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A 43-year-old male patient with underlying diabetes mellitus presented with lower abdominal pain radiating to left thigh. He was hemodynamically stable, but appeared lethargic. Both iliac fossae were tender, and crepitus appreciated along the anteromedial aspect of the left thigh. The patient initially responded well to treatment and was discharged; however, he was re-admitted several months later due to recurrent collection showing the growth of Klebsiella pneumoniae in the culture and succumbed to sepsis due to deep-seated intramuscular abscess and lung empyema. In conclusion, psoas abscess is a condition that can mimic various pathologies related to the lower abdomen and, therefore, clinicians should always have a high index of suspicion to prevent a missed diagnosis. Early detection may yield good outcomes, if managed with adequate surgical drainage and appropriate antibiotics.

Introduction: Our objective is to highlight the role of the semi-membranosus muscle, which is surprisingly not described in the major books of anatomy, as main thigh pump in the venous return [1]. Material and methods: Latex injection of fresh cadavers followed by anatomical dissection and colored segmentation of the whole venous network of 300 lower limbs, 3D reconstructions by CT venography of 1000 CVD patients are at the basis of this study. Results: The venous arcades of the semi-membranosus muscle constitute a main deep collateral route by-passing the narrowed area of the Hunter’s canal. This anatomical study clearly shows that these venous arcades are regularly connected:(Figure 1) • By their 2 lower branches to the popliteal vein • By their 2 higher branches to the deep femoral vein. Consequently, they constitute a derivative route of the femoral axis, explaining their dilatation in case of stenosis of the Hunter’s canal outlet. Similarly, in a physiological situation, the whole amount of blood ejected by the powerful calf pump through the popliteal vein cannot always reach the femoral vein through the Hunter’s canal: the arcades then play the role of a safety valve. Moreover, the veins of the semi-membranosus muscle constitute a main thigh pump: they push up the blood towards the femoral crossroad at the root of the limb. Discussion and conclusion: The veins of the semi-membranosus should be systematically investigated by USD : their dilatation is the witness of venous outlet syndrome of the Hunter’s canal which is a major cause of femoral vein thrombosis. USD investigation should be systematically carried out at that levels to prevent future deep vein obstruction.

Introduction: “Adductor canal syndrome”, or “Jogger’s syndrome” has been described as an unusual cause of acute arterial occlusion in younger men. It is also been identified as a cause of compressive neuropathy of the saphenous nerve. Nevertheless, femoral vein compression in the canal has never been described. Our aim is to describe the anatomy and physiology of Hunter’s canal, and to show that the femoral vein is much more exposed than the artery to compression inside the adductor hiatus, particularly at the outlet [1]. Material and methods: Fifty fresh cadavers were used to surgically expose the adductor hiatus for anatomical study. A series of 200 phlebographies and 100 CT venographies were also used to study the 3D morphology of the adductor hiatus. Results: Anatomically, in all cases we found that an abnormal musculotendinous band arose from the adductor magnus muscle, and joined the adductor tendon to the vastus medialis. The femoral vein is located more posteriorly and is frequently narrowed at this level : the edge of the vasto-adductor membrane. This was particularly true when the artery was calcified. Different types of anatomical compression of the femoral vein could by described, but the main is in the Hunter’s outlet: the edge of the vasto-adductor membrane. The resultant anatomical structure creates a notch with venous stenosis frequently occurring at the lower part of the hiatus, well seen in the cast of a femoral vein injected with latex and on the phlebographies In a majority of cases where such a stenosis was found, it was at the lower part of the canal, 13 to 15 cm above the femoral condyle. Compression by the artery or higher inside the canal could also be identified, but they are often ignored. Discussion and conclusion: Physiological hypothesis: The cadaveric simulations showed that contraction of the adductor longus closes the hiatus, and the adductor magnus opens it. Our hypothesis is that Hunter’s canal prevents femoro-popliteal axis reflux by synchronizing with calf pump ejection during ambulation. So in clinical practice, USD investigation should be a routine, seeking for a dilatation of the derivative routes, particularly the arcades of the semi-membranosus muscle: Compression of the femoral vein in the adductor canal is an underestimated cause of venous obstruction and deep vein thrombosis. Ultrasound investigation of both limbs should systematically be carried out at this precise level to prevent future venous obstruction from occurring here.

Background The “Adductor canal syndrome” has been described as an unusual cause of acute arterial occlusion inside the Hunter’s canal in young sportsmen. It may also produce a compressive neuropathy of the saphenous nerve. To our knowledge, femoral vein compression in the canal has never been reported. Objective To describe the anatomy, to propose a physiology of this canal, and to show that the femoral vein is much more exposed than the artery to compression inside this adductor hiatus, particularly at the outlet. Material and methods The whole adductor canal was exposed in 100 limbs for anatomical study following latex injection. A series of 200 phlebographies and 100 CT venograms were also analyzed. Results Anatomically, we found a musculotendinous band called the “vastoadductor membrane,” which jointed the adductor tendon to the vastus medialis in all the cases. The femoral vein, located more posteriorly, was frequently narrowed at this level. This band can create a notch with a venous stenosis at the outlet of the Hunter’s canal, usually located 12–14 cm above the femoral condyle. Two femoral valves constitute the landmark of the canal on the venograms: the lower is just below the outlet, 9 cm above the condyle. The second valve is 3 cm higher inside the canal. Functionally, the cadaveric simulations showed that the contraction of the adductor longus closes the hiatus, while the adductor magnus opens it. Our hypothesis is that Hunter’s canal prevents femoropopliteal axis reflux by synchronizing with calf pump ejection during ambulation. Conclusion Compression of the femoral vein inside the adductor’s canal is an underestimated and misdiagnosed cause of postural stenosis of the femoral vein. Ultrasound investigation of both limbs in patients with chronic venous disease (CVD) should be systematically carried out at this precise level in order to prevent future occlusion and onset of acute deep vein thrombosis.

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