The Medicine Forum Volume 26 Article 1 2025 The Medicine Forum: Volume 26 Follow this and additional works at: https://jdc.jefferson.edu/tmf Part of the Internal Medicine Commons Let us know how access to this document benefits you Recommended Citation (2025) "The Medicine Forum: Volume 26," The Medicine Forum: Vol. 26, Article 1. Available at: https://jdc.jefferson.edu/tmf/vol26/iss1/1 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in The Medicine Forum by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: JeffersonDigitalCommons@jefferson.edu. The Medicine ForumVolume 26, 2024–2025 Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital , 1et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 20252The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1To Friends of the Department of MedicineThe Jefferson Forum is a reflection of our residents' dedication to patient care, education, resilience, and research. Within these pages, you’ll find a unique combination of hard work, intellectual curiosity, and personality. As Program Director, I have the privilege of watching their transformation from learners to skilled clinicians and scholars, a journey marked by perseverance and a sense of purpose.In a time of rapid political and societal change, this publication stands as a testament to our renewed commitment to science, well-being, and the pursuit of knowledge. As physicians and researchers, we remain steadfast in our mission to improve health outcomes and advance equitable care. The Jefferson Forum embodies this mission, highlighting the thoughtful inquiry, innovation, and compassion that define our profession.To our alumni, your continued support and mentorship are invaluable to the success of this program. Your guidance helps shape the next generation of physicians, ensuring they are prepared to meet the evolving challenges of medicine. To our current residents, your dedication is evident in every article, case study, artistic endeavor, and research contribution. Your work strengthens this community, and your enthusiasm fuels our efforts to remain steadfast in our commitment.Looking ahead, we celebrate both where we’ve been and where we are going. The Jefferson Forum remains a testament to the strength found in knowledge, collaboration, and the unique camaraderie and excellence our residency is built on. I look forward to seeing how this tradition continues to grow in the years to come.Christopher Henry, MD, FACPAssistant Professor of Medicine Program Director, Internal Medicine Residency ProgramFrom the Desk oF the resiDency Program Director3et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025Dear Readers, It is with great enthusiasm that we present to you the 26th edition of our internal medicine residency journal. As chief editors, we have the privilege of curating the latest insights, research, and reflections from the ever-evolving world of medicine, all to enrich our shared knowledge and foster meaningful discussions within our community.Over the years, this journal has served as a platform for scholarly exploration, clinical advancements, and the voices of residents shaping the future of internal medicine. With each edition, we strive to uphold the highest standards of academic excellence while embracing the diversity of thought and expertise that make our field so dynamic.This issue brings together a compelling collection of articles, case studies, and editorials that highlight the ingenuity and dedication of our contributors. From groundbreaking research to insightful perspectives on patient care, we hope these pieces will inspire, inform, and ignite conversation.We extend our deepest gratitude to our contributors, reviewers, and readers for making this journal a cornerstone of medical scholarship. Your engagement and passion are what drive us forward. As we celebrate this milestone, we remain committed to providing a space where ideas flourish and knowledge continues to grow.Thank you for your unwavering support. We look forward to many more editions to come!Sincerely,Marina Gonzalez, MDVirginia Gonzalez, MDDevin Vasoya, MDMarc Yorker, MDFrom the eDitorsLeft to right: Devin Vasoya, MDVirginia Gonzalez, MDMarina Gonzalez, MDMarc Yorker, MD4The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1We sincerely thank the physicians who generously dedicated their time and expertise to reviewing and editing the work featured in this journal. Your thoughtful feedback and commitment to academic excellence were instrumental in shaping the quality of these contributions. Lastly, we thank Tim Flanagan for his dedication and creative vision in designing this journal and bringing our ideas to life.Sincerely, Marina Gonzalez, MDVirginia Gonzalez, MDDevin Vasoya, MDMarc Yorker, MDeDitorial staFFGregary Marhefka, MD Darius Farzad, MDSung-Hae Cho, MDMichael Foster, MDDaniel Underberg, MDAnna Chen, MDKatherine Duffey, MDDagan Coppock, MDSean Reilly, MDEmily Hansinger, MDTara Rakiewicz, MDMichael Dong, MD Gautam George, MD Vincent Chan, MDMarta Bean, MDEvan Nardone, MDJillian Zavodnick, MDFrienDs oF the ForumDr. Mark S. Berger and Ms. Jane R. EisnerDrs. Alan H. and Sheila Wang5et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025A Message from the Chiefs, It is with great pride that we present this year’s edition of The Medicine Forum, a reflection of the passion, intellectual curiosity, and multidimensional talents that define our Internal Medicine residency program.This journal continues to be more than a collection of case reports and research findings — it is a celebration of who we are as a community. It reflects our shared commitment to inquiry, creativity, and the art of medicine. From the rigor of original research to the introspection of narrative writing and the vibrancy of visual art, this edition captures the full spectrum of our residents’ voices.We would like to extend our deepest appreciation to this year's editorial team. Their leadership, vision, and meticulous dedication have elevated this publication year after year. Their work behind the scenes has ensured that each contribution — whether scientific or expressive — is shared with the care and intention it deserves.A special thank you is owed to Dr. Coppock, whose mentorship remains a cornerstone of The Medicine Forum. His encouragement and guidance continue to inspire the next generation of physician-scholars and educators.As chiefs, we’ve had the unique privilege of watching our colleagues grow — not only as physicians but as thinkers, writers, and advocates. You’ve brought energy and thoughtfulness to everything from journal club debates to QI projects and national presentations. Your achievements speak not only to your individual excellence but also to the strength of our collective community.As you flip through these pages, we hope you find inspiration in the work of your peers. May this edition remind us of the value of reflection, the importance of storytelling in medicine, and the joy of learning from one another.To our residents: thank you for all you do to shape this program. Your curiosity, compassion, and drive will continue to push the boundaries of what’s possible in medicine.Best, Akash Patel, DOAshley Traczuk, MDMark Liotta, MDClaire Zurlo, MD From the chieF resiDentsLeft to right: Mark Liotta, MDClaire Zurlo, MD Ashley Traczuk, MDAkash Patel, DO6The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1Dear Trainees and Faculty, We are honored to present this latest edition of The Medicine Forum. This platform is in its twenty-sixth year serving as an outlet for our medical community’s scholarly and creative efforts. This year, it has been my pleasure to work with Marc, Marina, Virginia, and Devin on this project. I have not only worked with them on the Forum, but also on the wards. It is impressive to see the same excellence they bring to patient care applied to this academic publication.This journal serves as a showcase for the efforts of our Department. It is always exciting to see the names of colleagues we see every day caring for patients all collected in this single publication. The Medicine Forum serves as a reminder of the depth of talent possessed by the physician-scientists and artists with whom we share our day-to-day work-lives.We owe our gratitude to a number of people who have helped bring this issue to publication. We thank the Department of Medicine leadership for their guidance and support. We want to thank all of the residents, students, and faculty who submitted their work. We express our gratitude to Timothy Flanagan for his design and editorial support. Finally, we thank the readers of this journal for turning the page and becoming participants in this community.Sincerely,Dagan Coppock, MD, MSCEForeworD From Faculty aDvisor7et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025CARDIOLOGYRESEARCH STUDIES3D-printeD coronary arteries: an effective tool in meDical eDucationZachary Pang, MD, Shreyas Chandragiri, MD, Shumpei Mori, MD, PhD, Alexander Hajduczok, MD, Cannon Greco Hiranaka, MD, Jesse Ottaway, MD, Zachary Mace, MD, Michael Wong, MD, Tammy Yoshioka, MD, Noah Haroian, MD, PharmD, Guiyun Zhang, MD, PhD ..................................................................12EVALUATING MORTALITY AND BLEEDING RISK AFTER PERCUTANEOUS LEFT ATRIAL APPENDAGE CLOSURE IN ATRIAL FIBRILLATION: A PROPENSITY-MATCHED ANALYSIS USING A MULTI-INSTITUTIONAL DATABASE Youssef Elfatatry, MD and Ryan Gardner, MD ..............................................................................................................................16preDicting in-hospital mortality in patients with hypertensive emergency: a retrospective cohort stuDyJay Satasiya, BS, Devin Vasoya, MD, Darius Farzad, MD ..........................................................................................................20CASE REPORTSa case of type 4 spontaneous coronary artery Dissection (scaD)Virginia Gonzalez, MD, Kashka Mallari, MD, Marina Gonzalez, MD, Svenja Schneider, MD, Sung-Hae Cho, MD, Paulina Gorodin Kiliddar, MD .....................................................................................................................21Be afraiD of severe pulmonary hypertension anD right ventricular failure in the peri-op patientAvish Patel, MD, Lily Ackermann, MD ........................................................................................................................................... 24hot coffee-inDuceD takotsuBo carDiomyopathy: a case report Zachary Pang, MD, M. Duncan Kilpatrick, MD, Jasmine Lee, MD, Gregary D. Marhefka, MD........................................ 28mitral annular Disjunction as a cause of carDiac arrest in young patient: a case reportSheraz Qamar, MD ..............................................................................................................................................................................31power outage: acute suBtotal occlusion of the left circumflex artery with minimal ecg changesDaniel D. Moylan, MD and Brady L. Houtz, MD ........................................................................................................................ 33protamine sulfate-inDuceD coronary vasospasm resulting in takotsuBo carDiomyopathyMatthew J. Bierowski, MD, Andre Cunningham, DO, Jordan Feingold-Link, MD ............................................................. 36a shock to the heart? a case of phantom shocks in a patient with BrugaDa synDromeVirginia Gonzalez, MD, Rebecca Goldfinger-Chanin, MD, Behzad B. Pavri, MD ............................................................... 39williams synDrome presenting with pericarDial effusion anD left ventricular apical aneurysm: a case report Zachary Pang, MD, M. Duncan Kilpatrick, MD, Sairamya Bodempudi, MD, David L. Fischman, MD, Gregary D. Marhefka MD ........................................................................................................................................................41table oF contents8The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1GASTROENTEROLOGY & HEPATOLOGYRESEARCH STUDIESracial Disparities in response to iBD DirecteD therapy in crohn’s Disease anD ulcerative colitis: a single center experienceAnanya Venkatesh, MD, Justin Robbins, MD, Zach Breslin, MD, Cuckoo Choudhary, MD ............................................ 45use of novel agent purastat® for post ampullectomy BleeDingBertilia Tavarez, MD, MS, Ananya Venkatesh, MD, Pedro Palacios Argueta, MD, Anand Kumar, MD, Alana Persaud, MD, Yasi Xiao, MD, Alexander Schlachterman, MD, Thomas Kowalski, MD, Faisal Kamal, MD ....................47use of novel agent purastat® for post sphincterotomy BleeDing Ananya Venkatesh, MD, Bertilia Tavarez, MD, MS, Pedro Palacios Argueta, MD, Donna Leet, MD, Afshin Khan, MD, Abdul Kouanda, MD, Anand Kumar, MD, Alana Persaud, MD, Yasi Xiao, MD, Alexander Schlachterman, MD, Thomas Kowalski, MD, Faisal Kamal, MD .......................................................................49CASE REPORTScomplexities in alcoholic necrotizing pancreatitis: a case report of severe vascular anD infectious complicationsDawood Tahir, MD, Shravya Ginnaram, MD, Jacob Lipkin, MD ..............................................................................................51investigating the link Between ulcerative colitis anD papillary thyroiD carcinoma: a case reportSonali Shah, MD, Emily Chiacchiaro, MD, Priya Sehgal, MD .................................................................................................. 56HEmATOLOGY & ONCOLOGYcase report of gastritis as a complication of immunotherapy treatment of metastatic enDometrial cancer with lenvatiniB anD pemBrolizumaBBret McCarty, MD, Nia Johnson, BS, Suchit Bhutani, MD........................................................................................................ 59ITP IN THE SETTING OF NEWLY DIAGNOSED COLORECTAL CANCER: A CASE REPORTBeatriz Torre, MD, Karlie Brasch, MD, Christopher Henry, MD ............................................................................................... 62an unusual complication of metastatic colorectal cancer: port-site hematoma as the first sign of Bone marrow involvement anD DisseminateD intravascular coagulationMichael Predi, DO, Julia Palecki, MD, Jordan M. Isaacs, BA, Ruben Rhoades, MD ..........................................................64WHEN THE CURE COMPLICATES: IFOSFAMIDE, METHYLENE BLUE, AND A LIFE-THREATENING DILEMMAMichael Predi, DO, Sarah Sulkowski, MD, Anika Patel, BA, Evan Nardone, MD .......................................................679et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025INfECTIOuS DISEASES & ENvIRONmENTAL mEDICINE a case of varicella zoster virus meningitis presenting as iDiopathic vocal folD paralysisDustin Sneed, MD, M. Duncan Kilpatrick, MD, Alicia Bao, MD ................................................................................................71a patient with recently DiagnoseD hiv founD to have cryptococcus meningitis with course complicateD By pneumocystis jirovecii pneumonia, cmv colitis, anD kaposi sarcoma Benjamin Richter, MD ........................................................................................................................................................................ 74from cure to crisis: a case of severe hypoxic respiratory failure Due to Daptomycin-associateD eosinophilic pneumonitis Muneeba Ali, MD, Enad Haddad, MD, Warda Naqvi, MD, Conrad Reed, MD ......................................................................77NEGATIVE URINE NAAT IN A CASE OF DISSEMINATED GONOCOCCAL INFECTION PRESENTING AS MIGRATORY ARTHRITISBenjamin Richter, MD ........................................................................................................................................................................80string theory - a case of hypermucoviscous kleBsiella pneumoniaeNatasa Kostic, MD and Marina Gonzalez, MD ............................................................................................................................82FROM ER TO MORTALITY IN 48 HOURS: A FATAL CASE OF OVERWHELMING POST-SPLENECTOMY INFECTIONMiriam Stern, BA, Blaise O’Malley, BS, Amry Majeed, MD, Michael Grodsky, MD .................................................. 85mEDICAL EDuCATION & HEALTH SYSTEmS SCIENCE enhancing community health center safety through participatory co-DesignArman Afifi, BS, Kelsey Smith, BS, Megan Reed, PhD, MPH, Lara Weinstein, MD, MPH .................................................88the factor viii DeBate: an auto-cancelleD laB near missAvish Patel, MD, Daniel Elchediak, MD, Zachary Pang, MD, Charlotte Shields, MD, Bethanne Venkatesan, MD, Ananya Venkatesh, MD, Michael J. Alessandro, BSN, Jeffrey Riggio, MD, MS, Alexis Wickersham, MD ..........................91heart core: a framework for leaDing with empathy in meDical eDucationAkash Patel, DO and Mark Liotta, MD ........................................................................................................................................... 93PuLmONARY, ALLERGY & CRITICAL CARE mEDICINEa complex case of multifactorial hypoxemia from metastatic testicular cancerSusanna Betti, MD .............................................................................................................................................................................96a case of streptococcus pneumoniae necrotizing pneumonia with pneumothorax anD aBscess formationSusanna Betti, MD ............................................................................................................................................................................. 97mcconnell’s sign in the aBsence of pulmonary emBolismAlicia Bao, MD and Tendai Marume, MD ....................................................................................................................................9810The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1RHEumATOLOGYrecurrent post-viral rhaBDomyolysis in a 36-year-olD male: a case reportWarda Naqvi, MD, David J. Walz, MD, Lucy Checchio, DO ................................................................................................. 102unmasking the Dvt mimic: a rare case of DiaBetic myonecrosis in a young patientAvish Patel, MD, Paul Endres, MD, Alexander Marchese, MD, Dianna Cheney-Peters, MD .......................................... 104HumANITIES & REfLECTION eternal lightAnurag Modak, MD .........................................................................................................................................................................108existential painKian Waddell .....................................................................................................................................................................................109navigating care anD loss through aging, Disease, anD Decision-making in the coviD eraMichael Predi, DO ............................................................................................................................................................................110small gifts, Big Questions: the ethical Dilemma in accepting gifts in meDicineMeiqi Luo, MD ...................................................................................................................................................................................11211et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202512 | The Medicine Forum, Volume 26 3D-Printed Coronary Arteries: An Effective Tool in Medical EducationZachary Pang, MD1, Shreyas Chandragiri, MD2, Shumpei Mori, MD, PhD3, Alexander Hajduczok, MD4, Cannon Greco Hiranaka, MD2, Jesse Ottaway, MD2, Zachary Mace, MD2, Michael Wong, MD2, Tammy Yoshioka, MD2, Noah Haroian, MD, PharmD4, Guiyun Zhang, MD, PhD51. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA3. University of California Los Angeles (UCLA) Cardiac Arrhythmia Center, UCLA Health System, David Geffen School of Medicine at UCLA, Los Angeles, CA4. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA5. Department of Pathology and Genomic Medicine, Sidney Kimmel Medical College, Philadelphia, PACARDIOLOGYINTRODUCTIONAnatomy and physiology can be a challenging topic due to their inherent complexity. Anatomy is most effectively learned through a combination of memorization, comprehension, and visualization.1 Lectures and textbooks provide ef f icient means for memorization and comprehension but can often be challenging for three-dimensional (3D) visualization. Conceptualizing 3D structures from two-dimensional (2D) textbook figures poses difficulty for many students. Anatomical education can be accompanied by dissection of cadavers, which can aid in visualization, but can be time-consuming and expensive.2 3D printing technology, however, holds the potential to solve this problem and enhance the anatomical education experience.3D printing refers to a technique where a printer constructs tangible, three-dimensional models. Creating 3D rendit ions involves image acquis i t ion, image post-processing, and 3D printing.3 Once an image, such as a computed tomography (CT) scan, is completed, it undergoes processing via specialized software that instructs the 3D printer to layer materials in the x-y plane and the z-plane. The x-y plane creates a 2D flat object, and the z-plane creates a layering effect, which produces a third dimension or 3D object.4 The versatile technology of 3D printing has been used in many fields, including medical education, where it is increasingly recognized for its transformative potential.3D printed models can help students learn anatomy. The use of 3D printed models has been shown to improve knowledge and skill in surgical training and can enhance the understanding of anatomy for both physicians and students.5-8 However, the use of 3D printing in the focused teaching of coronary anatomy remains relatively unexplored. Coronary anatomy can be challenging to comprehend because of the complexity, variability, and three-dimensionality of coronary arteries. The purpose of this teaching workshop was to investigate the efficacy of 3D printed coronary artery models in teaching coronary anatomy to medical students.METHODSPrior to 3D printing, virtual 3D coronary artery models were derived from the digital imaging and communications in medicine datasets obtained via CT coronary angiography. The virtual anatomy was meticulously reviewed for accuracy and then converted into standard tessellation language format (Figure 1). The segmented coronary arteries were then transformed into tangible 3D models using fused deposition modeling on the Ultimaker S5 3D printer. The production of the 3D models involved a dual extrusion process using polylactic acid as the primary material for the base structure and polyvinyl alcohol (PVA) for the support structures. Each model required approximately 20 hours of printing time, followed by an additional 12 hours to dissolve the PVA support structures. In total, 27 models were printed: nine of right-dominant, left-dominant, and co-dominant coronary circulations (Figure 2).The 3D models served as the basis for a coronary artery workshop for first-year medical students at the Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia, Pennsylvania. Twenty-six students voluntarily participated, each receiving their own model. The workshop occurred during the second week of their cardiology educational block. Prior to the workshop, the medical students had multiple cardiac anatomy lectures and participated in cadaver dissection of the heart and coronary arteries.The workshop lasted one hour, consisting of a pre-quiz, a hands-on workshop session with the models, and a post-quiz. The quizzes consisted of 10 multiple-choice questions identifying coronary dominance and major coronary arteries. The hands-on workshop started with a 10-minute lecture about coronary anatomy, followed by 30 minutes of time working with the 3D models. As students familiarized themselves with the models, they were encouraged to quiz each other and practice identifying the major coronary arteries on the 3D models. Students were encouraged to interchange models to observe the different coronary dominance patterns 12The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 13 Figure 1: Computerized representations of the 3D coronary artery models showing different patterns of dominance Figure 2: 3D printed coronary artery model made of polylactic acid. The right picture with right-dominant (top row), co-dominant (middle row), and left-dominant (bottom row). 