Pediatric Resident Curriculum for the PICU

UTHSCSA

HEAD INJURY AND

INTRACRANIAL
HYPERTENSION

Pediatric Resident Curriculum for the PICU

UTHSCSA

HEAD INJURY
Major cause of morbidity and mortality in
children
Leading cause of death in children > 1 yr is
trauma
Head injuries responsible for most trauma deaths
Adverse outcomes result from
Primary injury
Result of mechanical forces producing tissue
deformation at the moment of injury
Secondary ischemic injury
Associated with post injury hypotension,
hypoxemia, and intracranial hypertension

Pediatric Resident Curriculum for the PICU

UTHSCSA

ETIOLOGIES
Motor vehicle accidents
Responsible for most severe head injuries
Falls
Usually in children < 4 yrs and usually
mild
Recreational activities
Half of these are bicycle accidents
Assault or nonaccidental trauma
Most head injuries in kids < 1 yr are from
NAT and falls

Pediatric Resident Curriculum for the PICU

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ANATOMY
Uniquely susceptible to injury
Brain
Inelastic and noncompressible
Has no internal support
Cranium
Rigid and unyielding after sutures fused
Bony buttresses at anterior poles and temporal
poles
Membranous slings
Falx cerebri compartmentalizes R and L
hemispheres
Tentorium separates infra- and supratentorial
regions

Pediatric Resident Curriculum for the PICU

UTHSCSA

MECHANISM OF BRAIN INJURY

Brain is thrown against bony
irregularities or membranous slings or
compressed against these surfaces by
Contact injury
Head strikes or is struck by an
object
Acceleration/deceleration injury
Violent head motion causes
compressive, tensile, and shear
strain in brain tissue

Pediatric Resident Curriculum for the PICU

UTHSCSA

COUP - CONTRECOUP
INJURY

LifeArt: Williams & Wilkins

http://www.lifeart.com

Pediatric Resident Curriculum for the PICU

UTHSCSA

TYPES OF PRIMARY INJURIES

Focal injuries
Diffuse injuries
Skull fracture
Diffuse axonal
injury
Parenchymal
contusion
Diffuse vascular
Parenchymal
injury
laceration
Vascular injury
resulting in
hematoma (subdural,
extradural, or
parenchymal)

Pediatric Resident Curriculum for the PICU

UTHSCSA

SKULL FRACTURES
Most are uncomplicated
Basilar skull fractures

Battles sign, raccoon eyes

CSF rhinorrhea, CSF otorrhea possible
Cranial nerve injury possible

Depressed skull fractures represent more severe injury

1/3 are associated with dural laceration

1/3 are associated with cortical laceration
May require surgical elevation

Fracture crossing path of major vascular structure

increases risk for significant bleeding
Middle meningeal artery
Large dural sinus

Pediatric Resident Curriculum for the PICU

UTHSCSA

CONTUSION
Usually frontal or
temporal lobe
Small cortical
vessels and neural
tissue damaged
Damaged vessels
may thombose,
leading to ischemia

WebPath: University of Utah

http://www-medlib.med.utah.edu/WebPath/webpath.html

Pediatric Resident Curriculum for the PICU

UTHSCSA

INTRACEREBRAL
HEMORRHAGE
Usually frontal or
temporal lobe
Can be bilateral
(contracoup injury)
Can act as mass
lesions and cause
intracranial
hypertension

Pediatric Resident Curriculum for the PICU

UTHSCSA

EPIDURAL HEMATOMA
Usually arterial in origin
Between skull and dura,
limited by suture lines
Often from tear in middle
meningeal artery
Initial injury may seem
minor, followed by lucid
interval, then neurologic
deterioration
May expand rapidly and
require emergency
craniotomy
WebPath: University of Utah
http://www-medlib.med.utah.edu/WebPath/webpath.html

Pediatric Resident Curriculum for the PICU

UTHSCSA

SUBDURAL HEMATOMA
Usually venous bleeding
(bridging veins)
On surface of cortex, beneath
dura and outside arachnoid, not
limited by suture lines.
Typically requires greater force
to produce than epidural
hematoma
Usually associated with severe
parenchymal injury
WebPath: University of Utah
http://www-medlib.med.utah.edu/WebPath/webpath.html

Pediatric Resident Curriculum for the PICU

UTHSCSA

. ...... . ..

