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Brain and Spinal Cord Trauma


Brain and Spinal Cord Trauma Mani K.C Vindhya M.D Asst Prof of Anesthesiology Nova Southeastern University Spinal shock Spinal shock (Ezekiel MR. – PowerPoint PPT presentation

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Title: Brain and Spinal Cord Trauma

Brain and Spinal Cord Trauma
  • Mani K.C Vindhya M.D
  • Asst Prof of Anesthesiology
  • Nova Southeastern University

ABCs of Anesthesia for Traumatic Brain Injury
  • 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)
  • Principles for Resuscitating the Head-Injured
  • First ABC, then ICP.
  • 1. The ABCs initially take priority over ICP
  • (JC Drummond, ASA Refresher
    Course Lecture 144 1-7, 2000).
  • Secure the airway.
  • Breathing Guarantee gas exchange, oxygenation
    and ventilation.
  • Stabilize the circulation
  • Think associated injuries.
  • 2. Unstable C-spine injury could lead to a
    cervical cord injury
  • (Doolan LA,OBrien JF. Anaesth Int
    Care 13 319-24, 1985).
  • If a rapid sequence induction and intubation,
  • Cricoid pressure (Sellick maneuver) Manual
    in-line stabilization

  • Which patients need immediate intubation?
  • Empirically, patients with a Glasgow Coma Scale
    (GCS) lt 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)
  • C. Cervical Fractures are Common in Along with
    Traumatic Brain Injury
  • Cervical spine injury occurs in 2 of victims of
    blunt trauma (Crosby ET.Anesthesiology 104
    1293-1318, 2006.)
  • Higher incidence of cervical injury in patients
    who have experienced severe traumatic brain
    injury, as determined by
  • low Glasgow Coma Scale (GCS) and B.
  • Association between GCS and cervical spine injury
  • (Demetriades D et al. J Trauma 48 724-7, 2000).

  • 4. Of those patients who need emergent
    intubation (GCS lt 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).
  • 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

  • Intubating the Head-Injured Patient
  • 1. If pentothal (or etomidate)-sux-tube...
    (Drummond JC, ASA Refresher Course Lecture 144
    1-7, 2000)
  • a. Manual in-line stabilization (no pillow, head
    held rigid on backboard)
  • Axial traction could lead to extension injury
  • Cricoid pressure
  • Back of collar in place
  • Optimum exposure of vocal cords may be limited
    with in-line stabilization
  • Not sniffing position
  • Case report Neurologic Deterioration with
    Airway Management in a C-spine-injured Patient
    (Hastings RH, Kelley SD. Anesthesiology 78
    580-3, 1993).
  • MVA neck pain 3 views normal
  • Delayed respiratory distress Succinylcholine,
    intubation Paraplegic
  • CT C6-C7 prevertebral hematoma

  • 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
  • a. Complication from a naso-pharyngeal airway in
    a patient with a basilar skull fracture. (Muzzi
    DA et al. Anesthesiology 74 366-8,1991)
  • 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
  • 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., Millers
    Anesthesia, 6th ed., Churchill Livingstone,
    Philadelphia, 2005 pp. 2127-73.)

(No Transcript)
  • 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 lt 8) at time of hospital arrival
    (Chesnut RM et al. J Trauma 34 216-22, 1993)

  • 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
  • surgeons reading anesthesia records
  • retrospective methodology
  • If SBP gt 90 mm Hg intraoperatively, mortality
  • If SBP lt 90 mm Hg intraoperatively, mortality
    82 (P lt 0.001)

  • 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
  • Guideline Hypotension (SBP lt 90 mm Hg) or
    hypoxia (apnea or cyanosis in the field or a paO2
    lt 60 mm Hg) must be scrupulously avoided, if
    possible, orcorrected immediately
  • Option MAP should be maintained above 90 mm Hg
    throughoutthe patients course

