Hyperbaric, Crush Injury, Compartment Syndrome

Article Author:
Todd May
Article Editor:
Jeffrey Cooper
Updated:
10/27/2018 12:31:38 PM
PubMed Link:
Hyperbaric, Crush Injury, Compartment Syndrome

Introduction

Human limbs are composed of muscle groups divided into compartments by fascial membranes. If a limb sustains trauma (i.e., crush injury, fractures, or overuse), swelling and inflammation within a compartment may increase rapidly. Consequently, skeletal muscle compartment syndrome (SMCS) results when compartment pressures increase to the point that circulation and tissue function is compromised. Treatment of compartment syndrome remains challenging as there is no well-defined point at which performing a fasciotomy is optimal. Fasciotomies prolong hospital stays and require intensive post-surgical treatment; however, they provide limb-saving care. They prevent myonecrosis or ischemic neuropathy when indicated.

Etiology

SMCS has both traumatic and nontraumatic etiologies. Long bone fractures, especially comminuted fractures and location, account for the highest proportion of SMCS cases. In one study 414 acute tibial fractures were evaluated based on location. Mid-shaft tibial fractures had the highest rate of compartment syndrome and required a fasciotomy (8%) compared to 25% for proximal/distal metaphysis fractures. Trauma without fracture that can predispose a patient to SMCS includes crush injury, severe thermal burns, overly constrictive bandages, penetrating trauma, and injury to vascular structures in the extremities. Potential nontraumatic causes include ischemia-reperfusion injury, thrombosis, bleeding disorders, vascular disease, nephrotic syndrome, certain animal envenomations and bites, extravasation of intravenous fluids, injection of recreational drugs, and prolonged limb compression.

Epidemiology

SMCS occurs more often in patients younger than 35 years. The highest incidence is seen in young men, particularly after fractures of the tibial diaphysis and distal radius. Crush injuries among civilians occur most often due to falls, including 50% to 60% of lower extremity injuries and 30% of upper extremity injuries; industrial or work-related accidents, up to 20% of upper extremity injuries; or motor vehicle crashes. Military personnel most commonly suffer crush injuries from explosions (81%) or gunshot wounds (17%).

Pathophysiology

SMCS occurs when tissue fluid pressure exceeds capillary perfusion pressure to the muscle and nerves within a compartment. The muscle fascia and other connective tissues are inelastic. As the pressure builds, the venous return eventually is halted which results in transudation of fluid. This sets off a cascade of events, leading to an edema-hypoxia cycle. Once edema is severe enough to cause hypoxia, adhesion molecules are activated, leading to attachment of neutrophils, a release of reactive oxygen species, and severe vasoconstriction. This process constitutes reperfusion injury and is the basis behind the no-reflow phenomenon. It is estimated muscle necrosis starts to occur within 2 hours of injury in as many as 35% of patients.

History and Physical

Patient history should focus on determining if one of the traumatic or nontraumatic events mentioned above has occurred, thus placing a patient at risk for SMCS. On physical exam, impending SMCS is characterized by increasing pain, hyperesthesia, muscle weakness, discomfort with passive stretch, and/or tenseness of a muscle compartment. Established SMCS is characterized by increasingly severe pain, anesthesia, paralysis, extreme discomfort with passive stretch, rigid swelling of a muscle compartment, encephalopathy, myelopathy, and/or traumatic neuropathy. These signs and symptoms are noted in the literature as being unreliable and inconsistent.

Evaluation

Laboratory values are not used to diagnose SMCS; however, abnormalities such as elevated serum creatine phosphokinase (CPK) and myoglobinuria are typically seen as muscle breakdown ensues. Diagnosis is established by clinical findings and measurement of compartment pressures if available. Variability exists in pressure measurement interpretation and the threshold for fasciotomy. One approach is to calculate the delta pressure by subtracting the compartment pressure from the diastolic blood pressure. A delta pressure less than 20 to 30 mmHg indicates the need for fasciotomy. Alternatively, patients can be classified by their health status (See SMCS Table 1) to guide compartment pressure measurement interpretation. Measurements greater than 45 mmHg in a healthy host, less than 30 to 40 mmHg in an impaired host, and less than 20 to 30 mmHg in a decompensated and/or host in shock indicate established SMCS and need for fasciotomy. There are some pitfalls in the use of compartment pressures. In a study using a standardized cadaver model, 38 physicians were asked to monitor pressures. The correct technique was used only 31% of the time, and 30% of the measures were associated with a catastrophic error. Even when the correct technique was used, only 60% of the measurements were accurate.

Treatment / Management

For a limb at risk for SMCS, any dressing, splint, cast, or other restrictive covering should be removed. The limb should be placed at the level of the heart to avoid both reductions in arterial flow and dependent swelling. Frequent neurocirculatory checks should be performed every few hours in a limb in with suspected SMCS. Progression of SMCS from suspected stage to impending stage is based on clinical findings and/or compartment pressure measurements (See SMCS Figure 1a). In the impending stage, hyperbaric oxygen (HBO2) therapy can be implemented to prevent possible progression to the established stage. The typical treatment regimen consists of 3 HBO2 treatments (twice daily on day one, single treatment on day two). However, the use of HBO should never delay fasciotomy if a patient progresses to established SMCS. If fasciotomy is performed, HBO2 can be applied for various post-fasciotomy complications including:

  • ischemic muscle
  • unclear demarcation of viable and non-viable muscle
  • massive swelling
  • prolonged ischemia (less than six hours)
  • a compromised flap or graft
  • residual neuropathy
  • a markedly impaired or decompensated host (See SMCS Figure 1b)

Differential Diagnosis

  • infection
  • rhabdomyolysis

Prognosis

If caught and treated early with a decompressive fasciotomy, the outcomes are favorable. One study in 1976 found a fasciotomy done within 12 hours of onset of clinical symptoms (motor weakness, stretch pain, etc.) resulted in the normal function of 68% of patients. If the fasciotomy was delayed beyond 12 hours, only 8% of patients had normal function. Fasciotomies have complications like additional surgeries from delayed wound closure, skin grafting, pain, cosmetic problems, nerve injury, muscle weakness and chronic venous insufficiency. Additionally, repeated debridement is performed every 48 to 72 hours for muscle necrosis until the wound remains stable.

Pearls and Other Issues

In the most severe presentations, complications including osteomyelitis, non-union fractures, amputations, and failed flaps occur in approximately 50% of SMCS cases with the standard of practice and medical interventions. According to the American Heart Association level of classification, HBO2 for crush injury meets criteria for level b, class I evidence. HBO2 for SMCS meets criteria for level c, class I evidence.