Brain
and
Spinal Cord Trauma
Mani K.C Vindhya M.D
Asst Prof of Anesthesiology
Nova Southeastern University
ABC’s of Anesthesia for Traumatic Brain Injury (TBI)
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Airway management
Blood pressure management
CO2 (Hyperventilate or not?)
Diuretics or Dexamethasone?
Early decompressive craniectomy
Fluid management
Glucose management
Hypothermia (Is it “cool” or not?)
IV and Inhaled Anesthetics
Airway Management in TBI
Issues in Intubating the Head-Injured Patient
(JC Drummond, ASA Refresher Course Lecture 144: 1-7, 2000)
Head
Intracranial pressure (ICP),
altered mental status,
uncooperative/combative patient
Neck
Assume unstable C-spine
Airway
Blood,
injury,
skull base fracture
Breathing
Hypoxemia
Circulation
Assume hypovolemia
Digestive Juices
Assume full stomach
Principles for Resuscitating the Head-Injured Patient
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First ABC, then ICP.
1. The ABC’s initially take priority over ICP
(JC Drummond, ASA Refresher Course Lecture 144: 1-7, 2000).
Secure the airway.
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Breathing: Guarantee gas exchange, oxygenation and ventilation.
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Stabilize the circulation
Think associated injuries.
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2. Unstable C-spine injury could lead to a cervical cord injury
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(Doolan LA,O’Brien JF. Anaesth Int Care 13: 319-24, 1985).
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If a rapid sequence induction and intubation, then...
Cricoid pressure (Sellick maneuver) & Manual in-line stabilization
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Which patients need immediate intubation?
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Empirically, patients with a Glasgow Coma
Scale (GCS) < 8 require intubation and controlled
ventilation for airway and/or ICP control.
Patients with a GCS of 9-12 require close observation.
Some of these will “talk and die”
Delayed deterioration observed up to 48 hours after
initial injury (Marshall LF et al. J Neurosurg 59: 285-8, 1983).
Glasgow Coma Scale (GCS)
Eyes open
Never
To pain
To speech
Spontaneously
1
2
3
4
Best verbal responses
None
Garbled, incomprehensible sounds
Inappropriate words
Confused but converses
Oriented
1
2
3
4
5
Best motor responses
None
Extension (decerebrate rigidity)
Abnormal flexion (decorticate rigidity)
Withdrawal
Localizes pain
Obeys commands
1
2
3
4
5
6
Total
3-15
C. Cervical Fractures are Common in Along with Traumatic
Brain Injury
1. Cervical spine injury occurs in 2% of victims of blunt trauma
(Crosby ET.Anesthesiology 104: 1293-1318, 2006.)
2. Higher incidence of cervical injury in patients who have
experienced severe traumatic brain injury, as determined by:
A. low Glasgow Coma Scale (GCS) and B. Unconsciousness
Association between GCS and cervical spine injury
(Demetriades D et al. J Trauma 48: 724-7, 2000).
Injury Severity (GCS Score)
% of Patients with C-Spine Injury
13-15
9-12
<8
1.4 %
6.8 %
10.2 %
4. Of those patients who need emergent intubation (GCS < 8),
roughly10% (1 in 10) have an associated C-spine injury!
5. C-spine injuries may be missed by neck films or CT scans
(Crosby ET, Lui A. Can J Anaesth 37: 707-9, 1990; Drummond JC, ASA Refresher Course Lecture144:
1-7, 2000).
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Lateral X-ray misses 20% of C-spine fractures.
Lateral and AP and odontoid views miss only 7%.
7 to 14% of C-spine fractures involve C7 and/or T1.
Intubating the Head-Injured Patient
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1. If pentothal (or etomidate)-sux-tube... (Drummond JC, ASA Refresher Course
Lecture 144: 1-7, 2000)
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a. Manual in-line stabilization (no pillow, head held rigid on backboard)
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Axial traction could lead to extension injury
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Cricoid pressure
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Back of collar in place
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Optimum exposure of vocal cords may be limited with in-line
stabilization
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Not sniffing position
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Case report: “Neurologic Deterioration with Airway Management in a
C-spine-injured Patient” (Hastings RH, Kelley SD. Anesthesiology 78: 580-3, 1993).