DIFFUSE BRAIN INJURY

Diffuse axonal injury
Usually from rapid acceleration/deceleration
Shear forces disrupt small axonal pathways

After disruption, axons degenerate, fragment, then

disappear
The neurons then undergo Wallerian degeneration

Spectrum from mild to severe

Diffuse vascular injury
Microvasculature more resistant to shear than
axons
Results in multiple small hemorrhages throughout
brain
Usually seen in fatal head injuries

Pediatric Resident Curriculum for the PICU

UTHSCSA

SECONDARY ISCHEMIC
BRAIN INJURY
Compounds the potential for adverse
neurologic outcome
Caused by:
Post injury hypotension
Hypoxemia
Intracranial hypertension which
impairs cerebral blood flow

Pediatric Resident Curriculum for the PICU

UTHSCSA

INTRACRANIAL
HYPERTENSION
Vascular etiologies
Vasogenic edema

BBB impaired,
protein rich fluid
leaks to ECF

Hyperemia

Occurs days 1 to 3
after injury

Obstructed venous
drainage

Hydrostatic pressure
increased, protein
poor fluid leaks into
ECF

Nonvascular etiologies
Cytotoxic edema
Ionic gradients
impaired and cells
swell

Obstruction to CSF
outflow
Hematoma
Osmotic brain edema

Decreased osmolality
from iatrogenic
hemodilution or
SIADH

Pediatric Resident Curriculum for the PICU

UTHSCSA

INTRACRANIAL
HYPERTENSION
Normal intracranial pressure:

Adults: < 10 mm Hg
Infants/children: somewhat lower,
depending on age

Elevated ICP impairs cerebral perfusion

Risk for herniation with ICP > 40 mm Hg
Herniation can occur at lower ICPs when
mass lesion is present

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF HEAD
INJURY
Goals of resuscitation and treatment
is to minimize secondary ischemic
brain injury by promoting and
preserving cerebral perfusion

Prevent or treat post injury hypotension

Prevent or treat hypoxemia and reduce
oxygen demand of the brain
Prevent or treat intracranial hypertension
Avoid measures that decrease cerebral
perfusion

Pediatric Resident Curriculum for the PICU

UTHSCSA

RESUSCITATION
A, B,Cs
Major early risk is hypotension

Adequate fluid resuscitation to restore

normal BP does NOT worsen neurologic
outcome
Avoid hypotonic fluids

Emergent airway control for

GCS 8 or less
GSC 10 or less with abnormal head CT
Rapid neurologic deterioration
If needed for other injuries

Pediatric Resident Curriculum for the PICU

UTHSCSA

INTUBATION OF PATIENT WITH

HEAD INJURY
Preserve cerebral oxygenation
Maintain cerebral perfusion

Adequate analgesia and anxiolysis

Avoid meds that increase ICP
Avoid meds that cause hypotension
Avoid Trendelenburg position

Avoid aggravating C spine injury

C-spine injuries in as many as 10% of head

injury patients
In-line axial stabilization by an assistant
recommended

Pediatric Resident Curriculum for the PICU

UTHSCSA

DRUGS FOR RAPID

SEQUENCE INTUBATION
Analgesia/sedation
Neuromuscular blockade
Fentanyl, etomidate
Succinyl choline
little effect on BP
short acting
Thiopental
muscle fasciculations
decreases ICP but can
can increase ICP
drop BP
use with
Anxiolysis
defasciculating dose
Midazolam
of nondepolarizing
little effect on BP
Non depolarizing
Lidocaine IV
vecuronium
blunts sympathetic
longer acting and no
response to
increase in ICP
intubation

Pediatric Resident Curriculum for the PICU

UTHSCSA

RULE OUT & PREVENT NEUROSURGICAL

EMERGENCIES
Head CT as soon as possible
Initial CT may be normal in severe head
injury
Repeat CT in 12 to 24 hours
Moderate hyperventilation advisable during
transport and initial evaluation
If signs of impending herniation develop
(lateralizing signs, pupil asymmetry)
Hyperventilate
Give mannitol

