pathophysiology

In 1881, Richard von Volkmann first described development of contractures and paralysis when injured limbs were placed in constrictive dressings 17 . 25 years later, physicians began to suspect that these permanent neuromuscular sequelae were likely caused by elevated tissue pressures. 18 Since that time, marked advances in the understanding of compartment syndrome have been elucidated.

Compartment syndrome may develop whenever there is an increase in intrinsic pressure within a relatively fixed compartmental space, or whenever overwhelming external forces are applied. An increase in intracompartmental pressure leads to impaired microcirculation and tissue perfusion. Subsequently, cellular injury and capillary damage develop, and osmotically active substances are released into the interstitium. A viscious cycle ensues from this osmotic shift pulling more fluid into the interstitial space, causing further pressure increase, and progressive compromise of tissue perfusion. This ultimately leads to nerve injury, muscle infarction, scarring and contractures 19-21 .

Human studies have demonstrated application of an arm tourniquet for two hours can lead to tissue edema that increases the weight of an extremity by 30% 22 . Animal studies have shown that reversible nerve dysfunction may begin to develop as early as 30 minutes after onset of ischemia, and muscle deficits may be seen in as a little as 2-4 hours 23 . Early identification and decompression is paramount as many clinical human studies have reported the development of permament neuromuscular damage when delay of treatment exceded 12 hours from the onset of symptoms. 1-5 One study demonstrated that only 8% of individuals undergoing fasciotomy after 12 hours of symptom onset had complete recovery 1 . Furthermore, complication rates (infection, need for amputation, death) were significantly higher when treatment occurred later than 12 hours after symptom onset (54% vs 4.5%).

clinical findings

Classic teaching for the identification of compartment syndrome has traditionally emphasized the "5 P's" of pain, paresthesias, paralysis, pallor, and pulselessness. Many studies of compartment syndrome have demonstrated these findings to be highly variable, unreliable, and they often are only present in advanced stages. 25,28,29 One study found that when motor paralysis was present on examination, only 13% of patients regained function. 30 Furthermore, trauma patients often present with an altered level of consciousness making sensory and motor testing difficult if not impossible.

One clinical clue to the development of compartment syndrome is the development of unremitting pain that appears disproportionate to the apparent injury, though this is highly variable and many at risk for compartment syndrome have multiple traumatic injuries that may confound the assessment. 3,14,27,31 Pain on passive stretching of the muscles of a given compartment may be a reliable indicator, but not all authors agree. 4,14,20 Many investigators assert diminished sensation and two-point descrimination are more reliable early findings. 32-34 A tense "wooden" compartment, when present, may be suggestive. 35 Skin bullae may also be present. 35,36

Pallor and pulselessness are NOT common findings of compartment syndrome and, if they are present, the physician should immediately search for a primary vascular injury or cause. 25,29

Because of the lack of reliable historical and physical findings in the diagnosis of compartment syndrome, a physician must have a low threshold to perform direct compartment pressure measurement.