13et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202514 | The Medicine Forum, Volume 26 among the three model types. Following the hands-on workshop, students took the post-quiz, and a brief feedback evaluation survey concluded the workshop.The student's quiz scores were subjected to statistical analysis using a paired two-sample t-test for means. A two-sided p-value of <0.05 was considered statistically significant. Microsoft Excel 2022 was utilized for performing the analysis.RESULTSTwenty-six first-year medical students started and completed the workshop, including the pre-quiz, 3D model workshop, and post-quiz evaluation. There was a significant increase in quiz scores comparing pre-quiz to post-quiz scores on a paired two-tailed t-test for means (p<0.001). The pre-quiz average was 5.70 (CI = 1.41) out of 10 questions. The post-quiz average was 9.04 (CI = 0.69) out of 10 questions. Regarding individual performance, 23 of the 26 students improved their scores from pre-quiz to post-quiz. The remaining three students scored the same on the pre-quiz and post-quiz. None of the participants experienced a decrease in scores from the pre-quiz to the post-quiz. Feedback was collected through a post-workshop evaluation based on a 5-point Likert scale. These results evaluated the perceived efficacy and value of the 3D printed models. The results showed that 96% of students agreed or strongly agreed that the 3D printed models helped them better learn coronary anatomy. A similarly high proportion, 92% of students agreed or strongly agreed that they developed a stronger understanding of coronary anatomy after working with the models. Additionally, 96% of students endorsed the workshop as a worthwhile investment of their time. Lastly, in a testament to the perceived value of this innovative teaching approach, 96% of students recommended this workshop for future medical students.DISCUSSIONIt is important for health care providers to have a strong understanding of human anatomy. Thus, health care providers in training often spend an extensive amount of time learning the various anatomical intricacies of the human body. Anatomy is often taught through a multimodal approach of lectures, textbooks, and dissection. Lectures and textbooks are great tools for memorization and understanding but can often be challenging for visualization. 2D anatomical figures represent a fundamental limitation of textbooks, as conceptualizing 3D structures from 2D figures pose difficulty for students. Cadaver dissection laboratories can help bridge the gap. Cadaver laboratories remain a cornerstone of most medical school curriculums and are often considered the ‘gold standard’ for anatomical education.2-10 However, the financial burden of cadaver dissection laboratories is substantial and potentially beyond the reach of some institutions, ranging from hundreds of thousands of dollars to over a million dollars for larger medical schools or for state-of-the-art cadaver laboratories.12The cost of 3D printing is significantly less than operating a cadaver laboratory. The Ultimaker 5S used in this study costs approximately $5,000 USD. A computer to manage the 3D printing software costs under $500 USD. Each 3D printed model costs approximately $2 USD. Thus, the total cost of 3D printing is a few thousand dollars. When compared to cadaver laboratories, 3D-printed anatomical models represent a low-investment, high-yield tool in anatomical education.Not only are 3D printed models cost-effective, but the versatility of 3D printing also allows for the teaching of various anatomical systems. Online databases like the National Institutes of Health 3D Print Exchange provide access to many anatomical models designed by experts. 3D printed models have the potential to help students better understand and visualize complex anatomical topics. Future studies should aim to evaluate the impact of other 3D printed anatomical regions to help identify and utilize the learning potential of 3D printed models. There are some limitations to this study. First, this study evaluates a single anatomical region of focus, the coronary arteries. This limits the generalizability of this study to anatomy as a whole. However, prior studies have shown the efficacy of other 3D printed anatomical regions in medical education. Secondly, this study design does not have the ability to discern if the statistically significant increase in quiz scores was due to the 3D models, the workshop, or the combination of both. However, considering that students had already received over one week of cardiac anatomy lectures and had extensive experience in the cadaver dissection laboratory, we can infer that the improved quiz scores were attributed to the 3D printed models in the setting of the workshop. Thirdly, this study does not evaluate 3D printed models on long-term memory, which could be a topic of interest in future studies. Lastly, it is important to address the limitations of 3D printing technology. Despite its capacity to produce detailed and patient-specific models, 3D-printed models exhibit fundamental differences in weight, texture, color, and tactile feedback compared to cadaver specimens.9 For these reasons, the role of 3D printing should act as an additional tool in anatomical education but not as a replacement for cadaver-based learning. 14The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 15 CONCLUSIONThis study suggests that 3D printed models of the coronary arteries are effective and highly rated teaching tools. 3D printed models represent a relatively low-cost, high-yield tool that have the potential to enhance the existing multimodal approach of anatomical education. The use of 3D printing in anatomical education is worth further exploration. ACKNOWLEDGMENTSThe authors would like to thank the Jefferson Health Design Laboratory, the Jefferson Heart Institute, and the Thomas Jefferson University Department of Medical Education for supporting this project. The authors would also like to thank Dr. Mori, Dr. Chandragiri, and Dr. Haroian for their tireless efforts in producing the 3D-printed coronary artery models. REFERENCES1. Pandey P, Zimitat C. Medical students' learning of anatomy: memorisation, understanding and visualisation. Med Educ. 2007;41(1):7-14. 10.1111/j.1365-2929.2006.02643.x2. Estai M, Bunt S. Best teaching practices in anatomy education: A critical review. Ann Anat. 2016;208:151-157. 10.1016/j.aanat.2016.02.0103. Rengier F, Mehndiratta A, von Tengg-Kobligk H, et al. 3D printing based on imaging data: review of medical applications. Int J Comput Assist Radiol Surg. 2010;5(4):335-341. 10.1007/s11548-010-0476-x4. Ursan ID, Chiu L, Pierce A. Three-dimensional drug printing: a structured review. J Am Pharm Assoc (2003). 2013;53(2):136-144. 10.1331/JAPhA.2013.122175. Lee H, Nguyen NH, Hwang SI, Lee HJ, Hong SK, Byun SS. Personalized 3D kidney model produced by rapid prototyping method and its usefulness in clinical applications. Int Braz J Urol. 2018;44(5):952-957. 10.1590/S1677-5538.IBJU.2018.01626. Pugliese L, Marconi S, Negrello E, et al. The clinical use of 3D printing in surgery. Updates Surg. 2018;70(3):381-388. 10.1007/s13304-018-0586-57. Garcia J, Yang Z, Mongrain R, Leask RL, Lachapelle K. 3D printing materials and their use in medical education: a review of current technology and trends for the future. BMJ Simul Technol Enhanc Learn. 2018;4(1):27-40. 10.1136/bmjstel-2017-0002348. Chen Y, Qian C, Shen R, et al. 3D Printing Technology Improves Medical Interns' Understanding of Anatomy of Gastrocolic Trunk. J Surg Educ. 2020;77(5):1279-1284. 10.1016/j.jsurg.2020.02.0319. Lim KH, Loo ZY, Goldie SJ, Adams JW, McMenamin PG. Use of 3D printed models in medical education: A randomized control trial comparing 3D prints versus cadaveric materials for learning external cardiac anatomy. Anat Sci Educ. 2016;9(3):213-221. 10.1002/ase.157310. Sotgiu MA, Mazzarello V, Bandiera P, Madeddu R, Montella A, Moxham B. Neuroanatomy, the Achille's Heel of Medical Students. A Systematic Analysis of Educational Strategies for the Teaching of Neuroanatomy. Anat Sci Educ. 2020;13(1):107-116. 10.1002/ase.186615et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202516 | The Medicine Forum, Volume 26 Evaluating Mortality and Bleeding Risk After Percutaneous Left Atrial Appendage Closure in Atrial Fibrillation: A Propensity-Matched Analysis Using a Multi-Institutional DatabaseYoussef Elfatatry, MD1* and Ryan Gardner, MD1*1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA * These authors contributed equally to this workCARDIOLOGYINTRODUCTIONPercutaneous left atrial appendage closure (pLAAC) has emerged as an effective treatment strategy for stroke prevention in patients with atrial fibrillation (AF) who otherwise cannot tolerate anticoagulation (AC) therapy. The American College of Cardiology, American Heart Association, American College of Chest Physicians, and Heart Rhythm Society combined guidelines offer a class 2a recommendation to pursue pLAAC in patients with an elevated risk of stroke from AF and a contraindication to oral AC, and a class 2b recommendation for pLAAC in patients with elevated risk of stroke from AF and elevated risk of life-threatening bleeding from AC.1 The predominant pLAAC device on the market currently is the Watchman implant (Boston Scientific, St. Paul, Minnesota), which has been shown to be non-inferior to oral AC for stroke prevention in multiple landmark trials.2The Watchman device first gained approval in 2015 after the results of the PROTECT AF trial were published, which showed that the intervention was non-inferior to warfarin therapy in preventing stroke and death.3 The PREVAIL trial was established later to address some of the safety concerns presented in PROTECT AF regarding peri-procedural complication rates and procedural success.4 pLAAC was also found to be non-inferior to direct oral anticoagulants (DOACs) with respect to rates of stroke, major bleeding, and cardiovascular death in the PRAGUE-17 trial that enrolled 402 patients with both higher risks of stroke and bleeding.5 Based on the protocols presented in these landmark trials, guidelines recommend that patients be continued on anticoagulation for 45 days after implantation, followed by 6 months of dual antiplatelet therapy.6 This highlights the need for established long-term efficacy of pLAAC, given the overlap in initial AC management in both groups of patients in practice.Long-term outcomes from PROTECT AF and PREVAIL were evaluated in a 2017 study by Reddy et al., and demonstrated statistically significant lower rates of both hemorrhagic stroke and post-procedural bleeding (Hazard ratio [HR]: 0.20, p=0.0022; HR: 0.48, p<0.001) as well as a reduction all-cause mortality (HR: 0.73; p=0.035) in the pLAAC arm after 5 years.7 However, a 2023 meta-analysis comparing outcomes of pLAAC versus oral AC showed that while there was also a reduction in both all-cause and cardiovascular mortality (HR: 0.68, p=0.002, HR: 0.5; p<0.01) with LAAC strategy, there was no statistically significant difference in rates of major bleeding and hemorrhagic strokes (HR: 0.94, p=0.71; HR: 1.07; p= 0.74).8 Of note, the mean follow-up of the seven studies included in this meta-analysis was 22 months. A more recent 2024 meta-analysis of 68,171 patients with AF by Neto et al. failed to show a statistical difference in a composite outcome of stroke, systemic embolism, cardiovascular death, all-cause mortality, ischemic stroke, and thrombo-embolic events.9 We aimed to perform a real-world data analysis of patients who underwent pLAAC to address some of the heterogeneity seen in the literature.METHODSWe conducted a retrospective observational cohort study using the TriNetX Research Network, a global federated health research platform aggregating de-identified electronic health records from 102 healthcare organizations. This Compare Outcomes Analysis was performed to evaluate clinical outcomes in patients with AF who did and did not undergo pLAAC.Cohort DefinitionsPatients in the LAAC group (Cohort 1) were identified by the presence of AF diagnosis codes (ICD-10-CM: I48.x) and a procedural code for LAAC (CPT: 33340 or corresponding ICD-10-PCS/SNOMED codes). The comparison group (Cohort 2) consisted of patients with a diagnosis of AF who did not undergo LAAC, as defined by the absence of any LAAC procedural codes.Propensity Score MatchingOne-to-one propensity score matching was performed using nearest-neighbor matching without replacement. Matching variables included demographics (age, sex, race) and clinical comorbidities such as chronic kidney disease, ischemic heart disease, cerebrovascular disease, diabetes mellitus, chronic obstructive pulmonary disease, obesity, and other systemic conditions (ICD-10 categories). Results are summarized in Table 1.16The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 17 RESULTS Baseline CharacteristicsFollowing propensity score matching, baseline character-istics were well-balanced between the LAAC and No LAAC cohorts (Table 1). The mean age was 74.8 ± 8.8 years, and 59% of patients were male in both groups. Comorbidities, including ischemic heart disease, cerebrovascular disease, and GI disorders, were similarly distributed between cohorts (all standardized differences < 0.02). The median follow-up duration was 575 days [IQR: 956] in the LAAC group and 715 days [IQR: 1,431] in the No LAAC group.OutcomesLAAC was associated with significantly lower all-cause mortality compared to no LAAC (14.0% vs. 25.4%, p<0.001). The adjusted odds ratio (OR) for death was 0.48 (95% CI: 0.46–0.50), with a hazard ratio (HR) of 0.61 (95% CI: Index Event and Follow-UpThe index event was defined as the first documented instance of AF diagnosis (for the No LAAC group) or LAAC procedure (for the LAAC group). Outcomes were evaluated beginning one day after the index event and followed for up to 5 years (1,825 days).Outcomes and Statistical AnalysisPrimary outcomes included all-cause mortality, intracerebral hemorrhage (ICH), ischemic stroke, and gastrointestinal (GI) bleeding. Outcomes were defined using standard ICD-10 codes. Risk analysis, Kaplan-Meier survival curves, and hazard ratios (HR) with 95% confidence intervals (CI) were calculated. Patients with the outcome prior to the index event were excluded from the corresponding analyses. Statistical significance was set at p < 0.05.Table 1: Baseline Characteristics After Propensity Matching Category Cohort 1 (n = 31,360) Cohort 2 (n = 31,360) P-ValueAge at Index 74.8 ± 8.8 74.7 ± 9.3 0.165White 25,850 (82.4%) 26,166 (83.4%) 0.001Unknown Race 2,079 (6.6%) 1,931 (6.2%) 0.016Female 12,079 (38.5%) 12,081 (38.5%) 0.987Black or African American 1,688 (5.4%) 1,647 (5.3%) 0.466Male 18,518 (59.0%) 18,510 (59.0%) 0.948Asian 984 (3.1%) 907 (2.9%) 0.072Acute kidney failure & CKD 12,378 (39.5%) 12,352 (39.4%) 0.832Other COPD 6,527 (20.8%) 6,485 (20.7%) 0.679Diabetes mellitus 10,075 (32.1%) 10,058 (32.1%) 0.884Obesity and hyperalimentation 11,896 (37.9%) 11,904 (38.0%) 0.948Ischemic heart diseases 18,324 (58.4%) 18,346 (58.5%) 0.859Cerebrovascular diseases 10,956 (34.9%) 10,909 (34.8%) 0.694Diseases of digestive system 22,221 (70.9%) 22,347 (71.3%) 0.267Musculoskeletal diseases 22,205 (70.8%) 22,413 (71.5%) 0.067Blood/immune disorders 18,051 (57.6%) 18,059 (57.6%) 0.948Endocrine/metabolic diseases 26,676 (85.1%) 26,540 (84.6%) 0.13Circulatory system diseases 30,932 (98.6%) 30,925 (98.6%) 0.81Nervous system diseases 20,950 (66.8%) 21,080 (67.2%) 0.27Mental/behavioral disorders 14,388 (45.9%) 14,508 (46.3%) 0.33617et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202518 | The Medicine Forum, Volume 26 0.59–0.63). Kaplan-Meier analysis demonstrated improved survival probability in the LAAC group at 5 years (70.0% vs. 62.2%, Log-rank p<0.001). The risk of ischemic stroke was slightly lower in the LAAC group (4.9% vs. 5.4%, p=0.002), with an OR of 0.89 (95% CI: 0.82–0.96). However, Kaplan-Meier curves did not show a statistically significant difference in stroke-free survival (Log-rank p=0.662). Rates of ICH were similar between groups (1.0% vs. 1.1%, p=0.218), with no significant difference in hazard (HR: 1.02, 95% CI: 0.87–1.19). GI bleeds occurred less frequently in the LAAC group (9.8% vs. 11.5%, p<0.001), with an OR of 0.83 (95% CI: 0.79–0.89). Figure 1 presents the Kaplan-Meier survival curves for all primary outcomes.DISCUSSIONOur results are compatible with most of the current literature supporting that pLAAC through Watchman implantation may confer both a mortality and morbidity benefit in AF patients at higher risk of stroke. It is important to note that our results showed a significant early divergence in survival, with Kaplan-Meyer curves separating within the first 50 days of follow-up (Figure 1). This raises concerns for some undetected differences in baseline characteristics between the two groups that were not mitigated by propensity matching for comorbidities or excluding patients with a history of examined outcomes. This finding could also suggest that patients who were offered LAAC were likely healthier and thought to be at lower risk of post-procedural complications, conferring a perceived survival advantage. This is especially prudent since our cohort had a relatively advanced mean age. There was a small but significant reduction in rates of GI bleeding; however, this was less likely to account for the magnitude of difference in mortality, especially since there were no differences between rates of ICH and stroke-free survival in both groups.These findings suggest that further studies are needed to expand the potential patient population outside the current recommendations and look beyond potential bleeding risk and intolerance of AC management. The highly anticipated and currently underway CHAMPION AF trial has enrolled 3,000 patients with aim of determining whether the newer Watchman FLX device can be implanted as first-line treatment for AF patients who otherwise would have required lifelong DOAC therapy.10LimitationsWhile our cohorts included a large number of AF patients and were able to detect small differences, several limitations were inherent to the study design. Misclassification and inaccuracy of ICD codes in the database do not allow for the assessment of disease severity and disease-specific mortality. The clinical endpoints assessed in this study, such as stroke, ICH, and GI bleeding, vary widely in clinical presentation and prognosis, making it difficult to assess the clinical significance of the findings. Besides the risk of stroke, other thromboembolic events associated with AF were also not included in this study.Figure 1: Five year Kaplan-Meier survival analysis of primary outcomes. 18The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 19 REFERENCES1. Joglar JA, Chung MK, Armbruster AL, et al; Peer Review Committee Members. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e1–e156. doi:10.1161/CIR.00000000000011932. Fountain RB, Holmes DR, Chandrasekaran K, et al. The PROTECT AF (WATCHMAN Left Atrial Appendage System for Embolic PROTECTion in Patients with Atrial Fibrillation) trial. Am Heart J. 2006;151(5):956–961. doi:10.1016/j.ahj.2006.02.0053. Reddy VY, Sievert H, Halperin J, et al. Percutaneous left atrial appendage closure vs warfarin for atrial fibrillation: a randomized clinical trial. JAMA. 2014;312(19):1988–1998. doi:10.1001/jama.2014.151924. Holmes DR Jr, Kar S, Price MJ, et al. Prospective randomized evaluation of the Watchman Left Atrial Appendage Closure device in patients with atrial fibrillation versus long-term warfarin therapy: the PREVAIL trial. J Am Coll Cardiol. 2014;64(1):1–12. doi:10.1016/j.jacc.2014.04.0295. Osmancik P, Herman D, Neuzil P, et al; PRAGUE-17 Trial Investigators. Left atrial appendage closure versus direct oral anticoagulants in high-risk patients with atrial fibrillation. J Am Coll Cardiol. 2020;75(25):3122–3135. doi:10.1016/j.jacc.2020.04.0676. Saw J, Holmes DR, Cavalcante JL, et al. SCAI/HRS expert consensus statement on transcatheter left atrial appendage closure. Heart Rhythm. 2023;20(5):e1–e16. doi:10.1016/j.hrthm.2023.01.0077. Reddy VY, Doshi SK, Kar S, et al; PREVAIL and PROTECT AF Investigators. 5-year outcomes after left atrial appendage closure: from the PREVAIL and PROTECT AF trials. J Am Coll Cardiol. 2017;70(24):2964–2975. doi:10.1016/j.jacc.2017.10.0218. Jiang H, Koh TH, Vengkat V, et al. An updated meta-analysis on the clinical outcomes of percutaneous left atrial appendage closure versus direct oral anticoagulation in patients with atrial fibrillation. Am J Cardiol. 2023;200:135–143. doi:10.1016/j.amjcard.2023.05.0449. Requião Radel Neto G, Bittar de Morais L, Hideki Sheguti R, Poci Liberato A. Revisiting left atrial appendage closure versus oral anticoagulants in recurrent atrial fibrillation management: an updated systematic review and meta-analysis. Cureus. 2024;16(10):e70854. doi:10.7759/cureus.7085410. Kar S, Doshi SK, Alkhouli M, et al. Rationale and design of a randomized study comparing the Watchman FLX device to DOACs in patients with atrial fibrillation. Am Heart J. 2023;264:123–132. doi:10.1016/j.ahj.2023.05.02219et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202520 | The Medicine Forum, Volume 26 Predicting In-Hospital Mortality in Patients with Hypertensive Emergency: A Retrospective Cohort StudyJay Satasiya, BS1, Devin Vasoya, MD2, Darius Farzad, MD31. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 2. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA3. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PACARDIOLOGYINTRODUCTIONApproximately 1 .3 bill ion adults worldwide have hypertension.1 Between 2006 and 2013, there was a two-fold increase in Emergency Department visits for hypertensive emergency.2 The prevalence of hypertensive emergency ranges from 0.08% to 0.76% in patients presenting to the Emergency Department.1,3-6 The estimated incidence of hospitalization with a hypertensive emergency is 111 per 100,000 patients.1,7 Hypertensive emergency is also associated with significant morbidity and mortality, often leading to ischemic stroke, pulmonary edema, acute heart failure.3-6 In-hospital mortality among patients with hypertensive emergency varies between 0.48% and 12.5%.5,7 This retrospective cohort study aims to further clarify hypertensive emergency presentation features associated with in-hospital mortality. METHODSThe National (Nationwide) Inpatient Sample (NIS) database for 2021 was analyzed for patients hospitalized with the primary diagnosis of hypertensive emergency. The sample was categorized into two distinct groups: patients who survived to discharge and those with in-hospital mortality. The two tailed T-test along with relative risk were used to compare both groups, both at the 95% confidence interval.RESULTSWe analyzed data from 11,715 patients diagnosed with a hypertensive emergency (51 with in-hospital mortality and 11,664 surviving to discharge). The average age was 59.5 years, 52.7% were female, 42.3% were African-American, 45.9% were Medicare users, and 42.8% were in the 0-25th income percentile. The in-hospital mortality rate was 4.35 per 1,000 patients. The in-hospital mortality group exhibited: higher mean age (68 vs 59.5 years, p<0.05), longer hospital stay (9.35 vs 3.7 days, p<0.05), larger proportion of Medicare users (61% vs 46%, p<0.05), increased hospital charges ($164,673 vs $48,823, p<0.05) when compared to the survived to discharge group. When compared to the surviving group, the deceased group had significantly higher rates (p<0.05) of acute hypoxic respiratory failure (33%), metabolic encephalopathy (12%), pneumonia (10%), cerebral edema (10%), coma (6%), acute on chronic hypoxic respiratory failure (6%), sepsis (6%), and acute on chronic systolic and diastolic heart failure (6%) as complications of their hypertensive emergency. Sequelae of hypertensive emergency most associated with in-hospital mortality include coma (RR 174, CI 97.16 to 311.40, p<0.0001), cerebral edema (RR 29, CI 12.41 to 65.66, p<0.0001), sepsis (RR 17, CI 5.51 to 49.68, p<0.0001), acute on chronic hypoxic respiratory failure (RR 7, CI 2.17 to 20.54, p=0.0009), pneumonia (RR 4.9, CI 2.03 to 11.74, p=0.0004), acute hypoxic respiratory failure (RR 4.8, CI 2.91 to 7.78, p<0.0001), metabolic encephalopathy (RR 4, CI 1.83 to 9.17, p=0.0006), and acute on chronic systolic and diastolic heart failure (RR 3.4, CI 1.11 to 10.58, p=0.0335).CONCLUSIONAlthough hypertensive emergency is a rare phenomenon, it is associated with significant in-hospital mortality and healthcare costs. Additional efforts must be made to ensure that complications of hypertensive emergency are accurately diagnosed and promptly treated.REFERENCES1. Miller JB, Hrabec D, Krishnamoorthy V, Kinni H, Brook RD. Evaluation and management of hypertensive emergency. BMJ. 2024;386:e077205. Published 2024 Jul 26. doi:10.1136/bmj-2023-0772052. Janke AT, McNaughton CD, Brody AM, Welch RD, Levy PD. Trends in the Incidence of Hypertensive Emergencies in US Emergency Departments From 2006 to 2013. J Am Heart Assoc. 2016;5(12):e004511. Published 2016 Dec 5. doi:10.1161/JAHA.116.0045113. Farley TM. Hypertensive Emergency: Parenteral Antihypertensives and Population Data. Curr Hypertens Rep. 2023;25(12):423-428. doi:10.1007/s11906-023-01280-24. Vallelonga F, Cesareo M, Menon L, et al. Hypertensive emergencies and urgencies: a preliminary report of the ongoing Italian multicentric study ERIDANO. Hypertens Res. 2023;46(6):1570-1581. doi:10.1038/s41440-023-01232-y5. Siddiqi TJ, Usman MS, Rashid AM, et al. Clinical Outcomes in Hypertensive Emergency: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2023;12(14):e029355. doi:10.1161/JAHA.122.0293556. Astarita A, Covella M, Vallelonga F, et al. Hypertensive emergencies and urgencies in emergency departments: a systematic review and meta-analysis. J Hypertens. 