Threatening Inferior Limb Ischemia: When to Consider Fasciotomy and What Principles to Apply?

Inferior limb compartmental syndrome (CS) gathers a constellation of symptoms that traditionally refers to pathologically increased intramuscular and surrounding tissue pressure generally contained in nonexpansile leg spaces. It associates oftentimes reperfusion or traumatic injury. Intrinsic rigidity of these leg and foot closed compartments may enhance critical pressure risings with deleterious effects on specific vascular and nervous supply, with two main presentations: acute versus chronic display. For these situations, early fasciotomy plays the major role of releasing specific compartment hypertension and prevents deleterious tissue necrosis. Intervention is effective only if required upon precise indications (measured tissue pressure within 20 to 30？mm？Hg of systemic diastolic pressure) and performed correctly in a timely fashioned approach. Any failure or delay in recognizing CS inevitably leads to adverse outcomes and jeopardy for secondary limb loss. When judiciously applied during or soon after limb-salvage revascularization technically successful fasciotomy may represent a major contributor in limb preservation. It accounts for a well-defined therapeutic proceeding available for any conscientious and well-briefed interventionist. 1. Introduction The compartmental syndrome (CS) is a morbid entity that can arise in any area of the body that has little or no capacity for tissue expansion, such as the lower and upper limbs, the abdomen, and some described cervical regions [1, 2]. The vascular practitioner becomes increasingly confronted with revascularization side effects [3] since new techniques and contemporary devices venture more extreme and challenging peripheral ischemic situations. Among the whole evoked CS etiologies [1–3], the revascularization subgroup represents a frequent and possibly devastating pathology, requiring urgent and appropriate therapeutic measures [2, 3]. It is generally accepted that one of the most common locations of all peripheral CS manifestations is represented by the lower leg [1–3]; this arises upon relative nondistensibility of local bones and surrounding dense connective septa and tissues, facing reactive “postischemic” vasodilatation and swelling [1–4]. Intrinsic rigidity of these leg and foot closed compartments in specific anatomical locations may enhance critical pressure risings with deleterious effects on the local vascular and nervous supply. Eventual failure or delay in recognizing CS inevitably leads to adverse outcomes for concerned patients and hinders early prognosis for limb preservation [1, 2].