Functional improvement is sustained following anatomical and reverse shoulder arthroplasty for fracture sequelae: a...

Shoulder arthroplasty for proximal humerus fracture sequelae is known to provide significant patient improvement, yet this outcome varies with time, prosthesis type, and fracture sequelae. We outline the expected course of postoperative shoulder pain and function in patients with anatomical (ASA) or reverse (RSA) shoulder arthroplasty following different fracture sequelae.

Of 111 consecutive patients from our local shoulder arthroplasty registry, 32 underwent ASA for Boileau type 1 sequelae and 77 RSA patients were identified with Boileau types I, III, and IV. By 5 year post-surgery, there were 72 patients available. All patients underwent standardised ASA or RSA procedures with anatomical (Promos Standard; Lima SMR™; Arthrex Eclipse™; Univers™ II) or reverse prostheses (Promos Reverse^®; Lima SMR™ Reverse; Univers Revers™; Aequalis^® Reversed). Range of motion, Constant-Murley, Disability of the Arm, Shoulder and Hand (DASH), and Shoulder Pain and Disability Index (SPADI) scores were compared at 6, 12, 24, and 60 months postoperatively. We used generalised linear mixed models or random-effects ordered logistic regression to investigate postoperative changes of outcome parameters from baseline to follow-up time points for each group as well as for group comparisons.

Range of motion and clinical scores improved until 24 months postoperatively and did not deteriorate thereafter, except for internal rotation of Boileau type III and IV patients and external rotation of RSA patients with type I and IV sequelae. At all follow-ups, ASA patients with Boileau type I sequelae had significantly better internal and external rotation versus patients with RSA and/or other Boileau types (p < 0.001), while Constant, DASH, and SPADI scores were not significantly different between groups.

In humeral fracture sequelae, ASA and RSA lead to sustained clinical improvements. Surgeons may primarily consider implantation of ASA in type I sequelae.