Citations

Background: An open Achilles tendon repair is performed in patients who have suffered an acute rupture. All patients with this injury should be counseled on their treatment options, which include open operative repair and functional rehabilitation. We prefer the use of an open repair in high-level athletes and those who have delayed presentation. Typically, this injury—and the resulting open repair—are seen in young or middle-aged patients as well as athletes. Operative repair of a ruptured Achilles tendon is associated with a much faster return to activity/sport when compared with nonoperative alternatives. This surgical procedure is especially useful in allowing this patient population to return to their previous activity level and functional capacity as quickly as possible. Description: Open repair of a ruptured Achilles tendon begins with a 6 to 8-cm incision over the posteromedial aspect of the lower leg. Superficial and deep dissections are performed until the 2 ends of the ruptured tendon are identified. Adhesions are debrided to adequately mobilize and define the proximal and distal segments of the tendon. With use of a fiber tape suture, a modified locking Bunnell stitch is utilized to secure both ends. The fiber tape is tied securely, and the repair is reinforced with Vicryl suture (Ethicon). Once the tendon is repaired, the paratenon layer is identified and repaired with a running 0 or 2-0 Vicryl suture. This is an important step to minimize postoperative wound complications. The wound is then closed, and the extremity is splinted in maximum plantar flexion. Alternatives: Alternative treatments include minimally invasive surgical techniques such as percutaneous Achilles tendon repair and nonoperative treatment with functional rehabilitation, which can provide excellent outcomes but can also lead to a slight decrease in explosiveness as the patient returns to sport 1,2 . Rationale: Nonoperative and operative treatment of Achilles tendon rupture can both result in excellent patient outcomes. Appropriate patient selection is critical. Younger patients hoping to return to more highly competitive athletics should consider operative repair 3 . Possible differences have been identified in peak torque when comparing operative versus nonoperative treatment, with patients who had undergone operative repair having greater peak torque (i.e., explosiveness) 2 . Otherwise, findings are similar between treatment options as long as the patients meet the criteria for nonoperative treatment. Expected Outcomes: Overall, the scientific literature demonstrates that the functional outcomes following operative repair are good to excellent. In a study by Hsu et al. 4 , 88% of patients were able to return to their baseline level of activity by 5 months postoperatively, with a complication rate of 10.6% and no reruptures. In a recent meta-analysis by Meulenkamp et al. 5 , the authors found that operative repair of Achilles tendon rupture was associated with a reduced risk of rerupture compared with primary immobilization (i.e., conventional cast immobilization with delayed weight-bearing for at least 6 weeks only). However, open surgical repair, minimally invasive repair, and functional rehabilitation all had similar risk of rerupture 5 . In a review by Ochen et al. 6 that analyzed 29 studies with a total of 15,862 patients, operative repair was associated with a significantly lower risk of rerupture compared with nonoperative treatment (2.3% versus 3.9%, respectively). However, operative treatment was also associated with a significantly higher complication rate compared with nonoperative treatment (4.9% versus 1.6%, respectively) 6 . Finally, in a meta-analysis by Soroceanu et al. 7 , the authors found that if early range-of-motion protocols and functional rehabilitation were utilized, operative and nonoperative treatment resulted in similar outcomes and equivalent rates of rerupture. Important Tips: To prevent rerupture of an Achilles tendon, remind patients to engage in adequate stretching and warming prior to physical activity. Palpate and locate the tendon defect prior to making the first incision. Immobilize the ankle joint in a splint for 2 weeks postoperatively in maximum plantar flexion. Pitfalls include: ○ Poor suture management leading to tangling in the repair. ○ Undertensioning or overtensioning of the repair, which can be avoided by sterilely draping out both legs and checking resting tension intraoperatively. ○ Failure to close the paratenon, causing scarring of the skin or surrounding tissues, which can be avoided by making a relieving incision on the deep surface of the paratenon. ○ Leaving suture knots on the dorsal side of the repair that may aggravate the skin. Acronyms & Abbreviations: MRI = magnetic resonance imaging ESU = electrosurgical unit

