Acute ischemia of an extremity occurs in several stages, a lack of oxygen being the primary contributor of the event. Although underlying patho-mechanisms are similar, it is important to determine whether it is an acute or chronic event. Healthy tissue does not contain enlarged collaterals, which are formed in chronically malperfused tissue and can maintain a minimum supply despite occlusion. The underlying processes for enhanced collateral blood flow are sprouting vessels from pre-existing vessels (via angiogenesis) and a lumen extension of arterioles (via arteriogenesis). While disturbed flow patterns with associated local low shear stress upregulate angiogenesis promoting genes, elevated shear stress may trigger arteriogenesis due to increased blood volume. In case of an acute ischemia, especially during the reperfusion phase, fluid transfer occurs into the tissue while the vascular bed is simultaneously reduced and no longer reacts to vaso-relaxing factors such as nitric oxide. This process results in an exacerbative cycle, in which increased peripheral resistance leads to an additional lack of oxygen. This whole process is accompanied by an inundation of inflammatory cells, which amplify the inflammatory response by cytokine release. However, an extremity is an individual-specific composition of different tissues, so these processes may vary dramatically between patients. The image is more uniform when broken down to the single cell stage. Because each cell is dependent on energy produced from aerobic respiration, an event of acute hypoxia can be a life-threatening situation. Aerobic processes responsible for yielding adenosine triphosphate (ATP), such as the electron transport chain and oxidative phosphorylation in the mitochondria, suffer first, thus disrupting the integrity of cellular respiration. One consequence of this is irreparable damage of the cell membrane due to an imbalance of electrolytes. The eventual increase in net fluid influx associated with a decrease in intracellular pH is considered an end-stage event. Due to the lack of ATP, individual cell organelles can no longer sustain their activity, thus initiating the cascade pathways of apoptosis via the release of cytokines such as the BCL2 associated X protein (BAX). As ischemia may lead to direct necrosis, inflammatory processes are further aggravated. In the case of reperfusion, the flow of nascent oxygen will cause additional damage to the cell, further initiating apoptosis in additional surrounding cells. In particular, free oxygen radicals are formed, causing severe damage to cell membranes and desoxyribonucleic acid (DNA). However, the increased tissue stress caused by this process may be transient, as radical scavengers may attenuate the damage. Taking the above into final consideration, it is clearly elucidated that acute ischemia and subsequent reperfusion is a process that leads to acute tissue damage combined with end-organ loss of function, a condition that is difficult to counteract.

In this study we investigated how hemostats such as oxidized regenerated cellulose (ORC, TABOTAMP) and oxidized non-regenerated cellulose (ONRC, RESORBA CELL) influence local cellular behavior and contraction of the extracellular matrix (ECM). Human stromal fibroblasts were inoculated in vitro with ORC and ONRC. Cell proliferation was assayed over time and migration was evaluated by Live Cell imaging microscopy. Fibroblasts grown in collagen-gels were treated with ORC or ONRC and ECM contraction was measured utilizing a contraction assay. An absolute pH decline was observed with both ORC and ONRC after 1 hour. Mean daily cell proliferation, migration and matrix contraction were more strongly inhibited by ONRC when compared with ORC (p < 0.05). When control media was pH-lowered to match the lower pH values typically seen with ORC and ONRC, significant differences in cell proliferation and migration were still observed between ONRC and ORC (p < 0.05). However, in these pH conditions, inhibition of matrix contraction was only significant for ONRC (p < 0.05). We find that ORC and ONRC inhibit fibroblast proliferation, migration and matrix contraction and stronger inhibition of these essential cellular processes of wound healing were observed for ONRC when compared with ORC. These results will require further validation in future in vivo experiments to clarify the clinical implications for hemostat use in post-surgical wound healing.

Congenital absence of the inferior vena cava (AIVC) is a rare malformation which may be associated with an increased risk for deep vein thrombosis (DVT). However, the role of thrombophilia in AIVC and DVT is unknown. Between 1982 and 2013 41 patients (12 female, 29 male, mean age 28 S.D. 11 years) were detected at the University of Düsseldorf, Germany, with AIVC. Based on medical history, clinical examination, imaging and coagulation studies, we performed on this collective a risk characterisation. Extensive literature research added further 123 published cases during 1993 and 2013. AIVC-patients were compared with iliocaval DVT-patients without AIVC (n = 168) treated during the same period in our clinic (90 female, 78 male, mean age 38 S.D. 17 years). In contrast to classical DVT younger men were more often affected. Factor-V-Leiden-mutation, 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphism and hyperhomocysteinemia individually are associated with an increased risk of DVT in patients with AIVC. Aplasia/hypoplasia of the right or left kidney is also associated with IVCA. AIVC should be considered in young patients who present with DVT involving the vena cava. Analysis of publications with AIVC and our patients yielded a typical spectrum of AIVC-associated DVT characteristics: AIVC occurs in young male adults, is revealed by proximal DVT, not necessarily accused by precipitating factors like immobilisation, and is mostly located bilateral. Hereditary coagulation abnormalities seem to be more often a contributing factor for DVT in AIVC.

