglycemia (glucose>200) found
in 45% of children
• Associated with <4 years, GCS <8, multiple
traumatic injuries
• Admission serum glucose > or = 300 mg/dL was
uniformly associated with death.

32. HYPERGLYCEMIA
• Randomized controlled trial N=1369 all critically ill children
in PICU (not specific to TBI).
• Insulin infusion (Glucose levels 70-120)
• Outcome: number of days alive and free from mechanical
ventilation at 30 days after randomization.
• Conclusion: no significant effect on major clinical outcomes,
although the incidence of hypoglycemia was higher

33. HYPEROSMOLAR
AGENTS: MANNITOL
• Reduces blood viscosity and has osmotic effect
(moving water from parenchyma into systemic
circulation) (Bouma et al. J Neurotrauma 1992)
• Mannitol may accumulate in injured brain
regions, where reverse osmotic shift may occur
with fluid moving from intravascular
compartment into the brain parenchyma-
worsening raised ICP (Kaieda R et al. Neurosurgery 1989; 24:671-678)
• Use of mannitol may risk development of ATN
and renal failure (The Brain Trauma Foundation. Use of Mannitol J
Neurotrauma 2000; 17:521-525)

34. HYPERTONIC SALINE
• Unlike mannitol, does not cause profound
osmotic diuresis, and the risk of
hypovolemia as a complication is
decreased.
• Restores normal cellular resting membrane
potential and cell volume, inhibits
inflammation, enhances cardiac output.
• Side Effects: osmotic demyelination
(central pontine myelinosis), heart failure.

35. CSF DRAINAGE
• An intracranial drain can be placed to
remove CSF and monitor ICP.

36. BARBITURATE COMA
• Can be used to treat intracranial
hypertension that is refractory to other
modalities.
• Pentobarbital is the barbiturate that is best
studied and most commonly used.
• Side Effects: Cardiac suppression,
hypotension (should be promptly treated
with IVF and vasopressors).

37. CONCLUSION
• Overall trend in improved outcomes after
severe TBI in children.
• Improved prehospital care, regionalization
of pediatric trauma care, adherence to EBM,
more aggressive care (ICP monitoring, early
surgical evacuation of mass lesions), MRI,
and advances in intensive care.