AbstractFrom a complex systems perspective, clinical syndromes emerging from neurodegenerative diseases are thought to result from multiscale interactions between aggregates of misfolded proteins and the disequilibrium of large-scale networks coordinating functional operations underpinning cognitive phenomena. Across all syndromic presentations of Alzheimer’s disease, age-related disruption of the default mode network is accelerated by amyloid deposition. Conversely, syndromic variability may reflect selective neurodegeneration of modular networks supporting specific cognitive abilities. In this study, we leveraged the breadth of the Human Connectome Project-Aging cohort of non-demented individuals (N = 724) as a normative cohort to assess the robustness of a biomarker of default mode network dysfunction in Alzheimer’s disease, the network failure quotient, across the aging spectrum. We then examined the capacity of the network failure quotient and focal markers of neurodegeneration to discriminate patients with amnestic (N = 8) or dysexecutive (N = 10) Alzheimer’s disease from the normative cohort at the patient level, as well as between Alzheimer’s disease phenotypes. Importantly, all participants and patients were scanned using the Human Connectome Project-Aging protocol, allowing for the acquisition of high-resolution structural imaging and longer resting-state connectivity acquisition time. Using a regression framework, we found that the network failure quotient related to age, global and focal cortical thickness, hippocampal volume, and cognition in the normative Human Connectome Project-Aging cohort, replicating previous results from the Mayo Clinic Study of Aging that used a different scanning protocol. Then, we used quantile curves and group-wise comparisons to show that the network failure quotient commonly distinguished both dysexecutive and amnestic Alzheimer’s disease patients from the normative cohort. In contrast, focal neurodegeneration markers were more phenotype-specific, where the neurodegeneration of parieto-frontal areas associated with dysexecutive Alzheimer’s disease, while the neurodegeneration of hippocampal and temporal areas associated with amnestic Alzheimer’s disease. Capitalizing on a large normative cohort and optimized imaging acquisition protocols, we highlight a biomarker of default mode network failure reflecting shared system-level pathophysiological mechanisms across aging and dysexecutive and amnestic Alzheimer’s disease and biomarkers of focal neurodegeneration reflecting distinct pathognomonic processes across the amnestic and dysexecutive Alzheimer’s disease phenotypes. These findings provide evidence that variability in inter-individual cognitive impairment in Alzheimer’s disease may relate to both modular network degeneration and default mode network disruption. These results provide important information to advance complex systems approaches to cognitive aging and degeneration, expand the armamentarium of biomarkers available to aid diagnosis, monitor progression and inform clinical trials.

As the incidence of hepatocellular carcinoma (HCC) and subsequent treatments with liver‐directed therapies rise, the complexity of assessing lesion response has also increased. The Liver Imaging Reporting and Data Systems (LI‐RADS) treatment response algorithm (LI‐RADS TRA) was created to standardize the assessment of response after locoregional therapy (LRT) on contrast‐enhanced CT or MRI. Originally created based on expert opinion, these guidelines are currently undergoing revision based on emerging evidence. While many studies support the use of LR‐TRA for evaluation of HCC response after thermal ablation and intra‐arterial embolic therapy, data suggest a need for refinements to improve assessment after radiation therapy. In this manuscript, we review expected MR imaging findings after different forms of LRT, clarify how to apply the current LI‐RADS TRA by type of LRT, explore emerging literature on LI‐RADS TRA, and highlight future updates to the algorithm.Evidence Level3.Technical EfficacyStage 2.

