Transcript Management of Closed Head Injury - refresher course in anesthesia

Management of Closed Head Injury
Nicholas Sadovnikoff, MD, FCCM
Refresher Course in Anesthesia and Critical Care
November 26, 2011
Kuwait City, Kuwait
Case Study
16 year-old right-handed male
Unrestrained driver auto vs. tree (tree victorious) 12/25/99
At scene: 40 minute extrication
in respiratory arrest
intubated, IV access & circulation established
Transported to BWH ED
Case Study
In BWH ED:
VS BP 140/86 HR 126 SpO2 – 100%
GCS – 6T
Plain films:
lateral neck - OK
CXR - OK
pelvis - L sup and inf pubic rami fx, sacral fx
T-spine, L-S spine series no vertebral injury
Abd/pel CT
pubic rami fx, sacral fx
C-spine CT – no injury
The Glasgow Coma Scale
Score
Eye Opening
Verbal
Motor
1
None
None
Flaccid
2
Pain
Moans
Extends
3
Voice
Flexes
4
Spontaneous
Garbled
Words
Confused
Withdraws
Oriented
Localizes
5
6
Follows
commands
Case Study
In BWH ED:
CT head: minimally displaced L temporal skull fx
small L subdural hematoma with significant
mass effect
punctate L cortical hemorrhages, lateral
ventricular effacement, ? intraventricular blood
TBI – Epidemiology (2010)
• Each year, an estimated 1.7 million people in
the US sustain a TBI annually. Of them:
–1.365 million, nearly 80%, are treated and
released from an emergency department.
–275,000 are hospitalized, and
–52,000 die, 73% at the scene or in the ED
Evidence-Based Practice
• For many decades, management of severe
head trauma was tyrannized by anecdote and
institutional or individual idiosyncrasy
• Regional disparities in care and outcomes
were abundant
• Established effective therapies were not being
utilized, whereas practices shown to be
ineffective or even harmful persisted
Survey of 219 hospital intensive care units in 45 states that
treated patients with severe head injury.
Centers %
Routine ICP monitoring (more in high volume centers) 28
Hyperventilation and osmotic diuretics routinely used
83
Aiming for PaCO2 < 25 mm Hg
29
Corticosteroids use more than half the time
64
Crit Care Med 23: 560-567, 1995
History
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11 authors and 14 topics
3 years of meetings
Over 3000 articles reviewed
1st edition completed in 1995
2nd edition published in 2000
3rd edition published in 2007
Funded and supported by the
Brain Trauma Foundation (BTF)
American Association of Neurological Surgeons
World Health Organization’s Committee on Neurotrauma
Congress of Neurological Surgeons
AANS/CNS Joint Section on Neurotrauma and Critical Care
Guidelines for Management of Severe TBI
Objectives:
• STATE and DISSEMINATE the current scientific
evidence for the OPTIMAL management of TBI.
• Highlight issues for further RESEARCH and
CLINICAL TRIALS.
• Improve OUTCOME.
