The Painful Truth about The Painful Truth about Compartment Syndrome, Causalgia, Compartment Syndrome, Causalgia, and Post-traumatic Pain Syndromesand Post-traumatic Pain Syndromes
Sharla Owens, M.D.Vascular ConferenceNovember 14, 2005
Compartment SyndromeCompartment 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
PathophysiologyPathophysiologyMechanism 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-ReperfusionIschemia-ReperfusionIschemia 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 MediatorsInflammatory Mediators
Released from ischemic skeletal muscleProduce local and systemic effectsLocal: increase capillary permeability,
activate coagulation cascade to produce more tissue damage
Magnitude of systemic response depends on amount of muscle mass involved
ConsequencesConsequences
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 CycleVicious Cycle
Increasing capillary pressure
Fluid transudation andcellular swelling
Increasing compartmentalpressure
Clinical PresentationClinical 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
Continued…Continued…
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
Continued…Continued…
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 TestsObjective 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 > 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, cont’d.Objective Tests, cont’d.
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, cont’d.Objective Tests, cont’d.
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, cont’d.Objective Tests, cont’d.
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, cont’d.Objective Tests, cont’d.
Additional noninvasive modalities include fiberoptic transducers, near-infrared spectroscopy, laser Doppler flowmetry, and tissue tonometry
Above approaches are experimental, and such data should not be used independently to exclude the presence of compartment syndrome
TreatmentTreatment
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 death.
Pretreatment with mannitol, catalase, superoxide dismutase, or other scavengers, has been shown in models to diminish cell damage after I-R injury
Treatment, cont’d.Treatment, cont’d.
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, cont’d.Treatment, cont’d. 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.
Treatment, cont’d.Treatment, cont’d. 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 response).
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 ManagementWound 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 Post-traumatic Pain SyndromesSyndromes
The Quick and Dirty
CausalgiaCausalgia
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”.
CRPSCRPS
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
CRPSCRPS
Complex- dynamic/varied presentation, autonomic, cutaneous, motor, inflammatory, and dystrophic changes
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 allodynia.
CPRS, cont’d.CPRS, cont’d. Type I (RDS) follows
inciting event Pain and allodynia
beyond territory of single nerve
disproportionate Edema/abnormal skin
blood flow in region
Type II (Causalgia) results from specific nerve injury
Pain and allodynia beyond territory of single nerve
Edema/abnormal skin blood flow in region
EtiologyEtiology
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 recovery)
Idiopathic
PathogenesisPathogenesis 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 stimuli.
This theory has difficulty explaining similar pain without over nerve injury (CRPS I)
Presentation and DiagnosisPresentation 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 DiagnosisPresentation 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 BlockDiagnostic Sympathetic BlockValidity 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 sympathectomy
TreatmentTreatment
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, cont’d.Treatment, cont’d.
Nonoperative therapy relies on early mobilization for susceptible patients, drug therapy (phenytoin, amytriptyline, and carbamazepine), intermittent sympathetic blocks, and physiotherapy.
TENS (Transcutaneous electrical nerve stimulation)
Steroids Neuromodulation
Treatment, cont’d.Treatment, cont’d.
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.
SummarySummary
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.
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