2020;38(7):1203-1210. doi:10.1097/HJH.00000000000023727. Watson K, Broscious R, Devabhakthuni S, Noel ZR. Focused Update on Pharmacologic Management of Hypertensive Emergencies. Curr Hypertens Rep. 2018;20(7):56. Published 2018 Jun 8. doi:10.1007/s11906-018-0854-220The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 21 CARDIOLOGYA Case of Type 4 Spontaneous Coronary Artery Dissection (SCAD)Virginia Gonzalez, MD, MS1, Kashka Mallari, MD1, Marina Gonzalez, MD1, Svenja Schneider, MD2, Sung-Hae Cho, MD2, Paulina Gorodin Kiliddar, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PACASE PRESENTATIONA 52-year-old female presented to the emergency department ten minutes after the development of sudden-onset crushing chest pain radiating to both of her arms, associated with dyspnea on exertion. Notably, she reported a several-month history of significant stress caring for her elderly mother with Alzheimer’s disease. On admission, her vital signs revealed sinus bradycardia with a heart rate of 56 beats/min. The patient reported a past medical history of hypothy-roidism, breast cancer status post lumpectomy, nicotine dependence, and anxiety. She did not have a prior history of cardiovascular disease or stroke, nor a family history of premature coronary disease. She also had no prior radiation or chemotherapy. Her medications included levothyroxine and propranolol as needed for panic attacks.Initial labs showed a negative high-sensitivity troponin T level of 9 ng/L (normal <19 ng/L) and a lipid panel that was within normal limits. Chest x-ray was unremarkable. However, an electrocardiogram (ECG) revealed hyperacute T waves with ST elevations concerning for anterolateral infarct (Figure 1). She received high-dose aspirin as well as heparin and nitroglycerin infusions without relief of angina. She emergently underwent a left heart catheterization (LHC), which revealed 100% occlusion of the mid-left anterior descending artery (LAD) (Figure 2). The occlusion lacked the usual irregular, hazy appearance of a thrombotic plaque seen in coronary artery disease (CAD). Moreover, other coronary vessels showed no significant CAD with only minimal luminal irregularities. Intracoronary nitroglycerin was administered without improvement in the obstruction, excluding coronary vasospasm. The mid-LAD occlusion was deemed suggestive of type 4 spontaneous coronary artery dissection (SCAD). An initial drug-eluting stent (DES) was deployed distal to the site of occlusion, which led to dissection propagation at the proximal end, further confirming the diagnosis of SCAD. A second DES was positioned proximal to the first stent, and again, dissection propagation was seen at the proximal end (Figure 3c). Finally, a third DES was positioned without further propagation of dissection. In total, three overlapping DES were successfully placed from the distal to proximal LAD, resulting in 0% residual stenosis and Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow representing complete perfusion (Figure 3d). The ECG post-reperfusion showed sinus bradycardia with continued left anterior fascicular block and resolution of both the hyperacute T waves and ST elevations in the anterior leads with new anterolateral Q waves (Figure 4). Figure 1: ECG on admission displayed sinus bradycardia at 56 beats/min, hyperacute T waves from V2-V6 with 1-2 mm ST elevation, left anterior fascicular block (LAFB), and poor R wave progression in precordial leads.Figure 2: LHC on admission showed 100% occlusion of mid-LAD, indicative of Type 4 SCADs.21et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202522 | The Medicine Forum, Volume 26 She was admitted to the cardiovascular intensive care unit. Her subsequent high-sensitivity troponin T level, which was initially negative, increased to 3474 ng/L and peaked at 5952 ng/L. The following day, a transthoracic echocardiogram (TTE) showed a preserved ejection fraction with apical septal and apical inferior akinesis. Doppler ultrasound of bilateral carotid arteries and kidneys showed no findings of fibromuscular dysplasia or stenosis. After monitoring for three days, she was discharged on a regimen of aspirin, prasugrel, atorvastatin, isosorbide mononitrate, metoprolol succinate, and nitroglycerin with smoking cessation counseling and a cardiac rehabilitation referral. During her outpatient cardiology visit, it was noted that she was still feeling overwhelmed by caregiving duties and had begun psychotherapy.DISCUSSION SCAD refers to the separation of layers within the coronary artery wall, leading to the formation of a hematoma that may obstruct blood flow and lead to myocardial ischemia and infarction.1 SCAD is a relatively rare disease and is often underrecognized. In a study spanning from 2004 to 2015 and involving thirteen million patients, SCAD accounted for only 0.49% of acute coronary syndrome (ACS) cases.2 Notably, SCAD predominantly affects women, with one prospective study involving 750 SCAD patients from 2014 to 2018 citing that 88.5% of patients affected were women with a mean age of 51.8 ± 10.2 years.3 Among women less than 50 years of age, SCAD accounts for nearly 35% of ACS cases.4The above case presents a scenario of SCAD in a middle-aged female patient with recent emotional stress as a potential predisposing factor. Emotional stress has been shown to precede SCAD events in about 50% of cases, as seen in our patient who experienced stress related to caregiving responsibilities.3 She is also a current smoker, which is a risk factor for atherosclerotic ACS, although the association with SCAD remains uncertain.5 Associated conditions may include pregnancy, postpartum status, endogenous and exogenous sex hormones, fibromuscular dysplasia, connective tissue disorders, and certain genetic mutations, although clear evidence linking these conditions to SCAD is limited. Coronary angiography is often sufficient to diagnose SCAD, with the Yip-Saw classification aiding in subcatego-rization based on angiographic features.6 For type 1 SCAD, there is a distinctive dual-lumen appearance within the coronary vessel caused by contrast staining of the false lumen. Type 2 SCAD is identified by a long, smooth narrowing of the artery, resulting from compression by intramural hematomas. Type 3 SCAD poses challenges for diagnosis via coronary angiography alone, as its appearance resembles atherosclerotic disease with a focal or tubular stenosis appearance. In contrast, the more recently defined type 4 SCAD has not been officially described in this classification system. As is seen in our patient, it is marked by complete vessel occlusion, often of a distal coronary territory.6 Intracoronary imaging, such as intravascular ultrasound and optical coherence tomography, may be necessary to confirm the diagnosis of SCAD. However, these imaging techniques are generally avoided due to the risk of worsening dissection.7 Figure 3: a. Selective angiography of the left coronary artery showing 100% occlusion in the midportion of the LAD with a guidewire advanced distal to the site of occlusion. b. A smooth, linear appearance of the LAD distal to the site of occlusion after first dilation. c. Propagation of the dissection is seen proximal to the site of the second stent placement. d. After the third stent placement, 0% residual stenosis with TIMI 3 flow in the LAD. Figure 4: ECG Day 0 Post-PCI showing resolution of hyperacute T waves and ST elevations 22The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 23 Management of SCAD differs significantly from other ACS etiologies. Stable patients receive conservative management with three to five days of inpatient monitoring with the goal of angiographic “healing.”1 Revascularization procedures like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) carry a risk of potentially advancing the dissection in patients with SCAD. These procedures are typically reserved for unstable patients, those with ongoing ischemia, or involvement of the left main coronary artery.8 For example, in the previously mentioned prospective study involving 750 SCAD patients, 86% of patients underwent conservative management, with the majority having favorable outcomes and only 3% requiring subsequent PCI for ongoing ischemia. For those that did undergo revascularization, 30% were unsuccessful.3 In another observation study of 81 patients with type 4 SCAD, 93% of patients who underwent PCI had ST-segment elevation, and only 33% of patients who underwent PCI were successfully revascu-larized.9 Although our patient had ongoing ischemia in the setting of antianginal therapy, an indication for coronary angiography, PCI led to propagation of the dissection, necessitating the placement of three separate DES. It is worthwhile to consider whether conservative management would have led to an equally successful outcome without dissection propagation. Pharmacological management often involves antiplatelets, beta-blockers, and antianginals, though evidence from randomized trials is lacking.10 For antiplatelet therapy, patients such as ours who undergo PCI should receive guideline-based dual antiplatelet therapy. However, for those managed conservatively, most experts suggest aspirin for at least one year following a SCAD event if tolerated. Statin therapy should typically be reserved for patients requiring primary prevention of atherosclerosis.8Screening for conditions associated with SCAD, such as fibromuscular dysplasia and connective tissue disease, is recommended. While our patient underwent Doppler ultrasound of her carotid arteries and kidneys, head-to-pelvic cross-sectional imaging was not performed, which is an essential first step to diagnosing fibromuscular dysplasia.1 Additionally, genetic counseling should be considered in the setting of suggestive history and physical examination to evaluate for inherited arteriopathies and connective tissue disorders such as Marfan, Ehlers-Danlos, and Loeys-Dietz syndromes.3 Psychosocial support is a crucial aspect of post-SCAD management aimed at reducing morbidity and preventing disease recurrence. SCAD survivors are at a heightened risk of developing anxiety, depression, and post-traumatic stress disorder due to the uncertainty surrounding management and long-term prognosis.1 Cardiac rehabili-tation is advised for all SCAD patients, regardless of baseline functional status to allow patients to gradually regain confidence in exercise while establishing specific limits regarding exertion and strain.1,8 CONCLUSION SCAD is a potentially life-threatening condition that requires a high index of suspicion for appropriate diagnosis and management. This case highlights the importance of early recognition of the recently defined type 4 SCAD, especially in patients with a typical phenotype. An important takeaway from this case is that when a diagnosis of SCAD is suspected with catheter-based coronary angiography, conservative management should be considered to minimize the risk of iatrogenic dissection propagation. Furthermore, additional research should be conducted to further clarify specific management strategies in patients with type 4 SCAD.REFERENCES1. Hayes SN, Tweet MS, Adlam D, Kim ESH, Gulati R, Price JE, et al. Spontaneous coronary artery dissection: JACC state-of-the-art review. J Am Coll Cardiol. Published online July 18, 2018. doi:10.1016/j.jacc.2018.06.0072. Krittanawong C, Kumar A, Virk HUH, Yue B, Wang Z, Bhatt DL. Trends in incidence, characteristics, and in-hospital outcomes of patients presenting with spontaneous coronary artery dissection (from a national population-based cohort study between 2004 and 2015). Am J Cardiol. 2018;122(10):1617-1623. doi:10.1016/j.amjcard.2018.08.0203. Hayes SN, Kim ESH, Saw J, et al. Spontaneous coronary artery dissection: current state of the science: a scientific statement from the American Heart Association. Circulation. 2018;137(19):e523-e557. doi:10.1161/CIR.00000000000005644. Saw J, Aymong E, Mancini GB, Sedlak T, Starovoytov A, Ricci D, et al. Canadian spontaneous coronary artery dissection cohort study: in-hospital and 30-day outcomes. Eur Heart J. 2018;39(34):2997-3006. doi:10.1093/eurheartj/ehy2495. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012;126(5):579-588. doi:10.1161/CIRCULATIONAHA.112.1057186. Adlam D, Tweet MS, Gulati R, Kotecha D, Rao P, Moss AJ, et al. Spontaneous coronary artery dissection: pitfalls of angiographic diagnosis and an approach to ambiguous cases. JACC Cardiovasc Interv. Published online July 31, 2013. doi:10.1016/j.jcin.2013.06.0117. Barbieri L, D'Errico A, Avallone C, et al. Optical coherence tomography and coronary dissection: precious tool or useless surplus? Front Cardiovasc Med. 2022;9:822998. doi:10.3389/fcvm.2022.8229988. Tweet MS, Kok SN, Hayes SN. Spontaneous coronary artery dissection in women: what is known and what is yet to be understood. Clin Cardiol. Published online June 19, 2018. doi:10.1002/clc.224629. Mori R, Macaya F, Giacobbe F, Salinas P, Rolfo C, Porto I, et al. Clinical and angiographic features of SCAD type 4. Int J Cardiol. 2023;377:22-25. doi:10.1016/j.ijcard.2023.01.06710. Saw J, Humphries K, Aymong E, et al. Spontaneous coronary artery dissection: clinical outcomes and risk of recurrence. J Am Coll Cardiol. 2017;70(9):1148-1158. doi:10.1016/j.jacc.2017.06.0523et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202524 | The Medicine Forum, Volume 26 Be Afraid of Severe Pulmonary Hypertension and Right Ventricular Failure in the Peri-Op PatientAvish Patel, MD1, Lily Ackermann, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Hospital Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PACARDIOLOGYINTRODUCTIONHeart failure (HF), particularly right ventricular (RV) failure, and pulmonary hypertension (PH) present significant risks during the perioperative period. Despite the fact that these comorbidities are not always considered in preoperative risk evaluation, they are very important when considering perioperative risk. Current risk assessment tools mainly include the Revised Cardiac Risk Index (RCRI); however, it does not effectively assess severity of HF or PH. This review aims to highlight the major points on peri-operative management in non-cardiac surgeries using a case of a patient with severe PH who experienced unexpected mortality from acute RV failure post-operatively. CASE OVERVIEWThe case includes a 92-year-old female patient with severe chronic heart failure (ejection fraction 10%), severe pulmonary hypertension, atrial fibrillation, and osteoporosis. The orthopedic team performed a surgery for a femur fracture while her preoperative risk assessment revealed an RCRI that indicated a 6% probability of major adverse cardiac event (MACE) occurrence during the next thirty days. It was noted that her RCRI likely underestimates her risk given her severe pulmonary hypertension, underweight status, and prior cerebrovascular event. Given the time sensitive nature of the procedure, additional testing was not recommended given it would not significantly alter her procedural risk. Cardiology provided preoperative medication recommen-dations of holding sodium-glucose co-transporter 2 (SGLT2) inhibitors and judicious administration of fluid to minimize congestive heart failure exacerbation preoperatively. Expected postoperative anemia in conjunction with chronic right ventricular failure in the setting of mobilization for physical activity contributed to cardiovascular collapse resulting in an unexpected patient mortality. This clinical scenario demonstrates that RV failure intensifies both PH and HF complications around a surgery.Heart Failure, RV Failure, and Pulmonary Hypertension: Pathophysiology and Risks:RV failure together with PH creates specific treatment challenges for surgical procedures that often remain underrecognized. RV failure causes the right side of the heart to malfunction which leads to reduced oxygenation and poor systemic blood flow.1 PH exacerbates this condition by creating excessive resistance in the pulmonary vessels that intensifies pressure on the right ventricle.2 The dual challenge of preserving surgical stability becomes extremely challenging because RV failure combined with PH leads to multiple postoperative complications with higher mortality.The event of hypotension with initial post-operative physical activity rooted from multiple physiologic processes. A decrease in hemoglobin after hip fracture surgery from 9.2 g/dL to 7.8 g/dL created a critical condition that obstructed blood oxygen transport while making it difficult to maintain effective forward flow given RV failure depends heavily on sufficient preload. Patients with RV dysfunction are very sensitive to volume status changes to the point which a lower preload blood volume can acutely cause decompen-sation.3 This unresponsive patient helped illustrate that acute RV failure does not always respond to conventional fluid therapy, making emergent management challenging.Blood loss is common after orthopedic procedures as seen in this patient. Prior studies found that patients undergoing femoral fracture surgeries experience an average hemoglobin drop of 1.4 g/dL.4 The median number of blood transfusions was 2.0 with a median postoperative hemoglobin level of 7.7 g/dL.5 The blood loss that a standard patient may tolerate can cause rapid hemodynamic decompensation in RV failure or PH patients as noted in this case. It is imperative to consider patient specific approaches when defining transfusion goals and mobilization protocols. Clinicians should consider pre-physical therapy blood transfusions for patients with compromised RV function to prevent fatal hemodynamic instability. We next review risk stratification and optimized perioperative care practices that can improve outcomes in high-risk patients. Current ACC/AHA Guidelines on Risk Stratification:The current perioperative risk assessment guidelines from the American College of Cardiology (ACC) and the American Heart Association (AHA) demonstrate a major change in how clinicians should manage patients with HF and PH. The guidelines support extensive multidisci-plinary team management given the high risk of perioperative complications.2Within HF, non-ischemic HF and RV failure demonstrate increased potential for postoperative complications in comparison to typical ischemic cardiac events including myocardial infarction (MI). In a study with over 38,000 patients, non-ischemic and ischemic HF result in 9.3% and 24The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 25 9.2% of deaths, respectively, during the first thirty days postoperatively whereas patients with coronary artery disease (CAD) without HF experience only 2.9% mortality. This represents over a 3-fold higher risk of perioperative death for patients with HF than CAD alone.6 HF and PH related risks are often underappreciated over ischemic events such as an MI when considering sending a patient to surgery. While MI remains a significant risk, it carries a lower incidence of perioperative mortality when compared to HF. The risk of perioperative MI decreases over time following the last myocardial event with the highest risk occurring within the first 30 days.7 This underscores the critical need for more careful perioperative evaluation and optimization of HF, as it is often the primary driver of postoperative complications. By placing a greater emphasis on HF in the preoperative setting, we can help mitigate its impact on outcomes. The 2024 guidelines recommend considering any risk modifiers after assessing for acute conditions including severe PH. Pre-operative biomarker assessment is recommended followed by further testing.8 These evaluations help classify the heart failure stage and guide therapies. Maximizing medical treatments before surgery is crucial, especially for patients with severe pulmonary hypertension, where interventions to decrease afterload and improve ventricular performance are essential to reduce right ventricular strain. RV failure together with PH are very important risk factors that can lead to surgical decompensation. Perioperative cardiac risk assessments need to inspect both ischemic heart disease as well as RV failure and PH specifically for patients who have reduced ejection fraction along with advanced heart failure.3 The underappreciation of these risk factors can result in fatal consequences as seen in the case of this 92-year-old patient. Management Strategies: Preoperative, Intraoperative, and Postoperative Considerations: (Referenced from ACC/AHA Guidelines, Figure 1)1, 3, 7-81. Preoperative Management: i. Risk Assessment:a. Detect symptoms of RV failure and PH early b. Consider checking NT-proBNP levels pre-operatively as a pre-operative predictor and baseline c. Consider echocardiogram and right heart catheterization for risk stratification d. Cardiology consultation for risk assessment e. If severe PH undergoing high risk non-cardiac surgery (NCS), then consult PH specialist (Class 2a ACC/AHA 2024)8f. Deferral of surgery or Palliation are options to consider in high-risk patients ii. Optimization of Medical Therapy:a. Volume management and continue guideline directed medical therapy if compensated HFb. Continue targeted therapies for PH with NCS (Class 1 indication ACC/AHA 2024)8c. Hold SGLT inhibitors 3 to 4 days prior to surgery (Class 1 indication ACC/AHA)8 iii. Anemia Management:a. Should receive blood transfusions if acute change in anemia especially with mobilization to be able to compensate iv. Multidisciplinary Collaboration: a. Communication with Cardiology and PH specialists early pre-operatively is important for risk stratifi-cation into a procedure, intra-operative consider-ations and contingencies, and for post-operative planning and management. Considerations to discuss would be diuresis, invasive hemodynamic monitoring, and inotrope indications. b. Communication with Surgery team and Anesthesia, specifically Cardiac Anesthesia with elevated risk procedures on peri-operative management and considerations 2. Intraoperative Considerations i. Hemodynamic Monitoring: a. Invasive hemodynamic monitoring with severe PH during and post-operatively (Class 2a indication ACC/AHA 2024)8b. Short-acting inhaled pulmonary vasodilators for pre-capillary PH (Class 2b indication ACC/AHA 2024)8c. Coordination with Cardiac Anesthesia for high-risk cases to optimize hemodynamics ii. Fluid Management: a. Cautious volume management balancing decreased preload and volume overload state b. Consideration of volume via blood products especially with studied high blood loss procedures such as a femur fracture 3. Postoperative Management: i. Monitoring and Early Intervention: a. Appropriate post-operative disposition to critical care unit if need for continued invasive hemodynamic monitoring b. Consider higher blood transfusion goal given patients with PH and RV failure are more sensitive to change in pre-load c. Consider repeating echocardiogram to assess RV post-operatively25et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202526 | The Medicine Forum, Volume 26 Limitations ofCurrent ToolsThe RCRI inadequatelyassesses severity of HF or PH.92-year-old female with EF10%, severe PH, atrialfibrillation, osteoporosis.Patient OutcomeCardiovascular collapse post-opdue to RV failure, exacerbated byanemia during mobilizationConventional tools maymiss critical right-heartpathologiesLearning PointProcedureFemur fracture repairwith underestimatedrisk per RCRIACC/AHA 2024 GUIDELINES RISK STRATIFICATION PulmonaryHypertension (PH) INTRODUCTION HF, RV failure, and PH areunder-recognized but criticalperioperative risk factors.ObjectiveRaise awareness using a case-based lens on how to improve outcomesthrough multidisciplinary strategies and guideline-driven care. CASE OVERVIEW RCRI must evolve to account for PH, RV dysfunction, andhemoglobin thresholds.Guideline-Based ImprovementClinical ImperativesIdentify RV dysfunction and PH as high-risk.Use hemoglobin and preload-sensitive protocols.Involve cardiology, PH specialists, surgery, andanesthesia early.Future OutlookRaise transfusion targetsEmphasize preload before mobilizationStrengthen multidisciplinary protocolsConsider palliation or deferral of surgery.Perioperative Risk inPH & RV FailureLEARNING FROM A CASE OFUNEXPECTED DECOMPENSATION CONCLUSION Category Recommendation/DetailGeneral RiskStratificationHF, especially non-ischemic and RV failure, poses greaterperioperative mortality risk than CAD or MI. HF-related 30-day postoperative mortality: 9.3% (non-ischemic)vs. 2.9% (CAD without HF). MI risk highest within first 30 days post-event; decreases over time.Risk AwarenessHF and PH are underappreciated compared to MI duringpreoperative planning. RV failure with PH increases chance of surgical decompensation.Guideline EmphasisMultidisciplinary team involvement is crucial. Assessment of acute conditions like severe PH is recommended. Use pre-operative biomarkers and functional testing for accuratestaging and therapy guidance.PERIOPERATIVE MANAGEMENT FOR HF, RV FAILURE & PHPREOPERATIVE MANAGEMENTCategory Action/GuidanceRisk AssessmentDetect RV failure/PH symptoms early and Check NT-proBNP pre-operatively. Echocardiogram and right heart cath as needed. Cardiology consult is recommended. If severe PH + high-risk NCS, involve PH specialist (Class 2a),consider surgery deferral or palliation for high-risk cases.Medical TherapyOptimizationContinue GDMT if HF is compensated. Continue PH-targeted therapies for NCS (Class 1). Hold SGLT2 inhibitors 3–4 days pre-op (Class 1).AnemiaManagement Transfuse in acute anemia changes, especially if mobilization isplanned.MultidisciplinaryCollaborationEarly communication with Cardiology/PH specialists for (a) Riskstratification (b) Diuresis planning (c) Hemodynamic monitoring(d) Inotrope use Coordinate with Surgery and Anesthesia, especially CardiacAnesthesia, for perioperative risk planning.HemodynamicMonitoringUse invasive monitoring in severe PH (Class 2a). Short-acting inhaled pulmonary vasodilators for pre-capillaryPH (Class 2b). Work with Cardiac Anesthesia for hemodynamic optimization.Fluid Management Cautious volume strategy to balance preload and avoidoverload. Consider blood products in high blood loss surgeries (e.g., femurfractures).Category Action/GuidanceMonitoring &InterventionAdmit to critical care unit if invasive monitoring continues. Higher transfusion thresholds may be appropriate due topreload sensitivity. Repeat echocardiogram to reassess RV function post-op.INTRAOPERATIVE CONSIDERATIONSCategoryPOSTOPERATIVE MANAGEMENTHEART FAILURE, RV FAILURE, AND PULMONARYHYPERTENSION: PATHOPHYSIOLOGY AND RISKSRight Ventricular(RV) FailurePostoperativePhysiologic StressReduced PreloadInadequateResponse to FluidTherapyMobilizationcontributed tocardiovascularcollapseUNEXPECTEDPATIENT MORTALITYPulmonary vascularresistanceRV pressure loadOxygenationSystemic blood flowHb drop from 9.2 →7.8 g/dL after hipsurgeryObstructed bloodoxygen transportBlood volume →Forward flowimpairmentPhysical activity in thesetting of anemia + RVfailure triggers collapseRV dysfunction may notimprove withconventional fluidresuscitationOften underrecognizedin surgeryPostoperativecomplications (RV+PH)PULMONARYHYPERTENSIONRIGHTVENTRICULARFAILURECARDIOGENICSHOCK1. 