Spinal Cord Injury & Spinal Shock

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Spinal Cord Injury Spinal Shock
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Epidemiology1 (USA)

• Annual incidence 28-55/million (with or without
  bony injury)
• Avg of 10,000 new cases/yr may be higher
  because this does not include those who die
  before they reach a hospital (16-30 of cases)
• Prevalence of 200,000
• Avg age at time of injury is 32
• MF 41
• 55 of acute SCI are cervical

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Epidemiology1 (USA)

• Causes
• Traffic accidents 40-50
• Assaults 10-25
• Falls 20
• Work-related 10-25
• Sports/recreation related 10-25
• 3 month mortality of traumatic SCI 20-21
• Most consistent long-term outcome predictor is
  severity of neurologic injury

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Epidemiology1 (USA)

• 20-60 of pts with SCI have a concomitant noncord
  injury
• 25-50 of pts with SCI have a traumatic brain
  injury (TBI), however only 5-10 of pts with a
  TBI have a SCI.
• Principal causes of death
• Respiratory disorders (including PE)
• Cardiovascular disorders
• Infections
• Suicide
• Survival has improved over the past years2
• Life expectancy of quadraplegics now 70 of
  that in non-injured individuals
• It is 84 for complete paraplegics, 92 for
  incomplete SCI

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Pathophysiology

• Primary injury
• Maximal at onset and unlikely to be changed by
  surgery or any other interventions
• Secondary injury
• Occurs after the initial injury
• Involves
• Vascular compromise
• Inflammatory changes
• Cellular dysfunction
• Spinal cord edema presents 3-6 days
  post-injury. Takes weeks to improve

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Spinal Shock

• It occurs immediately after a spinal injury and
  lasts hrs mths
• Due to loss of descending impulses from higher
  centers
• Flaccid areflexic paralysis and anesthesia to all
  modalities
• Present in 50 of pts with SCI
• Important to distinguish from neurogenic shock
• Spinal shock is acute and transient, and involves
  sensorimotor dysfunction that develops at any
  level
• Neurogenic shock involves hemodynamic instability
  bradycardia and decreased SVR, and is
  associated with injuries above T6

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Acute Manifestations of Spinal Injury

• Flaccid paralysis
• Duration 1 to 4 weeks
• Absence of neurologic function (motor, sensory,
  autonomics, relexes) below the lesion
• Periphery is atonic, and the peripheral blood
  vessels are dilated
• Loss of DTRs
• Bradycardia only efferent component of
  baroreflex pathway that remains intact is the
  vagus
• Hypotension
• Alveolar hypoventilation
• Hypoxemia

C-spine and high T-spine
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Acute Manifestations of Spinal Injury

• Decreased ability to protect airway gt aspiration
  risk
• Nml DiaphragmIntercostal 7030, but in
  C-spine injury, the intercosals are often lost,
  and VC is decreased 40
• Also be aware of
• Bladder and bowel incontinence
• Respiratory infections and dysfunction
• Compensatory enhancement of renin-angiotensin-aldo
  sterone system for BP maintenance, therefore v.
  sensitive to ACEI
• Hypothermia
• Anemia
• Dehydration
• Electrolyte imbalances
• Hyperkalemia

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Surgery

• Two reviews completed and published recently
  revealed the following points with regard to
  early surgical intervention3,4
• Data are insufficient to generate specific
  treatment standards or guidelines for surgical
  management
• In pts with cord compression and stable
  neurologic findings, ealry (lt24 hrs) surgical
  intervention has not been shown to change
  neurologic outcomes, when compared to delayed
  decompression
• Urgent decompression is recommended in pts with
  irreducible bilateral facet dislocation and
  incomplete quadraplegia, and in the presence of
  rapidly deteriorating neurologic deficits

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Hemodynamics

• Arteriolar dilatation, increased venous capacity,
  bradycardia (T1-T4 interruption) and a decreased
  myocardial contractility can be expected in
  patients with an acute spinal cord lesion at or
  above T6
• There is a direct correlation between the
  severity of the cord injury and the incidence and
  severity of cardiovascular problems 6
• In a study that looked at the frequency of
  cardiovascular abnormalities in 71 consecutive
  patients with acute SCI, it was found that marked
  sinus slowing, hypotension, supraventricular
  arrhythmias, and primary cardiac arrest were
  significantly more frequent in the severe
  cervical injury group 7

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Hemodynamics

• Interestingly, the tachycardic response to
  hypercapnia and hypoxemia remains intact
  possibly due to vagal inhibition rather than
  sympathetic activity9
• Causes of hemodynamic instability1
• Neurogenic shock
• Bleeding
• Tension PTX
• MI
• Pericardial tamponade
• Sepsis
• Impaired left ventricular fiunction

