Effects of intermittent claudication due to arterial disease on pain-free gait.

INTRODUCTION: Studies of intermittent claudication gait report inconsistent outcomes. Changes in gait are often attributed to degradation of calf muscles, but causation has not been proven through real-time electromyographic data. Neither have effects of walking speed been fully considered. This study aimed to investigate the effect of intermittent claudication on kinematics, kinetics and muscle activity during pain-free gait. METHODS: 18 able bodied individuals and 18 with intermittent claudication walked at their preferred speed while lower limb kinematic, kinetic and electromyography data were collected. FINDINGS: People with intermittent claudication walk slower and with reduced step length. Internal ankle plantarflexion moment (P = 0.004, effect size = 0.96) and ankle power generation (P < 0.001, effect size = 1.36) in late stance were significantly reduced for individuals with intermittent claudication. Significant moment and power reductions at the knee and power reduction at hip occurred in early stance, with similar reductions in early and late stance for ground reaction forces. Peak electromyography of soleus activity was significantly reduced in late stance (P = 0.01, effect size = 1.1, n = 13). Effects were independent of walking speed. INTERPRETATION: Reductions in ankle plantarflexion moments and power generation were consistent with reduced soleus electromyography activity and reduced peak vertical ground reaction forces during late stance. These effects are not due to a reduced walking speed. Changes in knee and hip function are also unrelated to walking speed. These outcomes provide a platform for the design and evaluation of interventions that seek to restore normal walking and improve pain-free walking distances for people with intermittent claudication.

Aorto-enteric fistula development secondary to mycotic abdominal aortic aneurysm following intravesical bacillus Calmette-Guerin (BCG) treatment for transitional cell carcinoma of the bladder.

INTRODUCTION: Intravesical BCG-instillation for bladder cancer is considered safe but is not without risk. While most side-effects are localised and self-limiting, the development of secondary vascular pathology is a rare but significant complication. PRESENTATION OF CASE: A 77-year-old male presented with a mycotic abdominal aortic aneurysm and associated aorto-enteric fistula 18 months after receiving intravesical BCG-instillations for early stage transitional cell carcinoma. DISCUSSION: Response rates to intravesical BCG for early stage transitional cell carcinoma are high. The procedure produces a localised inflammatory response in the bladder but the exact mechanism of action is unclear. The treatment is generally well tolerated but BCG-sepsis and secondary vascular complications have been documented. Mycotic abdominal aortic aneurysm with associated aorto-enteric fistula secondary to BCG is very rare. Few examples have been documented internationally and the extent of corresponding research and associated management proposals is limited. Surgical options include in situ repair with prosthetic graft, debridement with extra-anatomical bypass and, occasionally, endovascular stent grafting. Recommended medical therapy for systemic BCG infection is Isoniazid, Rifampicin and Ethambutol. CONCLUSION: Current screening methods must be updated with clarification regarding duration of anti-tuberculous therapy and impact of concomitant anti-tuberculous medication on the therapeutic action of intravesical BCG. Long-term outcomes for patients post graft repair for mycotic aneurysm are unknown and more research is required regarding the susceptibility of vascular grafts to mycobacterial infection. Recognition of the risks associated with BCG-instillations, even in immunocompetent subjects, is paramount and must be considered even several months or years after receiving the therapy.