the painful truth about compartment syndrome, causalgia, and

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


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.


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.


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


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


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.

the painful truth about compartment syndrome, causalgia, and

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