Abstract

Atypical claudication is a relatively uncommon problem within the general population. However, suspicion for the diagnosis is raised when young and athletic patients present with symptoms of claudication during exercise. The most common causes of atypical claudication are anatomical variants, including popliteal artery entrapment syndrome and tarsal tunnel syndrome. These variants result in impaired arterial flow and nerve compression, respectively. In this report, we present a seminal case of dorsalis pedis artery entrapment by the extensor hallucis brevis tendon during active dorsiflexion of the foot. The patient was a 42-year-old male without significant past medical history, who presented with claudication in both feet upon active dorsiflexion. He underwent dynamic arterial duplex studies that first revealed normal flow in the neutral position and then revealed complete cessation of flow in both duplex and Doppler modes on dorsiflexion of the foot. He also underwent dynamic magnetic resonance angiography of bilateral lower extremities that revealed an incomplete pedal arch with early termination of the posterior tibial artery on static images and termination of the dorsalis pedis artery at notching on the dorsum of the foot during dorsiflexion. The patient was taken to the operating room for bilateral dorsalis pedis artery exploration. During exploration, the patient was found to have entrapment of the dorsalis pedis artery by the extensor hallucis brevis (EHB) tendon. This was documented by both direct visualization and intraoperative cessation of Doppler signal on dorsiflexion. Since the EHB tendon provides only secondary function to the extensor hallucis longus (EHL) tendon, the EHB was transected near its insertion and transposed directly to the EHL tendon. This allowed for normal extensor function of the great toe and restored triphasic Doppler signals during dorsiflexion. Dorsalis pedis arterial entrapment is a novel cause of atypical claudication. It is extremely uncommon as patients must have both abnormal anatomy and an incomplete pedal arch to display symptoms. Similar to other entrapment syndromes, if identified before permanent arterial scarring, the treatment does not require a bypass procedure. Removal of the tendon along with transposition will allow cessation of symptoms without impaired dorsiflexion of the great toe.

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