Compartment Syndrome and its Management

Introduction

Compartment syndrome is a surgical emergency and a recognized complication of several conditions treated by vascular surgeons. Failure to arrive at a timely diagnosis increases the risk of short- and long-term morbidity, including limb loss or permanent disability. Conversely, appropriate recognition and management of a compartment syndrome will optimize the chances of a full recovery. This chapter addresses the pathogenesis, diagnosis, and treatment of compartment syndrome of the lower leg and other less common anatomic sites. Abdominal compartment syndrome is discussed in Chapter 182 (Vascular Trauma: Abdominal).

Pathogenesis of Compartment Syndrome

Local Hemodynamics of Compartment Syndrome

The unifying feature of all compartment syndromes, regardless of etiology or anatomic location, is an increase in intracompartmental pressure (ICP) within an unyielding fascial envelope that impairs tissue perfusion. The adverse consequence of elevated ICP on tissue perfusion may be understood by applying Poiseuille’s law ( F = πr ΔP/8ηL) to capillary blood flow within a muscle compartment. In this equation, F represents capillary blood flow, r is the radius of the capillary to the fourth power, and Δ P is the pressure gradient from the precapillary arteriole to the postcapillary venule. Increasing ICP alters two variables in this equation, Δ P and r . As ICP rises, pressure is transmitted to the postcapillary venules, increasing the venous pressure and decreasing the arterial–venous pressure gradient (Δ P ). Furthermore, increased ICP may collapse capillaries, decreasing their radius and further increasing resistance to flow. ^,

Compartment Pressures

Several theories exploring the role of ICP in the development of compartment syndrome have been proposed. The concept of a critical closing pressure was one of the earliest concepts, whereas more recent research suggests that the dynamic ICP threshold more accurately predicts which muscle compartments will develop compartment syndrome.

Critical Closing Pressure

Matsen suggested that there is a “critical closing pressure” above which capillaries collapse from transmural pressure and blood flow is arrested. The pressure at which capillary blood flow ceases has been debated over the decades. Using vital microscopy to observe the response of isolated rat cremasteric muscle to increased external pressure, Hartsock found that a pressure gradient between the ICP and mean arterial pressure (MAP) of 25.5 ± 14 mm Hg arrested capillary blood flow. Hartsock saw no significant collapse of arterioles, capillaries, or venules. This study and others disproved the “critical closing theory” proposed by Matsen, suggesting instead that the arterial–venous pressure gradient (Δ P ) is the critical determinant of capillary blood flow. ^, ^, This conclusion has direct implications for determining the threshold ICP that defines compartment syndrome.

Absolute intracompartmental pressure threshold

Defining the threshold ICP that produces tissue injury and cell death is an important step in determining the pressure at which fasciotomy is advisable. Hargens found that an absolute ICP of 30 mm Hg for 8 hours universally produced muscle necrosis in normotensive dogs, whereas pressures less than 30 mm Hg produced no muscle necrosis. Tissues differed in their susceptibility to increased ICPs. Early signs of endoneurial injury were observed at pressures of 30 mm Hg for 8 hours. ^, The differential susceptibility to injury between tissues may provide an explanation for those cases in which a delayed fasciotomy fails to restore full neurologic function despite viable muscle in the compartment.

Dynamic intracompartmental pressure threshold

Defining compartment syndrome based on an absolute pressure threshold is appealing in its simplicity but ignores the role of arterial blood pressure in affecting compartmental blood flow. Changes in arterial pressure affect the arterial–venous pressure gradient (Δ P ), altering compartment blood flow. Some authors have proposed defining compartment syndrome using a pressure threshold relative to MAP or diastolic pressure. Heppenstall found that healthy muscle in dogs developed evidence of tissue ischemia on P -magnetic resonance spectroscopy when the difference between MAP and ICP (MAP − ICP) dropped below 30 mm Hg. Injured muscle showed greater sensitivity to ischemia, as tissue ischemia became evident when the difference between MAP and ICP was less than 40 mm Hg ([MAP − ICP] <40 mm Hg).

Heppenstall found that a dynamic pressure threshold (MAP − ICP) <40 mm Hg, prevented unnecessary fasciotomy in a number of patients with absolute ICP exceeding 30 mm Hg. Another study found that use of a dynamic ICP threshold of 30 mm Hg less than diastolic pressure prevented unnecessary fasciotomies in most patients. Using the diastolic blood pressure as their reference point, Heckman observed a dramatic increase in tissue injury and necrosis when the difference between the diastolic blood pressure and ICP was less than 10 mm Hg in dogs. These studies offer compelling evidence that a dynamic ICP threshold relative to MAP or diastolic pressure is more appropriate for selecting patients for fasciotomy.

