Introduction

Acute compartment syndrome (ACS) is a condition of elevated pressure within the fascia‐limited compartments of a limb where microcirculation and tissue perfusion are compromised [1]. The disease is rare, with an estimated incidence of 7.3 per 100,000 in males and 0.7 per 100,000 in females [2]. The true incidence of ACS has not been determined because most clinical studies have used fasciotomy as a diagnostic criterion [1]. ACS usually occurs secondary to physical trauma, such as bone fracture or crush injury, but may also develop during ischemia (e.g., prolonged tourniquet use), eschar contracture after extensive burns, or muscle overexertion due to strenuous exercise [3, 4, 5]. Current understanding suggests that the rapid progression of ACS results from positive feedback within the compartment, in which initial trauma or hypoxia induces tissue damage, stimulating local oxidative and inflammatory responses and increasing vascular permeability [1, 6]. Fluid leaking into the compartment increases interstitial pressure and compression of venous drainage, further increasing tissue pressure [7]. Eventually, tissue pressure approaches average arterial pressure, thereby restricting tissue perfusion and increasing hypoxic injury [8]. As the cycle repeats, increased pressure, reduced tissue perfusion, and hypoxic injury progress, culminating in extensive tissue damage and necrosis, leading to loss of muscle, nervous, and vascular tissues within the compartment [9]. The final result is often disability or loss of the limb, and in particularly severe cases, renal failure due to rhabdomyolysis, and possible death. Clinical diagnosis relies on the typical presentation of the 5Ps (Pain, Pallor, Paresthesia, Paralysis, Pulselessness) [10]. However, in clinical practice, these symptoms are poor predictors, and when present, they are terminal, losing the opportunity for surgical neuromuscular salvage [11].

Various types of animal models have been developed in the past, with dogs, pigs, rats, and turkeys as commonly used species, and the construction methods differ [12, 13, 14]. For example, the intrafascial fluid infusion method is more commonly used to simulate the pathology of high intracompartmental pressure (ICP) after trauma by continuous dripping of fluid in the intrafascial compartment [15]. The direct increase of ICP by external devices to simulate clinically high ICP is also one of the classic modeling approaches, with catheterized balloons placed within the intrafascial compartment or with an inflatable cuff around the limb [16, 17, 18]. However, these models have certain shortcomings. On the one hand, the reliance on tourniquets or vascular clamps to restrict arterial supply for creating ischemic injury and the need for surgical removal of blood vessels to eliminate collateral circulation to the compartment increase surgical complexity. On the other hand, the inflammatory reperfusion injury triggered by the sudden restoration of blood flow after removal of the tourniquet or vascular clamp is different from the diffuse focal ischemia commonly seen in limb trauma [19]. Some studies have attempted to simulate ACS by continuously infusing fluids into muscle areas to artificially increase interstitial pressure and swelling [15, 20]. While diffuse injury does occur, large volumes of fluid are reabsorbed into the circulation, again raising questions of systemic effects, which in turn limit their suitability and accuracy for simulating ACS in humans.

In past ICP measurements in animal studies, the Whitesides method or its modifications were used to obtain pressure data by injecting approximately 0.3–0.5 mL of fluid into the fascial compartment in discontinuous injections [21]. However, due to the rapid absorption of the injected fluid into the tissue, multiple measurements must be averaged, and continuous measurements are not possible, leading to large measurement errors. Multiple discontinuous injections of saline can also affect pathophysiologic processes within the tissue. Notably, previous models have mostly focused on the pathophysiologic changes following ACS formation, whereas the process of ACS formation following limb trauma has been less studied. An in‐depth understanding of this process is of great value for early intervention in ACS, reducing surgical rates, and improving long‐term prognosis.

In this study, we first developed a novel ACS injury model using limb crush to simulate the natural progression of ACS following trauma, thereby filling a major gap in preclinical research. Meanwhile, we continuously monitored ICP using a balloon catheter that did not require repeated fluid injections. Compared with previous studies, our model reproduces the development of clinical ACS and provides a physiologically relevant platform for studying the dynamic physiological changes during ACS formation.