Compartmental Syndromes.

Edited By: Frederick A. Matsen III, M.D., Winston J. Warme, MD
Last updated Thursday, February 10, 2005

Etiologies

Etiologies of compartmental syndromes

A compartmental syndrome may occur whenever tissue pressure within a limited space rises to the point that it compromises local circulation and function.

The two prerequisites for a compartmental syndrome are (a) a limiting envelope surrounding tissue and (b) a cause of increased tissue pressure within that envelope.

A wide variety of etiologies may produce a sufficient increase in local tissue pressure to cause a compartmental syndrome.

The relative frequency of the different etiologies may differ dramatically in different patient populations.

Postischemic swelling is a particularly sinister cause of a compartmental syndrome.

By definition, a compartmental syndrome is produced when the tissue pressure within a limited space rises to the point where the circulation and function of the tissues within that space are compromised.

There are therefore two prerequisites for the production of a compartmental syndrome: (a) an envelope limiting the available space and (b) a cause of increased pressure within that envelope.

The first prerequisite, a limiting envelope, may be any structure of limited compliance that surrounds tissue. Several different materials may compose these limiting envelopes. Envelopes may consist of fascia and bone, as in the anterior compartment of the leg, or may consist of fascia alone, as in the gluteal compartment. l The skin may serve as a limiting envelope in burned extremities or in cases in which the skin has been closed after surgical opening of the fascia. 2-7 Even the connective tissue layer that surrounds each muscle, the epimysium, may serve as the limiting envelope in a compartmental syndrome. 8- 9 Limiting envelopes may also be produced by the physician in the form of tight external dressings or casts. In 1881, Volkmann provided one of the first written descriptions of circulatory compromise from tight dressings. His identifications of externally applied pressure as a cause of muscle ischemia is important, even though he incorrectly attributed the ischemia to arterial occlusion. Edgar Bick's translation of this description is reproduced below: 10

For many years I have noted on occasion, following the use of bandages too tightly applied, the occurrence of paralysis and contraction of the limb, not, as has been previously assumed, due to paralysis of the nerve by pressure, but as a quick and massive disintegration of the contractile substance and the effect of the ensuing reaction and degeneration. The paralysis and contracture are to be understood as purely myogenic.

A series of new experiences has merely confirmed the correctness of this assertion, and also produced certain views about the character of the process here in question. Accordingly, I might summarize my views in the following sentences:

1. The paralyses and contractures appearing after too tight bandaging of the forearm and hand, less frequently in the lower extremity, are to be considered ischemic. They are caused by prolonged blocking of arterial blood. The almost simultaneous occurrence of massive venous stasis manifests itself at the beginning of the paralysis only to accelerate its progress.
2. The paralysis is based upon the fact that the muscle bundles, too long deprived of their acids become necrotic. The contractile substance coagulates, disintegrates into clumps and will be resolved later. The ensuing contracture is thereby to be understood above all as simply rigor mortis and shows the paralyzed and contracted limb-if as usual the entire musculature of a limb or part of a limb is affected-always in the same position which we find in the limbs of rigor mortis.
3. Characteristically, the paralysis and contracture appear simultaneously or follow immediately after one or the other, while in paralysis of nerve origin in the extremity the contracture develops gradually, and often much later; months and years pass before a deformity develops that cannot be overcome by immediate passive hand-power.
4. On the contrary, ischemic contracture shows its nature from the first moment by the great resistance it opposes to straightening the limb. The affected muscles have already completely and immediately lost their elasticity as in rigor mortis and are completely stiff.
5. The reactive and regenerating processes, always very imperfect in man, following the disintegration of the contractile substance, make the diseased muscles even more unyielding and further increase the contracture by cicatrization.
6. Ischemic paralysis and contraction of similar character also occur after application of any tight bandage, too long continuation of an Esmarch constriction of the limbs, and also after lacerations and contusions of large vessels, and perhaps also after long periods of severe cold.

The second prerequisite for a compartmental syndrome, a cause of increased pressure within the envelope, may be a decrease in the volume of the envelope, an increase in the content within the envelope, or the application of pressure to the outside of the envelope. Whitesides et al 11 and Hargens et al 12 sequentially increased the content of a dog's anterior compartment while observing the resulting changes in intracompartmental pressure. The initial increases in compartmental content produced only small increments in intracompartmental pressure; thus lax fascia appears to have a significant compliance. With increasing compartmental content, intracompartmental pressure rose more steeply, that is, the fascial compliance progressively diminished. This pressure content relationship is further emphasized by data of Whitesides et al 11 from an amputated human leg: a 30% increase in the content of the anterior compartment from 110% to 140% of normal raised the intracompartmental pressure only 20 mm Hg (from 10 to 30 mm Hg), whereas a 30% increase in content from 150% to 180% of normal caused the intracompartmental pressure to rise 75 mm Hg (from 45 to 120 mm Hg).

Any cause of locally increased tissue pressure is a potential cause for a compartmental syndrome:

Decreased compartmental volume:

• closure of fascial defects
• application of excessive traction to fractured limbs.

Increased compartmental content:

• bleeding
• vascular injury
• bleeding disorder
• anticoagulants
• increased capillary filtration
• increased capillary permeability
• post ischemic reperfusion
• trauma
• intensive use of muscles
• burns
• intraarterial drugs
• cold
• surgery
• snakebites
• increased capillary pressure
• venous obstruction
• diminished serum osmolarilty
• nephrotic syndrome
• infiltrated infusions
• muscle hypertrophy
• popliteal cysts

Externally applied pressure:

• tight casts, dressings
• air splints
• lying on limb

The relative frequency of these different etiologies may vary markedly from one geographical location to another. For example, in our series from the University of Washington affiliated hospitals, l3 extremity trauma was the etiology in 24 of 44 cases. By contrast, in the series from the University of California in San Diego, limb compression in association with drug overdose accounted for 5 of 11 cases, l4 an etiology not seen in our series.

Whereas the mechanism by which most of the etiologies produce increased tissue pressure is apparent, postischemic swelling deserves some additional discussion. Like other tissues, capillary endothelium is damaged by prolonged ischemia. This damage is reflected by an increase in capillary permeability. If the circulation is restored through ischemically damaged capillaries, the increased capillary permeability results in extravasation of fluid with an increase in extracellular volume. Cell volume may also be increased because ischemia may deprive cells of their normal membrane integrity and ionic pump functions. This postischemic swelling has been demonstrated by two laboratory investigations. Fuhrman and Crismon 83 measured the water content of rabbit muscle two hours after different periods of tourniquet ischemia. They found that three hours of ischemia gave rise to postischemic swelling of 30 to 60%. Whitesides et al 11 measured tissue pressures in the compartments of dog hindlimbs after a period of tourniquet ischemia. The postischemic increment in pressure was higher the longer the tourniquet had been applied. Whereas only a few of the animals with four hours of ischemia showed a significant increase in tissue pressure, most of the six-hour and all of the eight-hour animals showed significant pressure increases after the release of the tourniquet.

Compartmental syndromes resulting from postischemic swelling can present a diagnostic challenge. Because the tissue is injured by the initial period of ischemia, neuromuscular function may already be abnormal. Thus, the detection of additional deficits from a superimposed compartmental syndrome requires very close observation of the patient's nerve and muscle function.

Surgery for Compartmental Syndromes at the University of Washington

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