Abstract Purpose To estimate the risk of contralateral breast cancer (CBC) among women in the general population with germline pathogenic variants (PVs) in ATM, BRCA1, BRCA2, CHEK2, and PALB2. Methods Among 15,104 prospectively followed women within the CARRIERS study treated with ipsilateral surgery for invasive breast cancer, a subset of 14,237 women were identified from population-based studies. The risk of CBC was estimated for PV carriers in each gene compared to women without PVs in a multivariate proportional hazard regression analysis accounting for the competing risk of death and adjusting for patient and tumor characteristics. The primary analyses focused on the overall cohort and on women from the general population. Secondary analyses examined associations by race/ethnicity, age at primary breast cancer diagnosis, menopausal status, and tumor estrogen receptor status. Results Germline BRCA1, BRCA2, and CHEK2 PV carriers with breast cancer were at significantly elevated risk (Hazard ratio ≥ 1.9, p< 0.05) of CBC, whereas only the PALB2 PV carriers with ER-negative breast cancer had elevated risks. In contrast, ATM PV carriers did not have significantly increased CBC risks. African American PV carriers had similarly elevated risks of CBC as non-Hispanic White PV carriers. Among premenopausal women, the 15-year cumulative incidence of CBC was >20% for BRCA1, BRCA2 and CHEK2 PV carriers with breast cancer, and for PALB2 PV carriers with ER-negative breast cancer. The 15-year cumulative incidence of CBC among postmenopausal PV carriers was < 20% for PV carriers in any of the 5 genes. Conclusions Women diagnosed with breast cancer and known to carry germline PVs in BRCA1, BRCA2, CHEK2, or PALB2 are at substantially increased risk of CBC and may benefit from enhanced surveillance and risk-reduction strategies. Citation Format: Siddhartha Yadav, Nicholas J. Boddicker, Jie Na, Eric C. Polley, Chunling Hu, Steven N. Hart, Rohan D. Gnanaolivu, Nicole Larson, Carolyn Dunn, Susan Holtegaard, Huaizhi Huang, Lauren R. Teras, Alpa V. Patel, James V. Lacey Jr., Susan Neuhausen, Leslie Bernstein, Elena Martinez, Christopher Haiman, Fei Chen, Kathryn Ruddy, Janet Olson, Esther John, Allison W. Kurian, Dale P. Sandler, Katie M. O’Brien, Jack A. Taylor, Clarice R. Weinberg, Hoda Anton-Culver, Argyrios Ziogas, Gary R. Zirpoli, David E. Goldgar, Katherine L. Nathanson, Susan Domchek, Julie R. Palmer, Jeffrey Weitzel, Peter Kraft, Fergus J. Couch. Population-based Estimates of contralateral Breast Cancer Risk among Carriers of Germline Pathogenic Variants in ATM, BRCA1, BRCA2, CHEK2, and PALB2 [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr GS4-04.

Background: The National Institute on Aging-Alzheimer’s Association Research Framework proposes defining Alzheimer’s disease by grouping imaging and fluid biomarkers by their respective pathologic processes. The AT(N) structure proposes several neurodegenerative fluid biomarkers (N) including total tau (t-tau), neurogranin (Ng), and neurofilament light chain (NfL). However, pathologic drivers influencing each biomarker remain unclear. Objective: To determine whether cerebrospinal fluid (CSF)-neurodegenerative biomarkers (N) map differentially to Alzheimer’s disease pathology measured by Aβ 42 (an indicator of amyloidosis, [A]), p-tau (an indicator of tau deposition, [T]), and MRI vascular pathology indicators (measured by white-matter integrity, infarcts, and microbleeds [V]). Methods: Participants were from Mayo Clinic Study of Aging (MCSA) with CSF measures of NfL, Ng, t-tau, Aβ 42 , and p-tau and available MRI brain imaging. Linear models assessed associations between CSF neurodegeneration (N) markers, amyloid markers (A), tau (T), and vascular pathology (V). Results: Participants ( n = 408) had a mean age of 69.2±10.7; male, 217 (53.2%); cognitively unimpaired, 359 (88%). All three neurodegeneration biomarkers correlated with age ( p < 0.001 for NfL and t-tau, p = 0.018 for Ng). Men had higher CSF-NfL levels; women had higher Ng ( p < 0.001). NfL and t-tau levels correlated with infarcts ( p = 0.009, p = 0.034 respectively); no biomarkers correlated with white-matter integrity. N biomarkers correlated with p-tau levels (T, p < 0.001). Higher Aβ 42 levels associated with higher N-biomarker levels but only among cognitively unimpaired (A, p < 0.001). Conclusion: The influence of vascular pathology in the general population on CSF (N) biomarkers is modest, with greater influence of infarcts than white-matter disruption. Neurodegeneration markers more closely correlated with tau than amyloid markers.

