This document provides an overview of pediatric traumatic brain injury (TBI) management. It describes the case of a 13-year-old male involved in a motor vehicle collision. Key goals in management include maintaining cerebral perfusion pressure, decreasing intracranial pressure, and preventing secondary injury. Early management focuses on airway protection, oxygenation, imaging, and treating hypotension and elevated ICP. Refractory elevated ICP may be treated with osmotherapy, barbiturates, or decompressive craniectomy. Ongoing intensive care involves careful monitoring and treatment of ICP, CPP, seizures, and other complications. Outcomes depend on age, injury severity, and development of secondary insults like hypot

1. Pediatric Traumatic Brain Injury
Rob Parker, DO
Pediatric Critical Care Fellow

2. Overview
 Case
 Epidemiology
 Pathophysiology
 Management
– Early
– ICU
– Refractory

3. Case
 13 yo male on back of tandem bicycle
 Struck by pick up going 40 mph with father DOA
and pt thrown against building
 Pt moving all extremities on arrival and moaning
 Brought to ED as accident 1 min down street from
hospital

4. ED Course
 Mannitol given
 Intubated using
ketamine and sux and
brought to CT
– Intraparenchymal
contusions affecting entire
L hemisphere with massive
edema
– Uncal herniation
– Shift of midline structures
of R side
– Compression of ventricular
system
– Extensive fracture of L side
of skull
 Neurosurg and PICU
consults

5. OR Course
 Taken urgently to
OR for
decompressive
craniectomy
 Placement of ICP
monitor/drain

6. ICU Course
 Intracranial Pressure Control
– CSF Drainage
– Osmotherapy (Mannitol, 3%NaCl)
– Sedation (fentanyl, midazolam, barbiturates)
– Normothermia (cooling blanket)
– Normocarbia (mechanical ventilation)
 Maintenance of cerebral perfusion pressure
– Norepi infusion, fluid boluses
 Seizure prophylaxis
– Keppra

7. ICU Course cont
 Refractory ICP
– Hypertonic infusion
– Propofol then pentobarb coma
– Bilateral hemicraniectomy
 Refractory seizures
– Induced coma
 Neuroimaging
– MRI showing severe DAI

8. Rehab
 Extubation
– NPL reveals intact vocal cord function
 Rehab
– Neuropsych rehab
– PT/OT/ST, PEG tube, no trach
– Seizures controlled with Keppra
– Executive functioning issues
– Return to school 2 years later

9. Epidemiology
 Incidence of 230 cases per 100,000 with 475,000
new cases yearly
– One case every 2 to 3 minutes
– 10-15% of cases are severe TBI
– Even distribution within age groups: 0 to 4 years, 5 to
10 years, and 11 to 15 years
 Outcomes
– 3000 to 4000 pediatric deaths annually
– 5 to 15 years more favorable
– Under 2 years old most likely to have severe injury
Patrick M. Kochanek, Michael J. Bell, Hülya Bayir, Michael J. Forbes, Randall Ruppel, P. David Adelson and Robert
S.B. Clark, Chapter 61 - Severe Traumatic Brain Injury in Infants and Children, In Pediatric Critical Care (Fourth
Edition), edited by Bradley P. Fuhrman and Jerry J. Zimmerman, Mosby, Saint Louis, 2011, Pages 849-870

10. Pathophysiology
 Direct injury
 Disruption of
vascular anatomy or
neuronal elements
 Initiation of cytotoxic
cascade and
proinflammatory
cytokines

11. Pathophysiology

13. Goals of Management
 Maintain cerebral perfusion pressure and support
blood pressure
 Decrease brain metabolism
 Decrease the pressure
 Prevent Secondary Injury!!
• Jennett et al. (1977): 50% mortality rate. ICP
monitoring not routinely used.
• Becker et al. (1977): 30% mortality rate. Intensive
management protocol, including ICP monitoring.

14. Signs and Symptoms
Early
 Vomiting
 Headache
 Mental status changes
 Acute neurologic
deterioration
 Respiratory
irregularities
Late
 Cushing’s Reflex
 III or IV palsy
 Motor posturing
 Pupillary dilation
 Papilledema

16. ABC’s
 ABC’s
– Secure the airway if
GCS < 8
– Use of appropriate
induction agents
– Restore perfusion using
isotonic fluids (NS), and
pressors
 Induction agents
– Etomidate, propofol
– Ketamine?
 Muscle relaxant
 Rocuronium
 Succinylcholine?
 ATLS evaluation
– C-spine, associated
injuries
 Emergent non-
contrast head CT
 Pursue surgical
remedies
– Decompressive
craniectomy
– Clot evacuation
 Minimize ED and intra-
hospital transport time

17. Hypoxia
 Incredibly common
 Can result in increased mortality
Manley G - Arch Surg (2001) Hypotension hypoxia and head injury frequency duration and
consequences

