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The Painful Truth about Compartment Syndrome, Causalgia, and Post-traumatic Pain Syndromes


The Painful Truth about Compartment Syndrome, Causalgia, and Post-traumatic Pain Syndromes Sharla Owens, M.D. Vascular Conference November 14, 2005 – PowerPoint PPT presentation

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Title: The Painful Truth about Compartment Syndrome, Causalgia, and Post-traumatic Pain Syndromes

The Painful Truth about Compartment Syndrome,
Causalgia, and Post-traumatic Pain Syndromes
  • Sharla Owens, M.D.
  • Vascular Conference
  • November 14, 2005

Compartment Syndrome
  • Defined as increased tissue pressure contained in
    a nonexpansile space
  • Raised pressure within a closed fascial space
    reduces capillary perfusion, placing the enclosed
    structures at risk
  • Most commonly observed after acute injury or
    ischemia in upper and lower extremities
  • Abdominal, epidural, CHI, and angle-closure
    glaucoma are better defined and treated as
    variants of classic compartment syndrome

  • Mechanism of tissue volume increasing within a
    confined space, available tissue space
    decreasing, or a combination of both
  • Space-occupying lesions such as hematoma,
    abscess, PSA, muscle edema/fluid
  • Decreased space by circumstances where external
    devices are placed (cast, dressing) or with
    circumferential burns

  • Ischemia results in depletion of intracellular
    energy stores, which, after reperfusion will
    generate toxic oxygen radicals.
  • Results in cascade of activation of
    leukocytes/platelets, inflammatory mediators,
    calcium influx, disruption of cell membrane, and
    fluid transudation
  • All culminate in excess fluid formation

Inflammatory Mediators
  • Released from ischemic skeletal muscle
  • Produce local and systemic effects
  • Local increase capillary permeability, activate
    coagulation cascade to produce more tissue damage
  • Magnitude of systemic response depends on amount
    of muscle mass involved

  • Venular pressure, normally 4-7 mm Hg, increases
    progressively because of venous outflow
    obstruction from increased tissue pressure
  • Ultimately, when intracompartmental pressure
    equals capillary pressure, nutrient blood flow is
    reduced to 0, cellular perfusion ceases, and
    tissue infarction commences

Vicious Cycle
Increasing capillary pressure
Fluid transudation and cellular swelling
Increasing compartmental pressure
Clinical Presentation
  • Most frequently occurs with major extremity
    trauma (crush or closed fractures) or reperfusion
    after acute arterial insufficiency
  • Has also been reported with electrical injuries,
    massive volume resuscitation, and prolonged
    operative positioning
  • Symptoms include severe pain, which worsens
    despite appropriate care for underlying injury,
    and neurologic signs

  • Early neurologic dysfunction explained by the
    fact that tissues most sensitive to hypoxia are
    nonmyelinated type C sensory fibers (fine touch)
    and result in symptoms such as paresthesias.
  • If hypoxia continues, then affects myelinated
    nerves, skeletal muscle, and then skin and bone.
  • Muscle cell dysfunction fuels the progression of
    compartment syndrome

  • Physical findings commonly include tense muscle
    compartments that are tender to palpation, as
    well as passive flexion and extension
  • Numbness and weakness in the distribution of
    nerves passing through compromised compartments

Objective Tests
  • Objective measurement of compartment pressure
    using needles/catheters was developed in the
    1970s. Today, many still use needle manometry,
    and wick catheters
  • Traditionally, absolute measures were used to
    guide therapy pressures gt 40-45 mm Hg at any
    point, or sustained at greater than 30 mm Hg for
    more than 3-4 hours mandated fasciotomy.
  • Compartment syndrome (CS) occasionally develops
    at lower tissue pressures in hypotensive patients

Objective Tests, contd.
  • Isolated measurement of compartment pressure is
    neither sensitive nor specific for determining
    muscle ischemia
  • Important variable is the gradient between
    diastolic blood pressure and compartment pressure

Objective Tests, contd.
  • CS cannot exist without derangements of venous
    flow dynamics
  • Jones and coworkers determined that venous duplex
    scanning focused on tibial veins might be an
    accurate means of indirectly determining presence
    of compartmental pressures.

Objective Tests, contd.
  • Subsequent work by Ombrellaro showed that loss of
    normal respiratory venous phasicity correlates
    well with elevated tissue pressures.
  • The finding of normally phasic tibial venous flow
    on duplex scanning could effectively rule out
    elevated tissue pressures in that compartment.

Objective Tests, contd.
  • Additional noninvasive modalities include
    fiberoptic transducers, near-infrared
    spectroscopy, laser Doppler flowmetry, and tissue
  • Above approaches are experimental, and such data
    should not be used independently to exclude the
    presence of compartment syndrome

  • Reactive oxygen species play a key role in the
    development of compartment syndrome by producing
    DNA damage, which triggers complex energy
    consuming DNA repair mechanisms, leading to more
    inflammatory mediators, and potentially cell
  • Pretreatment with mannitol, catalase, superoxide
    dismutase, or other scavengers, has been shown in
    models to diminish cell damage after I-R injury

Treatment, contd.
  • Although these experimental observation have
    implications as adjunctive therapies, surgical
    decompression, or fasciotomy remains the mainstay
    of therapy.
  • Fasciotomy is indicated when compartment pressure
    is within 20-30 mm Hg of diastolic pressure
  • Sole purpose is to release compartment HTN and
    prevent necrosis of compressed tissue

Treatment, contd.
  • In the lower extremity, four compartment
    fasciotomy of the calf can be performed through a
    single lateral incision, started one
    fingerbreadth anterior to fibula and carried out
    to the lateral malleolus.
  • Access to anterior, lateral, and superficial
    posterior compartments is straightforward after
    raising narrow skin flaps. Access to deep
    posterior is best obtained distally where the
    gastrocnemius and soleus muscles become tendinous.

