Fasciotomy for Compartmental Hypertension and Acute Compartment Syndrome



Fasciotomy for Compartmental Hypertension and Acute Compartment Syndrome



Kaj H. Johansen


The term compartment syndrome invokes the concept of a pathophysiologic process in which elevated tissue pressures within inelastic surroundings result in neurovascular or muscular damage. The development of compartment syndrome is commonly anticipated in certain clinical scenarios, particularly in patients with blunt (or occasionally penetrating) extremity trauma and patients with severe acute limb ischemia that is successfully revascularized.



Pathophysiology


Two separate biophysical phenomena can result in compartmental hypertension and the development of compartment syndrome (Box 1). First, and relatively uncommonly, muscle compartment size may be limited or restricted. Examples include the occasionally deleterious effects of casts, splints, or other circumferential dressings; surgical closure of muscle fascial defects; or circumferential scars resulting from thermal injury.



BOX 1   Mechanisms Associated with Development of Compartment Syndrome




Much more common are the various forms of injury that increase the volume of tissues within an inexpansile compartment. This may be a result of edema, hematoma or blood or, occasionally, iatrogenic causes such as unintended extravasation of intravenous fluids or misdirected irrigation volumes. The vast majority of patients with clinically evident compartment syndrome develop this problem either in the calf muscles or the forearm muscles because these two sets of muscle compartments (four in the leg, three in the upper extremity) are bound by fascia that is much more inelastic than that surrounding muscles elsewhere in the body.


Patients with severe acute arterial insufficiency of the extremities that is successfully reversed are at risk for developing compartment syndrome. The ischemia–reperfusion pathophysiology that underlies this particular form of compartmental hypertension has been extensively studied by Hobson, Walker, and Blaisdell, among others. The underlying mechanism in post–ischemia–reperfusion compartmental hypertension appears to arise from the generation of toxic oxygen radicals, the effect of which, among others, is to render capillary beds leaky. When blood flow is restored (reperfusion), intravascular fluid—plasma—extravasates into the extracellular space. In most sites in the body, the affected tissues simply swell. However, in the forearm and the calf, the inelastic fascia surrounding the muscle compartments prevents such tissue expansion, resulting instead in an inexorable rise in tissue pressure, increasing encroachment on venous outflow and later on arteriolar inflow, producing a reduction in capillary perfusion pressure and a resulting loss of tissue nutrition. Unrelieved compartmental hypertension inevitably results in tissue necrosis diffusely throughout the affected compartment.


Skeletal muscle undergoes infarction initially at its depths, dying from the inside out. Muscle that is initially healthy and viable appearing at the time of initial decompression may be found to have proceeded to complete infarction at subsequent assessment. Ischemia itself does not result in compartmental hypertension. Rather, the ischemic tissue bed, once it is successfully revascularized, should be considered at risk for developing compartmental hypertension if the inevitable post-reperfusion tissue swelling could potentially occur within an inelastic fascial envelope.



Clinical Presentation and Diagnosis


Vascular specialists most commonly are confronted by the potential development of the clinical scenario of compartment syndrome in patients with acute arterial insufficiency, such as arterial embolism or acute thrombosis of a native artery or of a bypass graft, which is then successfully reversed by arterial embolectomy, thrombectomy, or even catheter-directed thrombolysis. Less commonly, trauma victims who had suffered crush injuries, closed fractures, or joint dislocations in the extremities should be considered at risk for developing symptoms associated with compartmental hypertension. Rarely, compartment syndrome complicates the management of severe lower extremity deep vein thrombosis (phlegmasia cerulea dolens), predominantly because diffuse occlusion of venous outflow results in pathologically elevated tissue pressures within calf muscle compartments. Likely for similar reasons, patients undergoing extended or prolonged operations, particularly in the dorsal lithotomy position, may be at increased risk for developing compartment syndrome.


The clinical presentation of compartment syndrome is stereotypical. Such patients are described as having pain out of proportion to physical findings and often recalcitrant even to major parenteral doses of opiate analgesic medication. Muscles of the affected compartment are tense and are diffusely tender to palpation; passive stretch of the muscles (e.g., downward traction on the foot) increases the patient’s discomfort. Importantly, neurologic dysfunction (e.g., numbness in the first dorsal web space of the foot associated with anterior compartment syndrome of the leg, often accompanied by weakness of foot dorsiflexion) is an important hallmark of an established compartment syndrome.


Unfortunately, a substantial number of patients at risk for developing compartment syndrome have extremity pain, tenderness, or neuromuscular dysfunction as a consequence of their underlying trauma or ischemia. Accordingly, although all the above clinical findings should be sought in the patient at risk for developing compartment syndrome, their presence is not necessarily very useful in a diagnostic sense. Ulmer has demonstrated that clinical findings may primarily be of value in their absence: In a meta-analysis of patients with tibial fractures, symptoms and signs of compartment syndrome had a sensitivity of only 13% to 19% but a specificity of 97% to 98%.


Further complicating the assessment of patients potentially harboring incipient compartment syndrome is the fact that such patients may be anesthetized, intubated, intoxicated, spinal-cord injured, or unconscious, and the clinical assessment may be untrustworthy or unobtainable. Clinical assessment for compartment syndrome can be similarly challenging in infants and children or in the demented elderly.

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Fasciotomy for Compartmental Hypertension and Acute Compartment Syndrome

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