  • BP Management in TBI Whats the Bottom Line for
  • 1. Avoid hypotension (SBP lt 90 mm Hg) if
    possible, or correct itimmediately
  • 2. MAP gt 70-80 mm Hg is reasonable

  • 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
  • Some studies showing that hyperventilation may be
    deleterious in TBI
  • Does acute hyperventilation provoke cerebral
    oligaemia in comatose patients after acute head
  • (Cold GE. Acta Neurochir 96 100-6, 1989)
  • 27 comatose head injury patients Intra-carotid
    133Xe to measure CBF paCO2 From 35 to 25
  • CBF lt 20 Foci went from 9/27 to 15/27 CBF lt 15
    Foci went from 2/27 to 9/27

  • 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
    gt 35, 25-35, and lt 25 mm Hg Baseline CBF (Xe CT)
    slightly decreased CMRO2 1/3rd of normal
  • ischemic Normocapnia (28.9) vs. hypocapnia
  • Moderate hyperventilation induced a harmful
    reduction in brain tissue PO2 (Imberti R et al.
    J Neurosurg 96 97-102, 2002).

  • Brain Trauma Foundation Recommendations
    Regarding Hyperventilation
  • Standard (One of the few) In the absence of
    increased ICP, chronic prolonged hyperventilation
    therapy (paCO2 lt 25 mm Hg) should be avoided
    after severeTBI
  • Guideline The use of prophylactic
    hyperventilation therapy (paCO2 lt 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 Whats the Bottom Line
    for Us?
  • Dont routinely hyperventilate the TBI patient
  • A paCO2 of 35 mm Hg is reasonable.
  • Hyperventilate to paCO2 of 25 only if needed
  • (i.e., swollen brain).

  • Diuretics or Dexamethasone in TBI?
  • Diuretics in TBI?
  • The osmotic diuretic mannitol is often employed
    in the setting of TBI.
  • Mannitol requires an intact bloodbrain barrier
    to work
  • The bloodbrain barrier is probably not intact in
    areas of severe TBI.
  • But we use mannitol anyway, hoping it will
    shrink normal brain.
  • 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).
  • Bottom Line? Dont use steroids in TBI! (But do
    use high-dose Solumedrol methylprednisolone for
    acute spinal cord injury!)

  • Early Decompressive Craniectomy
  • Early decompressive craniectomy for intractable
    intracranial hypertension is whats 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 46979, 2006).
  • ...insufficient data to support the routine use
    of DC decompressive craniectomy in TBI
    (Schirmer CM et al. Neurocritical Care 8 456-70,
  • Bottom line for us? More midnight specials
    while on call?

  • 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 31 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)
  • Fluid balance lt -594 ml
  • Mean arterial pressure lt 70 mm Hg Intracranial
    pressure gt 25 mm Hg

  • Which fluid is best in TBI?
  • Usually normal saline is recommended as the
    crystalloid for resuscitation.
  • NSS is slightly hypertonic.
  • Lactated Ringers
  • Is slightly hypotonic
  • Lactate converted to glucose in liver
  • Give blood or colloid as needed.
  • 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 88993-1002, 1998).

  • 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 Whats the Bottom
  • Monitor glucose levels to maintain
    normoglycemia as rigidly as possible.
  • Avoid IV glucose infusions unless necessary (NB
    drug infusions)
  • Use insulin to treat hyperglycemia.
  • Dont allow a sustained glucose gt 250.
  • Avoid hypoglycemia and electrolyte abnormalities.

  • Hypothermia in TBI was hot, but now its not!
  • National Acute Brain Injury Study Hypothermia
    (NABISH) prospective, multicenter, randomized
    trial (Clifton GL et al. N Engl J Med 344
    556-63, 2001)
  • 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 dont 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.

