Chronic Achilles Tendon Avulsion Repair: Central Third Fascia Slide Technique with Flexor Hallucis Longus Transfer.

Background: Chronic Achilles tendon defects are commonly associated with substantial impairment in gait and push-off strength, leading to decreased function1. These injuries cause a unique surgical dilemma, with no consensus surgical reconstruction technique for >6-cm gaps3. There are a multitude of surgical reconstruction techniques that rely on gap size as a determinant for preoperative planning1,2. The present article describes a technique for chronic Achilles tendon defects of >6 cm. The central third fascia slide (CTFS) technique with flexor hallucis longus (FHL) transfer provides adequate excursion and strength while avoiding use of allograft.2.The CTFS technique is a reconstructive technique that is utilized to treat large chronically gapped Achilles tendon tears, usually larger than 5 to 6 cm; however, recent literature has shown that intermediate gaps can be fixed with use of a combination of tendon transfers. The technique described here is a variation of the V-Y tendinoplasty and fascia turndown method in which the gastrocnemius complex fascia is slid down rather than being "turned down." This reconstructive technique, like its predecessor, restores function in damaged Achilles tendons3. Chronic gapping from a chronic Achilles tendon rupture can lead to decreased function and weakness. Patients may also experience fatigue and gait imbalance, leading to the need for surgical reconstruction to help restore functionality. Description: The CTFS technique utilizes a posterior midline incision, maintaining full-thickness flaps. A complete debridement of the degenerative Achilles tendon is performed, and the gap is measured. If the gap is >6 cm, the central third of the remaining Achilles and gastrocnemius fascia are sharply harvested. The FHL is transferred to the proximal Achilles footprint and held with use of an interference screw. The ankle is held in 15° to 25° of plantar flexion while the FHL shuttling suture is pulled plantarly and secured with a bio-interference screw. The fascial graft is then anchored to the calcaneus with use of a double-row knotless technique, maximizing osseous contact potential healing. Soft-tissue clamps are placed on the graft and on the gastrocnemius complex harvest site. The ankle is tensioned in nearly 30° of plantar flexion to account for known postoperative elongation. FiberWire (Arthrex) is utilized to secure the tension, then the remaining suture tape from the proximal insertional row is run up each side of the fascial graft in a running locking stitch, continuing proximally to close the harvest site. The use of an anchor-stay stitch helps to prevent elongation and maximizes construct strength. Alternatives: For patients who are poor surgical candidates or those with acceptable function, alternatives include nonoperative treatment and/or the use of a molded ankle foot orthosis. Most chronic Achilles tendon ruptures require surgery. Generally, a gap of <2 cm can be treated through primary repair with use of longitudinal and distally applied traction. For an Achilles gap of >2 cm but <6 cm, a V-Y gastrocnemius-lengthening procedure can utilized. Other methods such as autologous and local tendon transfers, advancement procedures, or a combination of these have been described as ways to treat gaps within this range. For gaps of >6 cm, there is insufficient literature to establish a single gold-standard reconstructive technique. Some surgeons have opted to utilize the turndown flap procedure, the FHL tendon transfer technique, or a combination of both. Rationale: The Achilles turndown flap technique can lead to the formation of scar tissue at the focal point of the turndown, a region also known as the hinge joint, and thus can perpetuate scarring of the repair site. To avoid this scarring, the central third fascia slide technique with FHL transfer is presented as a suitable reconstructive technique for chronic tendon defects of >6 cm. Expected Outcomes: Postoperatively, patients are managed according to a standard protocol. The first 2 weeks are non-weight-bearing with the foot in equinus in an L & U splint. At 2 to 4 weeks postoperatively, a walking boot with a 1.5-cm heel lift is applied, and crutches are utilized as the primary weight-bearing aid. At 4 to 6 weeks, the patient is transitioned to a 1-cm heel lift and may discontinue the use of crutches if they are able to walk without a limp. At 8 weeks, the patient may discontinue the use of the walking boot. At week 6 to 12, no heel lift is required. By approximately 12 weeks postoperatively, the patient should have regained full range of motion and should be able to walk without a limp. The patient should be able to resume activities of daily living by 3 to 4 months, with a gradual return to all physical activities by 4 to 6 months This postoperative protocol has produced favorable results. Ahmad et al. have reported the use of a similar protocol, with patients showing increased Foot and Ankle Ability Measure scores and decreased visual analog scale pain scores compared with the preoperative measurement2. Important Tips: Debride the Achilles until viable tendon is reached, then measure the defect.Tension the FHL and the fascia slide with the foot in 15° to 25° of plantar flexion.Perform a meticulous layered closure, preserving the paratenon as much as possible.Incomplete debridement may result in incompetent tissue.Incomplete closure of the fascia harvest site may predispose to seroma or hematoma formation.Not splinting for 10 to 14 days potentially predisposes the patient to wound breakdown. Acronyms and Abbreviations: CTFS = central third fascia slideFHL = flexor hallucis longusATTF = Achilles tendon turndown flapHPI = history of present illnessNWB = non-weight-bearingCAM = controlled ankle motionDVT = deep vein thrombosisMRI = Magnetic resonance imagingPMHx = past medical historyHTN = hypertensionSHx = social historyPE = physical examinationDF = dorsiflexionNVI = neurovascularly intactROM = range of motion.