2.3.4.5.6.Action/GuidanceFigure 1: Summary graphic of case details, perioperative risk stratification and recommendations for pulmonary hypertension, and pathophysiology. 26The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 27 CONCLUSIONAccording to this case we need to reevaluate perioperative scoring models such as the Revised Cardiac Risk Index (RCRI) because they tend to overlook essential factors like right heart failure and PH. Additions of RV functional assessment, pulmonary hypertension classification, and hemoglobin thresholds to preoperative pathways would significantly reduce complication risks and possibly reduce poor outcomes like described in this case. The understanding and awareness of the ACC/AHA guidelines is crucial to be able to effectively optimize this category of patients perioperatively. Safe healthcare delivery depends on organized multidisciplinary collaboration amongst all teams involved in the steps through a surgery. The patient’s postoperative hemoglobin level of 7.8 g/dL exacerbated the right-sided decompen-sation. In patients with HF, especially those with RV dysfunction, even modest reductions in hemoglobin can trigger significant hemodynamic instability. Early transfusion protocols and pre-mobilization stabilization are essential to avoid catastrophic collapse, particularly in RV-dominant HF phenotypes. Future investigations should include raising postoperative hemoglobin goals and protocols for preload optimization before mobilization with physical therapy post-operatively. Patients with severe PH can experience rapid changes in their intra-cardiac hemodynamics that can trigger RV failure. This case hopefully enhances awareness of the importance of PH and RV failure perioperatively. The takeaway is the importance of engaging the correct multi-disciplinary team members to safely manage this high-risk patient population through a surgery.REFERENCES1. Murphy, E., & Shelley, B. (2019). Clinical presentation and management of right ventricular dysfunction. BJA education, 19(6), 183–190. https://doi.org/10.1016/j.bjae.2019.02.0042. Rajagopal, S., Ruetzler, K., Ghadimi, K., et al. (2023). Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association. Circulation, 147(17), 1317–1343. https://doi.org/10.1161/CIR.00000000000011363. McGlothlin, D. P., Granton, J., Klepetko, W., et al. (2022). ISHLT consensus statement: Perioperative management of patients with pulmonary hypertension and right heart failure undergoing surgery. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 41(9), 1135–1194. https://doi.org/10.1016/j.healun.2022.06.0134. Stacey, J., Bush, C., & DiPasquale, T. (2021). The hidden blood loss in proximal femur fractures is sizeable and significant. Journal of clinical orthopaedics and trauma, 16, 239–243. https://doi.org/10.1016/j.jcot.2021.02.0125. Smeets, S. J. M., Verbruggen, J. P. A. M., & Poeze, M. (2018). Effect of blood transfusion on survival after hip fracture surgery. European journal of orthopaedic surgery & traumatology : orthopedie traumatologie, 28(7), 1297–1303. https://doi.org/10.1007/s00590-018-2205-z6. Van Diepen, S., Bakal, J. A., McAlister, F. A., et al. (2011). Mortality and readmission of patients with heart failure, atrial fibrillation, or coronary artery disease undergoing noncardiac surgery: an analysis of 38 047 patients. Circulation, 124(3), 289–296. https://doi.org/10.1161/CIRCULATIONAHA.110.0111307. Fleisher, L. A., Fleischmann, K. E., Auerbach, A. D., et al. (2015). 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Developed in collaboration with the American College of Surgeons, American Society of Anesthesiologists, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Anesthesiologists, and Society of Vascular Medicine Endorsed by the Society of Hospital Medicine. Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology, 22(1), 162–215. https://doi.org/10.1007/s12350-014-0025-z8. Thompson, A., Fleischmann, K. E., Smilowitz, N. R., et al. (2024). 2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 150(19), e351–e442. https://doi.org/10.1161/CIR.000000000000128527et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202528 | The Medicine Forum, Volume 26 Hot Coffee-Induced Takotsubo Cardiomyopathy: A Case Report Zachary Pang, MD1, M. Duncan Kilpatrick, MD1, Jasmine Lee, MD1, Gregary D. Marhefka, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PACARDIOLOGYINTRODUCTIONTakotsubo cardiomyopathy is a well-known phenomenon due to physical or emotional stress, causing a catecholamine surge leading to myocardial wall motion abnormalities, most commonly apical ballooning of the left ventricle.1-3 The diagnosis of Takotsubo cardiomy-opathy can be challenging as its presentation often mimics acute coronary syndrome. This case highlights the classic presentation of the apical ballooning variant of Takotsubo cardiomyopathy and appropriate workup and diagnosis.CASE PRESENTATIONThe patient is a 72-year-old female with a past medical history of right-sided breast cancer status post lumpectomy five years prior, hyperlipidemia, hypertension, anxiety, and depression, who presented to the emergency department after a syncopal episode, which resulted in burns to her chest. The patient reported she was at home recovering from an upper respiratory infection when she suddenly felt warm, flushed, and passed out at her kitchen table, causing her to spill hot coffee on her chest. When the patient awoke, she noticed the skin over her chest wall was very red and painful, prompting her to go to the emergency department. The patient reported external chest tingling and burning like pain on the skin overlying her chest, but denied a sense of internal chest pain, shortness of breath, abdominal pain, or musculo-skeletal pain. The patient also denied confusion or post-ictal symptoms after her syncopal episode. On arrival to the hospital, the patient’s vital signs were stable. The patient was afebrile with heart rate of 90 beats per minute, blood pressure of 166/75 mm Hg, and oxygen saturation of 96% on room air. She appeared mildly uncomfortable but not in acute distress. The patient’s right breast and chest wall had second- and third-degree burns with diffuse erythema. Heart sounds were normal rate, regular rhythm, without rubs, murmurs, or gallops. Lungs were clear to auscultation bilaterally. Bilateral extremities were warm and well perfused, and there were no focal neurologic deficits on exam.The patient’s laboratory results showed a complete blood count, comprehensive metabolic panel, and lactate all within normal limits. The patient’s high sensitivity troponin was normal at 9 ng/L (normal < 19 ng/L). The patient’s electrocardiogram (ECG) showed normal sinus rhythm without ST elevations or depressions. Transthoracic echocardiogram (TTE) showed normal left ventricular (LV) chamber size, concentric remodeling, hyperdynamic LV systolic function without segmental wall motion abnormalities, and an estimated visual ejection fraction of 80% (Figure 1). The patient was seen by trauma surgery, who took her to the operating room for debridement of her burn wounds on her chest wall. Within an hour after surgery, while in the recovery suite, the patient developed severe nausea and hypotension to 64/56 mm Hg, which resolved to 130/60 mm Hg without intervention. The patient denied chest pain, but reported she felt extremely overwhelmed and stressed with all that had happened over the past 24 hours since admission. ECG postoperatively showed new anterior ST elevations with high sensitivity troponin 1,065 ng/L, compared to 9 ng/L preoperatively. Bedside point-of-care TTE showed new apical and anterolateral hypokinesis to akinesis. Due to new ST elevations on ECG with elevated troponins and new bedside TTE findings, the patient underwent urgent left heart catherization with concern for acute coronary syndrome post-debridement. The patient’s left heart catheterization showed no obstructive coronary artery disease. A formal bedside TTE showed moderately decreased LV systolic function with apical akinesis and ballooning of the LV apex with an estimated visual ejection fraction of 35%. (Figure 2). The patient was diagnosed with Takotsubo stress-induced cardiomyopathy, apical-type variant. With postoperative ST elevation on ECG, elevated troponin, and echocardiographic wall motion abnormalities that were out of proportion to the degree of coronary artery disease on left heart catheterization, acute coronary syndrome was ruled out, and Takotsubo cardiomy-opathy, a diagnosis of exclusion, was concluded. The Takotsubo cardiomyopathy was likely from a combination of the overwhelming emotional stress from the hot coffee-induced burns requiring hospitalization and the physical stress of the surgical debridement in the operating room. The patient’s initial syncopal event was likely vasovagal in the setting of recent upper respiratory infection and poor oral intake with prodromal symptoms of warmth and flushing. 28The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 29 DISCUSSIONTakotsubo stress-induced cardiomyopathy can have a dramatic presentation, often mimicking an acute coronary syndrome, and is usually triggered by intense emotional and or physical stress. Takotsubo cardiomyopathy was first described in Japan in the 1990s with the classical apical ballooning of the left ventricle.4 The shape of the LV gives the appearance of a Japanese octopus trap, which in Japanese translates to ‘Takotsubo’. The workup often includes EKG, cardiac biomarkers, TTE, and potentially a left heart catheterization. In the absence of obstructive coronary artery disease in a patient presenting with classic LV apical ballooning on TTE, with other causes excluded, a diagnosis of Takotsubo cardiomyopathy may be reached. Takotsubo cardiomyopathy can occur rapidly after the stressor or, in some cases, can occur up to a few days after a stressor. Both physical and emotional stress can play a significant role in Takotsubo cardiomyopathy, as Figure 1: A. TTE 4 chamber view in diastole on arrival to hospital with normal LV chamber size (traced in red). B. TTE 4 chamber view in systole with hyperdynamic LV systolic function without segmental wall motion abnormalities, visually estimated ejection fraction of 80%. Figure 2: TTE post-debridement after left heart catheterization showed no obstructive CAD. A. TTE 4 chamber view in diastole (LV traced in red). B. TTE 4 chamber view in systole showing moderately decreased LV systolic function, with mid to distal LV akinesis and ballooning of the LV apex (LV traced in red). Visually estimated ejection fraction of 35%. Right-hand corner with illustration of the Japanese “takotsubo” octopus trap, from which this LV appearance takes its name. 29et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202530 | The Medicine Forum, Volume 26 seen in this patient. There are four main known types of Takotsubo cardiomyopathy based on the location of the wall motion abnormalities seen on TTE.5 The most common and seen in this patient is the apical variant, which accounts for approximately 80% of cases. Other variants include wall motion abnormalities in the midven-tricular region, basal region, or other focal regions. The pathophysiology of Takotsubo cardiomyopathy is believed to be precipitated by a catecholamine surge, often triggered by a stressful event.3-5 An emotional or physically stressful event causes an upregulation of the hypothalamic-pituitary-adrenal axis, which releases catecholamines such as adrenaline and noradrenaline into the bloodstream. This surge in catecholamines can result in LV dysfunction, but the exact mechanism remains unclear. Some hypothesize that due to unequal distribution of beta-1 and beta-2 receptors between the apex and base of the LV, this contributes to the apical ballooning phenomenon. Others theorize that the catecholamine surge can lead to coronary vasospasm and increased microvascular dysfunction leading to stress on the heart, which can cause elevated troponin and ECG changes in addition to the classical apical ballooning. Further research is warranted to better understand the exact pathophysiology of Takotsubo stress-induced cardiomyopathy. Management of Takotsubo cardiomyopathy is often supportive, as there are currently no robust randomized clinical trials available to guide management. In the acute setting, management is focused on excluding acute coronary syndrome along with supportive care and treating possible complications that arise. These can include cardiogenic shock due to acute reduction in cardiac output, causing hypotension in approximately 10% of patients, ventricular arrhythmias in approximately 10% of patients, and acute or subacute thromboem-bolism in approximately 14% of patients.5-6 Long-term management is also based on symptomatology, as a majority of patients improve over time. Durowju et al. found that 83% of patients diagnosed with Takotsubo cardiomyopathy experienced normalization of ejection fraction with a median follow-up of 14 days. This study and others like it underscore the generally favorable long-term prognosis of Takotsubo stress-induced cardiomyopathy. CONCLUSION Takotsubo stress- induced cardiomyopathy is a well-documented phenomenon triggered by emotional and or physical stress. Its presentation often mimics acute coronary syndrome with clinical findings including chest pain or pressure, shortness of breath, hypotension, and abnormal electrocardiogram, troponin, and echocar-diography findings, so appropriate workup to exclude acute coronary syndrome is often warranted. This case demonstrates the classical apical variant Takotsubo stress-induced cardiomyopathy, which presented very similarly to an acute coronary syndrome, that was triggered by combined emotional and physical stress after the patient spilled hot coffee on her chest, inducing second- and third-degree burns requiring operating room debridement. REFERENCES1. Alcaraz-Mor R, Gasche E, Villa A, Lehucher-Michel MP. Takotsubo syndrome in a teen health centre. Occup Med (Lond). 2019;69(2):146-148.2. Durowoju R, Li S, Huang GS. Outcomes in Takotsubo syndrome following left ventricular ejection fraction improvement. Am J Cardiol. 2022;169:136-142.3. Ghadri JR, Wittstein IS, Prasad A, et al. International expert consensus document on Takotsubo syndrome (Part I): clinical characteristics, diagnostic criteria, and pathophysiology. Eur Heart J. 2018;39(22):2032-2046.4. Sato H, Tateishi H, Uchida T. Tako-tsubo-like left ventricular dysfunction due to multivessel coronary spasm. In: Kodama K, Haze K, Hon M, eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure. Tokyo, Japan: Kagakuhyouronsha; 1990:56-64.5. Shadmand M, Lautze J, Md AM. Takotsubo pathophysiology and complications: what we know and what we do not know. Heart Fail Rev. 2024;29:497-510.6. Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med. 2015;373(10):929-938.30The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 31 Mitral Annular Disjunction as a Cause of Cardiac Arrest in Young Patient: A Case ReportSheraz Qamar, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONMitral annular disjunction is a structural abnormality where there is a separation of the mitral valve annulus and left atrial wall. We present a case of cardiac arrest in a young patient with known mitral valve prolapse that was now found to have mitral annular disjunction due to myxomatous mitral valve disease. This case highlights the importance of finding the etiology of cardiac arrest, which in this case, is myxomatous mitral valve disease causing mitral annular disjunction. It also highlights the importance of secondary prevention of sudden cardiac death with defibrillator placement in these patients. CASE DESCRIPTIONA 43-year-old female with a past medical history of mitral valve prolapse, hypothyroidism, anxiety, migraines, and a high burden of premature ventricular complexes (PVCs) presented after witnessed cardiac arrest with immediate cardiopulmonary resuscitation performed via bystander. She suddenly collapsed and was found to be without a pulse while out with her husband and child for the Philadelphia Eagles parade. When emergency medical services arrived, they reported that she was in ventricular fibrillation and received three defibillations, epinephrine, and lidocaine. The morning of the cardiac arrest, the patient reported having a headache and took her as needed rizatriptan 10 mg. Per the patient’s husband, she has been on a stable dose of levothyroxine for some time and took rizatriptan for migraines as needed. She occasionally consumes cannabis gummies but has no significant alcohol or smoking history. Family history is significant for myocardial infarction in mother and hypertension in father. Upon presentation, the patient’s vital signs were notable for tachycardia to 104 beats per minute and hypoxia on non-rebreather which stabilized on non-invasive positive pressure ventilation (NIPPV). On physical examination, the patient was alert, anxious-appearing and restless. Jugular venous pressure was difficult to observe with NIPPV. On cardiac exam, heart sounds were normal with a regular rhythm. Lung exam notable for coarse rales anteriorly. Her abdomen was soft and non-distended. Extremities had no edema and she had warm extremities with normal pulses. Labs were notable for a high anion gap metabolic acidosis with pH of 7.14, pCO2 of 52 mmHg and bicarbonate 10 mEq/L. Lactate was elevated to 6.1 mmol/L, high sensitivity troponin T peaked at 111 ng/L, proBNP 450 pg/mL, creatinine 1.1 mg/dL with baseline of 0.8 mg/dL and WBC 21.1 cells/μL. Electrocardiogram (ECG) showed sinus rhythm with PVCs and slightly prolonged QT interval. The patient underwent computed tomography angiography (CTA) chest which was negative for pulmonary thrombo-embolism but did show multifocal pneumonia. Figure 1. A. Parasternal long axis view on TTE showing mitral annular disjunction of 11 mm. B. Pickelhaube sign seen in myxomatous mitral valve disease and bileaflet mitral valve prolapse depicting high velocity mid-systolic spike on doppler imaging of the lateral mitral annulusCARDIOLOGY31et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202532 | The Medicine Forum, Volume 26 As an outpatient, the patient had a transthoracic echocar-diogram (TTE) recently which showed an ejection fraction (EF) of 60-65%, normal left ventricle (LV) systolic and diastolic function, mild mitral valve prolapse of both leaflets and mild mitral regurgitation. She also had continuous cardiac monitoring around the same time which showed a 12% burden of PVCs. TTE in the hospital showed a mildly dilated left atrium, moderate bileaflet mitral valve prolapse with 11 millimeter mitral annular disjunction (Figure 1a). It also showed mitral leaflet thickening and redundancy consistent with myxomatous mitral valve disease. It also showed mild to moderate late systolic mitral regurgitation. Otherwise, systolic and diastolic function of the left ventricle was normal. DISCUSSIONIn cases of mitral valve prolapse, it is important to assess if there is underlying mitral annular disjunction, as the two are frequently associated and can present with symptoms of syncope, palpitations, or even ventricular arrhythmias, as seen in this case.1 Mitral annular disjunction is also associated with non-sustained ventricular tachycardia (NSVT) and PVCs. It has been found that mitral annular disjunction of greater than 8.5 mm was associated with NSVT, which is also another finding in this case presentation.1 Ventricular arrhythmias occur due to the fibrosis and inflammation of the mitral apparatus, which can be seen on cardiac magnetic resonance imaging (MRI). This fibrosis develops due to the mechanical stress exerted by the excessively mobile left ventricular segments as a result of the mitral annular disjunction. This results in Pickelhaube sign, as seen in Figure 1B, which is a high velocity mid-systolic spike at the lateral mitral annulus on tissue doppler. An especially important consideration to detect mitral annular disjunction in cases of mitral valve prolapse is when planning for mitral valve repair surgeries. Surgery is recommended for mitral annular disjunction with severe mitral regurgitation. It is important to assess the annular disjunction so that it can be addressed during surgery in order to limit the mechanical stress on the left ventricular wall which causes fibrosis. We know that myocardial scarring and fibrosis is a known cause for ventricular fibrillation, and patients with longer mitral annular disjunction are at higher risk of developing more fibrosis.2It is also important to address the possible genetic component of mitral valve prolapse.3 Mitral valve prolapse is thought to include syndromic forms, such as in Marfan syndrome and non-syndromic forms, such as myxomatous valve disease. Further research into the pathophysiology and development of mitral annular disjunction is needed to understand what can be done to diagnose it at an earlier age and prevent sudden cardiac death in these patients. CONCLUSIONMitral valve prolapse is associated with mitral annular disjunction, which is a structural abnormality where there is a separation of the mitral valve annulus and left atrial wall. This structural abnormality causes mechanical stress on the left ventricular wall, leading to scarring and fibrosis. As a result, ventricular arrhythmias can occur, including sudden cardiac death with ventricular fibrillation. This case presentation highlights the importance of identifying mitral annular disjunction on imaging. It also highlights the different objective findings such as PVCs, NSVT and intermittent palpitations that can be observed in cases of mitral annular disjunction. Having a clinical suspicion in the right clinical context can help prevent sudden cardiac death and make sure patients have adequate secondary prevention for ventricular arrhythmias if needed through an implantable cardioverter-defibrillator (ICD). REFERENCES1. Zhu L, Yeow Leng Chua. Mitral Annular Disjunction: Clinical Implications and Surgical Considerations. Cardiology research. 2023;14(6):421-428. doi:https://doi.org/10.14740/cr15842. Bennett S, Thamman R, Griffiths T, et al. Mitral annular disjunction: A systematic review of the literature. Echocardiography. 2019;36(8):1549-1558. doi:https://doi.org/10.1111/echo.144373. Carmo P, Andrade MJ, Aguiar C, Rodrigues R, Gouveia R, Silva JA. Mitral annular disjunction in myxomatous mitral valve disease: a relevant abnormality recognizable by transthoracic echocardiography. Cardiovascular Ultrasound. 