18. Protect the Airway
 All should receive
O2
 Prehospital
intubation leads to
improved neurologic
outcomes
– Decreased airway
tone, bleeding,
inability to protect
airway
 Intubate all with GCS
≤8 Bossers SM - PLoS ONE (2015) Experience in Prehospital Endotracheal Intubation
Significantly Influences Mortality of Patients with Severe Traumatic Brain Injury A Systematic
Review and Meta Analysis..
Bernard SA - Ann Surg (2010) Prehospital rapid sequence intubation improves functional
outcome for patients with severe traumatic brain injury a randomized controlled trial

19. RSI
 Induction drugs:
– Etomidate 0.3 mg/kg
– Ketamine 2-4 mg/kg
– Propofol 1-2 mg/kg
 Paralytics:
– Rocuronium 1 mg/kg
– Vecuronium 0.1 mg/kg
– ? succinylcholine – increased mortality
 Pretreatment:
– ? Lidocaine

20. Ketamine
Study Study Size Setting Finding
Jabre
2009
655 Etomidate vs Ketamine for intubation No differences between groups
Smischeney
2012
84 Propofol or ketofol for induction Ketofol provided better hemodynamic
stability
Mayberg
1995
20 Intraoperative administration during
craniotomy
Reduction in intracranial pressure
Grathwohl
2008
214 Total intravenous anesthetic vs inhalational
anesthetic
No difference in mortality or
neurosurgical outcome
Roberts
2011
380 Systematic review of different agents used for
sedation in ICU
No evidence that one agent over
another is better at improving
neurological outcome
Albanese
1997
8 Propofol sedation with additional of ketamine No difference in CPP compared to
baseline, slight decrease in ICP
Kolenda
1996
35 Sedation with ketamine/midazolam vs.
fentanyl/midazolam
Non-significant increase in ICP but
improved CPP in ketamine group
Bourgoin
2003
25 Sedation with ketamine/midazolam vs.
sufentanyl/midazolam
No difference in ICP or CPP
Bourgoin
2005
30 Target controlled sedation with
ketamine/midazolam vs. sufentanil/midazolam
No difference in ICP or CPP
Chang LC - CNS Neurosci Ther (2013) The emerging use of ketamine for
anesthesia and sedation in traumatic brain injuries

21. Imaging
Acute Subdural Acute Epidural

22. ICP Monitoring
• Recommended for GCS <8

23. Monro-Kellie Doctrine

24. Cerebral Perfusion Pressure
 CPP = MAP – ICP
– Low CPP (<40mmHg) and
hypotension have both been
associated with worsened
clinical outcomes
 Studies have shown that
increasing blood pressure
does not significantly increase
ICP
 Suggested critical adult
threshold: 70 – 80 mmHg
 Optimal pediatric threshold
may be lower (50 – 65 mmHg)

25. Vasodilatory Cascade
Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion
pressure: management protocol and clinical results. J
Neurosurg. 1995;83(6):949-62.

26. Reversing the Vasodilatory Cascade
Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion
pressure: management protocol and clinical results. J
Neurosurg. 1995;83(6):949-62.

27.  ICP-directed
– No specified CPP
– Keep ICP < 20 mmHg
– Keep BP normal, treat
hypertension
 CPP-directed (Rosner)
– Maintain CPP > 70 mmHg
– Volume expansion
– Vasopressors

28. Hypotension
 Even a single episode
of hypotension
drastically increases
mortality
 Early hypotension is
common and more
dangerous than late
hypotension
– Can double mortality
rates
 Efforts to avoid
hypotension must be
made
Coates BM - Crit Care Med (2005) Influence of definition and location of hypotension on
outcome following severe pediatric traumatic brain injury
Manley G - Arch Surg (2001) Hypotension hypoxia and head injury frequency duration and
consequences

29. Hypotension and Hypoxia
American Heart Association Scientific Sessions 2014
Resuscitation Science Symposium. Abstract 4. Presented
November 15, 2014

30. ICP or CPP or Both
 ICP
– No set numbers but poorer
outcomes when ICP greater
than 20
 Potentially should be
lower with younger
children
– Infant 0 – 2 yo
 Goal <15 mm Hg
– Children 2 – 8 yo
 Goal <18 mm Hg
– Adolescents 8+ yo
 Goal <20 mm Hg
 CPP
– No set numbers but
consensus agreement is not
below 40
 Post 2012 guidelines,
studies suggest:
– Infant 2 – 6 yo: >50
– Children 7 – 10 yo : > 55
– Adolescents 11 – 16 yo: >60
Mazzola CA - Crit Care Med (2002) Critical care management of head trauma in children

31. 1st Tier Strategies
 Head of Bed 30⁰
– Improved outflow
lowers ICP without
change in CBF or CPP
 Head midline
– Improved outflow via
jugular venous and
CSF drainage
 Adequate sedation
– Decreased metabolic
demand
– Decreased
responsiveness to
noxious stimuli

