Purpose: Vascular injuries in lower extremity trauma, especially with involvement of the popliteal artery, are associated with considerably high rates of limb loss, especially with blunt trauma mechanisms. The aim of this study was to evaluate the risk of amputation in patients with traumatic popliteal artery lesions with special focus on the validity of the Mangled Extremity Severity Score (MESS). Methods: In this retrospective study, all patients treated for isolated lesions of the popliteal artery following trauma between January 1990 and December 2020 at a high-volume level I trauma center were included. Primary outcome was limb salvage dependent on MESS and the influence of defined parameters on limb salvage was defined as secondary outcome. The extent of trauma was assessed by the MESS. Results: A total of 50 patients (age 39.2 ± 18.6 years, 76% male) with most blunt injuries (n = 47, 94%) were included. None of the patients died within 30 days and revascularization was attempted in all patients with no primary amputation and the overall limb salvage rate was 88% (44 patients). A MESS ≥ 7 was observed in 28 patients (56%) with significantly higher rates of performed fasciotomies (92.9% vs. 59.1%; p < 0.01) in those patients. MESS did not predict delayed amputation within our patient cohort (MESS 8.4 ± 4.1 in the amputation group vs. 8.1 ± 3.8 in the limb salvage group; p = 0.765). Conclusion: Revascularization of limbs with isolated popliteal artery injuries should always be attempted. MESS did not predict delayed amputation in our cohort with fasciotomy being an important measure to increase limb salvage rates.

Recent evidence demonstrates an involvement of impaired mitochondrial function in peripheral arterial disease (PAD) development. Specific impairments have been assessed by different methodological in-vivo (near-infrared spectroscopy, ³¹P magnetic resonance spectroscopy), as well as in-vitro approaches (Western blotting of mitochondrial proteins and enzymes, assays of mitochondrial function and content). While effects differ with regard to disease severity, chronic malperfusion impacts subcellular energy homeostasis, and repeating cycles of ischemia and reperfusion contribute to PAD disease progression by increasing mitochondrial reactive oxygen species production and impairing mitochondrial function. With the leading clinical symptom of decreased walking capacity due to intermittent claudication, PAD patients suffer from a subsequent reduction of quality of life. Different treatment modalities, such as physical activity and revascularization procedures, can aid mitochondrial recovery. While the relevance of these modalities for mitochondrial functional recovery is still a matter of debate, recent research indicates the importance of revascularization procedures, with increased physical activity levels being a subordinate contributor, at least during mild stages of PAD. With an additional focus on the role of revascularization procedures on mitochondria and the identification of suitable mitochondrial markers in PAD, this review aims to critically evaluate the relevance of mitochondrial function in PAD development and progression.

Background & objective: Arterial vascular trauma bears a great risk of poor functional outcome or limb loss. The aim of this study was to analyze amputation rates of patients after vascular trauma and to perform a predictor analysis for the risk of major amputation. Methods: In a single-center retrospective analysis of 119 extremities treated for arterial vascular injury between 1990 and 2018 amputation rates and factors associated with limb loss were assessed. All patients were treated for traumatic vascular injuries; iatrogenic injuries were not included in the study. Results: During the study period, a total of 119 legs in 118 patients were treated after arterial vascular trauma. The in-hospital major amputation rate was 16.8% and the mortality rate was 2.5%. In the predictors analysis, vascular re-operation (amputation rate 53.8% vs 12%, odds ratio = 8.56), a Rutherford category ⩾IIb (25.4% vs 4.2%, odds ratio = 6.43), work-related or traffic accidents (28.2% vs 0%, odds ratio = 4.86), concomitant soft tissue or bone injuries (26.7% vs 7.3%, odds ratio = 4.64), polytrauma (33.3% vs 12%, odds ratio = 3.68), and blunt trauma (18.9% vs 0% for penetrating trauma, odds ratio = 1.64) were found to be associated with amputation. Conclusions: Lower extremity arterial vascular trauma was associated with a significant major amputation rate. Several predictors for limb loss were identified, which could aid in identifying patients at risk and adapting their treatment.

Objective: We aimed to predict patient-specific rupture risks and growth behaviors in abdominal aortic aneurysm (AAA) patients using biomechanical evaluation with finite element analysis to establish an additional AAA repair threshold besides diameter and sex. Methods: A total of 1219 patients treated between 2005 and 2024 (conservative and repaired AAAs) were screened for a pseudo-prospective single-center study. A total of 15 ruptured (rAAA) vs. 15 non-ruptured AAAs (control group) were matched for pre-rupture imaging (first rAAA) and the initial post-rupture imaging (second rAAA) with two images in the asymptomatic control group (first and second control). The matching criteria were as follows: aneurysm diameter, sex, and time period between imagings. The biomechanical properties were analyzed with the finite element method (A4clinicsRE, Vascops GmbH, Graz, Austria). Results: Both groups had the same median aortic diameter of 5.5 cm in the first imaging but had significantly different aneurysm progressions with 6.9 cm (5.5–9.4 cm) in the second rAAA vs. 6.0 cm (5.1–7.3 cm) in the second control group (p = 0.006). The first rAAA, compared to the first control, showed significantly a higher peak wall stress (PWS) (211.8 kPa vs. 180.5 kPa, p = 0.029) and luminal diameter (43.5 mm vs. 35.3 mm; p = 0.016). The second rAAA, compared to the matched second control, showed a significantly higher PWS (281.9 kPa vs. 187.4 kPa, p = 0.002), luminal diameter (58.3 mm vs. 39.7 mm; p = 0.007), PWRR (0.78 vs. 0.49, p = 0.014) and RRED (79.8 vs. 56.5, p = 0.014). The rAAA group showed over-proportional averages, over the observation time, and an increase in PWS (nearly 10× faster in rAAA) and luminal diameter (nearly 4× faster in rAAA) per month. Conclusions: The finite element analysis of biomechanical properties could be used for the early prediction of an increased rupture risk in AAA patients. This was confirmed by matched imaging analyses before and after AAA rupture. Further multicenter data are needed to support these findings.

Spinal cord ischemia (SCI) is a devastating and unpredictable complication of thoracoabdominal aortic repair. Postischemic Toll-like receptor 3 (TLR3) activation through either direct agonists or shock wave therapy (SWT) has been previously shown to ameliorate damage in SCI models. Whether the same applies for pre- or postconditioning remains unclear. In a model of cultured SHSY-5Y cells, preconditioning with either poly(I:C), a TLR3 agonist, or SWT was performed before induction of hypoxia, whereas postconditioning treatment was performed after termination of hypoxia. We measured cytokine expression via RT-PCR and utilized Western blot analysis for the analysis of signaling and apoptosis. TLR3 activation via poly(I:C) significantly reduced apoptotic markers in both pre- and postconditioning, the former yielding more favorable results through an additional suppression of TLR4 and its downstream signaling. On the contrary, SWT showed slightly more favorable effects in the setting of postconditioning with significantly reduced markers of apoptosis. Pre- and post-ischemic direct TLR3 activation as well as post-ischemic SWT can decrease apoptosis and proinflammatory cytokine expression significantly in vitro and might therefore pose possible new treatment strategies for ischemic spinal cord injury.