Background:The posterior interosseous artery (PIA) flap has been widely reported to cover defects at the dorsal aspect of the hand. However, the use of this flap to cover elbow defects has been rarely reported. The purpose of this study was to analyze the anatomical feasibility of the PIA flap to cover elbow soft-tissue defects and, additionally, to review the clinical outcomes of patients treated with this flap.Methods:An anatomical study was performed on 14 cadaveric specimens to assess the number of PIA perforators at the distal third of the forearm, along with the distance of the perforators from the ulnar styloid. Additionally, the pedicle distance from the pivot point to the lateral epicondyle was recorded. A clinical study in 4 patients with elbow soft-tissue defects treated with the antegrade PIA was also performed to assess viability and clinical outcomes.Results:A mean of 3 perforators (range, 2–4) of the PIA were found in the distal third of the forearm. The pedicle distance from the pivot point to the lateral epicondyle was 10 cm (range, 8–11.5 cm). In the clinical study, all cases treated with the antegrade PIA flap showed satisfactory outcomes without loss of the flap or significant partial necrosis.Conclusion:In this limited series, the antegrade PIA flap has shown to be a reliable and effective alternative for treatment of soft-tissue defects at the elbow. The PIA perforators in the distal forearm and the pedicle length allow the flap to easily reach the elbow.
Muscle herniation in the upper extremity is a rare but recognized phenomenon with a paucity of reports in the current literature. In the majority of cases, the herniation is secondary to trauma, with some of the cases due to muscle hypertrophy and increased intra-compartmental pressure from the forced exertion. Treatment for this condition ranges from nonsurgical, repair, or reconstruction to fasciotomy of the flexor carpi ulnaris fascia. Here, we present a case of flexor carpi ulnaris herniation after an open in situ cubital tunnel release in a 57-year-old male 6 years after initial surgery. The patient’s symptoms did not improve with conservative management, and the patient subsequently underwent endoscopic fasciotomy with resolution of his symptoms and maintenance of his wrist and grip strength. The rationale for the treatment chosen is discussed.
Surgical treatment of trigger finger involves release of A1 pulley. Some authors have theorized that the loss of A1 pulley can lead to ulnar subluxation of flexor tendons, which can be prevented by release of A1 pulley radially, even in a nonrheumatoid hand. However, there is no evidence in literature to either support or oppose this hypothesis. Occasionally, difficulty is encountered to precisely identify where A1 ends and A2 begins. While incomplete release of A1 can cause relapse of triggering, release of substantial A2 can cause bowstringing. Knowledge of the safe limit of concomitant A2 release is beneficial. The study was conducted in 12 cadaver upper extremity specimens. A1 pulleys of 48 fingers were divided at the radial (24 fingers) or ulnar (24 fingers) attachment. A 20lb traction force was applied on the flexor tendons. Any subluxation or bowstringing was noted. The experiment was repeated following serial release of the A2—initially 25%, followed by 50% and 100%. No bowstringing or subluxation was noted when A1 pulley was opened, either by radial or ulnar incision. The same was true for A1 + 25% A2 release. When A1 + 50% A2 pulley were released, bowstringing was observed in 3/48 fingers. When A1 + 100% of the A2 pulley were released, bowstringing occurred in all cases. The location of incision for release of the A1 pulley has no effect on bowstringing or tendon subluxation. Release of additional 25% of the A2 pulley can be performed safely, which corresponds to the level of palmar digital crease.
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