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MVA; neck pain; 3 views “normal”
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Delayed respiratory distress Succinylcholine, intubation Paraplegic
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CT: C6-C7 prevertebral hematoma
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Remember other intubation options (JC Drummond, ASA Refresher
Course Lecture 144: 1-7, 2000):
Fiberoptic oral / nasal
 Blind nasal (not if basilar skull fracture)
 Light wand / stylettes
 Augustine guide
 Glidescope, Bullard scope, etc.
 Retrograde cannulation
 LMA (as backup for failed intubation)
 Cricothyrotomy
Case reports: “Beware of the basilar skull fracture!”
a. “Complication from a naso-pharyngeal airway in a
patient with a basilar skull fracture.” (Muzzi DA et al. Anesthesiology 74:
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366-8,1991)
b. “Intracranial placement of a nasotracheal tube after
facial fracture: a rare complication” (Marlow TJ, Goltra DD Jr, Schabel SI.
J Emerg Med 15: 187-91, 1997)
Blood Pressure (BP) Management in TBI
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Three historical strategies to manage MAP after TBI.
The strategy depends on the relationship of cerebral blood
flow (CBF) to MAP after head injury (Drummond JC, Patel PM.
“Neurosurgical Anesthesia,” Chap. 53 in Miller RD ed., Miller’s Anesthesia, 6th ed., Churchill
Livingstone, Philadelphia, 2005: pp. 2127-73.)
Approach
Assumption About
Autoregulation
Assumption About MAP
“Lund” Approach
Abolished (steep rise)
Avoid hyperemia, keep
MAP down
“Edinburgh” Approach
Abolished (gradual rise)
Avoid decreased CBF,
keep MAP up
“Birmingham” Approach
Intact (but plateau lower)
Avoid decreased CBF,
keep MAP up
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A new and evolving theme in neurosurgical management of
TBI (JC Drummond, ASA Refresher Course Lecture 144: 1-7, 2000)
1. We used to worry about cerebral hyperemia (too much
CBF), and tended to decrease BP.
2. Now we worry about cerebral ischemia (not enough CBF),
and tend to increase BP.
Hypoperfusion is very common after TBI (on the first day)
Autoregulation is impaired.
Brain is very vulnerable to secondary injury.
Hypotension after TBI is associated with particularly “bad” outcomes.
Impact of Hypoxia and/or Hypotension on Outcome after
Closed Head Injury (GCS < 8) [at time of hospital arrival]
(Chesnut RM et al. J Trauma 34: 216-22, 1993)
Number % Good or Moderate % Poor or Dead
Total
699
43%
57%
Normotension/normoxia
456
51%
49%
Hypotension (SBP<90)
113
24%
76%
Hypoxia (paO2 < 60)
78
45%
55%
Hypoxia and hypotension
52
6%
94%
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“Deleterious effects of intraoperative hypotension on
outcome in patients with severe head injuries” (Pietropaoli JA et al, J
Trauma 33: 403-7, 1992)
53 blunt head injuries
 All required surgery.
Problems
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surgeons reading anesthesia records
retrospective methodology
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If SBP > 90 mm Hg intraoperatively, mortality = 25%
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If SBP < 90 mm Hg intraoperatively, mortality = 82% (P < 0.001)
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Brain Trauma Foundation: Recommendations to
Manage Severe TBI (Joint Section on Neurotrauma and
Critical Care, The Brain Trauma Foundation, Surgeons
AAoN: Guidelines for the Management of Severe Head
Injury. Park Ridge, IL, The American Association of
Neurological Surgeons, 1995.)
Standards, Guidelines, and Options
Standards – represent principles that reflect a high degree of
clinical certainty
Guidelines – reflect a moderate degree of clinical certainty
Options – represent principles for which there is unclear
clinical certainty
Resuscitation of BP and Oxygenation Standard – none
Guideline – Hypotension (SBP < 90 mm Hg) or hypoxia
(apnea or cyanosis in the field or a paO2 < 60 mm Hg) must
be scrupulously avoided, if possible, orcorrected
immediately
Option – MAP should be maintained above 90 mm Hg
throughoutthe patient’s course
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BP Management in TBI: What’s the Bottom Line
for Us?
1. Avoid hypotension (SBP < 90 mm Hg) if possible,
or correct itimmediately
2. MAP > 70-80 mm Hg is reasonable
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CO2 Management in TBI
Should we hyperventilate?
