Introduction

Acute compartment syndrome (ACS) is a surgical emergency, regardless of etiology or anatomic location. It is caused by an increase in intracompartmental pressure (ICP) within an unyielding fascia envelope, which impairs tissue perfusion [1]. Increased ICP reduces the pressure gradient between the vascular bed and the surrounding soft tissues, compromising the circulation and function of the compartment’s contents. When ICP remains elevated, capillary perfusion is reduced through the transmission of the pressure to the postcapillary venules, which increases venous pressure and decreases the arterial–venous pressure gradient. Furthermore, increased ICP may collapse capillaries, decreasing their radius and further increasing resistance to flow. This results in inadequate tissue oxygenation of the nerves and muscles within the affected compartment [1–8].

ICP can be elevated by conditions that either increase compartment volume or exert external compression. Trauma is, by far, the most common cause (fractures, crush injuries, contusions or gunshot wounds). The National Trauma Data Bank (USA) reveals that 1.22% of patients with forearm fractures and 3.79% of those with tibial fractures underwent fasciotomy for compartment syndrome. Other causes such as tight casts, dressings, external wrappings, extravasation of intravenous fluids/infusions, burns, bleeding disorders, post-ischemic swelling and arterial injuries are also well-documented [1, 3, 7, 8]. Although rare, compartment syndromes of the hand or forearm secondary contrast extravasation have been reported. Key factors affecting the severity of extravasation injuries include osmolality, the ionic or non-ionic nature of the compound, and the volume of the extravasation. Causes for extravasation may be technique-related (high-volume or high-rate injection via infusion pumps) or patient-related (inability to communicate or fragile blood vessels in patients undergoing chemotherapy) [6, 9, 10].