Pediatric Resident Curriculum for the PICU

UTHSCSA

MONITORING OF INTRACRANIAL
PRESSURE
Ventriculostomy catheter
Catheter tip in frontal horn of lateral
ventricle
Can drain CSF
Can be recalibrated as necessary
Transducer tipped catheter
Intraparenchymal or subdural
Cannot drain CSF
Cannot be recalibrated
Exhibits drift in values measured over time

Pediatric Resident Curriculum for the PICU

UTHSCSA

MONITORING OF INTRACRANIAL
PRESSURE
Indications

GCS < 8 after resuscitation

Abnormal head CT
Rapid neurologic deterioration

ICP monitoring is continued for as

long as treatment of intracranial
hypertension is required

Pediatric Resident Curriculum for the PICU

UTHSCSA

CEREBRAL PERFUSION
PRESSURE
Can be determined from ICP and mean
arterial pressure:
CPP = MAP - ICP
Calculated CPP does not reflect perfusion of
entire brain
CPP further decreased in areas of injury
Factors that cause cerebral
vasoconstriction without lowering MAP
result in a falsely low calculated CPP

Pediatric Resident Curriculum for the PICU

UTHSCSA

CEREBRAL PERFUSION
PRESSURE
Goal of therapy

CPP > 60 mm Hg if
or
CPP > 70 mm Hg if

ICP < 22 mm Hg
ICP > 22 mm Hg

Lowering ICP while maintaining MAP will

increase CPP
Increasing MAP will increase CPP

Pediatric Resident Curriculum for the PICU

UTHSCSA

FACTORS AFFECTING
INTRACRANIAL PRESSURE
Increases ICP
Decreases ICP
hypercarbia
hyperoxia
hypoxia (pO2 < 50)
hypothermia
seizures or shivering
barbiturates
hyperthermia
hypocapnia
arousal
via cerebral
pain, anxiety
vasoconstrictio
venous congestion
n
fluid overload
intrathoracic
lowers CPP and
pressure
is undesirable

Pediatric Resident Curriculum for the PICU

UTHSCSA

EFFECT OF pCO2 and pO2 ON

CBF AND CPP
Hypoxia increases
CBF by vasodilation
Hypercapnia
increases CBF
Hyperventilation and
resulting hypocapnia
decrease CBF
Hyperventilation
is useful to
prevent impending
herniation but will
worsen secondary
ischemic injury

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Head position
Head elevated 30 degrees and midline
Sedation and pain control
Analgesic + anxiolytic
Fentanyl, morphine, or propofol plus a
benzodiazepine
Continuous infusions or scheduled
doses to maintain sedation
Watch for and treat hypotension
Seizure prophylaxis
Phenytoin or phosphenytoin

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF INCREASED
ICP
Neuromuscular blockade
Facilitates mechanical ventilation and control
of pCO2
Prevents shivering
Use if movement increases ICP
Temperature control
A rise in temp of 1o C increases cerebral
metabolic rate by 10%, increasing ICP by
several mm Hg
Maintain temp < 37.5 o C
Scheduled acetaminophen, body exposure,
cooling blanket

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Osmotherapy with mannitol
Decreases extracellular fluid in brain
Intermittent doses for ICP spikes or scheduled
if elevated ICP is persistent
Adverse effects:

Hypernatremia, hypokalemia
Hyperosmolality
Hemodilution and drop in hematocrit
Hypotension

Follow serum osmolality and Na

Hold mannitol if serum osm > 320 mOsm/l

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Drainage of CSF

Possible if ventricular catheter is in

place
CSF drainage pressure usually set at 20
cm H2O
CSF drains when ICP exceeds drainage
pressure
Ventricular catheters cannot be placed if
cerebral edema has obliterated or
significantly compressed ventricles

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Second tier therapies for intracranial
hypertension refractory to sedation,
muscle relaxation, osmotherapy, and
moderate hypothermia:

barbiturate coma
induced hypertension
decompressive craniotomy
hypothermia

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Barbiturate coma
ICP control is the principal endpoint
EEG burst suppression is a useful guide to
optimal barbiturate dosage
Pentobarbital 10mg/kg followed by infusion
at 1 mg/kg/hr, titrated to effect
May give additional boluses during infusion
for acute spikes in ICP
Moderate doses cause sluggishly reactive
pupils while large doses may cause mid
position to 5 mm nonreacting pupils
Watch for hypotension