Abstract Staging the severity of Alzheimer’s disease pathology using biomarkers is useful for therapeutic trials and clinical prognosis. Disease staging with amyloid and tau PET has face validity; however, this would be more practical with plasma biomarkers. Our objectives were, first, to examine approaches for staging amyloid and tau PET and, second, to examine prediction of amyloid and tau PET stages using plasma biomarkers. Participants (n = 1136) were enrolled in either the Mayo Clinic Study of Aging or the Alzheimer’s Disease Research Center; had a concurrent amyloid PET, tau PET and blood draw; and met clinical criteria for cognitively unimpaired (n = 864), mild cognitive impairment (n = 148) or Alzheimer’s clinical syndrome with dementia (n = 124). The latter two groups were combined into a cognitively impaired group (n = 272). We used multinomial regression models to estimate discrimination [concordance (C) statistics] among three amyloid PET stages (low, intermediate, high), four tau PET stages (Braak 0, 1–2, 3–4, 5–6) and a combined amyloid and tau PET stage (none/low versus intermediate/high severity) using plasma biomarkers as predictors separately within unimpaired and impaired individuals. Plasma analytes, p-tau181, Aβ1–42 and Aβ1–40 (analysed as the Aβ42/Aβ40 ratio), glial fibrillary acidic protein and neurofilament light chain were measured on the HD-X Simoa Quanterix platform. Plasma p-tau217 was also measured in a subset (n = 355) of cognitively unimpaired participants using the Lilly Meso Scale Discovery assay. Models with all Quanterix plasma analytes along with risk factors (age, sex and APOE) most often provided the best discrimination among amyloid PET stages (C = 0.78–0.82). Models with p-tau181 provided similar discrimination of tau PET stages to models with all four plasma analytes (C = 0.72–0.85 versus C = 0.73–0.86). Discriminating a PET proxy of intermediate/high from none/low Alzheimer’s disease neuropathological change with all four Quanterix plasma analytes was excellent but not better than p-tau181 only (C = 0.88 versus 0.87 for unimpaired and C = 0.91 versus 0.90 for impaired). Lilly p-tau217 outperformed the Quanterix p-tau181 assay for discriminating high versus intermediate amyloid (C = 0.85 versus 0.74) but did not improve over a model with all Quanterix plasma analytes and risk factors (C = 0.85 versus 0.83). Plasma analytes along with risk factors can discriminate between amyloid and tau PET stages and between a PET surrogate for intermediate/high versus none/low neuropathological change with accuracy in the acceptable to excellent range. Combinations of plasma analytes are better than single analytes for many staging predictions with the exception that Quanterix p-tau181 alone usually performed equivalently to combinations of Quanterix analytes for tau PET discrimination.

