RESUMEN
Chronic life-threatening ischemia (CLTI), characterized by chronic severe ischemic ulcers or gangrene in the legs with arterial occlusive disease, has a high rate of amputation and mortality. However, how lower extremity artery disease (LEAD) leads to CLTI is not fully understood yet. Here, we report a 79-year-old man with resting pain and gangrene in the left first and fifth toes for a year who had undergone repetitive endovascular treatment (EVT) that temporarily improved the ischemia. Non-obstructive general angioscopy (NOGA) revealed yellow and red floating emboli at the occluded left superficial femoral artery (SFA). Although a second EVT for the reoccluded SFA was successful, amputation of the left lower knee remained necessary because of osteomyelitis of the left heel. Cholesterol crystals (CCs) associated with innate inflammation were detected in spontaneously ruptured aortic plaques (SRAPs) via aortic screening using the NOGA, in occluded SFAs, and on the surface of the muscle cross-section of the amputated legs via a polarizing microscope. Histopathological analysis demonstrated CCs in small vessels in various stages of patchy necrosis and muscle regeneration. In this case, the process of CC embolization, such as the embolic source of CCs, occlusion in arteries, small arteries, and deposition in muscles, was confirmed in CLTI. CCs are the principal trigger of IL-6 production through the innate inflammatory response in spontaneously ruptured aortic plaques. Mechanical ischemia and chronic inflammation due to embolized CCs may cause chronic limb damage. In this case, the CC embolization might exacerbate CLTI.
RESUMEN
BACKGROUND: The acromioclavicular (AC) and coracoclavicular (CC) ligaments are important stabilizers of the AC joint. We hypothesized that AC and trapezoid ligament injuries induce AC joint instability and that the clavicle can override the acromion on cross-body adduction view even in the absence of conoid ligament injury. Accordingly, we investigated how sectioning the AC and CC ligaments contribute to AC joint instability in the cross-body adduction position. METHODS: Six fresh-frozen cadaveric shoulders were used in this study, comprising five male and one female specimen, with a mean age of 68.7 (range, 51-87) years. The left side of the trunk and upper limb, and the cervical and thoracic vertebrae and sternum were firmly fixed with an external fixator. The displacement of the distal end of the clavicle relative to the acromion was measured using an electromagnetic tracking device. We simulated AC joint dislocation by the sequential resection of the AC ligament, AC joint capsule, and CC ligaments in the following order of stages. Stage 0: Intact AC and CC ligaments and acromioclavicular joint capsule; stage 1: Completely sectioned AC ligament, capsule and joint disc; stage 2: Sectioned trapezoid ligament; and stage 3: Sectioned conoid ligament. The superior clavicle displacement related to the acromion was measured in the horizontal adduction position, and clavicle overriding on the acromion was assessed radiologically at each stage. Data were analyzed using a one-way analysis of variance and post-hoc tests. RESULTS: Superior displacement was 0.3 mm at stage 1, 6.5 mm at stage 2, and 10.7 mm at stage 3. On the cross-body adduction view, there was no distal clavicle overriding at stages 0 and 1, and distal clavicle overriding was observed in five cases (5/6: 83%) at stage 2 and in six cases (6/6: 100%) at stage 3. CONCLUSION: We found that AC and trapezoid ligament sectioning induced AC joint instability and that the clavicle could override the acromion on cross-body adduction view regardless of conoid ligament sectioning. The traumatic sections of the AC and trapezoid ligament may lead to high grade AC joint instability, and the distal clavicle may subsequently override the acromion.