Abstract
Compartment syndrome is a rare but potentially life-threatening pathology that requires high suspicion. Although there are limited objective measurements, this remains a clinical diagnosis. Traditionally the 6 “Ps” (pain, pulselessness, paresis, paresthesia, pressure, pallor) are listed as symptoms; however, the majority of cases can present without some—or all. Prompt diagnosis and consultation to an orthopaedic surgeon is necessary for definitive treatment.
Key Concepts
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Skeletal muscles are contained within distinct osseofascial compartments throughout the body.
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Compartment syndrome is caused by an increase in pressure within these relatively noncompliant compartments.
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Compartment syndrome can be acute or chronic.
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Acute compartment syndrome (ACS) is an emergency and can lead to permanent functional loss if not treated.
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Chronic exertional compartment syndrome usually presents with exercise-induced symptoms that resolve with rest.
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Elevated compartment pressures in ACS can result from internal or external factors.
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Internal: Fluid accumulation within the compartment, secondary to hemorrhage or edema, diminishes the space available for the muscles and nerves.
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External: Compression or traction of the limb can lead to change in the size/volume of the compartments.
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Epidemiology
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3.1 per 100,000 in Western populations
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Male-to-female predominance of 10 : 1, which is believed to be reflective of the increased male presence in acute trauma
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Higher incidence in younger (<35 years old) men, which may reflect the increased muscle mass within the compartments in this population
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Equal incidence of both high- and low-energy injuries
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Fractures are the most common cause of ACS (69% of cases)
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Occurs in both open and closed fractures
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Most common fractures
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Tibial diaphyseal fractures
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1-11% incidence of ACS (approximately 40% of all compartment syndromes)
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Forearm (radius/ulna) diaphyseal fractures
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3% incidence of ACS
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Distal radius fractures
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0.25% incidence of ACS
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Etiology
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Fractures
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Soft-tissue trauma/crush injury
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Vascular injury
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Bleeding diatheses or anticoagulation leading to hemorrhage/hematoma
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Burns (soft-tissue contracture)
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Constrictive circumferential dressings/casts
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Skeletal traction for fracture reduction
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Fluid extravasation (e.g., intravenous fluids, contrast dye)
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Intramedullary reaming during fracture fixation (forces blood and marrow into surrounding compartments)
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Surgical positioning (through direct pressure or certain positioning; i.e., Lloyd-Davies for colorectal surgery)
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Prolonged recumbent position leading to limb compression (e.g., drug overdose)
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Reperfusion after prolonged ischemia
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Abscess/infection
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Pathophysiology
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Increased intracompartmental pressure results in a progressive pathologic pathway:
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Alteration in arteriovenous pressure gradient
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Diminished capillary perfusion
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Cellular anoxia
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Muscle and nerve ischemia
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Tissue necrosis
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Functional impairment of the limb
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Elevated intracompartmental pressure leads to a reduction in venous outflow, which in turn increases interstitial pressure, contributing to edema formation—a continuously worsening cycle.
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Tissue ischemia can also lead to an increase in vascular permeability and exacerbate the intracompartmental pressure elevations.
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The innermost muscle fibers are the first to become ischemic, with progression to peripheral muscle involvement in a centrifugal fashion.
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The magnitude and duration of elevated intracompartmental pressure that determines the extent of muscle and nerve ischemia and necrosis.
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Locations
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Upper extremity
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Shoulder girdle
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Arm (two compartments: anterior and posterior)
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Forearm (three compartments: dorsal, volar, and mobile wad)
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Hand (10 compartments)
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Lower extremity
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Buttock
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Thigh (three compartments: anterior, posterior, and adductor)
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Leg (four compartments: anterior, lateral, superficial, and deep posterior)
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most common location
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Foot (nine compartments)
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Spinal musculature
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History
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ACS is a clinical diagnosis that is supported by compartment measurements; making the diagnosis and deciding when to treat can be a challenge.
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A high clinical suspicion must be maintained so that the diagnosis is not missed.
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It is important to understand the mechanism of injury; ACS most often occurs after a traumatic event.
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Inquire about other risk factors such as age, anticoagulants, bleeding diatheses (i.e., hemophilia), or other medical comorbidities (i.e., neuropathy, hypotension, or shock).
Physical Examination
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Swelling, discoloration, or blistering of the skin ( Fig. 13.1 )
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Limb compartment palpation/manual compression to estimate tension
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Active and passive motion of involved limb
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Muscle strength
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Sensory function
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Vascular status:
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Close monitoring with serial examinations is critical because the development of compartment syndrome can occur over hours to days.
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The diagnosis is made by considering the entire clinical picture, because no examination finding is pathognomonic.
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Individually the classic P signs ( p ain, p ulselessness, p aresis/ p aralysis, p aresthesias, p ressure, and p allor) can be absent or equivocal. However, together, the constellation of signs and symptoms including severe or intensifying pain, firm compartments, and sensory changes are strong indicators of an ACS.
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Early Signs
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Pain:
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Pain with passive movement—one of the most sensitive signs ( Fig. 13.2 )
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May not be elicited in the involved extremity if the patient has altered mental status, a concomitant nerve injury, other distracting injuries, or received anesthesia
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Severe or progressive pain, especially with an increasing narcotic requirement
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Pressure:
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Increased tension of muscle compartments may be the only sign
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Difficult to quantitate clinically—assessment subjective and unreliable
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Deep posterior compartment cannot be palpated
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Paresthesias ( Fig. 13.3 ):
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Herald ischemia of the nerves within the involved compartments
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Occurs early because nerves are sensitive to anoxia
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Can progress to hypoesthesia and, later, irreversible motor and sensory loss
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Can also be present with nerve injuries and are not specific for ACS
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