Postdural puncture headache is a frequently encountered complication following procedures such as lumbar puncture, neuraxial anesthesia, or intrathecal drug delivery device implantation. It classically presents as a painful orthostatic headache that is exacerbated when a patient is upright. For treatment, patients are often started on conservative options such as hydration, caffeine, bedrest, and NSAID analgesics; however, certain patients who fail these therapies may require intervention with an epidural blood patch. The epidural blood patch remains the gold standard for treating refractory postdural puncture headache. Contraindications to epidural blood patch include severe coagulopathy, patient refusal, or infection at the intended site of entry. There are no clear consensus recommendations regarding patients with a hematological malignancy and potential risk that autologous blood may seed malignant cells into the neuraxis. In this case report, we present a patient with acute myeloid leukemia who developed a postdural puncture headache after receiving subarachnoid administration of antineoplastics. The patient was refractory to conservative therapy, prompting multidisciplinary consultation and discussion with the patient about the risks and benefits of proceeding with an epidural blood patch. Ultimately, the patient elected to proceed with the offered epidural blood patch which led to complete resolution of his painful headaches and did not cause any spread of malignant cells into his neuraxis or cerebral spinal fluid.

Background: Meniscal and chondral damage is common in the patient undergoing revision anterior cruciate ligament (ACL) reconstruction. Purpose: To determine if meniscal and/or articular cartilage pathology at the time of revision ACL surgery significantly influences a patient’s outcome at 6-year follow-up. Study Design: Cohort study; Level of evidence, 3. Methods: Patients undergoing revision ACL reconstruction were prospectively enrolled between 2006 and 2011. Data collection included baseline demographics, surgical technique, pathology, treatment, and scores from 4 validated patient-reported outcome instruments: International Knee Documentation Committee (IKDC), Knee injury and Osteoarthritis Outcome Score (KOOS), Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), and Marx Activity Rating Scale. Patients were followed up at 6 years and asked to complete the identical set of outcome instruments. Regression analysis assessed the meniscal and articular cartilage pathology risk factors for clinical outcomes 6 years after revision ACL reconstruction. Results: An overall 1234 patients were enrolled (716 males, 58%; median age, 26 years). Surgeons reported the pathology at the time of revision surgery in the medial meniscus (45%), lateral meniscus (36%), medial femoral condyle (43%), lateral femoral condyle (29%), medial tibial plateau (11%), lateral tibial plateau (17%), patella (30%), and trochlea (21%). Six-year follow-up was obtained on 79% of the sample (980/1234). Meniscal pathology and articular cartilage pathology (medial femoral condyle, lateral femoral condyle, lateral tibial plateau, trochlea, and patella) were significant drivers of poorer patient-reported outcomes at 6 years (IKDC, KOOS, WOMAC, and Marx). The most consistent factors driving outcomes were having a medial meniscal excision (either before or at the time of revision surgery) and patellofemoral articular cartilage pathology. Six-year Marx activity levels were negatively affected by having either a repair/excision of the medial meniscus (odds ratio range, 1.45-1.72; P≤ .04) or grade 3-4 patellar chondrosis (odds ratio, 1.72; P = .04). Meniscal pathology occurring before the index revision surgery negatively affected scores on all KOOS subscales except for sports/recreation ( P < .05). Articular cartilage pathology significantly impaired all KOOS subscale scores ( P < .05). Lower baseline outcome scores, higher body mass index, being a smoker, and incurring subsequent surgery all significantly increased the odds of reporting poorer clinical outcomes at 6 years. Conclusion: Meniscal and chondral pathology at the time of revision ACL reconstruction has continued significant detrimental effects on patient-reported outcomes at 6 years after revision surgery.

