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Spinal Cord Injury & Spinal Shock


Spinal Cord Injury & Spinal Shock Epidemiology1 (USA) Annual incidence = 28-55/million (with or without bony injury) Avg of 10,000 new cases/yr may be higher ... – PowerPoint PPT presentation

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Title: Spinal Cord Injury & Spinal Shock

Spinal Cord Injury Spinal Shock
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

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

Epidemiology1 (USA)
  • 20-60 of pts with SCI have a concomitant noncord
  • 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

  • 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

Spinal Shock
  • It occurs immediately after a spinal injury and
    lasts hrs mths
  • Due to loss of descending impulses from higher
  • Flaccid areflexic paralysis and anesthesia to all
  • 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
  • Neurogenic shock involves hemodynamic instability
    bradycardia and decreased SVR, and is
    associated with injuries above T6

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
  • Hypotension
  • Alveolar hypoventilation
  • Hypoxemia

C-spine and high T-spine
Acute Manifestations of Spinal Injury
  • Decreased ability to protect airway gt aspiration
  • 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

  • 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
  • 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
  • Urgent decompression is recommended in pts with
    irreducible bilateral facet dislocation and
    incomplete quadraplegia, and in the presence of
    rapidly deteriorating neurologic deficits

  • 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

  • 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

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

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

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

Anesthetic Agents
  • There is no clinical data to support the use of
    one anesthetic agent over another, however,
  • 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))

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
  • 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

Chronic SCI
  • Autonomic hyperreflexia
  • Physical signs
  • HTN due to centrally mediated sympathetic
    stimulation, not increased catecholamines
  • Bradycardia - 2º to HTN acting on the carotid
  • 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

  • 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

Tx for Autonomic Hyperreflexia
  • Stop surgery
  • Deepen anesthesia
  • Empty the bowel/bladder
  • Control HTN

  • 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
  • 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
  • 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
  • Troll GF, Dohrmann GJ. Anaesthesia of the spinal
    cord-injured patient cardiovascular problems and
    their management. Paraplegia. 1975
  • Pokorski, M et al. Cardiac responses to hypoxia
    and hypercapnia in spinal man. Eur Heart J.
    199011 611-618
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