Introduction: Acquired pes planus is caused by mechanical uncoupling of the bones of the tarsus due to failure of the osseoligamentous complex that maintains the medial longitudinal arch of the foot. The most common cause of acquired flat foot deformity in adults is posterior tibialis tendon dysfunction. A solitary previous case report has documented an alternative aetiology of acquired flat foot in adults due to isolated spring ligament rupture; in that case diagnosis was made intra-operatively.

Materials and Methods: We present 9 cases of acquired flat foot deformity that were caused by isolated spring ligament insufficiency, mainly presenting after an eversion injury of the ankle. We present the clinical sign of ability to single leg tiptoe, but with persistent forefoot abduction and heel valgus, that allows differentiation of this diagnosis from posterior tibialis tendon dysfunction. In addition we illustrate the radiological features of this condition which have not been previously described and allow confirmation of the diagnosis non-operatively.

Results: Six patients have been managed with orthotics and three underwent surgery; one patient who presented early had an isolated repair of the spring ligament complex and has done well. The remaining two patients required a calcaneal osteotomy and Flexor Digitorum Longus transfer as for a PTT reconstruction. In all these three patients the spring ligament was found to be completely ruptured during surgery.

Discussion: This type of injury may not be as rare as previously thought and demonstrates the importance of the spring ligament on its own in maintaining the medial longitudinal arch. Awareness of this condition could lead to earlier diagnosis and better prognosis with earlier treatment.

Conclusion: We propose that early diagnosis (with ultrasound confirmation) and management of this condition would offer a better prognosis and allow less interventional surgery.

The purpose of this study was to investigate the role that genetics play in the aetiology and symptomatology of full thickness tears of the rotator cuff.

From a retrospective, cohort study of 205 patients diagnosed with full thickness rotator cuff tears, we determined, using ultrasound, the prevalence of full thickness tears in their 129 siblings. Using 150 spouses as controls, the relative risk of full thickness rotator cuff tear in siblings v controls was 2.42 (p< 0.0001, 95 % CI 1.77 to 3.31). The relative risk of symptomatic full thickness rotator cuff tear in siblings v controls was 4.65 (p< 0.0001, 95 % CI 2.42 to 8.63).

The significantly increased risk for tears in siblings implies that genetic factors play a major role in the development of full thickness tears of the rotator cuff.

From a retrospective, cohort study of 205 patients diagnosed with full-thickness tears of the rotator cuff, we determined, using ultrasound, the prevalence of such tears in their 129 siblings. Using 150 spouses as controls, the relative risk of full-thickness tears in siblings versus controls was 2.42 (95% CI 1.77 to 3.31). The relative risk of symptomatic full-thickness tears in siblings versus controls was 4.65 (95% CI 2.42 to 8.63).

The significantly increased risk for tears in siblings implies that genetic factors play a major role in the development of full-thickness tears of the rotator cuff.