Topics
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Trauma systems
Initial management
Resuscitation of blood pressure and oxygenation
Indications for ICP monitoring
ICP treatment threshold
ICP monitoring technology
Cerebral perfusion pressure
Topics
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Hyperventilation
Mannitol
IV fluids
Barbiturates
Hypothermia
Steroids
Nutrition
Antiseizure prophylaxis
ICP treatment algorithm
Guidelines for the Management
of Severe Traumatic Brain Injury
Topics list
• Electronic literature search
• All relevant articles:
– Screened for scientific and statistical validity
– Classified according to a three point scale
• Class I
• Class II
• Class III
• Recommended ONLY what the literature supports
Guidelines for the Management
of Severe Traumatic Brain Injury
Class I
• Prospective, randomized, controlled trials
Class II
• Non-randomized, prospective controlled trials
• Observational studies
Class III
• Case series
• Case reports
• Expert opinion
Guidelines for the Management
of Severe Traumatic Brain Injury:
3rd edition changes
“Standards” became “Level I recommendations”
• Class I evidence
“Guidelines” became “Level II recommendations”
• Class II evidence
“Options” became “Level III recommendations”
• Class III evidence
Guidelines for the Management
of Severe Traumatic Brain Injury
Level I recommendations
• Represent principles that reflect a high degree
of clinical certainty
Level II recommendations
• Represent principles that reflect a moderate degree
of clinical certainty
Level III recommendations
• Represent principles for which there is unclear
clinical certainty
Topics
Blood pressure and oxygenation
Brain Trauma – It’s a two-way street
• Failure to support the CNS renders remaining organ
system support a futile exercise, but
Brain Trauma – It’s a two-way street
• Failure to support the CNS renders remaining organ
system support a futile exercise, but
• The first steps in supporting the brain actually
involve tending to the ABC’s
Brain Trauma – It’s a two-way street
• Failure to support the CNS renders remaining organ
system support a futile exercise, but
• The first steps in supporting the brain actually
involve tending to the ABC’s, because
• Hypotension and hypoxemia are the leading causes
of secondary injury
Secondary Injury
• In the recent decades, medical research has
demonstrated that all brain damage does not occur
at the moment of impact, but evolves over the
ensuing hours and days. This is referred to as
secondary injury.
• The injured brain is extremely vulnerable to
hypotension, hypoxia, and increased intracranial
pressure which are causes of secondary injury.
McHugh GS et al. Prognostic value of secondary insults in traumatic brain
injury: results from the IMPACT study. J Neurotrauma. 2007;24(2):287.
• Prospective prehospital and E.R. study of 717
severe head injury patients in the Traumatic Coma
Data Bank.
• Hypotension (SBP < 90 mm Hg) occurred in 35%
of patients and was associated with a two fold
increase in mortality.
J. Trauma 34:216-222, 1993
Resuscitation of Blood Pressure
& Oxygenation
Level II recommendation
• Blood pressure should be monitored and hypotension
(systolic blood pressure < 90 mm Hg) avoided.
Level III recommendation
• Oxygenation should be monitored and hypoxemia
(PaO2 < 60 mm Hg or O2 saturation < 90%) avoided.
Initial Management
Don’t forget the c-spine!
Initial Management
Don’t forget the c-spine!
5-7% of severe head trauma patients have a
concomitant c-spine injury
This increases to 8-10% of patients whose head
injury is from a MVC
Topics
Indications for ICP monitoring
ICP Physiology
ICP Physiology
• Intracranial Contents (normal)
–Brain 80%
–CSF 10%
–Blood 10%
ICP Physiology
• Intracranial Contents (normal)
–Brain 80%
–CSF 10%
–Blood 10%
• Munro-Kellie Doctrine – the volume of the cranial
contents is constant :
Vbrain + VCSF + Vblood (+ Vmass) = K
ICP Physiology
• Intracranial Contents (normal)
–Brain 80%
–CSF 10%
–Blood 10%
• Munro-Kellie Doctrine – the volume of the cranial
contents is constant :
Vbrain + VCSF + Vblood (+ Vmass) = K
• When brain injury occurs, brain expands, other