(No Transcript)
Treatment, contd.
  • Muscle viability is assessed by color, presence
    of arterial bleeding, and contraction to galvanic
    (electrocautery) stimulation.(Muscle relaxing
    anesthetic agents do not interfere with this
  • Muscles that do not contract should be debrided.
  • Myoglobinuria should be sought and treated with
    volume expansion, mannitol/loop diuretics as
    needed, and urine alkalinization by NaHCO3 to
    prevent renal complications.

Wound Management
  • Early and complete closure of the fasciotomy
    wound is a critical step to maintaining a
    functional limb
  • Sterile, moist dressings applied until swelling
    has diminished to allow closure
  • Closure delayed primary vs. secondary vs. skin
    graft vs. flap

Post-traumatic Pain Syndromes
  • The Quick and Dirty

  • Derived from Greek causos, meaning heat, and
    algos, meaning pain. First case reported in
    early 16th century.
  • Early reports from American Civil War described
    incomplete peripheral nerve injury secondary to
    penetrating trauma with subsequent burning pain,
    autonomic dysfunction, and limb atrophy.

  • Term developed at consensus committee to replace
    causalgia and RSD. Hallmarks of syndrome include
    dysfunction and pain of duration or severity out
    of proportion to what might have been expected
    from initiating event.
  • Cause of pain and underlying pathophysiology
    remain obscure

  • Complex- dynamic/varied presentation, autonomic,
    cutaneous, motor, inflammatory, and dystrophic
  • Regional- wide distribution beyond the area of
    lesion distal part of limb usually affected
  • Pain- out of proportion to initiating event,
    hallmark of condition. Refers to spontaneous
    burning and thermally or mechanically induced

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CPRS, contd.
  • Type I (RDS) follows inciting event
  • Pain and allodynia beyond territory of single
  • disproportionate
  • Edema/abnormal skin blood flow in region
  • Type II (Causalgia) results from specific nerve
  • Pain and allodynia beyond territory of single
  • Edema/abnormal skin blood flow in region

  • Traumatic- fractures, dislocations, sprains,
    burns, crush injuries (Majority of cases)
  • Nontraumatic- prolonged bed rest, neoplasms,
    metabolic bone disease, MI, CVA (15 of pts s/p
    MI develop persistent pain in the UE during their
  • Idiopathic

  • Not well understood
  • Most popular theory is that of artificial
    synapses occurring at site of injury, where a
    short circuit occurs at the point of partial
    nerve interruption that allows efferent
    sympathetic impulses to be relayed back along
    afferent somatic fibers.
  • Stimulation of a sensory nerve may make the nerve
    more sensitive to the usual types of sensory
  • This theory has difficulty explaining similar
    pain without over nerve injury (CRPS I)

Presentation and Diagnosis
  • Stage I, acute warmth, erythema, burning, edema,
    hyperalgesia, hyperhidrosis, patchy osteoporosis.
    Good result with chemical sympathectomy,
    spontaneous resolution possible.
  • Stage II, dystrophic Coolness, mottling of skin,
    cyanosis, brawny edema, brittle nails, diffuse
    osteoporosis. Good response to sympathetic block,
    symptoms present for fixed interval, spontaneous
    resolution rare.

Presentation and Diagnosis
  • Stage III, atrophic- Pain always extends beyond
    area of injury, florid trophic changes, atrophy
    of skin, fixed joint contractures, severe
    demineralization and ankylosis on plain films.
  • Diagnosis of CRPS II certain when clinical
    presentation includes superficial burning pain in
    distribution of single somatic sensory nerve,
    hyperesthesia, vasomotor abnormalities,
    radiographic evidence of osteoporosis, and a good
    response to local sympathetic blockade.

Diagnostic Sympathetic Block
  • Validity of clinical diagnosis can be
    strengthened by a positive response to
    sympathetic block
  • Patients should quantify the degree of pain
    relief experienced (e.g., 100, 50)
  • Degree of pain relief is an excellent predictor
    of how much relief can be expected from surgical

  • Depends on clinical stage of development,
    severity of symptoms, and degree and duration of
    relief by sympathetic block
  • Disabling pain, several month duration, relief
    from block for typical duration, should be
    considered candidates for surgical sympathectomy
  • Pain of recent onset, with relief from blockade
    that lasted beyond duration of anesthetic,
    continue with nonoperative

Treatment, contd.
  • Nonoperative therapy relies on early mobilization
    for susceptible patients, drug therapy
    (phenytoin, amytriptyline, and carbamazepine),
    intermittent sympathetic blocks, and
  • TENS (Transcutaneous electrical nerve
  • Steroids
  • Neuromodulation

Treatment, contd.
  • Stage I PT /- TENS, sympathetic block for
    severe pain or pts unable to undergo PT. If above
    fails, possible course of steroids.
  • Stage II PT, TENS, steroid therapy combined.
    Sympathetic blocks and surgical sympathectomy
    considered if measures fail.
  • Stage III Steroid or sympathetic block and
    surgical sympathectomy should be considered, but
    may be unsuccessful.

  • Key to Compartment Syndrome is a high index of
    suspicion, and early intervention
  • CRPS- no one really knows what it is, or what
    causes it, but once diagnosed, the patient should
    seek therapy, get on medication, and potentially
    have surgery.