2010;8(1). doi:https://doi.org/10.1186/1476-7120-8-5332The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 33 Power Outage: Acute Subtotal Occlusion of the Left Circumflex Artery with Minimal ECG ChangesDaniel D. Moylan, MD1* and Brady L. Houtz, MD1*1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA * These authors contributed equally to this workINTRODUCTIONAcute coronary syndrome (ACS) represents one of the most recognizable causes of death in the United States. Despite significant advances in cardiovascular preventative health, an American will have a myocardial infarction approximately every 40 seconds.1 Fortunately, rapid diagnosis and treatment of ACS have allowed for significant reductions in both morbidity and mortality of myocardial infarctions.2 Thus, prompt identification of ACS is crucial, and nonetheless, it can still present a noteworthy challenge to physicians. In this case, we present a near-electrically silent acute thrombotic coronary subtotal occlusion. It constitutes a stark reminder that diagnosis of an acute myocardial infarction extends beyond the electrocardiogram (ECG). CASE DESCRIPTIONA 77-year-old female with a past medical history of hypertension, hyperlipidemia, type 2 diabetes mellitus, a ten-pack-year smoking history, and a remote history of paroxysmal atrioventricular block status-post pacemaker presented to the emergency department with an acute onset of substernal chest pain. On the day of presentation, the patient was in her usual state of health when she suddenly experienced sharp substernal chest pressure associated with lighthead-edness, dizziness, and diaphoresis while preparing a meal. The patient attempted to rest without improvement and subsequently noticed significant dyspnea with exertion. Therefore, she called emergency medical services and was brought to a large tertiary medical center for further care. En route, she received aspirin. Upon arrival at the hospital, the patient was hemody-namically stable. Vital signs included a heart rate of 75 beats per minute, a blood pressure of 134/75 mmHg, and 98% oxygen saturation on room air. Her physical examination was unremarkable aside from continued chest pain during examination. Initial workup was significant for a high sensitivity troponin T of 26 ng/L, D-dimer within normal limits, and a normal chest x-ray. Additional testing was unremarkable. Treatment in the emergency department was initiated with sublingual nitroglycerin as needed for chest pain. Initial ECG on admission was reassuring due to overall similarity to baseline and a lack of significant ST segment changes, although mild ST depressions were noted in leads I and aVL (Figure 1).Point of care ultrasound (POCUS) revealed a normal appearing ejection fraction and no wall motion abnormalities. Repeat troponin demonstrated a mild increase to 35 ng/L. The patient was subsequently admitted to cardiology for further management of non-ST elevation myocardial infarction (NSTEMI). She was started on a heparin continuous infusion as well as metoprolol tartrate 12.5 mg twice daily, atorvastatin 80 mg daily, and continued aspirin 81 mg daily, with initial improvement in symptoms.CARDIOLOGYFigure 1: ECG demonstrating sinus rhythm with first-degree AV block and ST depressions in leads I and aVLFigure 2: Repeat ECG demonstrating sinus rhythm with first-degree AV block and left axis deviation33et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202534 | The Medicine Forum, Volume 26 Overnight, concern arose as the patient’s troponin continued to incrementally increase to 221, 610, and 1,178 ng/L. Although the patient’s chest pain had improved since arrival, and she appeared comfortable, a dull left-sided chest pain persisted. ECG revealed resolution of ST depressions and no concerning ST segment abnormalities (Figure 2). Repeat POCUS again demonstrated a normal appearing ejection fraction without wall motion abnormalities. Intravenous nitroglycerin was added with near resolution of chest pain. Despite continued improvement in symptoms and hemodynamic stability, the patient’s troponins increased to a peak of 3,683 ng/dL. Therefore, the decision was made to expedite left heart catheterization.Left heart catheterization was significant for an acute thrombotic 99% occlusion of the proximal left circumflex artery (LCx). The proximal portion of the lesion was aneurysmal. Additionally, there was mild to moderate diffuse atherosclerosis throughout the left anterior descending and right coronary arteries, with a right-dominant posterior descending artery. Following identifi-cation, there was successful placement of a drug-eluting stent with excellent angiographic results as Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow was restored (Figure 3).The patient’s chest pain resolved nearly immediately following her catheterization. On the morning of the second day following admission, the patient was noted to feel excellent with no recurrence of her symptoms. Formal transthoracic echocardiogram demonstrated low-to-normal ejection fraction with anterolateral and inferior wall motion abnormalities consistent with LCx infarction. The patient was discharged on daily aspirin 81 mg, twice daily ticagrelor 90 mg, twice day metoprolol tartrate 25 mg, daily lisinopril 5 mg, and daily atorvastatin 80 mg. One week later, at a follow-up visit, she reported recovering well with no chest pain or complications from her medications.DISCUSSIONThe traditional model for acute myocardial infarction dictates that acute total coronary occlusions cause transmural infarctions, resulting in ST-segment elevation on ECG. In clinical practice, this paradigm is not always accurate. Recent large meta-analyses have demonstrated that up to 30% of patients diagnosed with NSTEMI were found to have a total occluded coronary artery.3 The lack of significant ST changes in this patient population can lead to delayed interventions compared to patients diagnosed with STEMI. Furthermore, these patients were demonstrated to have poorer outcomes than patients without total occlusion, including increased major cardiac adverse events and all-cause mortality.4 Therefore, management of patients with acute severe occlusions without significant ST-segment changes is not only challenging, but also crucial to patient outcomes. The left circumflex artery is especially obfuscating as it has been identified as the most likely culprit artery for acute occlusions without ST-segment elevations.5 Additionally, percutaneous coronary intervention within Figure 3: Coronary angiography demonstrating acute 99% proximal LCx occlusion before (left) and after (right) deployment of a drug-eluting stent with restoration of flow.34The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 35 24 hours has been demonstrated to be significantly less likely for LCx occlusions as opposed to other territories.6 It is not yet clear why LCx lesions more frequently present without significant electrophysiologic changes relative to other territories. Geffin et al. propose one intriguing explanation in a retrospective review that identified proximal LCx lesions to be particularly less likely to produce ECG changes – the expected ST elevations in leads I and aVL may be cancelled out by reciprocal forces in the limb leads.7In this case, an acute 99% occlusion of the proximal LCx presented a significant dilemma that highlights the diagnostic challenges described. Although the patient presented with symptoms consistent with acute coronary syndrome, further evaluation was falsely reassuring. Notably, initial ECG demonstrated only mild ST segment depressions in leads I and aVL that resolved with repeat ECG even as troponin levels rose. Furthermore, symptoms improved, and the point-of-care ultrasound was reassuring. Although delays in troponin elevation and wall motion abnormalities can be observed with acute infarction, the patient’s lack of significant ECG changes made an acute subtotal occlusion unexpected. Fortunately, strong clinical intuition allowed this patient to receive intervention within 24 hours and recover well. What else could be done to prevent this and similar presentations from being overlooked?Retrospectively, a posterior ECG could have led to an expedited diagnosis in this case. At the time of presentation, the lack of anterior ST changes and rapid normalization of ECG in addition to the clinical stability and improvement, did not raise suspicion for an occult myocardial infarction. Nonetheless, it is possible that the mild ST depressions in leads I and aVL may have represented reciprocal changes to a subtle posterior myocardial infarction that may have been revealed with immediate posterior ECG. For high-risk patients, early assessment with additional posterior and right-sided leads (18-lead ECG) should be strongly considered. Various methods have been proposed to improve diagnostic accuracy for ECG leads. As noted, an 18-lead ECG can be considered in patients with a high clinical suspicion for acute infarction despite minimal ECG changes. Body surface potential maps, which include 80 ECG leads, have been shown to significantly improve sensitivity relative to a traditional ECG.8 Other case reports have also highlighted LCx incidentally detected on CT, thus providing a reminder for the astute diagnostician to use all the tools at their disposal.9 In the future, continued technological development and improved techniques may allow for more diagnosis and rapid management of acute coronary occlusions without significant electro-graphic changes. For now, as in the case of this patient, astute clinical judgment must continue to be emphasized when a case does not fit the traditional picture. CONCLUSIONAcute occlusion of the coronary artery without electro-graphic changes represents a significant challenge to timely diagnosis and management that is likely underrec-ognized and undertreated. A significant portion of patients with NSTEMI have a total occluded coronary artery, and these patients have worse cardiovascular outcomes, including mortality. Although additional diagnostic techniques have been proposed, current methods are still limited. It is imperative to maintain a strong clinical acumen and expedite intervention for patients even when they do not demonstrate traditionally recognized ischemic patterns on ECG. REFERENCES1. Martin SS, Aday AW, Almarzooq ZI, et al. 2024 heart disease and stroke statistics: a report of US and global data from the American Heart Association. Circulation. 2024;149(8):e347–e913. doi:10.1161/CIR.0000000000001209 Erratum in: Circulation. 2024;149(19):e1164. doi:10.1161/CIR.00000000000012472. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025;151(13):e771–e862. doi:10.1161/CIR.0000000000001309 Erratum in: Circulation. 2025;151(13):e865. doi:10.1161/CIR.00000000000013283. Tziakas D, Chalikias G, Al-Lamee R, Kaski JC. Total coronary occlusion in non-ST elevation myocardial infarction: time to change our practice? Int J Cardiol. 2021;329:1–8. doi:10.1016/j.ijcard.2020.12.0824. Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082–3089. doi:10.1093/eurheartj/ehx4185. Hung CS, Chen YH, Huang CC, et al. Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded "culprit" artery: a systemic review and meta-analysis. Crit Care. 2018;22(1):34. doi:10.1186/s13054-018-1944-x6. From AM, Best PJ, Lennon RJ, Rihal CS, Prasad A. Acute myocardial infarction due to left circumflex artery occlusion and significance of ST-segment elevation. Am J Cardiol. 2010;106(8):1081–1085. doi:10.1016/j.amjcard.2010.06.0167. Geffin R, Triska J, Najjar S, Berman J, Cruse M, Birnbaum Y. Why do we keep missing left circumflex artery myocardial infarctions? J Electrocardiol. 2024;83:4–11. doi:10.1016/j.jelectrocard.2023.12.0118. Daly MJ, Scott PJ, Harbinson MT, Adgey JA. Improving the diagnosis of culprit left circumflex occlusion with acute myocardial infarction in patients with a nondiagnostic 12-lead ECG at presentation: a retrospective cohort study. J Am Heart Assoc. 2019;8(5):e011029. doi:10.1161/JAHA.118.0110299. Mahabir S, Samra G, Bucklew E, et al. An electrically silent STEMI diagnosed on cardiac CT. J Am Coll Cardiol. 2023;81(8 Suppl):3619. doi:10.1016/S0735-1097(23)04063-935et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202536 | The Medicine Forum, Volume 26 Protamine Sulfate-Induced Coronary Vasospasm Resulting in Takotsubo Cardiomyopathy Matthew J. Bierowski, MD1, Andre Cunningham, DO1, Jordan Feingold-Link, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PACARDIOLOGYINTRODUCTIONTakotsubo syndrome (TTS), also known as stress-induced cardiomyopathy, is characterized by new left ventricular (LV) dysfunction out of proportion to any known coronary artery disease that usually follows an emotional or physical stress. The disease process mimics acute coronary syndrome (ACS), with acute chest pain, moderate elevations in serum troponins, and electrocardiographic changes. While spontaneous return to normal left ventricular function is typical, the morbidity and mortality of TTS is significant, with increased risk for major adverse cardiac events and disease recurrence.1The understanding of the pathogenesis of TTS is incomplete, although recent work has identified that several processes likely occur to produce the characteristic findings. During periods of acute stress, excessive catecholamine release can cause intense vasoconstriction of coronary microcirculation, impairing myocardial perfusion despite open epicardial coronary arteries. Microvascular dysfunction leads to regional myocardial ischemia and stunning, particularly in the apical segments of the heart.2 Additionally, coronary vasospasm can further reduce blood flow and contribute to myocardial injury, and its role in the development of TTS is an area of investigation.2-3Protamine sulfate is a commonly used agent to reverse anticoagulation with heparin during and following cardiac surgery. While numerous adverse reactions to protamine exist in the literature, a systematic review examining drugs associated with TTS did not identify protamine sulfate as a possible trigger.4 However, one case report detailed a woman who developed TTS following a severe protamine sulfate reaction requiring extracorporeal membrane oxygenation (ECMO) therapy.5 To our knowledge, no case reports have definitively shown coronary vasospasm to be the driving mechanism for TTS cardiomyopathy secondary to protamine sulfate administration.We herein present the case of a 78-year-old female who developed stress-induced cardiomyopathy secondary to coronary vasospasm in the setting of an adverse reaction to protamine after completion of mitral valve replacement surgery. The characteristic findings of TTS were observed on intraoperative transesophageal echocardiography (TEE), and left heart catheterization (LHC) immediately post-op demonstrated active coronary vasospasm. The patient would require rescue with ECMO before eventually regaining full myocardial function. CASE PRESENTATIONA 78-year-old female with long-standing mitral annulus and leaflet calcification along with mild prolapse presented for mitral valve replacement for severe mitral regurgitation. Other medical history included hyperlip-idemia and migraines. Known allergies included paper adhesive tape and oxycodone-acetaminophen, neither of which had been associated with anaphylactic reactions. Notably, preoperative echocardiogram demonstrated normal LV function without segmental wall motion abnormalities and an estimated ejection fraction (EF) of 70%, as well as normal right ventricular function. Preoperative LHC revealed non-obstructive coronary artery disease with left anterior descending (LAD) artery stenosis at 40%. The patient underwent an uncomplicated mitral valve replacement with a bioprosthetic valve while on cardio-pulmonary bypass (CPB), followed by successful closure of the atriotomy and left atrial appendage without complications. Cross-clamp time was 124 minutes, and bypass time was 135 minutes.The patient was then weaned from CPB without difficulty. Protamine sulfate was then given to reverse the heparin. Within minutes, the patient developed severe hypotension to 66/46 mmHg, with notable severe global LV dysfunction seen on intraoperative TEE (EF 5-10%). She was given epinephrine (0.04 mcg/kg/min), milrinone (0.125 mcg/kg/min), norepinephrine (0.02 mcg/kg/min), and phenylephrine (400 mcg total). Given hemodynamic instability, the patient was placed back on CPB. After achieving hemodynamic stability for 30 minutes, another attempt was made to wean off CPB, while being supported on milrinone (0.125 mcg/kg/min) and epinephrine (0.04 mcg/kg/min). She was given methyl-prednisolone 125 mg, diphenhydramine 50 mg, and famotidine 20 mg prophylactically. Heparin reversal was again attempted, this time with a small amount of protamine injected directly into the aorta. Again, a severe reaction was seen within minutes in which the patient became profusely hypotensive to 53/33 mmHg and was started on vasopressin (0.04 units/min). She was also noted to be in atrial fibrillation with rapid ventricular response for which amiodarone was given (122 mg total load). At this point, given continued hemodynamic instability (cardiac index noted to be 1.67), she was placed on ECMO using the existing cannulae. Protamine was 36The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 37 reversed with blood products and factors. Intraoperative TEE demonstrated severely reduced LV function with akinesis of the distal two-thirds of the ventricle and relative preservation of wall motion at the anterior and inferior base (Figure 1). Due to concern for ACS, the chest incision was left open, and the patient was urgently transported to the catheter-ization lab. Emergent LHC revealed no evidence of coronary artery occlusion, but severe left coronary arterial vasospasms were observed and intracoronary nitroglycerin and nicardipine were administered (Figure 2 A/B).The patient was transferred to the cardiac intensive care unit on ECMO with epinephrine, phenylephrine, and vasopressin support. On post-op day (POD) 0, she was switched to milrinone and epinephrine to maintain pulsatility with norepinephrine for mean arterial pressure (MAP) goals > 65. Repeat TEE demonstrated biventricular failure with LV function unchanged from intraoperative TEE. Over the next few days, ECMO flow rates were weaned successfully (able to maintain a cardiac index (CI) of > 2.2 on inotropic support alone). Repeat TTE on POD 3 demonstrated substantially improved LV function with EF 45% and improved right ventricular function. On POD 4, she returned to the operating room (OR) for chest washout, closure, and decannulation. She was successfully decannulated. Intraoperative TEE at the time of decannulation demonstrated near complete recovery of her LV function, with EF now at 65%, and a well-functioning mitral valve prosthesis. After successful weaning off intravenous inotropes, she was eventually discharged to a long-term care facility. Figure 1. Intraoperative TEE demonstrating severely reduced LV function with global akinesis of the distal two-thirds of the ventricle and relative preservation of wall motion at the anterior and inferior base. Figure 2A (left). Coronary angiography demonstrating diminutive appearance of the branches of the left coronary artery, likely due to severe vasospasm. Figure 2B (right). Coronary angiography demonstrating improvement in caliber following administration of intracoronary nicardipine and nitroglycerin, consistent with coronary vasospasm. Figure 1: Intraoperativ TEE demonstrating severely reduced LV fu ction with global akinesis of the distal two-thirds of the ventricle and relative preservation of wall motion at the anterior and inferior base.Figure 2A: Coronary angiography demonstrating diminutive appearance of the branches of the left coronary artery, likely due to severe vasospasm.Figure 2B: Coronary angiography demonstrating improvement in caliber following administration of intracoronary nicardipine nd nitroglycerin, consistent with coronary vasospasm. 37et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202538 | The Medicine Forum, Volume 26 DISCUSSION The hemodynamic collapse observed during protamine administration was likely perpetuated by severe coronary vasospasm leading to a stunned myocardium. The intraop-erative TEE findings of LV distal akinesis with relative preservation of the basal segments of the myocardium, absence of significant coronary disease, and complete ventricular recovery in only a few days are suggestive of Takotsubo cardiomyopathy. Given that a near identical reaction occurred on two separate occasions immediately following heparin reversal, it can be postulated that the patient had a severe reaction to protamine sulfate.Adverse reactions to protamine sulfate have been well documented in the literature, with such cases including: Abrupt pulmonary hypertension leading to RV failure,6 takotsubo cardiomyopathies,4, and anaphylaxis leading to circulatory shock.7Although it is believed that the initial pathophysiologic insult leading to stress cardiomyopathies is usually triggered by a catecholamine surge, for our patient that was unlikely the case. Rather, protamine was the likely trigger that initiated the degenerative cascade, as it preceded the severe coronary spasm that led to LV failure. Efforts by the surgical team to then support the patient’s hemodynamics with both inotropes and catecholamines may have further decreased cardiac function as well.While the exact mechanism leading to coronary vasospasm is unclear, it may have been a type 1 Kounis reaction. This array of syndromes postulates that an allergenic pathway, triggered by an external precipitant, can lead to acute coronary syndrome-like presentations.8 Specifically, in type I, the vasospastic endothelial dysfunction is thought to be due to mast cell degranulation. Unfortunately, these syndromes are very hard to diagnose and are almost universally first treated as an anaphylactic reaction, as was the case for our patient. However, given the severe myocardial dysfunction and oxygen demand mismatch associated with coronary spasm, administration of beta-adrenergics likely further augmented the deleterious process. In such cases, fluids, afterload reduction, antihistamines, and corticosteroids are preferred treatments.9 Ultimately, if weaning off CPB becomes too dangerous, prompt initiation of ECMO is critical, as was the case for our patient.TTS carries a significant mortality burden with both 30-day and 24-month mortality risk comparable to ACS.1 Major complications that can occur include ventricular arrhythmia and cardiogenic shock.1 Patients are generally treated with supportive therapies such as antiarrhythmics, inotropes, and diuretics in the acute phase, with later addition of guideline-directed medical therapy (GDMT) in hopes of regaining myocardial function. In extreme cases, mechanical circulatory support (MCS) may be required. Interestingly, the use of ECMO as a bridge for stress cardiomyopathy recovery has been increasing, with one study estimating a nearly 95% survival rate.10 In our case, the patient was able to have LV functional recovery only four days post-op, illustrating the importance of prompt initiation of MCS. Although challenging, if Kounis syndrome is considered to be a cause of hemodynamic collapse, prompt initiation of ECMO, rather than the use of inotropes and catechol-amines, may contribute to faster myocardial recovery. Additional studies are needed to validate this hypothesis. In conclusion, the above case discusses a rare cause of stress-induced cardiomyopathy precipitated by severe coronary vasospasm from protamine sulfate. Prompt recognition by the surgical team that the patient was likely experiencing an adverse medication reaction led to the administration of steroids and antihistamines. Additional hemodynamic support with vasopressors and inotropes may have caused further cardiac insult. In such cases, prompt initiation of ECMO may be a better treatment option to facilitate quick myocardial recovery and stabilize hemodynamics.REFERENCES1. Redfors B, Vedad R, Angerås O, et al. Mortality in takotsubo syndrome is similar to mortality in myocardial infarction: a report from the SWEDEHEART1 registry. Int J Cardiol. 2015;185:282–289.2. Patel SM, Lerman A, Lennon RJ, Prasad A. Impaired coronary microvascular reactivity in women with apical ballooning syndrome (Takotsubo/stress cardiomyopathy). Eur Heart J Acute Cardiovasc Care. 2013;2(2):147–152. doi:10.1177/20488726134758913. Patel VI, Sobnosky S. Multivessel coronary artery vasospasm-induced Takotsubo cardiomyopathy. Case Rep Cardiol. 2022;2022:2192863. doi:10.1155/2022/21928634. Kido K, Guglin M. Drug-induced Takotsubo cardiomyopathy. J Cardiovasc Pharmacol Ther. 2017;22(6):552–563. doi:10.1177/10742484177086185. Li S, Koerner MM, El-Banayosy A, Soleimani B, Pae WE, Leuenberger UA. Takotsubo’s syndrome after mitral valve repair and rescue with extracor-poreal membrane oxygenation. Ann Thorac Surg. 2014;97(5):1777–1778. doi:10.1016/j.athoracsur.2013.08.0326. Protamine sulfate: Protamine reaction in the form of pulmonary hypertension and cardiovascular collapse: case report. Reactions Weekly. 2022;1887(1):594.7. Levy JH, Adkinson NF. Anaphylaxis during cardiac surgery: implications for clinicians. Anesth Analg. 