components must diminish, or pressure will rise
ICP Physiology
• CSF
–Formed in choroid plexus
ICP Physiology
• CSF
–Formed in choroid plexus
–Normal cerebral complement ~150ml
ICP Physiology
• CSF
–Formed in choroid plexus
–Normal cerebral complement ~150ml
–Quantity produced 0.3 ml/kg/hr = ~500ml/day
ICP Physiology
• CSF
–Formed in choroid plexus
–Normal cerebral complement ~150ml
–Quantity produced 0.3 ml/kg/hr = ~500ml/day
–Indifferent to ICP
ICP Physiology
• CSF
–Formed in choroid plexus
–Normal cerebral complement ~150ml
–Quantity produced 0.3 ml/kg/hr = ~500ml/day
–Indifferent to ICP
–Slight decrease with furosemide, acetazolamide
ICP Physiology
• CSF
–Formed in choroid plexus
–Normal cerebral complement ~150ml
–Quantity produced 0.3 ml/kg/hr = ~500ml/day
–Indifferent to ICP
–Slight decrease with furosemide, acetazolamide
–Drainage is only meaningful way to affect this
intracerebral component
ICP Physiology
• Intracranial pressure-volume curve
Topics
Indications for ICP monitoring
• 207 severely head injured patients who had ICP monitoring
and head CT scans
• Patients with a normal head CT had a 13% chance of ICP >
20 mm Hg
• Risk of intracranial hypertension (with normal CT) increased
to 60% if two or more of the following were noted:
– 1) Age over 40 years
– 2) SBP < 90 mm Hg
– 3) motor posturing
• Study 29 years old – ~4 generations of CT scanners ago
J. Neurosurg 56: 650-659, 1982
Indications for ICP Monitoring
Level II recommendation
• ICP monitoring is appropriate in severe head injury
patients with an abnormal CT, or
Level III recommendation
• a normal CT scan if 2 or more of the following are
noted on admission:
– SBP < 90 mm Hg
– Age > 40 years
– Uni-/Bilateral motor posturing
• Surveyed 34 academic trauma centers in the US (28
Level I and 6 Level II)
• Defined “aggressive” management centers as those
where ICP monitors were placed in >50% of patients
with an initial GCS of <9 and and abnormal head CT
• 11 centers “aggressive”, 20 “nonaggressive”
• Mortality: 27% vs. 45% (p=.01)
• No differences in outcome among survivors
Intraventricular Catheter
Topics
ICP treatment threshold
• The ICP threshold that was most predictive of 6 month
outcome was analyzed in 428 severely head injured patients.
• The proportion of hourly ICP reading greater than 20 mm Hg
was a significant independent determinant of outcome.
J. Neurosurg 75:S59-S66, 1991
ICP Treatment Threshold
Level II recommendation
• Treatment should be initiated with intracranial
pressure (ICP) thresholds above 20 mm Hg.
Level III recommendation
• A combination of ICP values, and clinical and brain
CT findings, should be used to determine the need
for treatment.
Topics
ICP monitoring technology
ICP Monitoring Technology
Recommendation (no level)
• In the current state of technology, the ventricular
catheter connected to an external strain gauge is
the most accurate, low cost, and reliable method
of monitoring ICP. It also allows therapeutic
CSF drainage.
• ICP transduction via fiberoptic or strain gauge
devices placed in ventricular catheters provide
similar benefits but at a higher cost.
Topics
Cerebral perfusion pressure
CPP Physiology
• Cerebral blood volume – hard to measure
• Cerebral blood flow – surrogate for volume
– Also hard to measure
• TCD
• Xenon scans – not commercially viable
• Cerebral perfusion pressure
– Easy to measure (MAP – ICP (or CVP))
– Target of therapy – traditionally to maintain > 70mmHg
– Not rigorously validated as a therapeutic strategy
CPP Treatment Strategy
• Where did the goal of a CPP of 70 come from?
CPP Treatment Strategy
• Where did the goal of a CPP of 70 come from?
CPP Treatment Strategy
Where did the goal of a CPP of 70 come from?
Rosner and Becker 1984
Cat percussive injury model
Elimination of plateau waves at CPP > 70mmHg
Plateau waves (Lundberg A waves)
Plateau waves – lethal cycle hypothesis
ICP
CBV
CPP
Vasodilation
• 158 patients with GCS < 7 managed according to a
CPP protocol:
– Maintain euvolemia (CVP 8-10 mm Hg)
– Ventriculostomy CSF drainage at 15 mm Hg
– Systemic vasopressors to maintain CPP at least 70 mm Hg
– Hyperventilation, barbiturates, hypothermia not used.