 Concepts in TBI have totally changed
 Hyperventilation and hypocapnia (paCO2 of 25):
Decreases ICP
But also decreases CBF, predisposing to cerebral ischemia
Some studies showing that hyperventilation may be
deleterious in TBI:
 “Does acute hyperventilation provoke cerebral oligaemia in
comatose patients after acute head injury?”
(Cold GE. Acta Neurochir 96: 100-6, 1989)
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27 comatose head injury patients Intra-carotid 133Xe to
measure CBF paCO2: From 35 to 25
CBF < 20: Foci went from 9/27 to 15/27 CBF < 15: Foci went
from 2/27 to 9/27
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“Effect of hyperventilation on regional cerebral blood flow
in head- injured children” (Shippen P et al. Crit Care Med 25: 1402-9, 1997)
23 children; isolated TBI; GCS from 3 to 7 paCO2 > 35, 2535, and < 25 mm Hg Baseline CBF (Xe CT) slightly
decreased CMRO2 1/3rd of normal
% ischemic: Normocapnia (28.9%) vs. hypocapnia (73.1%)
Moderate hyperventilation induced a harmful reduction in
brain tissue PO2 (Imberti R et al. J Neurosurg 96: 97-102, 2002).
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Brain Trauma Foundation: Recommendations Regarding
Hyperventilation
Standard: (One of the few) In the absence of increased ICP,
chronic prolonged hyperventilation therapy (paCO2 < 25 mm
Hg) should be avoided after severeTBI
Guideline: The use of prophylactic hyperventilation therapy
(paCO2 < 35 Hg) during the 1st 24 hours after severe TBI
should be avoided because it can compromise cerebral
perfusion during a time when CBF is decreased.
Option: Hyperventilation therapy may be necessary for brief
periods when there is acute neurologic deterioration, or for
longer periods of time if there is intracranial HTN refractory to
sedation, paralysis, CSF drainage, and osmotic diuretics.
Hyperventilation in TBI: What’s the Bottom Line for Us?
 Don’t routinely hyperventilate the TBI patient intraoperatively.
 A paCO2 of 35 mm Hg is reasonable.
 Hyperventilate to paCO2 of 25 only if needed
(i.e., “swollen brain”).
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Diuretics or Dexamethasone in TBI?
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Diuretics in TBI?
 The osmotic diuretic mannitol is often employed in
the setting of TBI.
 Mannitol requires an intact blood:brain barrier to work
 The blood:brain barrier is probably not intact in areas
of severe TBI.
 But we use mannitol anyway, hoping it will “shrink”
normal brain.
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Dexamethsone in RBI? Corticosteroids are thought to
be beneficial to shrink edema around solid brain tumors.
They are not beneficial, and may even be harmful, in TBI
(Dearden NM et al. J Neurosurg 64: 81-8, 1986; Alderson P, Roberts I. BMJ 314: 1855-9, 1997;
Yates RI et al, Lancet 364 (9442): 1321-8, 2004).
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Bottom Line? Don’t use steroids in TBI! (But do use
high-dose Solumedrol [methylprednisolone] for acute
spinal cord injury!)
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Early Decompressive Craniectomy
Early decompressive craniectomy for intractable
intracranial hypertension is “what’s new” in TBI.
2006 Study: “better-than-expected functional
outcome in patients with medically uncontrollable
ICP and/or brain herniation, compared with outcomes
in other control cohorts...” (Aarabi B et al. J Neurosurg 104: 469:79, 2006).
“...insufficient data to support the routine use of DC
[decompressive craniectomy] in TBI” (Schirmer CM et al.
Neurocritical Care 8: 456-70, 2008).
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Bottom line for us? More “midnight specials” while
on call?
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Fluid Management in TBI
Basic principles of fluid management in TBI
 The mantra in intracranial neuro used to be “Run ‘em dry.”
 Now the mantra is “Run ‘em even.”
 Avoid hypovolemia with fluid replacement.
 For normal craniotomy,
Deficit +
Hourly maintenance +
Cover urine cc for cc
Cover blood loss 3:1 with crystalloid
 A negative fluid balance is associated with a bad outcome.