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Induced hypertension
Inotropes to increase MAP, even beyond normal
for age, to achieve an optimal CPP
Dopamine
Norepineprine

Rise in ICP in tandem with a rise in MAP

implies total loss of autoregulation and is a
poor prognostic sign
Decompressive craniotomy
Large portion of cranium removed to allow
room for brain to swell and minimize ischemia
Dura must be opened as well

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF
INCREASED ICP
Hypothermia
Core body temp of 32o to 33o C
Reduced cerebral metabolic activity,
reducing ICP
Also has cytoprotective effects
Adverse effects
Arrythmias
Coagulopathies
Hypokalemia
Increased risk of infection

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Respiratory

Maintain normocapnia

Hyperventilation only appropriate during early

diagnosis and management or if herniation is
impending

Maintain oxygenation
pO2 > 100 is optimal

PEEP to maintain alveolar recruitment

ARDS, neurogenic pulmonary edema frequent

complications
Hypoxemia has more deleterious effects on brain
than modest venous congestion caused by PEEP
PEEP of 5 to 10 cm H2O not shown to have
detrimental effect on neurologic outcome

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Cardiovascular
Maintain normal blood pressure
Hypotension significantly reduces CPP
Inotropes if necessary to maintain normal BP
Induced hypertension if necessary
Gastrointestinal
Stress gastritis prophylaxis with H 2 blocker
Jejunal feeds to maintain healthy intestinal
mucosa and prevent bacterial translocation
from gut

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Fluids, Electrolytes, Nutrition

Goal is NORMOVOLEMIA
Total fluid intake should be @ 100% maintenance
Bolus as necessary to achieve normal CVP
Avoid hypotonic fluids
Lactated Ringers and 0.9% saline w/ 20 mEq
KCl/l are good choices for maintenance fluids
Follow electrolytes closely
Avoid hyponatremia
Mannitol can cause electrolyte abnormalities
Watch for SIADH, diabetes insipidus, cerebral salt
wasting

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Fluids, electrolytes, nutrition

Provide calories to meet metabolic demands of

patient
Increased metabolic demands during acute phase
of injury
Heavily sedated, relaxed, cooled patient has
decreased metabolic demands
Enteral feedings via nasojejunal catheter preferable
to TPN if gut deemed to be healthy
Avoid hyperglycemia
Associated with poor neurologic outcome
Watch serum glucose closely if dextrose containing
fluids used

Pediatric Resident Curriculum for the PICU

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MANAGEMENT OF OTHER
SYSTEMS
Renal

Place foley for strict Is and Os

Hematologic

Coagulopathy common with head injuries

Brain derived thromboplastin activator
substances released
Follow PT/PTT or DIC screens
Blood component replacement if evidence of active
bleeding or if surgical intervention anticipated
Maintain normal hematocrit to optimize oxygen
delivery

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Endocrine

DIABETES INSIPIDUS
Complete or partial failure of ADH secretion
from shearing of pituitary stalk
Polyuria, hypernatremia, urine osm < plasma
osm
Treatment:
Run maintenance fluids @ 100%
Replace urine output cc for cc with dextrosecontaining fluids
Continuous vasopressin infusion or DDAVP
(subQ or intranasal) q 12 to 24 hrs

Pediatric Resident Curriculum for the PICU

UTHSCSA

MANAGEMENT OF OTHER
SYSTEMS
Endocrine

CEREBRAL SALT-WASTING
ANP-like substance released from brain,
inducing natriuresis and diuresis
SIADH
Elevated level of ADH inappropriate for
prevailing osmotic or volume stimuli
Hyponatremia, hypo-osmolality, urine osm
> plasma osm, high urine Na
Treatment is water restriction

Pediatric Resident Curriculum for the PICU

UTHSCSA

SUMMARY
Identify and treat primary brain injury
Rule out neurosurgical emergency

Minimize secondary ischemic brain injury by

promoting cerebral perfusion
Maintain normovolemia and adequate BP
Maintain normal electrolytes and euglycemia
Maintain normocapnia and adequate
oxygenation
Avoid factors that increase ICP
Treat intracranial hypertension