2008;106(2):392–403. doi:10.1213/ane.0b013e3181602e0d8. Kounis NG. Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clin Chem Lab Med. 2016;54(10):1545–1559. doi:10.1515/cclm-2016-00109. Cevik C, Nugent K, Shome GP, Kounis NG. Treatment of Kounis syndrome. Int J Cardiol. 2010;143(3):223–226. doi:10.1016/j.ijcard.2010.02.04010. Mariani S, Richter J, Pappalardo F, et al. Mechanical circulatory support for Takotsubo syndrome: a systematic review and meta-analysis. Int J Cardiol. 2020;316:31–39. doi:10.1016/j.ijcard.2020.05.03338The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 39 A Shock to the Heart? A Case of Phantom Shocks in a Patient with Brugada SyndromeVirginia Gonzalez, MD1, Rebecca Goldfinger-Chanin, MD1, Behzad B. Pavri, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONBrugada syndrome is an inherited condition characterized by an increased risk of sudden cardiac death (SCD) secondary to lethal ventricular arrhythmias occurring most often in the fourth decade of life. Implantable cardioverter-defibrillators (ICDs) are recommended in patients who have documented ventricular tachycardia (VT) or ventricular fibrillation (VF) and in patients presenting with a spontaneous type 1 Brugada pattern on electrocar-diogram (ECG) and a history of arrhythmic-sounding syncope.1 However, patients with ICDs are at risk of developing “phantom shocks” which occur when a patient reports the sensation of receiving a shock that is not confirmed upon subsequent device interrogation.2 One retrospective study of 38 patients demonstrated that patients who reported phantom shocks had a higher prevalence of documented depression, anxiety and substance use and that patients who had previous ICD shocks for “arrhythmia storm” were more likely to experience phantom shocks.3 Prior studies have described the increased incidence of anxiety and decreased quality of life in patients diagnosed with Brugada syndrome alone with some patients developing post-traumatic stress disorder (PTSD).4 We present a case of a patient with previously diagnosed Brugada syndrome who suffered from phantom shocks after a defibrillation event. This case highlights the importance of recognizing phantom shocks for improving patient outcomes, to provide a multidisciplinary approach and to optimize both cardiac and psychological well-being of these patients.CASE DESCRIPTIONA 59-year-old male with a past medical history of Brugada syndrome status-post ICD implantation, hypertension, and hyperlipidemia presented to the emergency room after a perceived ICD shock. Notably, the patient had experienced an appropriate defibrillation by his ICD one month prior in response to an episode of ventricular fibrillation. Before the most recent episode of perceived shock, the patient had been resting at home when he began to feel palpitations, followed by shortness of breath and chest pressure. He denied recent fevers, nausea, vomiting, or diarrhea. He had been diagnosed with Brugada syndrome almost 20 years prior in the setting of recurrent syncopal episodes. An ECG at that time showed a type 1 Brugada pattern, and further electrophysiology testing confirmed an inducible rhythm. He had not undergone genetic testing and had no known family history of Brugada syndrome, SCD, or recurrent syncope. He had an ICD placed approximately 17 years ago, and his medications included quinidine gluconate 324 mg twice daily, hydrochlorothiazide 12.5 mg daily, and valsartan 320 mg daily. On admission, labs were notable for a potassium level of 2.8 mmol/L (normal 3.3-4.8). ECG demonstrated a type 1 Brugada pattern (Figure 1). During this hospitalization, ICD interrogation demonstrated no arrhythmias, and no shocks had been delivered. He was monitored on telemetry, which failed to demonstrate arrhythmic events correlating with symptoms that occurred prior to presentation. In the absence of true shocks, a diagnosis of phantom shocks was made. Education on the benign nature of phantom shocks was provided. Additionally, he was switched from hydrochlorothiazide to spironolactone to minimize hypokalemia, started on daily potassium supplementation, and discharged with close outpatient electrophysiology follow-up. Of note, the appropriate defibrillator shock the patient had experienced a month prior had manifested with similar symptoms. At that time, he had been resting on his couch when he began to feel lightheadedness and palpitations with subsequent loss of consciousness. He had consumed multiple alcoholic beverages prior to that event. He was awoken by his son and transported to the emergency department. Device interrogation at the time was remarkable for an episode of ventricular fibrillation. A single 35-joule shock was delivered, which converted him back to sinus rhythm.CARDIOLOGYFigure 1: Type 1 Brugada pattern on ECG characterized by coved ST-segment elevation of ≥2 mm in leads V1–V2, followed by T-wave inversion, without significant QRS widening or PR prolongation39et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202540 | The Medicine Forum, Volume 26 He did not remember feeling the shock and said that this was his first defibrillation delivered after implantation of his automatic implantable cardioverter-defibrillator (AICD) in 2008, with a generator change in 2014. During the subsequent hospitalization, he was started on quinidine gluconate. He was discharged and re-presented the following day with symptoms of chest pressure and syncope, followed by perceived ICD firing. Device interrogation at the time showed a single brief episode of supraventricular tachycardia with a maximum heart rate of 150 beats per minute without a defibrillator shock. He was subsequently discharged from the emergency department to his home. On follow-up outpatient appointment, this episode was diagnosed as a “stress reaction” secondary to undergoing defibrillator shock. It is important to highlight that this patient’s history is negative for psychiatric conditions, including anxiety or depression.DISCUSSION Brugada syndrome is a rare but potentially fatal inherited cardiac condition most often related to a loss-of-function SCN5a mutation and is associated with an increased risk of SCD due to ventricular arrhythmias. The cornerstones of management for high-risk individuals include quinidine and ICD placement. ICDs can be lifesaving, but can also result in traumatic experiences for patients who receive shocks. In Brugada syndrome, antiarrhythmic therapy, especially quinidine, can improve the quality of life of these patients by decreasing the probability of developing VT/VF and thus, the likelihood of receiving a shock and suffering from phantom shocks in the future. However, long-term quinidine therapy has its own risks (QRS widening, QT prolongation, syncope, etc.) and the medication is sometimes not tolerated.The incidence of phantom shocks varies widely across literature from 5.1% to 21% of patients with ICDs.4,5 While the exact pathophysiology remains unclear, it has been hypothesized to be similar to that of post-traumatic stress disorder with an initial traumatic insult, such as an actual ICD shock, memory consolidation, and memory retrieval in the setting of heightened somatosensory perception leading to the misinterpretation of benign symptoms as shocks.3 In this case, the patient had received an appropriate shock due to ventricular fibrillation one month prior, followed by recurrent episodes of perceived ICD shocks without corroborating evidence on device interrogation. This sequence of events supports the observation that previous shock exposure increases susceptibility to phantom shocks.The management of phantom shocks primarily involves patient education and reassurance, as there is no specific treatment. Studies have demonstrated a strong association between phantom shocks and underlying anxiety or depression, suggesting that psychological support, cognitive behavioral therapy, and, in some cases, pharmacologic intervention may be beneficial.7 In our case, the patient was reassured of the benign nature of phantom shocks and provided close electro-physiology follow-up. Additionally, his hydrochloro-thiazide was switched to spironolactone to reduce the risk of hypokalemia, an arrhythmogenic trigger in Brugada syndrome.This case underscores the importance of recognizing phantom shocks as a potential complication of ICD therapy in Brugada syndrome and emphasizes the need for a multidisciplinary approach, including electrophysiol-ogists, mental health professionals, and primary care providers, to optimize both cardiac and psychological outcomes in these patients.REFERENCES1. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: the Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Eur Heart J. 2015;36(41):2793–2867. doi:10.1093/eurheartj/ehv3162. Prudente LA, Reigle J, Bourguignon C, et al. Psychological indices and phantom shocks in patients with ICD. J Interv Card Electrophysiol. 2006;15(3):185–190. doi:10.1007/s10840-006-9010-z3. Jacob S, Panaich SS, Zalawadiya SK, et al. Phantom shocks unmasked: clinical data and proposed mechanism of memory reactivation of past traumatic shocks in patients with implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2012;34(2):205–213. doi:10.1007/s10840-011-9640-74. Sears SF, Hauf JD, Kirian K, Hazelton G, Conti JB. Posttraumatic stress and the implantable cardioverter-defibrillator patient: what the electrophysi-ologist needs to know. Circ Arrhythm Electrophysiol. 2011;4(2):242–250. doi:10.1161/CIRCEP.110.9576705. Kraaier K, Starrenburg AH, Verheggen RM, van der Palen J, Scholten MF. Incidence and predictors of phantom shocks in implantable cardioverter defibrillator recipients. Neth Heart J. 2013;21(4):191–195. doi:10.1007/s12471-012-0345-z6. Berne P, Usai F, Silva E, et al. Diagnosis of Brugada syndrome affects quality of life and psychological status. Front Cardiovasc Med. 2024;11:1429814. doi:10.3389/fcvm.2024.14298147. Galo J, Feroze R, Almas T, Morera J, Sahadevan J. Understanding phantom shocks in implantable cardioverter-defibrillator recipients. Cureus. 2024;16(1):e53161. doi:10.7759/cureus.5316140The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 41 Williams Syndrome Presenting with Pericardial Effusion and Left Ventricular Apical Aneurysm: A Case ReportZachary Pang, MD1, M. Duncan Kilpatrick, MD1, Sairamya Bodempudi, MD2, Darius Farzad, MD2, David L. Fischman, MD2, Gregary D. Marhefka, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Cardiology, Jefferson Heart Institute, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONWilliams syndrome (WS) is a genetic disorder caused by a gene deletion involving the protein elastin on chromosome 7q11.23. WS is associated with intellectual disability and characteristic facial features, including a short nose with a flat nasal bridge, medial eyebrow flare, and long philtrum.1-2 WS is also associated with cardiovascular manifestations, most commonly supravalvular aortic stenosis. Patients with WS have an estimated risk of sudden cardiac death that is 25 to 100 times greater than the healthy age-matched population.3 This case highlights the importance of keeping acute coronary syndrome on one’s differential when caring for patients with Williams syndrome, regardless of prior cardiac history.CASE DESCRIPTIONThe patient is a 49-year-old male with a past medical history of Williams syndrome, type 2 diabetes mellitus, gastroesophageal reflux disease, and diverticulosis who was sent to the hospital for a pericardial effusion. Three weeks prior to admission, the patient had experienced excruciating left arm pain that woke him up from his sleep, along with abdominal pain and nausea. The patient was evaluated by his primary care physician, who attributed his symptoms of abdominal pain and nausea to recurrent diverticulitis, for which the patient received a course of oral antibiotics. Despite completion of antibiotic therapy, his symptoms progressed, and he developed throat pain that radiated to his back. The patient underwent a CT scan of his abdomen due to his unrelenting symptomatology. He was found to have a pericardial effusion, for which he was sent to the hospital for further evaluation. On arrival to the hospital, the patient’s vital signs were stable. On physical exam, the patient was not in acute distress, cardiovascular exam revealed tachycardia with distant heart sounds, lungs were clear to auscultation bilaterally, and bilateral lower extremities were warm and well perfused with trace edema. Laboratory results showed a comprehensive metabolic panel and complete blood count grossly within normal limits. Initial high sensitivity troponin-t was 248 ng/L (normal <19 ng/L) with subsequent troponin of 211 ng/L. Electrocardiogram (ECG) showed sinus tachycardia, left anterior fascicular block, and deep Q waves in V1-V4 with < 2 mm ST elevation in V2-V4 with no prior ECG for comparison (Figure 1). A transthoracic echocardiogram (TTE) showed an ejection fraction of 20% with akinesis of the apical, anterior, anteroseptal, inferior, and inferoseptal walls with layering of a mural thrombus within the left ventricle (LV), and a moderate pericardial effusion with early right ventricular diastolic inversion concerning for cardiac tamponade. TTE also showed concern for an LV apical pseudoaneurysm with Doppler color flow through the possible LV pseudoa-neurysm (Figure 2). In addition, TTE was performed with DEFINITY® contrast, but it did not show a frank flow of contrast from the LV into the possible pseudoaneurysm.A multidisciplinary shock team, including critical care cardiology, cardiac surgery, advanced heart failure, and interventional cardiology, convened to decide the best course of action. The mechanism of this patient’s LV apical pseudoaneurysm versus aneurysm was thought to be a complication of a previous anterior myocardial infarction (MI), as deep Q waves were seen on ECG. As the patient was stable and there was diagnostic uncertainty whether there was a LV pseudoaneurysm or true LV aneurysm, the team concluded emergent cardiac surgery or pericardio-centesis would result in higher mortality, given that the patient was hemodynamically stable and not in cardiogenic shock. Thus, the consensus was to obtain further imaging to better characterize the LV pseudoaneurysm versus true aneurysm to help guide management. Figure 1. ECG on arrival with sinus tachycardia, left anterior fascicular block, and deep Q waves in V1-V4. CARDIOLOGY41et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202542 | The Medicine Forum, Volume 26 Computed tomography angiography (CTA) of the heart showed a true LV apical aneurysm measuring 7 cm and a large thrombus measuring 1.5 cm adherent to the akinetic anterior wall without features of LV rupture, and a moderate pericardial effusion that by Hounsfield units did not resemble blood (Figure 3). cardiac magnetic resonance imaging (MRI) showed thinning of the LV wall predominantly involving the left anterior descending (LAD) territory with akinesis of the anterior wall and hypokinesis of the apex and anterior inferior segments (Figure 3). The patient underwent a left heart catheterization, which showed complete occlusion of the mid-LAD, 99% stenosis of the first diagonal branch, 100% stenosis of the first obtuse marginal branch, and 50% stenosis of the proximal right coronary artery (Figure 4).The patient was diagnosed with a true LV apical aneurysm likely secondary to his acute myocardial infarction that occurred in the weeks prior to admission, possibly the night that he awoke with excruciating left arm pain. Percutaneous coronary intervention was not performed given evidence of completed infarct with suspected non-viable myocardium in the LAD distribution, and the plan was for outpatient follow-up and coronary artery bypass graft evaluation. The patient was started on a heparin infusion for LV thrombus and bridged to warfarin. The patient was started on metoprolol succinate and spironolactone for guideline-directed medical therapy for newly diagnosed heart failure with reduced ejection fraction and discharged with an external wearable defibrillator vest. The patient was scheduled for outpatient appointments with his primary care doctor, cardiologist, and cardiothoracic surgeon.Four days after being discharged, the patient presented to an outside hospital for decreased oral intake and dizziness. He was admitted to the intensive care unit for pressor requirement due to undifferentiated shock. The next morning, the patient was found to be in pulseless electrical activity, and advanced cardiovascular life support was administered, but after 40 minutes, the patient expired. The cause of death was attributed to cardiogenic shock. The family declined an autopsy.DISCUSSIONCardiovascular disease is a significant cause of morbidity and mortality in patients with Williams syndrome. The pathophysiology in these specific patients is related to reduced or abnormal deposition of the protein elastin within developing vessels, a process that leads to recurrent injury and fibrosis.3-5 Case reports of myocardial infarction in WS have been associated with known concomitant supravalvular aortic stenosis (SVAS) or present in patients with known coronary artery disease (CAD) at an early age Figure 2. A. TTE four-chamber apical view with akinesis of the apical, anterior, anteroseptal, inferior, and inferoseptal walls. Moderate pericardial effusion with estimated visual ejection fraction of 20%. B.: TTE four-chamber apical view with Doppler color flow through what was thought to be a possible ruptured LV apical pseudoaneurysm and layering of a mural thrombus within the LV. Figure 4. Left heart catheterization with 100% occlusion of the LAD (red arrow), 99% stenosis of the first diagonal branch, and 100% stenosis of the first obtuse marginal branch. Figure 3. A. CT Angiography with LV apical true aneurysm measuring 7 cm with a large amount of thrombus measuring 1.5 cm in thickness adherent to the anterior akinetic wall. Low-density pericardial effusion consistent with fluid rather than blood by Hounsfield units. B. Cardiac MRI consistent with a true LV aneurysm and transmural late gadolinium enhancement in the LAD distribution. 42The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 43 due to progressive elastin arteriopathy. However, this patient was 49 years old and did not have SVAS or previous known cardiovascular abnormalities. Thus, this case highlights the importance of keeping CAD and acute coronary syndrome on the differential for patients with WS regardless of cardiac history.The initial evaluation of an LV aneurysm is often via echocardiography. However, differentiating an LV aneurysm from pseudoaneurysms can sometimes be difficult. LV apical aneurysms and pseudoaneurysms are distinct entities with different pathophysiological mechanisms.6-9 LV aneurysms are true aneurysms containing all three layers of the heart wall. LV aneurysms are one of the most common complications to occur post myocardial infarction due to an outpouching of the weakened myocardium and are characterized by a broad neck. In contrast, pseudoaneurysms or false aneurysms are often a result of contained rupture of the ventricular free wall. LV pseudoaneurysms are characterized by a narrow neck and are prone to rupture, which can make them a surgical emergency. When echocardiography is unable to differentiate LV aneurysm from pseudoan-eurysm, further imaging is warranted. CTA and MRI can be valuable adjunctive imaging modalities for differentiating LV aneurysm from pseudoaneurysm in hemodynamically stable patients post-myocardial infarction. This case highlights the ability to use Hounsfield units on CTA and MRI to make the diagnosis of a true LV apical aneurysm when echocardiography is indeterminate. Patients with intellectual disabilities (ID) require special attention and a holistic care approach. As patients with ID can have a difficult time expressing symptoms and the timeline of symptom onset, involving the caregiver and other members of the care team in elucidating a history is crucial in determining what is normal versus abnormal for a patient. When a communication barrier is in place, there is an extra challenge in determining what critical diagnoses need to be ruled out. Thus, it is important to keep a broad differential when caring for a patient with an intellectual disability.Patients with ID not only can have difficulty expressing themselves, but they also have an increased risk of cardiovascular disease and overall mortality.9-10 Patients with ID have higher rates of obesity, diabetes, and hyperlipidemia compared to age-matched individuals, and the risk of cardiovascular disease directly increases with the severity of ID. In addition, other major barriers include socioeconomic status and limited access to health care. At Thomas Jefferson University Hospital, to help ameliorate this healthcare disparity, there is the For Adolescents and Beyond (FAB) Center for Complex Care, which is a clinic dedicated to the care of adolescent and post-adolescent patients with ID and other complex conditions. This case highlights the complexity of caring for patients with ID. CONCLUSIONWilliams syndrome is associated with characteristic facial features, intellectual disability, and SVAS. However, Williams syndrome should also be regarded as an arteriopathy, which can present as stenosis of small to large-sized blood vessels, including the coronary arteries. Coronary artery disease in Williams syndrome is often associated with SVAS, but this case demonstrates the importance of keeping acute coronary syndrome on one’s differential diagnosis when caring for patients with Williams syndrome, regardless of prior cardiac history. In addition, this case highlights the ability of CTA and MRI in helping differentiate an LV apical aneurysm from a pseudoaneurysm when an echocardiogram is indeterminate. REFERENCES1. Wessel A, Gravenhorst V, Buchhorn R, Gosch A, Partsch CJ, Pankau R. Risk of sudden death in the Williams-Beuren syndrome. Am J Med Genet A. 2004;127A(3):234-237.2. Pieles GE, Ofoe V, Morgan GJ. Severe left main coronary artery stenosis with abnormal branching pattern in a patient with mild supravalvar aortic stenosis and Williams-Beuren syndrome. Congenit Heart Dis. 2014;9(3):E85-E89.3. Kawai C, Kondo H, Miyao M, et al. Fatal cardiac dysfunction in a child with Williams syndrome. Leg Med (Tokyo). 2024;67:102387.4. Keating MT. Genetic approaches to cardiovascular disease: supravalvular aortic stenosis, Williams syndrome, and long-QT syndrome. Circulation. 1995;92(1):142-147.5. Conway EE Jr, Noonan J, Marion RW, Steeg CN. Myocardial infarction leading to sudden death in the Williams syndrome: report of three cases. J Pediatr. 1990;117(4):593-595.6. Sattar Y, Alraies MC. Ventricular aneurysm. In: StatPearls. Treasure Island, FL: StatPearls Publishing; April 3, 2023.7. Serrano CV Jr, Ramires JA, Soeiro Ade M, et al. Efficacy of aneurys-mectomy in patients with severe left ventricular dysfunction: favorable short- and long-term results in ischemic cardiomyopathy. Clinics (Sao Paulo). 2010;65(10):947-952.8. Velazquez EJ, Lee KL, Deja MA, et al; STICH Investigators. Coronary-artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med. 2011;364:1607-1616.9. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm: a review of the literature. Chest. 1997;111(5):1403-1409.10. Wang H, Lee PMY, Zhang J, Svendsen K, Li F, Li J. Association of intellectual disability with overall and type-specific cardiovascular diseases: a population-based cohort study in Denmark. BMC Med. 2023;21(1):41.43et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202544 | The Medicine Forum, Volume 26 "Violet-capped Woodnymph" – Bret McCarty, MD 44The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 45 Racial Disparities in Response to IBD Directed Therapy in Crohn’s Disease and Ulcerative Colitis: A Single Center ExperienceAnanya Venkatesh, MD1, Justin Robbins, MD2, Zach Breslin, MD3, Cuckoo Choudhary, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Gastroenterology & Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA3. