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

Abstract

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.

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“…Reported DFS singularities include (1) the regular tibial trunks calcifications [2,30,31,57] that match the extent of local neuropathy [25,31], (2) the "end-artery occlusive disease" (EAOD) concept [59], (3) an impaired arterio-and angiogenesis [60], (4) a specific collateral deprivation following chronic inflammation and septic thrombosis of small vessels [31,35,[57][58][59], (5) intrinsic vascular or matrix impaired regeneration [61], and (6) characteristic neuro-ischemic compartmental hyper pressure foot syndromes [62].…”

“…Modern diabetic ulcer understanding builds a complete design of multifaceted and potentially devastating CLI effects in these patients [2,31,[57][58][59][60][61][62].…”

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“…Additionally, recent clinical research unveils original macro-and microcirculatory arterial modifications frequently associating CLI neuro-ischemic diabetic foot wounds [26,27]. Among these characteristics, regular tibial trunks calcifications [26,28] (corroborating the local neuropathic involvement), [26,29] the "end-artery occlusive disease" (EAOD) concept [29], impaired arterio-and angiogenesis [30], specific foot collateral decay following chronic inflammation and septic thrombosis of small vessels [16,29,30], intrinsic vascular or matrix impaired regeneration [31] and specific compartmental ischemic foot syndromes [32] structure nowadays a more complete and bigger picture of devastating diabetic CLI effects [1,6,[26][27][28][29][30][31][32][33]. Contemporary clinicians are also able nowadays to designate alternative strategies [16] for revascularization, in addition to basic technical preparation of interventions [4,18,28].…”

“…Future diagnostic tools focusing on the topographic superficial (the skin level) [16,40] also on deep foot structures (bones, tendons and fascial compartments) [32] can complete this new "regional" and more unitary view of the neuro-ischemic diabetic foot [33,39].…”