  • Inhaled Anesthetics
  • Reasonable maintenance regimens for intracranial
    neuroanesthesia (going from routine to desperate)
  • N2O isoflurane (1/2) fentanyl?
  • N2O the first agent to go if theres brain
    swelling or venous air emboli or danger of
    ischemia (i.e., head trauma)
  • MAC equivalents of sevoflurane or desflurane
    might also be substituted for isoflurane
  • Sufentanil could be substituted for fentanyl.
  • Isoflurane (1) fentanyl
  • Isoflurane (1/2) propofol fentanyl
  • The volatile agents are next to go if the brain
    is compromised (i.e. markedly increased ICP or
    brain swelling).
  • Total IV anesthetic propofol fentanyl
  • Barbiturate coma for intractable brain swelling
    (titrated to EEG burst suppression)
  • Thiopental
  • Pentobarbital?

  • ICP Monitoring in TBI
  • Brain Trauma Foundation Guideline. ICP monitoring
    is appropriate in severe head injury patients
    (GCS lt 8) with an abnormal CT, or a normal CT
    scan if 2 or more are noted on admission
  • Systolic BP lt 90 mm Hg
  • Age gt 40 years
  • Uni- or bilateral motor posturing
  • What patients need ICP monitoring during
    non-neurologic surgery? (JC Drummond, ASA
    Refresher Course Lecture 144 1-7, 2000)
  • Level of consciousness? If loss of consciousness
    at any time or GCS lt 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).
  • 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)

  • Summary ABCs of Anesthesia for Traumatic Brain
  • Airway. Safely get control.
  • Blood pressure
  • Choose an anesthetic that maintains MAP.
  • Avoid hypotension (SBP lt 90 mm Hg) if possible,
    correct it immediately.
  • MAP gt 70-80 mm Hg is reasonable.
  • Carbon dioxide. Dont routinely hyperventilate,
    only if necessary for a swollen brain.
  • Diuretics or Dexamethasone?
  • We usually give diuretics (mannitol). We usually
    dont give steroids.
  • Early decompressive craniectomy may cause us many
    sleepless nights.
  • Fluids. Avoid hypovolemia.
  • Glucose. Treat hyperglycemia.
  • Hypothermia was hot, but now its not. Avoid
  • 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)

  • 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)
  • Rapid sequence induction and intubation with
    in-line cervical fixation
  • Fiberoptic oral / nasal intubation
  • Blind nasal intubation (not if basilar skull
  • Light wand/stylettes
  • Glidescope, Bullard scope, etc.
  • Retrograde cannulation
  • Laryngeal mask airway (backup for failed
  • Cricothyrotomy

  • Succinylcholine
  • Safe for use in first 24-48 hours
  • Contraindications to succinylcholine

  • 3. High-dose methylprednisolone (Bracken MB
    et al, N Engl J Med 3221405-11, 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

Spinal shock
  • Spinal shock (Ezekiel MR. Handbook of
    Anesthesiology, 2002-2003 Edition. Current
    Clinical Strategies Publishing, pp. 165-66)
  • Seen in high SCIs
  • Lasts a few hours to several weeks
  • Characterized by (below lesion)
  • Loss of sympathetic tone
  • Flaccid paralysis
  • Total absence of visceral and somatic sensation
  • Paralytic ileus
  • Loss of spinal cord reflexes

Autonomic hyperreflexia
  • Autonomic hyperreflexia (Stoelting RK, Miller RD.
    Basics of Anesthesia, 4th ed. Churchill-Livingsto
    ne 2000, pp. 328-9)
  • A complication of chronic spinal cord transection
  • (especially above T6)
  • Sudden hypertension reflex bradycardia
  • Distension of hollow viscus (e.g. bladder)
  • 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

(No Transcript)
  • Basic Principles of SCI
  • Difficult airway can be problematic.
  • Unstable cervical spine. Dont break the
    patients neck!
  • Cant use succinylcholine after 24-48 hours.
    Dont cause a hyperkalemic code!
  • Hemodynamic instability is common with anesthesia
    and surgery.
  • Acute SCI spinal shock and hypotension
  • Chronic SCI autonomic hyperreflexia and

End of NeuroAnesthesiology
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