• Mortality 29% and 2% vegetative for entire group. Favorable
outcome in GCS 3 of 35% ranging up to 75% for GCS 7.
J. Neurosurg 83: 949-962, 1995
Comparison of CPP-targeted therapy
with ICP-targeted therapy
• CPP targets
• ICP targets
– CPP > 70
– ICP < 20
– MAP > 90
– CPP > 50
– ICP < 20
– MAP > 70
Cerebral Perfusion Pressure
• Conclusions:
– With ICP-targeted therapy, 2.4-fold greater risk of
“secondary ischemic insults” defined as jugular venous
desaturations
– No difference between the two groups in neurologic
outcome
– 5-fold higher incidence of ARDS (3% vs. 15%) in CPPtargeted group
– “…potential adverse effects of this management strategy
may offset these beneficial effects.”
Robertson et al, CCM 1999; 27:2086-2095
Cerebral Perfusion Pressure
“...the critical threshold for CPP seems to be
60 rather than 70 mmHg.”
Marion DW (editorial) CCM 2002 30:7; 1671-1672
Cerebral Perfusion Pressure
Level II recommendation
Aggressive attempts to maintain cerebral perfusion
pressure (CPP) above 70 mm Hg with fluids and
pressors should be avoided because of the risk of
adult respiratory distress syndrome (ARDS).
Cerebral Perfusion Pressure
Level III recommendation
CPP of <50 mm Hg should be avoided.
The CPP value to target lies within the range of 50-70
mm Hg. Patients with intact pressure autoregulation
tolerate higher CPP values.
Ancillary monitoring of cerebral parameters that include
blood flow, oxygenation, or metabolism facilitates CPP
management.
What about jugular venous saturation or
brain tissue oxygenation monitoring?
What about jugular venous saturation or
brain tissue oxygenation monitoring?
Level III recommendation
Jugular venous saturation (<50%) or brain tissue
oxygen tension (<15 mm Hg) are treatment
thresholds.
Jugular venous saturation or brain tissue oxygen
monitoring measure cerebral oxygenation.
Topics
Hyperventilation
Hyperventilation
• Is hyperventilation an appropriate strategy in
management of intracranial hypertension?
– Reliably lowers ICP
• But…
– Works by cerebral vasoconstriction
– Fatigable phenomenon
– Doesn’t work in injured brain
– Rebound phenomenon
Hyperventilation
Level I recommendation
• In the absence of increased intracranial
pressure (ICP), chronic prolonged
hyperventilation therapy (PaCO2 of 25 mm Hg
or less) should be avoided after severe
traumatic brain injury (TBI).
Hyperventilation
Level II recommendation
• The use of prophylactic hyperventilation
(PaCO2 < 35 mm Hg) therapy during the first
24 hours after severe TBI should be avoided
because it can compromise cerebral perfusion
during a time when cerebral blood flow (CBF) is
reduced.
Hyperventilation
Level III recommendation
• Hyperventilation therapy may be necessary for
brief periods when there is acute neurologic
deterioration, or for longer periods if there is
intracranial hypertension refractory to sedation,
paralysis, cerebrospinal fluid (CSF) drainage,
and osmotic diuretics.
Topics
Mannitol
Mannitol
• Advantages
– Non-metabolized, osmotically active alcohol
– Lowers ICP by osmotic mechanism
– Hydroxyl radical scavenger
• But…
– Osmotic effect only with intact blood-brain barrier
– May aggravate edema in injured brain tissue
– Diuretic – leads to volume depletion
– Hemodynamic instability at serum osmolality >~325
Mannitol
Level II recommendation
• Mannitol is effective for control of raised intracranial
pressure (ICP) at doses of 0.25 gm/kg to 1 g/kg
body weight. Arterial hypotension (systolic blood
pressure < 90 mm Hg) should be avoided
Level III recommendation
• Effective doses range from 0.25 - 1.0 gm/kg
body weight.