In humans,
exceeding certain thresholds was associated with an increased
percentage of patients with poor outcome (Clifton GL et al. Fluid thresholds
and outcome from severe brain injury. CritCare Med 30: 739-45, 2002):
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Fluid balance < -594 ml
Mean arterial pressure < 70 mm Hg Intracranial pressure > 25
mm Hg
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Which fluid is best in TBI?
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Usually normal saline is recommended as the crystalloid
for resuscitation.
 NSS is slightly hypertonic.
 Lactated Ringer’s
Is slightly hypotonic +
Lactate converted to glucose in liver
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Give blood or colloid as needed.
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In an experimental model of TBI, brain water content
was increased with both ½ NSS and NSS, relative to blood or
colloid (Drummond JC et al. Anesthesiology 88:993-1002, 1998).
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Glucose Management in TBI
Hyperglycemia is detrimental.
 Elevated glucose levels are deleterious in cerebral
ischemia.
In animal models, hyperglycemia at onset of ischemia worsens
outcome
In humans, hyperglycemia is associated with a worsening of
post-ischemic brain injury
 Why? Intracellular acidosis probably injures neurons and
glia (Wass CT, Lanier WL. Mayo Clin Proc 71: 801-12, 1996)
Glucose Management in TBI: What’s the Bottom Line?
 Monitor glucose levels to maintain “normoglycemia” as
rigidly as possible.
 Avoid IV glucose infusions unless necessary (NB: drug
infusions)
 Use insulin to treat hyperglycemia.
 Don’t allow a sustained glucose > 250.
 Avoid hypoglycemia and electrolyte abnormalities.
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Hypothermia in TBI was hot, but now it’s not!
National Acute Brain Injury Study: Hypothermia (NABIS:H)
= prospective, multicenter, randomized trial (Clifton GL et al. N Engl J Med 344:
556-63, 2001)
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“Treatment with hypothermia, with the body temperature reaching
33 oC within 8 hours after injury, was not effective in improving
outcomes in patients with severe brain injury.”
Patients that were hypothermic on admission and warmed did
poorly.
Patients that were hypothermic on admission and stayed
hypothermic seemed to do better.
So don’t rewarm hypothermic patients too quickly.
Bottom line?
 Mild induced hypothermia
 Not beneficial:
 After traumatic brain injury
 During clipping of intracranial aneurysms (Todd MM et al, New
Engl J Med 352: 135-45, 2005.
Beneficial after successful resuscitation from cardiac arrest
(New ACLS Guidelines)
 Avoid hyperthermia.
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Inhaled Anesthetics
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Reasonable maintenance regimens for intracranial
neuroanesthesia (going from routine to desperate)
 N2O + isoflurane (1/2%) + fentanyl?
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N2O = the first agent to go if there’s brain swelling or
venous air emboli or danger of ischemia (i.e., head trauma)
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MAC equivalents of sevoflurane or desflurane might also be
substituted for isoflurane
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Sufentanil could be substituted for fentanyl.
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Isoflurane (1%) + fentanyl
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Isoflurane (1/2%) + propofol + fentanyl
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The volatile agents are next to go if the brain is
compromised (i.e. markedly increased ICP or brain
swelling).
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Total IV anesthetic: propofol + fentanyl
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Barbiturate coma – for intractable brain swelling (titrated to
EEG burst suppression)
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Thiopental
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Pentobarbital?
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ICP Monitoring in TBI
Brain Trauma Foundation Guideline. ICP monitoring is
appropriate in severe head injury patients (GCS < 8) with an
abnormal CT, or a normal CT scan if 2 or more are noted on
admission:
 Systolic BP < 90 mm Hg
 Age > 40 years
 Uni- or bilateral motor posturing
What patients need ICP monitoring during nonneurologic surgery? (JC Drummond, ASA Refresher Course Lecture 144: 1-7, 2000)
 Level of consciousness? If loss of consciousness at any
time or GCS < 15, have neurosurgery check CT scan. ICP
monitoring is advisable if compressed basal cisterns,
midline shift, effaced ventricles, or any intracranial lesion
(i.e. contusion, small subdural).
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Time since injury. Delayed deterioration has been observed up
to 48 hourspost-injury
Intended aortic occlusion, i.e. repair of ruptured aorta
Nature and duration of intended procedure (i.e. short
debridement vs. long orthopedic procedure)
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Summary: ABC’s of Anesthesia for Traumatic Brain Injury
Airway. Safely get control.