Clinical Etiologies

Vascular Causes

ICP is elevated by conditions that either increase compartment volume or produce external compression on the compartment. The most common vascular etiologies for compartment syndrome are ischemia-reperfusion (IR) injury associated with acute ischemia, arterial and venous traumatic injuries, crush injuries, phlegmasia cerulea dolens, and hemorrhage within a compartment.

Ischemia-Reperfusion

The IR phenomenon, described in detail in Chapter 6 (Ischemia-Perfusion), plays a central role in the pathogenesis of compartment syndrome due to acute ischemia and crush injury. IR increases compartment volume by causing muscle tissue injury, which leads to increased microvascular permeability with efflux of plasma proteins and progressive interstitial edema. With reperfusion, oxygen radical generation exacerbates microvascular permeability and resulting interstitial edema.

Orrapin identified several risk factors for compartment syndrome after acute limb ischemia, including inadequate backflow from the distal arteries, high serum creatinine kinase levels, positive fluid balance, and advanced-stage and prolonged limb ischemia.

Trauma

Both arterial and venous trauma may produce compartment syndrome. Occlusive arterial injuries result in distal ischemia that initiates the IR phenomenon, whereas venous injuries may compromise venous outflow. The impact of compromised venous outflow is discussed next (Venous Outflow Obstruction). Fasciotomy rates vary according to the type of vascular injury, ranging from 29.5% for isolated arterial injuries, 15.2% for isolated venous injuries, and 31.6% for combined arterial and venous injuries. Injuries to the popliteal artery are notorious for a higher risk of compartment syndrome (61% incidence), compared with injuries above the knee (19% incidence).

Venous Outflow Obstruction

Uncomplicated deep venous thrombosis (DVT) often increases ICP, depending on the extent of DVT. Only when there is extensive, multilevel DVT with occlusion of venous collaterals is the venous outflow obstruction sufficient to increase ICP and produce compartment syndrome. With increased venous hypertension the arterial–venous pressure gradient (Δ P ) is altered and capillary blood flow is impaired. With reduced capillary blood, muscle cell injury ensues, exacerbating tissue edema. This cycle continues until eventually the postcapillary venules thrombose and venous gangrene develops.

Two examples of situations that may result in venous outflow obstruction and compartment syndrome include deep vein harvest for use as an arterial conduit and extracorporeal membrane oxygenation (ECMO). In a minority of cases, especially when there is concurrent great saphenous vein harvest or IR in the same limb, harvesting deep vein can produce compartment swelling sufficient to necessitate fasciotomy. ECMO may cause lower extremity compartment syndrome in 10.3% (7.3% to 14.5%) of patients. Compartment swelling during ECMO may be a result of venous outflow obstruction due to the presence of large bore cannula in the femoral vein and ischemia induced by a partially occlusive arterial cannula in the same extremity.

Hemorrhage

Hemorrhage may be a source of rapid increases in compartment pressure. Thigh compartment syndrome has been described as the presenting symptom for rupture of a popliteal artery aneurysm or postoperative hemorrhage after joint replacement surgery in an anticoagulated patient.

Nonvascular Etiologies

Fracture

Tibial or forearm fractures are the most common orthopedic causes of acute compartment syndrome. These fractures injure the surrounding muscles and cause bleeding within the compartment, elevating ICP. The incidence of compartment syndrome with fractures ranges from 1% to 29%. ^, The anterior compartment of the leg and the flexor compartment of the forearm are most prone to this phenomenon. Comminuted fractures are more likely to result in a compartment syndrome, owing to the greater energy absorbed in such injuries.

Crush Injury

Crush injuries are another form of trauma that may cause compartment syndrome. Reported mechanisms include crushing by equipment at industrial sites or large building structures during earthquakes and blunt trauma due to assault. ^, Compartment syndrome after crush injury results from a combination of direct muscle injury and IR due to direct compartment pressure with underlying muscle ischemia and subsequent reperfusion upon removal of the external compressive force. Large-volume crystalloid resuscitation can exacerbate the increase in ICP.

Iatrogenic

Iatrogenic causes of compartment syndrome include extravasation of large volumes of fluid within a muscle compartment, extravasation of caustic medications such as contrast agents, inadvertent arterial injections, and hemorrhage related to arterial or venous punctures in coagulopathic or anticoagulated patients. Additional mechanisms include the compression injuries associated with prolonged intraoperative immobilization, as occurs in the dorsal lithotomy position, and cast immobilization for fractures.

Secondary Compartment Syndrome

Rarely a compartment syndrome develops in a trauma patient without overt evidence of extremity trauma. This phenomenon has been termed “secondary compartment syndrome” and is believed to be a consequence of diffuse microvascular permeability due to trauma-induced systemic inflammatory response syndrome in concert with massive fluid resuscitation.

Clinical Presentation

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