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PAINTRODUCTIONCrohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases (IBD) associated with significant morbidity and mortality. Current clinical guidelines recommend a range of therapies, including tumor necrosis factor alpha (TNFα) antagonists, anti-integrins, interleukin-12/23 (IL12/23) inhibitors, Janus kinase (JAK) inhibitors, and/or corticosteroids for both induction and maintenance of remission. Determining the optimal medication for individual patients can be challenging due to the complexity of treatment options and the need to consider numerous phenotypic factors. While treatment guidelines do not address racial differences explicitly, prior research has highlighted significant phenotypic disparities based on race. This study aims to explore the racial disparities in treatment outcomes and medication selection between Caucasian and African American patients with UC or CD treated with IBD-directed therapies. METHODSWe conducted a retrospective chart review of patients with UC and CD treated at the Division of Gastroenterology & Hepatology at Thomas Jefferson University Hospital. Data on patient demographics, including age, race, and treatment modalities, were collected. Primary outcomes included baseline and post-treatment fecal calprotectin (FCP) levels and time to normalization of FCP. We stratified these outcomes by race, phenotypic characteristics of disease, and the specific IBD-directed medications used. RESULTSA total of 4,867 patients met the inclusion criteria, with 11% identifying as African American and 89% identifying as Caucasian. At the time of initial presentation both African American and Caucasian patients had similar baseline FCP levels (473 vs. 446); however, the time to normalization of FCP following treatment initiation differed by race. For UC, African American patients took longer to normalize FCP compared to Caucasian patients (378 vs. 334 days). In contrast, African American patients with CD experienced faster FCP normalization compared to their Caucasian counterparts (307 vs. 369 days). Regarding medication selection, a higher percentage of African American patients were started on infliximab compared to Caucasian patients (36.7% vs. 30.1%, p = 0.008). Conversely, a significantly higher percentage of Caucasian patients were started on vedolizumab compared to African American patients (17.3% vs. 12.9%, p = 0.016).CONCLUSIONOur data suggest significant racial disparities in both the treatment and outcomes of IBD among Caucasian and African American patients. These disparities underscore the need for further research to better understand how race and other phenotypic factors influence treatment responses in IBD. As precision medicine continues to evolve in gastroenterology, it is essential to refine treatment strategies that consider patient-specific characteristics, ensuring that all patients receive the most effective therapy tailored to their unique needs. REFERENCES1. Lichtenstein GR, Shahabi A, Seabury SA, et al. Lifetime economic burden of Crohn's disease and ulcerative colitis by age at diagnosis. Clin Gastroenterol Hepatol. 2020;18(4):889-897.e10. doi:10.1016/j.cgh.2019.07.0222. Feuerstein JD, Ho EY, Shmidt E, et al. AGA clinical practice guidelines on the medical management of moderate to severe luminal and perianal fistulizing Crohn's disease. Gastroenterology. 2021;160(7):2496-2508. doi:10.1053/j.gastro.2021.04.0223. Shi HY, Levy AN, Trivedi HD, Chan FKL, Ng SC, Ananthakrishnan AN. Ethnicity influences phenotype outcomes in inflammatory bowel disease: a systematic review and meta-analysis of population-based studies. Clin Gastroenterol Hepatol. 2018;16(2):190-197.e11. doi:10.1016/j.cgh.2017.05.0474. Basson A, Swart R, Jordaan E, Mazinu M, Watermeyer G. The association between race and Crohn's disease phenotype in the Western Cape population of South Africa, defined by the Montreal Classification System. PLoS One. 2014;9(8):e104859. doi:10.1371/journal.pone.01048595. Walker CH, Arora SS, Colantonio LD, et al. Rates of hospitalization among African American and Caucasian American patients with Crohn's disease seen at a tertiary care center. Gastroenterol Rep (Oxf). 2017;5(4):288-292. doi:10.1093/gastro/gow036GASTROENTEROLOGY & HEPATOLOGY45et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202546 | The Medicine Forum, Volume 26 6. Nguyen GC, LaVeist TA, Harris ML, Wang MH, Datta LW, Brant SR. Racial disparities in utilization of specialist care and medications in inflammatory bowel disease. Am J Gastroenterol. 2010;105(10):2202-2208. doi:10.1038/ajg.2010.2027. Flasar MH, Johnson T, Roghmann MC, Cross RK. Disparities in the use of immunomodulators and biologics for the treatment of inflammatory bowel disease: a retrospective cohort study. Inflamm Bowel Dis. 2008;14(1):13-19. doi:10.1002/ibd.202988. Murdoch T, O'Donnell S, Silverberg MS, Panaccione R. Biomarkers as potential treatment targets in inflammatory bowel disease: a systematic review. Can J Gastroenterol Hepatol. 2015;29(4):203-208. doi:10.1155/2015/3895489. Facciorusso A, Ramai D, Ricciardelli C, et al. Prognostic role of post-induction fecal calprotectin levels in patients with inflammatory bowel disease treated with biological therapies. Biomedicines. 2022;10(9):2305. doi:10.3390/biomedicines1009230510. GBD 2017 Inflammatory Bowel Disease Collaborators. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2020;5(1):17-30. doi:10.1016/S2468-1253(19)30333-446The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 47 Use of Novel Agent PuraStat® for Post-Ampullectomy Bleeding Bertilia Tavarez, MD, MS1, Ananya Venkatesh, MD1, Pedro Palacios Argueta, MD2, Anand Kumar, MD2, Alana Persaud, MD2, Yasi Xiao, MD2, Alexander Schlachterman, MD2, Thomas Kowalski, MD2, Faisal Kamal, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Gastroenterology & Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONEndoscopic ampullectomy is the first line treatment modality for major papilla neoplasms that have not invaded the muscularis propria.1 Complications of endoscopic ampullectomy include bleeding, pancreatitis, perforation, papillary stenosis, and cholangitis with the incidence of post-ampullectomy bleeding reported to be as high as 30%.1,2 PuraStat® is a new synthetic hemostatic gel being used for the prophylaxis and treatment of gastrointestinal bleeding.3-5 To date, there are no reports on the use of PuraStat® for post-ampullectomy bleeding. We hope to investigate the use and outcomes of PuraStat® for post-ampullectomy bleeding.METHODSWe conducted a retrospective review of medical records from Thomas Jefferson University Hospital. All adult patients who underwent endoscopic ampullectomy of the minor or major papilla for which PuraStat® was used for the treatment of bleeding at the post-ampullectomy resection site were included. The aim of this study is to report on the indication, procedural and technical parameters, any adverse effects, and the efficacy and safety of these agents for post ampullectomy hemorrhage.GASTROENTEROLOGY & HEPATOLOGYTable 1: Patient Characteristics Prior to Ampullectomy Female 75%Male 25%Average of patients’ age 46# of patients with cirrhosis 0%# of patients with normal international normalized ratio (INR) 25%# of patients with significant renal dysfunction (glomerular filtration rate <60)25%# of patients with recent discontinuation of anticoagulant 0%# of patients who had recently discontinued antiplatelet agent 0%# of patients on acetylsalicylic acid (ASA) 0%# of patients with normal platelets 100%Table 2: Post-Ampullectomy Patient OutcomesOne piece resection of ampulla 100%Snare tip soft coagulation 75%Ampullectomy complicationsPerforation 25%Cholangitis 0%Pancreatitis 25%Other 25% (nausea, vomiting, abdominal pain)Intraprocedural/immediate bleeding Total 25%Active bleeding at time of PuraStat® application25%Hemorrhagic modalities used for patients with immediate bleeding Snare tip soft coagulation 75%Bipolar cautery 0%Epinephrine injection 0%Through-the-scope (TTS) clip 0%Coagulation grasper 0%Hemostatic agent 25%Delayed bleeding (defined as bleeding <2 weeks)0%# of transfusion requirements for immediate bleeding0%Adverse events of endoscopic hemostasis for immediate bleeding Perforation 25%Cholangitis 0%Pancreatitis 25% however a month status-post ampullectomyOther 0%Hospitalization post-ampullectomy 50%Average length of stay in the hospital post-ampullectomy2.75 days47et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202548 | The Medicine Forum, Volume 26 RESULTSA total of 4 patients met inclusion criteria. Seventy-five percent of patients were female, and mean age was 46 years. One-quarter of patients had significant renal dysfunction (GFR <60) and all patients had normal platelets at the time of intervention (Table 1). A quarter of patients had post-ampullectomy complications including perforation, pancreatitis and abdominal pain. A quarter of the patients had active bleeding at the time of PuraStat®. None of the patients experienced delayed bleeding which was defined as bleeding <2 weeks after ampullectomy. 75% of the patients underwent snare tip soft coagulation as hemorrhagic modality for immediate bleeding (Table 2).CONCLUSIONOur study demonstrates the efficacy of PuraStat® in the management of post-ampullectomy bleeding, as none of the patients experienced recurrent bleeding after its use. The use of this agent proves to be safe and efficacious when used alongside other hemostatic methods. Larger scale studies are required to further validate these findings.REFERENCES1. Espinel J, Pinedo E, Ojeda V, Del Rio MG. Endoscopic management of adenomatous ampullary lesions. World J Methodol. 2015;5(3):127-135. doi:10.5662/wjm.v5.i3.1272. Bassan M, Bourke M. Endoscopic ampullectomy: a practical guide. J Interv Gastroenterol. 2012;2(1):23-30. doi:10.4161/jig.201313. Heise C, Abou Ali E, Hasenclever D, et al. Systematic review with meta-analysis: endoscopic and surgical resection for ampullary lesions. J Clin Med. 2020;9(11):3622. doi:10.3390/jcm91136224. Branchi F, Klingenberg-Noftz R, Friedrich K, et al. PuraStat in gastrointestinal bleeding: results of a prospective multicenter observational pilot study. Surg Endosc. 2022;36:2954-2961. doi:10.1007/s00464-021-08761-w5. Dhwani J, Rajesh VA. A review on extracellular matrix mimicking strategies for an artificial stem cell niche. Polym Rev. 2015;55(4):561-595. doi:10.1080/15583724.2015.104055248The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 49 Use of Novel Agent PuraStat® for Post-Sphincterotomy Bleeding Ananya Venkatesh, MD1, Bertilia Tavarez, MD, MS1, Pedro Palacios Argueta, MD2, Donna Leet, MD3, Afshin Khan, MD3, Abdul Kouanda, MD3, Anand Kumar, MD2, Alana Persaud, MD2, Yasi Xiao, MD2, Alexander Schlachterman, MD2, Thomas Kowalski, MD2, Faisal Kamal, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Gastroenterology & Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA3. Division of Gastroenterology, Department of Medicine, University of California San Francisco, San Francisco, CA INTRODUCTIONEndoscopic sphincterotomy is commonly performed during endoscopic retrograde cholangiopancreatography (ERCP). Endoscopic sphincterotomy (ES) is associated with adverse events such as bleeding.1 PuraStat® is a new synthetic hemostatic gel being used for treatment of gastrointestinal bleeding. We aim to report and outcomes of PuraStat® for post-sphincterotomy bleeding. METHODSWe conducted a retrospective review. All patients who underwent ES for which PuraStat® was used were included. GASTROENTEROLOGY & HEPATOLOGYTable 1: General Characteristics of Patients Prior to Undergoing Sphincterotomy Total number of patients N = 11 Average of patients’ age 59 Gender N= % Female 55 Male 45 Past medical history that could predispose to increase bleeding risk N = % Patients with history of cirrhosis 0 Patients with abnormal international normalized ratio (INR) 0 Patients with significant renal dysfunction (glomerular filtration rate <60)18 Patients with recent discontinuation of anticoagulant 36 Patients who had recently discontinued antiplatelet agent 27 Patients on acetylsalicylic acid (ASA) 27 Patients with abnormal platelets 9 Table 2: Procedural Details and Outcomes of Post-Sphincterotomy Procedural details N = % Sphincterotomy successfully completed 100 Intraprocedural/immediate bleeding 82 Active bleeding at time of PuraStat® application 55 Hemostatic modalities used for patients with immediate post-sphincterotomy bleeding N = % Snare tip soft coagulation 9 Bipolar cautery 36 Epinephrine injection 18 Through-the-scope (TTS) clip 9 Coagulation grasper 0 Hemostatic agent 100 Complete cessation of bleeding after application of hemostatic agent N = % Yes 82 No 18 Recurrent bleeding after use of hemostatic agent (defined as bleeding <2 weeks) N = % Yes 0 No 100 Percentage of patients requiring transfusion for immediate bleeding 14% Percentage of patients who require hospitalization for immediate or delayed bleeding 0 49et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202550 | The Medicine Forum, Volume 26 RESULTSA total of 11 patients met our inclusion criteria. 82% of patients had intraprocedural/immediate bleeding during sphincterotomy (Table 1). 18% of the patients required hospitalization due to immediate bleeding. 82% of the patients had complete cessation of the bleeding during index procedure after PuraStat® application. None of the patients experienced recurrent (<2 weeks) bleeding after hemostatic agent use (Table 2). CONCLUSIONOur study demonstrates the efficacy of PuraStat® in the management of post-sphincterotomy bleeding. Larger scale multicenter studies are required to further validate these findings. .REFERENCE1. Freeman ML, DiSario JA, Nelson DB, et al. Complications of endoscopic biliary sphincterotomy. Gastrointest Endosc. 1996;44(6):643–649. doi:10.1016/S0016-5107(96)70075-350The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 51 Complexities in Alcoholic Necrotizing Pancreatitis: A Case Report of Severe Vascular and Infectious ComplicationsDawood Tahir, MD1, Shravya Ginnaram, MD2, Jacob Lipkin, MD31. Division of Internal Medicine, Department of Medicine, Jefferson Abington Hospital, Abington, PA2. Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE3. Division of Gastroenterology & Hepatology, Department of Medicine, Jefferson Abington Hospital, Abington, PA INTRODUCTIONAcute pancreatitis (AP) incidence has been increasing, with an annual incidence of approximately 5 to 40 cases per 100,000.1 Several complications occur with AP, including splanchnic vein thrombosis (SVT), pseudocyst, and pseudoaneurysm (PSA). Moreover, 15-20% of patients develop necrotizing pancreatitis (NP) following an episode of AP with a mortality rate of up to 32%,2 which can be further complicated by infected necrosis in up to one-third of patients.2 Hemorrhage is estimated to occur in less than 6% of patients with NP by pseudoaneurysm.3 The endoscopic step-up approach is the standard treatment for walled-off necrosis, whereas alternative therapy includes percutaneous drainage followed by minimally invasive surgery.4 Although antibiotic prophylaxis in AP has been inconclusive, early initiation of antibiotic therapy has improved treatment outcomes by reducing infection-related morbidity and mortality by treating infected NP.5 In this case report, we present a complex case of a patient suffering from recurrent alcoholic pancreatitis leading to an infected NP requiring numerous endoscopic and interventional radiology procedures. The hospitalization was prolonged with various complications, not limited to methicillin-sensitive Staphylococcus aureus (MSSA) with vancomycin-resistant Enterococcus (VRE) peritonitis, portal vein thrombosis, and splenic artery pseudoan-eurysm bleeding. We highlight the need for prophylactic and early initiation of antibiotics in NP, the risks versus benefits of endoscopic versus surgical procedures, discuss the need for anticoagulation (therapeutic versus prophylactic) for SVT and venous thromboembolism (VTE) in the setting of pancreatic hemorrhage, and the importance of a multidisciplinary team approach with early goals of care discussion.CASE PRESENTATIONWe present a case of a female in her 40s with a past medical history significant for alcohol-induced pancreatitis who presented to the emergency department with abdominal pain associated with nausea and vomiting. The patient consumed four-to-five alcoholic beverages daily. See Table 1 for vital signs and lab results. On physical examination, she was ill-appearing with epigastric tenderness with voluntary guarding and positive bowel sounds in all four quadrants.GASTROENTEROLOGY & HEPATOLOGYTable 1: Admission Vital Signs and Labs Vital signsResult with reference ranges and unitsTemperature 98.5° FahrenheitHeart rate 140 beats per minuteBlood pressure 99/64 mmHgRespiratory rate 12 breaths per minuteOxygen saturation 99% on room airLab TestsResult with reference ranges and unitsWhite blood cell count 13.4 B/L (4.0-11.0 B/L)Hemoglobin 15.8 g/dL (12.0-16.0 g/dl)Platelet count 153 x 109/L (150-400 × 109/L)Sodium 127 mmol/L (135-146 mmol/L)Chloride 86 mmol/L (89-109 mmol/L)Creatinine 3.25 mg/dL (baseline of 0.7 mg/dL)Anion gap 29 mmol/L (6-14 mmol/L)Lactate 10.9 mmol/L (normal <2 mmol/L)Aspartate aminotransferase 67 IU/L (7-35 IU/L)Alanine aminotransferase 28 IU/L (0-30 IU/L)Alkaline phosphatase 45 IU/L (29-92 IU/L)Total bilirubin 1.3 mg/dL (0.1-0.9 mg/dL)Lipase 3000 U/L (13-60 U/L)Triglycerides 300 mg/dL (<150 mg/dL)Urine drug screen normalBlood alcohol level negative51et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202552 | The Medicine Forum, Volume 26 The patient had a prolonged, complicated hospital course (Table 2). CT abdomen/pelvis (A/P) without contrast unveiled pancreatitis with a diffusely enlarged pancreas and ascites. The patient received aggressive intravenous fluid (IVF) and was started on intravenous (IV) vancomycin, cefepime, and metronidazole for concerning severe sepsis. Despite fluid resuscitation, the patient remained hypotensive, requiring norepinephrine continuous infusion, and she was upgraded to the medical intensive care unit (ICU) for further management. She required mechanical ventilation for acute hypoxic respiratory failure. The Ranson criteria at 48 hours was 7. The following day, the patient was febrile to 103° Fahrenheit (F) with increased vasopressor requirements. A CT A/P with IV contrast unveiled a main portal vein thrombosis (PVT). A therapeutic heparin infusion was initiated, and broad-spectrum antibiotics were discontinued given negative cultures.In week 2, a repeat CT A/P unveiled extensive necrosis of the body of the pancreas without any evidence of infected NP, so endoscopic intervention was initially deferred. She remained febrile at 101.9°F with worsening leukocytosis; therefore, IV metronidazole and meropenem were restarted for three days before infectious disease (ID) consultants recommended monitoring off antibiotics as fever and leukocytosis were expected in the setting of severe pancreatitis with no superimposed infection (cultures remained negative). In week 3 of hospitalization, repeat CT A/P revealed resolution of PVT and persistent NP with peripancreatic necrotic fluid collections and ascites (worsened from prior). The patient underwent multiple paracentesis procedures, initially negative for infection with a serum ascites albumin gradient <1.1 g/dL. One month into her hospitalization, the patient underwent another paracentesis, which revealed a white blood cell count of 4104 cells/μL with 64% neutrophils and tested positive for MSSA, prompting cefazolin initiation.During the fifth week, an endoscopic ultrasound (EUS)/esophagogastroduodenoscopy (EGD) revealed a massive solid walled-off pancreatic necrosis. The patient underwent fine needle aspiration followed by a cystogastrostomy using lumen-apposing metal stents (LAMS). Blood-tinged purulent fluid (300cc) was suctioned from the stent. Since the risk of bleeding was higher, only deep vein thrombosis (DVT) prophylaxis was resumed. As the pancreatic tissue sample grew MSSA, the patient continued on cefazolin.During week six, the patient underwent EGD with necrosectomy (Figure 1). A semi-solid, maroon-colored necrosis was noted in the cavity. The next day, the patient developed right upper extremity swelling, and an extremity ultrasound (US) revealed a nonocclusive thrombosis of the right internal jugular and subclavian veins. Only a prophylactic dose of enoxaparin was continued. Later, in light of the infected NP with a necrotic cavity, an interven-tional radiologist (IR) placed two retroperitoneal (RP) drains. Abscess cultures grew MSSA with vancomycin-resistant Enterococcus faecium (VRE), prompting a change in antibiotics to linezolid.In the seventh week, another necrosectomy was performed. The following week, the patient was hypoxic, tachycardic, and febrile. A CT chest unmasked a filling defect in the left lower lobe pulmonary artery, suggestive of pulmonary embolism. Hematology recommended starting a low dose of argatroban.Two days after the final necrosectomy, the patient developed hemorrhagic shock, and a left RP drain produced 600 mL of blood. A massive transfusion protocol was activated, which included six units of packed red blood cells, seven units of fresh frozen plasma, one order of cryoprecipitate, and two pools of platelets. Anticoagulation was stopped, as the patient was noted to have bleeding per rectum and abdominal pain, and there was strong clinical suspicion of splenic artery pseudoaneurysm bleeding. A STAT CT angiogram A/P and splenic arteriogram revealed extravasation in the left upper quadrant adjacent to the pigtail catheter. IR embolized the mid-splenic artery Figure 1: Necrotic debris occluding the stent (top); necrosectomy: debridement (bottom).52The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 53 Table 2: Hospital Course with Significant EventsHospital Course Hospital Events Treatment PlanWeek 1Severe sepsis secondary to acute pancreatitis, acute hypoxic respiratory failure, acute renal failure, and later: development of portal vein thrombosis.Antibiotics with IVF; ventilator and vasopressor support with continuous venovenous hemofiltration; therapeutic heparin initiated for thrombosis. Antibiotics stopped by the end of the first week.Week 2 Progression of severe pancreatitis with fever and leukocytosis.Restarted antibiotics (vancomycin/meropenem) briefly before ID stopped them, as blood cultures were negative.Week 3Resolution of portal vein thrombosis, persistent necrotizing pancreatitis, and worsening ascites.Multiple paracenteses with SAAG <1.1 g/dLWeek 4Recurrent ascites with the ascitic fluid testing positive for Staphylococcus aureus.Paracentesis pertinent for elevated white cell count and neutrophils. Week 5Endoscopic ultrasound and EGD revealed a massive walled-off necrotic collection in the pancreas.FNA of fluid for bacterial culture and pancreatic tissue sample grew MSSA.Cystogastrostomy performed using lumen-apposing metal stents. Therapeutic heparin AC was held due to bleeding risk; DVT prophylaxis with enoxaparin was resumed. Cefazolin continued.Week 6EGD with necrosectomy and maroon, infected necroma observed.Right upper extremity swelling and diagnosis of multiple upper extremity DVTs. Abscess cultures grew MSSA with vancomycin-resistant Enterococcus faecium (VRE)Nasocystic catheter was placed to lavage the necrotic cavity. IR placed two RP drains. Thick, bloody, purulent material was collected.No therapeutic AC was started due to the higher bleeding risk, but a prophylactic dose of enoxaparin was continued.Change in antibiotic to linezolid.Week 7 Another necrosectomy with debridement and irrigation. Double pigtail stent to maintain drainage. Week 8Acute hypoxic respiratory failure and fever. Diagnosed with left lower lobe pulmonary embolism. Ventilator support; therapeutic AC not initiated.Week 9EGD with necrosectomy demonstrated extensive soft semi-solid debris throughout the cavityMechanical necrosectomy and lavage of the cavity with water and dilute peroxide solutionAC with argatroban started after the 4th procedure.Week 10EGD with necrosectomyHypovolemic and hemorrhagic shockDiagnosis of splenic artery pseudoaneurysm bleedingPost-IR embolization, she developed DICAC held and initiated massive transfusion protocol with vasopressor support. Splenic arteriogram followed by IR embolization of mid-splenic arteryThe family opted for transition to comfort care; the patient passed away the same day.IVF: Intravenous fluids; ID: infectious disease; SAAG: serum ascites albumin gradient; FNA: fine needle aspiration; MSSA: methicillin-sensitive Staphylococcus aureus; EGD: esophagogastroduodenoscopy; AC: anticoagulation; DVT: deep vein thrombosis; IR: interventional radiology; RP: retroperitoneal; DIC: disseminated intravascular coagulation53et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202554 | The Medicine Forum, Volume 26 with detachable coil placement, as general surgery deemed her unstable for a splenectomy. After the procedure, the patient was hemodynamically unstable and unresponsive. Disseminated intravascular coagulation (DIC) testing was positive. A goals-of-care discussion was held with the close family members to relay a guarded prognosis. The family opted for comfort care measures, and she passed away the same day.DISCUSSION20% of the patients develop severe necrotizing pancreatitis following AP. Morbidity resulting from local and systemic complications, as well as invasive interventions, results in mortality rates historically as high as 30%.6 Pseudocysts are pancreatic fluid collections (PFC) walled off with little to no inflammation/necrosis due to ductal obstruction. Walled-off PFCs with necrosis mature. Encapsulating peripancreatic or pancreatic necrosis is called walled-off pancreatic necrosis. These necroses progress over at least four weeks and can become infected.3 A recent study found that early intervention within four weeks for infected NP refractory