Download Head Injury and Intracranial Hypertension

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
UTHSCSA
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
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COUP - CONTRECOUP
INJURY
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Pediatric Resident Curriculum for the PICU
UTHSCSA
TYPES OF PRIMARY INJURIES
• Focal injuries
• Diffuse injuries
– Skull fracture
– Diffuse axonal
– Parenchymal
injury
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
• Nonvascular etiologies
– Cytotoxic 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
• 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 ICP’s 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,C’s
• 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 can
• decreases ICP but
increase ICP
can drop BP
• use with
• Anxiolysis
defasciculating
– Midazolam
dose of
• little effect on BP
nondepolarizing
• Lidocaine IV
– Non depolarizing
• blunts
• vecuronium
sympathetic
• longer acting and
response to
no 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 ICP < 22 mm Hg
or
CPP > 70 mm Hg if 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
– hypercarbia
– hypoxia (pO2 <
50)
– seizures or
shivering
– hyperthermia
– arousal
• pain, anxiety
– venous
congestion
• fluid overload
• intrathoracic
• Decreases ICP
– hyperoxia
– hypothermia
– barbiturates
– hypocapnia
• via cerebral
vasoconstrictio
n
• lowers CPP and
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 H2
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 Ringer’s 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,
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
UTHSCSA
MANAGEMENT OF OTHER
SYSTEMS
• Renal
– Place foley for strict I’s and O’s
• 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