Spinal cord ischemia (SCI) is a clinical complication following aortic repair that significantly impairs the quality and expectancy of life. Despite some strategies, like cerebrospinal fluid drainage, the occurrence of neurological symptoms, such as paraplegia and paraparesis, remains unpredictable. Beside the major blood supply through conduit arteries, a huge collateral network protects the central nervous system from ischemia—the paraspinous and the intraspinal compartment. The intraspinal arcades maintain perfusion pressure following a sudden inflow interruption, whereas the paraspinal system first needs to undergo arteriogenesis to ensure sufficient blood supply after an acute ischemic insult. The so-called steal phenomenon can even worsen the postoperative situation by causing the hypoperfusion of the spine when, shortly after thoracoabdominal aortic aneurysm (TAAA) surgery, muscles connected with the network divert blood and cause additional stress. Vessels are a conglomeration of different cell types involved in adapting to stress, like endothelial cells, smooth muscle cells, and pericytes. This adaption to stress is subdivided in three phases—initiation, growth, and the maturation phase. In fields of endovascular aortic aneurysm repair, pre-operative selective segmental artery occlusion may enable the development of a sufficient collateral network by stimulating collateral vessel growth, which, again, may prevent spinal cord ischemia. Among others, the major signaling pathways include the phosphoinositide 3 kinase (PI3K) pathway/the antiapoptotic kinase (AKT) pathway/the endothelial nitric oxide synthase (eNOS) pathway, the Erk1, the delta-like ligand (DII), the jagged (Jag)/NOTCH pathway, and the midkine regulatory cytokine signaling pathways.

Introduction: Popliteal artery aneurysms (PAA) are rare. Different surgical techniques for open surgical repair are possible. This study presents a single centre experience using open surgical repair with a medial approach (MA) and outlines differences between symptomatic (SLS) and asymptomatic (ALS) legs. Methods: Data collection was performed retrospectively. The investigation period was from 1 January 1996 to 1 January 2013. Patients presented in the Outpatient Department and received a questionnaire concerning their quality of life. Data are presented as mean ± standard deviation. Mann–Whitney test and Cochran–Armitage test for trend was used for data analysis. Kaplan–Meier method was used to calculate limb salvage rates. p < 0.05 was considered statistically significant. Results: We analyzed 16 ALS and 26 SLS with an average age of 63.5 ± 10 years. Preoperative ankle-brachial index (ABI) was 1.0 ± 0.2 for ALS (on control examination: 1.12 ± 0.24) and 0.08 ± 0.18 for SLS (on control examination 0.94 ± 0.14) (p < 0.05). Limb salvage rate was 100% for ALS and 86.7% for SLS (overall 93.3%). Primary patency rate for SLS was 85%, for ALS rate of 100%, respectively (overall 92.5%). ALS reached an average of 13.1 ± 2.7 points (SLS 11.4 ± 2.8) on a numeric point scale. Conclusion: Open surgery is therapy and prevention of acute ischaemia all in one, especially for asymptomatic patients and delivers good long-term results. Endovascular therapies offer an alternative but long-term results are pending. Open surgery should still be considered as a gold standard therapy.

Gelatin-based hemostats have been used in various surgical fields and showed advantageous effects on central aspects of wound healing when compared to cellulose-based hemostats. Nevertheless, the influence of gelatin-based hemostats on wound healing has not been fully explored yet. Hemostats were applied to fibroblast cell cultures for 5, 30, 60 min, 24 h, 7 and 14 days and measurements were taken at 3, 6, 12, 24 h and 7 or 14 days, respectively. Cell proliferation was quantified after different exposure times and a contraction assay was conducted to measure the extent of the extracellular matrix over time. We further assessed quantitative levels of vascular endothelial growth factor and basic fibroblast growth factor using enzyme-linked immunosorbent assay. Fibroblast counts decreased significantly at 7 and 14 days independent of the application duration (p < 0.001 for 5 min application). The gelatin-based hemostat did not have a negative impact on cell matrix contraction. After application of gelatin-based hemostat, the basic fibroblast growth factor did not change; yet, the vascular endothelial growth factor significantly increased after a prolonged 24 h application time when compared to controls or to a 6 h exposure (p < 0.05). Gelatin-based hemostats did not impair contraction of the extracellular matrix or growth factor production (vascular endothelial growth factor and basic fibroblast growth factor), while cell proliferation diminished at late time points. In conclusion, the gelatin-based material seems to be compatible with central aspects of wound healing. For further clinical assessment, future animal and human studies are necessary.