Pathophysiology of Compartment and Crush Syndromes


Thermal injuries (burns), in addition to decreasing compartment space, are associated with massive edema. Measurement of intramuscular pressure is needed to document the underlying compartment tamponade and the need for treatment with decompressive escharotomy.


Another cause of fluid accumulation is hemorrhage in patients who are receiving anticoagulant therapy after arterial puncture and in patients who have a bleeding diastasis such as hemophilia. Infiltration of exogenous intravenous fluid into the compartment and venomous snakebites may also produce compartment syndrome.


CONSTRICTION OF COMPARTMENT


Compartment syndrome may also result from surgical closure of a fascial defect. For example, a high performance runner may develop a muscle hernia and fascial defect. The hernias are usually bilateral and develop in the lower third of the leg overlying the anterior and lateral compartments, causing pain on exertion and often numbness. Unfortunately, some hernias are treated with surgical closure of the fascial defects, which decreases the volume of the compartment and increases intracompartmental pressure. The treatment of choice for a runner with exertional leg pain and muscle hernia is fascial release, not fascial closure.


Another cause of compartment volume is circumferential full-thickness (third-degree) burns. This injury decreases compartment size and coalesces the skin, subcutaneous tissue, and fascia into one tight, constricting eschar that requires immediate decompression.


EXTERNAL COMPRESSION


Unconsciousness after drug overdose can precipitate not only multiple compartment syndromes but also crush syndrome if the person lies with the limbs trapped beneath the torso or head. Compression of the forearm or leg produces persistent elevation of intracompartmental pressure, which often is greater than 50 mm Hg. Prolonged inflation of air splints and incorrect application of circumferential casts may also produce external compression that limits compartment swelling. Deflating the splint and splitting the cast quickly decrease the compressive pressure. Usually neither device causes compartment syndrome unless there is an underlying injury such as fracture or contusion.


DIAGNOSIS OF ACUTE COMPARTMENT SYNDROME


Clinical Manifestations


The clinical examination findings play an important role in the diagnosis of a compartment syndrome; where invasive pressure measurement formerly played a larger role, the diagnosis is now widely considered to be a clinical diagnosis. The most important symptom of an impending compartment syndrome is pain that is out of proportion to the primary problem or injury. However, pain may be absent if there is a superimposed deficit of the central or peripheral nervous system or if the process has been present for a sufficient amount of time to cause permanent nerve damage. Other early symptoms are best remembered by the six P’s of a compartment syndrome (see Plate 7-14).


Pressure. The earliest finding is a swollen, palpably tense compartment. Palpation is difficult to quantify and has poor interobserver reliability. Furthermore, significant subcutaneous edema may mask the underlying pressure.


Pain on Stretch. Passive movement of the digits may produce pain in the involved ischemic muscles, and this is now widely considered the most sensitive clinical finding. Increased tissue pressure (even below the ischemic threshold) causes significant pain with stretching of the involved muscles, and thus this is often the earliest finding. Additionally, the course of pain, that is, pain that is continually worsening, is an important indicator of a potential impending compartment syndrome. Pain will diminish late in the course when nerve conduction is affected by the ischemia.


Paresis. Muscle weakness may be due to primary nerve involvement, muscle ischemia, or guarding secondary to pain.


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Jul 3, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Pathophysiology of Compartment and Crush Syndromes
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