Mannitol
Level III recommendation
• Restrict mannitol use prior to ICP monitoring to
patients with signs of transtentorial herniation or
progressive neurological deterioration not
attributable to extracranial causes.
Topics
IV fluids
Original Article
Saline or Albumin for Fluid Resuscitation in
Patients with Traumatic Brain Injury
The SAFE Study Investigators
N Engl J Med
Volume 357(9):874-884
August 30, 2007
Kaplan-Meier Estimates of the Probability of Survival
The SAFE Study Investigators. N Engl J Med 2007;357:874884
Topics
Barbiturates and propofol
Barbiturates and propofol
Level II recommendation
• Prophylactic administration of barbiturates to induce
burst suppression EEG is not recommended.
• High-dose barbiturate administration is
recommended to control elevated ICP refractory to
maximum standard medical and surgical treatment.
Hemodynamic stability is essential before and
during barbiturate therapy.
Barbiturates and propofol
Level II recommendation (continued)
• Propofol is recommended for the control of ICP, but
not for improvement in mortality or 6 month
outcome. High-dose propofol can produce
significant morbidity.
Topics
• Hypothermia
Topics
Steroids
CRASH = Corticosteroid Randomisation After
Significant Head Injury
Steroids
Level I recommendation
• The use of steroids is not recommended for
improving outcome or reducing intracranial pressure
in patients with severe head injury.
Topics
Nutrition
Nutrition
Head injury is associated with elevated catabolic state
and nitrogen wasting
Starvation aggravates this process
Literature of relatively poor quality, but trend favors
early institution of nutrition
Nutrition
Level II recommendation
• Patients should be fed to attain full caloric
replacement by day 7 post-injury.
Topics
Antiseizure prophylaxis
• 404 post traumatic head injury patients (GCS 3-10 and
abnormal head CT) randomized to treatment with phenytoin
or placebo for one year with a two year follow up.
• In the first week after injury 4% of the patients receiving
phenytoin had seizures compared to 14% taking placebo.
• After the first week there was no significant difference
between the rate of seizures in the two groups.
N. Engl. J. Med 323:497-502, 1990
Antiseizure Prophylaxis
Level II recommendation
• Prophylactic use of phenytoin or valproate is not
recommended for preventing late posttraumatic
seizures (PTS).
• Anticonvulsants are indicated to decrease the
incidence of early PTS (within 7 days of injury).
However, early PTS is not associated with worse
outcomes.
Case Study
Admitted to 7D ICU
ICP monitor placed
ICP elevated, remained >35mmHg in spite of aggressive
management with mannitol, furosemide and
hypertonic saline
To OR for decompressive craniectomy
XXXXXXX
Decompressive Craniectomy for TBI
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Considered “salvage therapy” for refractory ICH
Poor quality data regarding efficacy
Encouraging pediatric trial
Recent trial in Australia/NZ disappointing
RESCUEicp (Randomized Evaluation of Surgery
with Craniectomy for Uncontrollable Elevation of
Intracranial Pressure) trial currently enrolling
Intracranial Pressure before and after Randomization.
Cooper DJ et al. N Engl J Med 2011;364:1493-1502
Cumulative Proportions of Results on the Extended Glasgow Outcome Scale.
Cooper DJ et al. N Engl J Med 2011;364:1493-1502
Conclusions
• In adults with severe diffuse traumatic brain injury
and refractory intracranial hypertension, early
bifrontotemporoparietal decompressive craniectomy
decreased intracranial pressure and the length of
stay in the ICU but was associated with more
unfavorable outcomes.
Case Study
Postoperatively localizing with both upper
extremities
Protracted ICU course complicated by MRSA
pneumonia
Tracheostomy 1/8/00 V-P shunt 1/21/00
Recovered consciousness, speech. Discharged
to rehab 1/29/00
Case Study
Rehab x 2 months
Special school x 2 months
Fall 2000 restarted junior year of high school
Seen in pre-operative clinic 11/00 for minor
GU procedure
No detectable cognitive deficit
PHEW!
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