Blood pressure
Choose an anesthetic that maintains MAP.
Avoid hypotension (SBP < 90 mm Hg) if possible, correct it immediately.
MAP > 70-80 mm Hg is reasonable.
Carbon dioxide. Don’t routinely hyperventilate, only if necessary for a “swollen
brain.”
Diuretics or Dexamethasone?
We usually give diuretics (mannitol). We usually don’t give steroids.
Early decompressive craniectomy may cause us many sleepless nights.
Fluids. Avoid hypovolemia.
Glucose. Treat hyperglycemia.
Hypothermia was “hot”, but now it’s not. Avoid hyperthermia.
IV and Inhaled Anesthetics.
N2O is first to go.
Volatile inhaled anesthetics are next to go.
TIVA (with fentanyl and propofol) is reasonable
Thiopental (for EEG burst suppression) if intractable brain swelling
Acute and chronic spinal cord injury
(SCI)
Effects of spinal cord lesions
( Ezekiel MR. Handbook of
Anesthesiology,2002-2003 Edition. Current Clinical Strategies Publishing, pp. 165-66):
LESION SITE
COMMON PROBLEM
C3-C5 (Phrenic nerve)
Usually apnea requiring intubation and
mechanical ventilation
Below C5-C6
Impaired oxygenation and ventilation (up
to 70% decrease in VC and FEV1)
T1-T4 (origin of cardio-accelerator fibers)
Bradycardia, bradydysrhythmias, AV
block, cardiac arrest
Above T7
Significant alveolar ventilation
impairment
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Issues in spinal cord injury (SCI):
1. Intubation options: Airway management of acute
C-spine injury (JC Drummond, ASA Refresher Course Lecture 144: 1-7, 2000)
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Rapid sequence induction and intubation with in-line
cervical fixation
Fiberoptic oral / nasal intubation
Blind nasal intubation (not if basilar skull fracture)
Light wand/stylettes
Glidescope, Bullard scope, etc.
Retrograde cannulation
Laryngeal mask airway (backup for failed intubation)
Cricothyrotomy
Succinylcholine
Safe for use in first 24-48 hours
Contraindications to succinylcholine:
AFTER 24-48 HOURS
AT ANY TIME
Quadri- or paraplegia
Hemiplegia (i.e., stroke)
rd
Extensive 3 degree burns
Multiple trauma
Chronic renal failure (K+ > 5.5)
History of malignant hyperthermia (MH)
Muscular dystrophy (such as Duchenne’s)
Routine use in pediatrics
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3. High-dose methylprednisolone (Bracken MB et al, N Engl J Med
322:1405-11, 1990)
May improve functional recovery if given within 8 hours
after SCI
 Loading dose = 30 mg/kg IV
Maintenance dose = 5.4 mg/kg/hr IV for 23 hours
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Spinal shock
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Spinal shock
(Ezekiel MR. Handbook of Anesthesiology, 2002-2003
Edition. Current Clinical Strategies Publishing, pp. 165-66)
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Seen in high SCI’s
Lasts a few hours to several weeks
Characterized by (below lesion):
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Loss of sympathetic tone
Flaccid paralysis
Total absence of visceral and somatic sensation
Paralytic ileus
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Loss of spinal cord reflexes
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Autonomic hyperreflexia
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Autonomic hyperreflexia (Stoelting RK, Miller RD. Basics of Anesthesia, 4th ed.
Churchill-Livingstone: 2000, pp. 328-9)
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A complication of chronic spinal cord transection
(especially above T6)
Sudden hypertension + reflex bradycardia
Distension of hollow viscus (e.g. bladder)
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common precipitating event
Prevented by spinal anesthesia (also by epidural or general
anesthesia and anti-hypertensives such as nitroprusside
Diagnosis may compel you to insert arterial line
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Basic Principles of SCI
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Difficult airway can be problematic.
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Unstable cervical spine. Don’t break the patient’s neck!
Can’t use succinylcholine after 24-48 hours. Don’t cause
a hyperkalemic code!
Hemodynamic instability is common with
anesthesia and surgery.
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Acute SCI: spinal shock and hypotension
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Chronic SCI: autonomic hyperreflexia and hypertension
End of NeuroAnesthesiology