Background: Open trigger finger release is an elective surgical procedure that serves as the gold standard treatment for trigger digits. The aim of this procedure is to release the A1 pulley in a setting in which the pulley is completely visible, ultimately allowing the flexor tendons that were previously impinged on to glide more easily through the tendon sheath. Although A1—or the first annular pulley—is the site of triggering in nearly all cases, alternative sites include A2, A3, and the palmar aponeurosis 1 . Description: Typically, the surgical procedure can be conducted in an outpatient setting and can vary in duration from a few minutes to half an hour. The surgical procedure involves the patient lying in the supine position with the operative hand positioned to the side. A small incision, ranging from 1 to 1.5 cm, is made on the volar side of the hand, just proximal to the A1 pulley in the skin crease in order to minimize scarring. Once the underlying neurovascular structures are exposed, the A1 pulley is released longitudinally at least to the level of the A2 pulley, followed by decompression of the flexor tendons that were previously impinged on. In order to confirm the release, the patient is asked to flex and extend the affected finger. The wound is irrigated and closed once the release is confirmed by both the patient and surgeon. Alternatives: Aside from an open release, trigger finger can be treated nonoperatively with use of splinting and corticosteroid injection. Alternative operative treatments include a percutaneous release, which involves the use of a needle to release the A1 pulley 2 . Trigger finger can initially be treated nonoperatively. If unsuccessful, surgical intervention is considered the ultimate remedy 2 . Rationale: Because of their efficacious nature, corticosteroid injections are indicated preoperatively, particularly in non-diabetic patients 3 . Splinting is often an appropriate treatment option in patients who wish to avoid a corticosteroid injection 1 . However, if nonoperative treatment modalities fail to resolve pain and symptoms, surgical intervention is indicated 2 . In comparison with a percutaneous trigger finger release, an open release provides enhanced exposure and may be safer with respect to avoiding iatrogenic neurovascular injury 2 . However, in a randomized controlled trial, Gilberts et al. found no difference in the rates of recurrence when comparing open versus percutaneous trigger finger release 4 . Expected Outcomes: With reported success rates ranging from 90% to 100%, the open release of the A1 pulley is considered a common procedure associated with minimal complications 2 . Complications of the procedure were assessed in a retrospective analysis of 43 patients who underwent 78 open trigger releases performed by 1 surgeon. In that study, the authors reported a minor complication rate of 28% and a major complication rate of 3% 5 . Specifically, the 2 major complications noted by the authors were a synovial fistula and a proximal interphalangeal joint arthrofibrosis. In a larger study that included 543 patients who underwent 795 open trigger releases, the authors reported a minor complication rate of 9.6% and major complication rate of 2.4% 6 . Furthermore, the most common complications involved persistent stiffness, swelling, or pain. In that analysis, the authors suggested that sedation, male gender, and general anesthesia may be associated with greater risk 6 . Important Tips: At the discretion of the surgeon, a longitudinal, transverse, or oblique incision is made directly on top of the tendon at the level of the metacarpophalangeal joint, which is the preferred incision site because it provides maximal accessibility to the A1 pulley. Local anesthesia is preferred because it allows the patient and surgeon to confirm the release immediately. If conducting an open trigger release on the thumb, the surgeon should identify and protect the radial digital nerve, which courses directly over the A1 pulley. Acronyms and Abbreviations: MCP = metacarpophalangeal

Background: The purpose of this study was to evaluate monetary trends in Medicare reimbursement rates for 30 abdominal wall reconstruction surgical procedures over a 20-year period (2000 to 2020). Methods: The Physician Fee Schedule Look-Up Tool from the Centers for Medicare and Medicaid Services was used for each of the 30 included current CPT codes, and reimbursement data were extracted. Monetary data were adjusted for inflation to 2020 U.S. dollars using changes to the United States consumer price index. The R2 values for the average annual percentage change and the average total percentage change in reimbursement were calculated based on these adjusted trends for all included procedures. Results: After adjusting for inflation, the average reimbursement for all procedures decreased by 17.1% from 2000 to 2020. The greatest mean decrease was observed for CPT code 49568 (the implantation of mesh or other prosthesis for open incisional or ventral hernia repair or mesh for closure of débridement for necrotizing soft-tissue infection, −34.4%). The only procedure with an increased adjusted reimbursement rate throughout the study period was CPT code 20680 (+3.9%). From 2000 to 2020, the adjusted reimbursement rate for all included procedures decreased by an average of 0.85% each year, with an average R2 value of 0.78, indicating a stable decline throughout the study period. Conclusions: Reimbursement rates are declining when adjusted for inflation. Increased awareness of these trends is helpful to maintain access to optimal abdominal reconstruction care in the United States.