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Hemodynamic Management

• If possible, avoid reverse Trendelenburg this
  can gt 60 decrease in BP
• Maintain spinal perfusion pressure, although
  there is no clinically useful method of measuring
  it requires vasopressors for BP augmentation,
  and careful fluid loading to prevent pulmonary
  edema, and CHF1,5
• Hypotension is very deleterious gt cord
  hypoperfusion, and increasing secondary injury

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Hemodynamic Management

• If SVR decreased, but CO and HR are adequate,
  then phenylephrine or norepinephrine can be used
• IF SVR decreases with impaired CO and HR, then an
  inotropic agent (dopamine) may be more useful
• Some advocate the use of a Swan-Ganz in patients
  with high SCI (T6 or above)4 , although there may
  be occasional difficulty in interpretation of
  measurements from the Swan-Ganz catheter if high
  airway pressures are used. However, it is a more
  sensitive monitor than C.V.P.
• A TEE should be considered in the presence of
  severe hemodynamic compromise

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Hemodynamic Management

• The minimal amount of invasive monitoring used
  should include a CVP and arterial line.

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Anesthetic Agents

• There is no clinical data to support the use of
  one anesthetic agent over another, however,
  remember
• Inhalational agents increase SCBF
• Thiopental decreases SCBF
• Do Not use succinylcholine if injury gt 24 hrs old
• The muscle membrane following SC injury becomes
  chemically sensitive (normally, only electrical)
  can be present for 1 day to 2 years
• Succinylcholine causes the release of K, both
  from the motor end plate and muscle membrane gt
  v. fib
• Treat v. fib caused by sux by CPR, DC shock , and
  treating the hyperkalemia (glucose, insulin,
  kaxylate, Ca2 (cardio-protective))

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Chronic SCI

• Autonomic hyperreflexia
• Occurs with the return of spinal cord reflexes
  after a spinal cord injury above T7
• Occurs anywhere from 6mths to 2 yrs after the
  injury
• The stimulus can be any endogenous or exogenous
  stimulus occurring below the lesion most
  commonly distension of the bladder or rectum
• The response is greater as the distance between
  the stimulus and the level of the lesion
  increases

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Chronic SCI

• Autonomic hyperreflexia
• Physical signs
• HTN due to centrally mediated sympathetic
  stimulation, not increased catecholamines
• Bradycardia - 2º to HTN acting on the carotid
  sinus
• Ventricular arrythmias
• Profuse sweating and flushing (vasodilation)
  above the lesion
• Blanching and vasoconstriction below it
• Clinical signs
• Severe headache, dyspnea, nausea, shivering and
  blurred vision

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Anesthesia

• Awake FOI followed by slow induction to decrease
  the risk of CV collapse
• Pt should be on OR table prior to induction if
  they have an unstable C-spine.
• Spinal anesthesia good option, if it is high
  enough it blocks afferent impulses, so that a
  stimulus will not cause autonomic hyperreflexia.
• Sodium nitroprusside is the anti-hypertensive of
  choice

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Tx for Autonomic Hyperreflexia

• Stop surgery
• Deepen anesthesia
• Empty the bowel/bladder
• Control HTN

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References

• Stevens RD et al. Critical Care and Perioperative
  Management in Traumatic Spinal Cord Injury. J
  Neurosurg Anes. 200315 (3)215-29.
• Yeo, JD et al. Mortality following spinal cord
  injury. Spinal Cord. 199836329-36
• Fehlings, MG, Sekhon LH, Tator C. The role and
  timing of decompression in acute spinal cord
  injury what do we know? What should we do?
  Spine. 200126 (suppl 24) 101-10.
• Guidelines of the American Association of
  Neurologic Surgeons and the Congress of
  Neurologic Surgeons. Treatment of subaxial
  cervical spine injuries. Neurosuirgery. 200250
  (suppl)156-65
• Moeschler O, Ravussin P. Anesthesia of patients
  with injury to the cervical spine. Ann Fr Anesth
  Reanim. 199211(6)657-65.
• Piepmeier JM, Lehmann KB, Lane JG. Cardiovascular
  instability following acute cervical spinal cord
  trauma. Cent Nerv Syst Trauma. 1985
  Fall2(3)153-60.
• Lehmann KG, Lane JG, Piepmeier JM, Batsford WP.
  Cardiovascular abnormalities accompanying acute
  spinal cord injury in humans incidence, time
  course and severity. J Am Coll Cardiol. 1987
  Jul10(1)46-52
• Troll GF, Dohrmann GJ. Anaesthesia of the spinal
  cord-injured patient cardiovascular problems and
  their management. Paraplegia. 1975
  Nov13(3)162-71.
• Pokorski, M et al. Cardiac responses to hypoxia
  and hypercapnia in spinal man. Eur Heart J.
  199011 611-618