32. Osmotic therapies
 Osmotic Agents are
solutions containing
simple, LMW
solutes;
hyperosmolar
relative to plasma
 Examples: mannitol,
glycerol, dextrose,
sorbitol, sucrose,
sodium chloride

33. Mannitol
Early <75min
 Plasma volume expansion
– Reduces blood viscosity
(rheology) lowering ICP
 Results from a viscosity-
mediated reflex vasoconstriction
(intact autoregulation), which
allows cerebral blood flow to be
maintained despite a reduced
level of cerebral blood volume
Late >75 min up to 6hrs
 Osmotic gradient
– Gradual movement of water from
the brain parenchyma into the
systemic circulation
– Requires intact BBB
 May act as a free radical
scavenger

34. Mannitol
 No controlled trials
with placebo or HTS
comparison
 2003 Cochrane review
of mannitol for acute
traumatic brain injury
– “There is not enough
evidence from trials to
show how best to use
mannitol for people with
head injury”

 Dose 0.25 – 1.0 g/kg
over 15-20 min
– May cause
hypotension
 Maintain Serum Osm
<320

35. Hypertonic Saline
 Mechanism:
– Rheologic effect
– Osmotic gradient
 Proposed additional
benefits:
– Restoration of cell
membrane potential
– Inhibition of
inflammation
– Enhancement of
cardiac output
 Dose:
– 3 – 5 ml/kg of 3%
 Can push serum
Osm to <360
 Can push [Na] to
>160
 May be beneficial if
CSW occurs

36. Hypertonic Saline
Study Size Description Findings
Fisher
1992
18 Randomized controlled crossover trial
comparing 3% and 0.9% saline;
outcome = ICP
Hypertonic saline was associated with a
lower ICP and reduced need for
additional interventions
Peterson
2000
68 Retrospective chart review using
continuous infusion of 3%
hypertonic saline to lower ICP;
outcome = ICP, GOS
Survival rate was higher than expected
53% had good outcome, 20%
moderate, 10% severe, 0.1%
vegetative, and 15% died
Simma
1998
35 Randomized controlled trial comparing
1.7% HTS solution vs LR as
continuous infusion; outcome = ICP,
cerebral perfusion pressure, need for
other interventions, fluid requirements,
intensive care unit stay, survival rate
No difference in survival or hospital
LOS
HTS has less interventions
HTS has shorter mechanical ventilation
days, PICU LOS and less complications
• Class II evidence: use of hypertonic saline (3%) for the acute treatment
• Class III evidence: use as a continuous infusion during the intensive care
unit course

37. Hyperventilation
 Used in 1970’s as first line to
induce cerebral
vasoconstriction and thereby
decrease CBF
 Ultimately found that CBF is
reduced early in course of
TBI and cerebral perfusion is
related to mortality
 Recommendation to maintain
normocarbia with pCO2 33-
38 mm Hg
– Some consider brief periods of
hyperventilation safe to “break”
acute ICP spikes

38. Additional Therapies
 Nutrition:
– Generally accepted to use dextrose free fluids/feeds but no evidence
supports this
 Thought is to decrease metabolic demand
– Excessive glucose control can lead to metabolic crisis increasing
metabolic demand
 Thermoregulation:
– Moderate hypothermia (32-33 C) should not be begun early and
continued for 24 hours followed by rapid rewarming
 Trend toward worse outcome and increased mortality
– Moderate hypothermia (32-33 C) for 48 hours followed by slow
rewarming can be considered
 Seizure Control/PPx
– Prophylactic treatment with phenytoin may be considered to reduce
the risk of early PTS
– Many clinicians use Keppra although neither has shown beneficial in
reducing early or seizure occurrence

39. Barbituates
 Barbiturates reduce ICP by metabolic suppression
(assuming flow-metabolism coupling is intact) and
changing vascular tone.
 The goal of barbiturate therapy is to achieve burst
suppression on EEG
 There is no clear evidence that barbiturate therapy
benefits patients
 Recommendation:
– High-dose barbiturate therapy may be considered in
hemodynamically stable patients with refractory intracranial
hypertension despite maximal medical and surgical
management

40. Decompressive Craniectomy
 8 small studies, mostly retrospective, with varying criterial
but mainly elevated ICP refractory to medical management
– All class III data with 5-23 pts in each series
 Most with decreases in ICP and some with good outcomes
 Large decompressive surgeries with duraplasty may be
effective in reversing early signs of neurologic deterioration
or herniation, and in treating intracranial hypertension
refractory to medical management
 Cautious interpretation of these outcomes suggests that
decompressive craniotomy may be effective in improving
outcome in patients with medically intractable intracranial
hypertension.

41. Additional Considerations
 Lumbar CSF drain
 Hypothermia
 Hyperventilation

45. Questions?