Failure of osteochondral lesions using bioabsorbable fixation in the adolescent patient: a case report.

Injury to the chondral surface and subchondral bone can be due to osteochondritis dissecans or traumatic injury. These lesions can lead to pain, swelling, and mechanical symptoms causing functional impairments for patients. Treatment can include nonoperative management or surgical intervention including internal fixation. Internal fixation can be performed through multiple methods including the use of bioabsorbable screw fixation, though there is concern for potential early failure of this method. We present three cases of osteochondral lesions treated with internal fixation with bioabsorbable screws, which experienced early failure of the bioabsorbable screws, leading to failure of fixation and requiring revision surgery with advanced cartilage restoration procedures. All patients had resolution of their symptoms and improved function postoperatively. While the use of bioabsorbable screw fixation can potentially decrease cost and morbidity, their mechanical properties may increase the risk of failure before lesion healing. We advocate caution with the use of these screws for the treatment of unstable osteochondritis dissecans lesion and recommend careful patient selection and meticulous surgical technique to avoid failure of fixation of these lesions.

Splicing factor deficits render hematopoietic stem and progenitor cells sensitive to STAT3 inhibition.

Hematopoietic stem and progenitor cells (HSPCs) sustain lifelong hematopoiesis. Mutations of pre-mRNA splicing machinery, especially splicing factor 3b, subunit 1 (SF3B1), are early lesions found in malignancies arising from HSPC dysfunction. However, why splicing factor deficits contribute to HSPC defects remains incompletely understood. Using zebrafish, we show that HSPC formation in sf3b1 homozygous mutants is dependent on STAT3 activation. Clinically, mutations in SF3B1 are heterozygous; thus, we explored if targeting STAT3 could be a vulnerability in these cells. We show that SF3B1 heterozygosity confers heightened sensitivity to STAT3 inhibition in zebrafish, mouse, and human HSPCs. Cells carrying mutations in other splicing factors or treated with splicing modulators are also more sensitive to STAT3 inhibition. Mechanistically, we illustrate that STAT3 inhibition exacerbates aberrant splicing in SF3B1 mutant cells. Our findings reveal a conserved vulnerability of splicing factor mutant HSPCs that could allow for their selective targeting in hematologic malignancies.

Great Toe Metatarsophalangeal Joint Arthroscopy: Simple Technique for Painful Nonunion.

Great toe metatarsophalangeal joint (MTPJ) arthroscopy was first described as a viable technique for a multitude of first MTPJ pathologies in the early 1970s; however, with improving arthroscopic technique and technology, these indications will continue to expand. Arthroscopy of the first MTPJ has increasingly become a new pursuit for foot and ankle specialists. Therefore, we have proposed a simple technique and illustration from our operating room setup to traction and to our procedural technique to make great toe arthroscopy simple and reproducible for arthroscopic foot and ankle surgeons.

Uncovering the Genomic Landscape in Newly Diagnosed and Relapsed Pediatric Cytogenetically Normal FLT3-ITD AML.

Fms-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD) mutations, common in pediatric acute myeloid leukemia (AML), associate with early relapse and poor prognosis. Past studies have suggested additional cooperative mutations are required for leukemogenesis in FLT3-ITD+ AML. Using RNA sequencing and a next-generation targeted gene panel, we broadly characterize the co-occurring genomic alterations in pediatric cytogenetically normal (CN) FLT3-ITD+ AML to gain a deeper understanding of the clonal patterns and heterogeneity at diagnosis and relapse. We show that chimeric transcripts were present in 21 of 34 (62%) of de novo samples, 2 (6%) of these samples included a rare reoccurring fusion partner BCL11B. At diagnosis, the median number of mutations other than FLT3 per patient was 1 (range 0-3), which involved 8 gene pathways; WT1 and NPM1 mutations were frequently observed (35% and 24%, respectively). Fusion transcripts and high variant allele frequency (VAF) mutants, which included WT1, NPM1, SMARCA2, RAD21, and TYK2, were retained from diagnosis to relapse. We did observe reduction in VAF of simple or single mutation clones, but VAFs were preserved or expanded in more complex clones with multiple mutations. Our data provide the first insight into the genomic complexity of pediatric CN FLT3-ITD+ AML and could help stratify future targeted treatment strategies.