to medical management using an endoscopic transluminal step-up approach, led to significant improvements in organ failure, an acceptable mortality rate, and no increase in complications such as perforation compared to interventions conducted after four weeks.7 Early intervention effectively stabilizes deteriorating patients with infected collections that were poorly demarcated or walled off.7 Our patient received antibiotic management intermittently for sepsis, and when she failed medical management during her fifth week of hospitalization, the gastroenterologist opted for endoscopic intervention. Afterward, the patient required weekly endoscopic necrosectomies (EN). The risk of death appears to be significantly lower for endoscopic and minimally invasive interventions than for open necrosectomy for necrotizing pancreatitis .8 The EUS-guided drainage with LAMS has similar clinical success to double pigtail plastic stent drainage for the management of PFCs; however, LAMS drainage has a lower rate of adverse events.9 In addition, the role of prophylactic antibiotics may reduce the incidence of secondary infections in AP. Still, the use of prophylactic antibiotics revealed no difference in NP, converting sterile to infected collections, mortality, surgical intervention, or positive blood culture, as suggested in meta-analysis from China.10 In contrast, if the patient clinically decompensates (fever, leukocytosis) or fails to improve within 7-10 days of hospitalization, then an infected NP is suspected, and initiating empiric antibiotics is recommended.11 However, antibiotics must be discontinued if blood and other cultures result as negative and no source of infection is identified.11 Carbapenem, metronidazole, and quinolone drug classes penetrate the infected wall well and are therefore recommended as an empiric therapy to delay surgical intervention.11 Our patient received broad-spectrum empiric antibiotic coverage; however, the ID and gastro-enterology specialists recommended stopping the antibiotics since her symptoms were expected in the early phase of pancreatitis, and the blood/urine cultures were negative. Later, the pancreatic tissue cultures and ascitic fluid tested positive for MSSA and VRE, which necessitated the initiation of specific antibiotics. This would indicate that early endoscopic intervention, ascitic fluid collection, or fine needle aspiration cultures are warranted to initiate and target specific microorganisms. Moreover, no current fixed guidelines exist for the duration of antibiotic therapy (discontinuation or extension). The American College of Gastroenterology suggests at least 14 days of antibiotics; however, these recommendations should be individualized.11 Apart from this, splanchnic vein thrombosis (SVT) is underreported and is found incidentally on imaging in 1-24% of cases. While it can resolve spontaneously in one-third of patients, pancreatologists recommend therapeutic AC for acute portal thrombosis, irrespective of other co-morbidities, including infected necrosis or pancreatic necrotic or fluid hemorrhaging.12 Despite these recommendations, we initially prescribed therapeutic AC but later withheld it for our patient due to the bleeding necroma seen and the higher risk of RP hemorrhage. There are no definite guidelines on AC choice and duration in the setting of AP, NP, or associated complications, such as pseudoaneurysm. This is a good topic for future research.One of the rare complications of NP is splenic artery pseudoaneurysm secondary to pancreatic enzymes and necrotic material eroding the arterial walls.3,13 Ruptured aneurysms have led to mortality and morbidity in 50% of cases.6,13 A high clinical suspicion is required and should be suspected in patients with active gastrointestinal bleeding, hemodynamic instability, decreasing hemoglobin, or bloody output from their drains. The treatment involves angiographic embolization with or without stenting of pseudoaneurysms. All these pertinent clinical findings were witnessed in our patient. Massive transfusion protocol was activated aptly, and IR was involved in emergent splenic embolization and coiling.CONCLUSIONProphylactic antibiotics have no role in NP; however, early endoscopic intervention, ascitic fluid, or fine needle aspiration cultures are warranted to initiate and target specific microorganisms. Moreover, there are no definite guidelines on the choice and duration of anticoagulation for portal vein thrombosis secondary to necrotizing pancreatitis or associated vascular complications/bleeding. In addition, due to the high mortality rate, high clinical suspicion is required for prompt diagnosis and management of pseudoaneurysms.54The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 55 REFERENCES1. Hammad AY, Ditillo M, Castanon L. Pancreatitis. Surg Clin North Am. 2018;98(5):895-913. doi:10.1016/j.suc.2018.06.0012. Petrov MS, Shanbhag S, Chakraborty M, Phillips ARJ. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139(3):813-820. doi:10.1053/j.gastro.2010.06.0103. Sabo A, Goussous N, Sardana N, Patel S, Zureikat A. Necrotizing pancreatitis: a review of multidisciplinary management. JOP. 2015;16(2):125-135. doi:10.6092/1590-8577/29474. Xiao NJ, Cui TT, Liu F, Li W. Current status of treatments of pancreatic and peripancreatic collections of acute pancreatitis. World J Gastrointest Surg. 2021;13(7):633-644. doi:10.4240/wjgs.v13.i7.6335. Severino A, Varca S, Airola C, Mezza T, Francavilla M. Antibiotic utilization in acute pancreatitis: a narrative review. Antibiotics (Basel). 2023;12(7):1120. doi:10.3390/antibiotics120711206. Trikudanathan G, Wolbrink DRJ, van Santvoort HC, Mallery S, Freeman M, et al. Current concepts in severe acute and necrotizing pancreatitis: an evidence-based approach. Gastroenterology. 2019;156(7):1994-2007.e3. doi:10.1053/j.gastro.2019.01.2697. Trikudanathan G, Tawfik P, Alali A, et al. Early (<4 weeks) versus standard (≥4 weeks) endoscopically centered step-up interventions for necrotizing pancreatitis. Am J Gastroenterol. 2018;113(10):1550-1558. doi:10.1038/s41395-018-0232-38. Van Brunschot S, Hollemans RA, Bakker OJ, Besselink MG, et al. Minimally invasive and endoscopic versus open necrosectomy for necrotising pancreatitis: a pooled analysis of individual data for 1980 patients. Gut. 2018;67(4):697-706. doi:10.1136/gutjnl-2016-3133419. Guzmán-Calderón E, Chacaltana A, Díaz R, Li B, Martinez-Moreno B, Aparicio JR. Head-to-head comparison between endoscopic ultrasound-guided lumen-apposing metal stents and plastic stents for the treatment of pancreatic fluid collections: a systematic review and meta-analysis. J Hepatobiliary Pancreat Sci. 2022;29(2):198-211. doi:10.1002/jhbp.100810. Ding N, Sun YH, Wen LM, Wang JH, et al. Assessment of prophylactic antibiotics administration for acute pancreatitis: a meta-analysis of randomized controlled trials. Chin Med J (Engl). 2020;133(2):212-220. doi:10.1097/CM9.000000000000060311. Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;108(9):1400-1415. doi:10.1038/ajg.2013.21812. Sissingh NJ, Groen JV, Timmerhuis HC, Besselink MG, et al. Therapeutic anticoagulation for splanchnic vein thrombosis in acute pancreatitis: a national survey and case-vignette study. World J Gastroenterol. 2023;29(21):3328-3340. doi:10.3748/wjg.v29.i21.332813. Evans RP, Mourad MM, Pall G, Fisher SG, et al. Pancreatitis: preventing catastrophic haemorrhage. World J Gastroenterol. 2017;23(30):5460-5468. doi:10.3748/wjg.v23.i30.546055et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202556 | The Medicine Forum, Volume 26 Investigating the Link Between Ulcerative Colitis and Papillary Thyroid Carcinoma: A Case ReportSonali Shah, MD1, Emily Chiacchiaro, MD1, Priya Sehgal, MD2 1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Gastroenterology & Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAGASTROENTEROLOGY & HEPATOLOGYINTRODUCTIONInflammatory bowel diseases (IBD) are chronic inflammatory conditions that primarily involve the gastro-intestinal tract, but also cause widespread systemic inflammation. There have been multiple studies investigating the link between ulcerative colitis (UC) and crohn’s disease (CD) and thyroid diseases, as the incidence is greater than the general population.1 In addition, patients with IBD have been found to be at increased risk of developing both intestinal malignancies and extraint-estinal malignancies.2 Literature review suggests a possible connection between ulcerative colitis and papillary thyroid cancer, with most studies concluding there is a higher risk of PTC in patients with UC, but no conclusive association has been truly established.3,4 In this case study, we report a unique case of an initial diagnosis of a thyroid cancer with a subsequent diagnosis of UC. CASE PRESENTATIONThe patient was a 22-year-old male with previously diagnosed metastatic papillary thyroid cancer status-post total thyroidectomy who presented to Thomas Jefferson University Hospital (TJUH) for evaluation of abdominal pain and hematochezia. Eight months prior to presenting to TJUH, the patient presented to their primary care physician (PCP) for an annual visit, where he was found to have an enlarged right cervical lymph node. Initial workup with a soft tissue neck ultrasound revealed atypical cervical adenopathy, suspicious for metastatic disease, as well as an enlarged, markedly heterogeneous appearance of the thyroid. Additional imaging evaluation with a computed tomography (CT) soft tissue of the neck revealed bilateral enlarged lymph nodes located in the upper jugular chain, middle jugular, lower jugular, and posterior triangle of the neck. Fine needle aspiration of a left-sided enlarged lymph node revealed atypical cells positive for thyroid transcription factor 1 (TTF-1) and thyroglobulin, confirming a diagnosis of metastatic papillary thyroid carcinoma. The patient underwent a total thyroidectomy with central and bilateral neck dissection two months prior to presentation to TJUH, with good recovery following surgery and future plan for radioactive iodine therapy.About a month prior to admission to TJUH, the patient started to experience diarrhea, which eventually progressed to frank hematochezia. Additional symptoms included left-sided abdominal pain, intermittent episodes of emesis, lethargy, and weight loss of ~20 lbs. A PCP visit for evaluation of these symptoms prompted a non-contrast CT of the abdomen and pelvis, which revealed diffuse wall thickening of the colon, with worse thickening along the sigmoid colon and associated mild pericolonic fat haziness. Continued symptoms led to two separate hospital admissions, the first admission at an outside hospital resulting in supportive care with fluid resuscitation. On initial admission, labs were notable for an elevated fecal calprotectin of 7,520 μg/g, as well as a negative gastroin-testinal infectious stool workup, including Salmonella, Shigella, Campylobacter, E. coli, and C. difficile. The patient was discharged but had a subsequent admission to TJUH about two weeks later due to worsening symptoms. Significant labs on admission included elevated white blood cell count 16,200/mm3, hemoglobin 8.2 g/dL, erythrocyte sedimentation rate 51 mm/hr, and C-reactive protein 1.03 mg/dL. Given the high clinical suspicion for a new diagnosis of IBD and current flare, the patient was empirically treated with intravenous (IV) methylprednisolone with a plan for further evaluation with colonoscopy. Endoscopic evaluation two days following steroid initiation demonstrated ulceration, friability, and erythema of the rectum and sigmoid colon, compatible with a Mayo score of 3-4, thereby confirming a new diagnosis of ulcerative colitis. The decision was made to administer infliximab inpatient for induction therapy, given the severity of the disease, and the patient was discharged with prednisone taper and close gastro-enterology follow-up. DISCUSSIONPapillary thyroid cancer (PTC) has been found to be one of the most common types of thyroid cancer in the general population, with certain studies investigating if there is an elevated risk of thyroid cancer in general in the IBD population.5 While there are certain studies that have found an elevated risk of thyroid cancers in patients with a history of IBD, others have been unable to find a significant relationship between the two, suggesting that 56The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 57 further research is necessary in order to determine the actual association.5-7 A handful of case studies have reported the association between ulcerative colitis and thyroid cancer, especially papillary thyroid cancer, but historically, the diagnosis of UC has predated the diagnosis of a thyroid carcinoma by multiple years.8,9 Our case study is a novel report on a primary diagnosis of PTC, followed by a diagnosis of IBD. The question of why patients with an IBD diagnosis could be at a higher risk of developing a thyroid malignancy has been investigated, with a few theories exploring this idea. Immunosuppressive therapy has been a mainstay of IBD treatment, and it has been well studied that the use of immunosuppressive agents generally can lend itself to increased rates of malignancy due to decreased immune surveillance, increased risk of general infections, DNA alterations, and even direct carcinogenic effects of certain medications, such as azathioprine and TNF-α antagonist agents.10 Given these known possible adverse outcomes of treatment, patients in conjunction with their medical team require a thorough risk-benefit analysis prior to starting any kind of treatment directed at their IBD. Alongside the potential link between the immunosuppressive medications used to treat IBD and general increased cancer risk due to impaired immune control, shared immune dysregulation by way of shared genetic mutations has also been theorized to be a causative reason as to why we see high rates of PTC in UC, but the exact mechanism and pathways involved require further elucidation.1 It is also pertinent to consider environmental factors and even the nutritional status of IBD patients and what the role is when it comes to increased cancer risk, specifically thyroid cancer risk. IBD patients often have impaired nutrition given the widespread intestinal inflammation that occurs as a result of the disease. The chronic inflammation can not only lead to nutritional deficits, including necessary nutrients for proper thyroid function, such as iodine, but also general stress on the body, leading to free radical production and possible damage to the thyroid as a result.1 Our case study highlights the rarely associated link between UC and PTC in a young patient who received the diagnosis of his thyroid cancer prior to any presenting symptom or diagnosis of UC. While research exists focusing on the possible link between these two conditions, specifically when a diagnosis of IBD precedes any cancer diagnosis, further investigation is needed to fully understand what links IBD and thyroid cancers together. REFERENCES1. Calcaterra V, Penagini F, Rossi V, et al. Thyroid disorders and inflammatory bowel disease: an association present in adults but also in children and adolescents. Front Endocrinol (Lausanne). 2025;16:1425241. doi:10.3389/fendo.2025.14252412. Lewine E, Katz S. Thyroid cancer in inflammatory bowel disease. Am J Gastroenterol. 2024;119(12S):S31.3. Lo B, Zhao M, Vind I, Burisch J. The risk of extraintestinal cancer in inflammatory bowel disease: a systematic review and meta-analysis of population-based cohort studies. Clin Gastroenterol Hepatol. 2021;19(6):1117-1138.e19. doi:10.1016/j.cgh.2020.08.0154. Mala A, Foteinogiannopoulou K, Koutroubakis IE. Solid extraintestinal malignancies in patients with inflammatory bowel disease. World J Gastrointest Oncol. 2021;13(12):1956-1980. doi:10.4251/wjgo.v13.i12.19565. Cao L. Assessment of thyroid cancer risk in more than 334,000 patients with inflammatory bowel disease: a case-control study and a meta-analysis. World J Surg Oncol. 2018;16(1):182. doi:10.1186/s12957-018-1485-46. Biancone L, Zuzzi S, Ranieri M, et al. Fistulizing pattern in Crohn's disease and pancolitis in ulcerative colitis are independent risk factors for cancer: a single-center cohort study. J Crohns Colitis. 2012;6(5):578-587. doi:10.1016/j.crohns.2011.11.0057. Biancone L, Armuzzi A, Scribano ML, et al; Italian Group for the Study of Inflammatory Bowel Disease. Inflammatory bowel disease phenotype as risk factor for cancer in a prospective multicentre nested case-control IG-IBD study. J Crohns Colitis. 2016;10(8):913-924. doi:10.1093/ecco-jcc/jjw0488. Casella G, Antonelli E, Di Bella C, et al. Papillary thyroid cancer and ulcerative colitis. Gastroenterol Hepatol Bed Bench. 2013;6(1):52-54. PMID:248342469. Evgenikos N, Stephen JG. Papillary thyroid carcinoma associated with ulcerative colitis. Postgrad Med J. 1996;72(852):621-622. doi:10.1136/pgmj.72.852.621. PMID:897794810. Moutinho BD, de Barros JR, Baima JP, Saad-Hossne R, Sassaki LY. Immunosuppression and malignant neoplasms: risk-benefit assessment in patients with inflammatory bowel disease. Am J Case Rep. 2020;21:e920949. doi:10.12659/AJCR.920949. PMID:3221841357et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202558 | The Medicine Forum, Volume 26 "A Mind in Bloom, A Body at Rest" – Jenny Chan58The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 59 Case Report of Gastritis as a Complication of Immunotherapy Treatment of Metastatic Endometrial Cancer with Lenvatinib and PembrolizumabBret McCarty, MD1, Nia Johnson, BS2, and Suchit Bhutani, MD31. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA3. Department of Medical Oncology, Sidney Kimmel Medical College, Philadelphia, PAINTRODUCTIONImmune checkpoint inhibitors (ICIs), such as pembrolizumab (a PD-1 inhibitor), have been shown to be effective in the treatment of a variety of malignancies, including progressive endometrial cancer. ICIs help to activate the patient’s immune system to attack neoplastic cells. However, this immune activation can trigger autoimmune side effects throughout the body, known as immune-related adverse events (irAEs). Immunotherapy-associated hepatitis, colitis and diarrhea have been well documented as irAEs, but gastritis is much less common.1 In this case report of immunotherapy-related gastritis, we attempted to better characterize this more rare condition to assist with early recognition and initiation of appropriate management of immunotherapy-related gastritis.We describe a case of a 73-year-old woman with stage IV uterine carcinosarcoma status post chemoradiation and adjuvant combination immunotherapy using lenvatinib/pembrolizumab. The patient developed moderate-severe gastritis after 13 cycles of lenvatinib/pembrolizumab with intractable nausea/vomiting. The patient's condition resolved after administration of intravenous (IV) corticosteroids.CASE PRESENTATIONThe patient is a 73-year-old female with a past medical history of metastatic uterine carcinosarcoma status-post total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH-BSO) with progression of disease despite two lines of chemotherapy and radiation now on adjuvant immunotherapy with lenvatinib and pembrolizumab. She presented to the emergency room with intractable nausea/vomiting and failure to thrive with thirty pounds of unintentional weight loss over seven months.She initially presented to her gynecologist with one month of worsening postmenopausal bleeding. Endometrial biopsy revealed serous endometrial cancer. She subsequently underwent robotic TAH-BSO, with pathology confirming a diagnosis of uterine carcino-sarcoma (tumor measuring 10 cm) invading the cervix, lymph/blood vessels, and 80% of the myometrium. The tumor was triple-negative for estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2).Chemotherapy was initiated with carboplatin and paclitaxel every 21 days with dose reduction due to neuropathy. She completed six cycles, followed by vaginal brachytherapy. Imaging showed progression of disease and she was subsequently started on carboplatin and doxorubicin every 28 days. Imaging after several cycles showed recurrent tumor at the left superior vaginal wall and further progression of disease. Given continued disease progression through two lines of chemotherapy, she was transit ioned to adjuvant immunotherapy with pembrolizumab and lenvatinib. After several cycles, imaging showed decreased lung metastases and reduction in the vaginal cuff mass with stable peritoneal implants.Her treatment course was uncomplicated until she received the twelfth cycle of immunotherapy, after which she was hospitalized due to worsening moderate-to-severe nausea and vomiting with resultant failure to thrive. Computed tomography (CT) abdomen and pelvis on hospital day two showed no evidence of malignant obstruction and stable cancer except for an enlarging hepatic lesion, and possible gastric wall thickening versus underdistention related to poor oral intake (Figure 1A-B). Her symptoms resolved with IV fluids and anti-nausea medications, and she was deemed medically stable for discharge on hospital day five. She received cycle thir teen of immunotherapy post-discharge but was readmitted one week later due to recurrence of severe nausea/vomiting and poor oral intake. On presentation to the emergency department, she was afebrile and hemodynamically stable. Physical examination revealed mild, diffuse abdominal tenderness without rebound or guarding. Initial labs showed hypomagnesemia, normal liver testing, and a normal lipase. Abdominal x-ray showed a non-obstructive bowel gas pattern. She was admitted to the hospital and received supportive treatment with IV fluids, antiemetics, and electrolyte replacement. CT abdomen and pelvis on hospital day one showed diffuse gastric edema throughout the stomach wall concerning for moderate-severe gastritis (Figure 1C-D). Gastroenterology HEMATOLOGY & ONCOLOGY59et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202560 | The Medicine Forum, Volume 26 red blood cells (1u pRBC). Given ongoing hematemesis, IV methylprednisolone dose was increased to 2 mg/kg/day and sucralfate was started per gastroenterology recommendations. On hospital day seven, Hgb again dropped, and another 1u pRBC was transfused. Hgb remained stable thereafter.Her symptoms gradually improved, along with her ability to tolerate oral intake. She was transitioned to oral prednisone 2 mg/kg/day on hospital day ten with significant improvement in her symptoms and oral intake. She was medically stable for discharge home on hospital day twelve with close follow up with medical oncology and gastroenterology.During follow-up in the medical oncology office, she reported tolerating a normal diet with resolution of her nausea and vomiting, and she began a slow prednisone performed esophagogastroduodenoscopy (EGD) on hospital day two, which showed diffuse erythema, edema, and friability of the entire stomach (Figure 2). Pathology from stomach biopsies demonstrated diffuse active chronic gastritis with ulceration. The biopsies were negative for malignancy or intestinal metaplasia, and immunohisto-chemical stains ruled out infection with cytomegalovirus, H. pylori, or spirochetes. The patient’s clinical picture was consistent with severe ICI-related gastritis based on high clinical suspicion from medical oncology and gastroen-terology, for which IV methylprednisolone 1 mg/kg/day was initiated as a treatment recommendation.Post-EGD course was complicated by worsening hematemesis, with hemoglobin (Hgb) down-trending over three days from 9.6 to 7.0 g/dL. On hospital day six, the patient had further hematemesis and an acute Hgb drop from 7.0 to 5.8 g/dL, requiring transfusion of 1 unit packed Figure 1: Representative images from CT abdomen and pelvis taken during the first admission (A-B) and during the second admission (C-D).Figure 2: Endoscopic findings of diffuse erythema, edema, and friability of the entire stomach.60The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 61 ICI-related toxicity had been included in the differential diagnosis during her near-identical presentation one month prior. irAEs most often appear within the first 6-12 months after initial exposure to immunotherapy. However, there is an increasing number of cases demonstrating that irAEs can present years after treatment initiation.4 Therefore, it is essential to always consider immune-related toxicity in any patient with prior exposure to immunotherapy. Moreover, this report emphasizes the importance of collaborating in a multidisciplinary approach with medical oncology, gastroenterology, radiology, and other specialties where appropriate. We hope that by sharing this case, we will help increase awareness among clinicians about the rare complications of immunotherapies.REFERENCES1. Goel N, Levine MD, Chambers LM, Nagel CI. Gastritis as an immuno-therapy-related toxicity in the treatment of endometrial cancer: A case report. Gynecol Oncol Rep. 2023 Mar 31;47:101174. doi: 10.1016/j.gore.2023.101174. PMID: 37102082; PMCID: PMC10123331.2. Makker V, Colombo N, Casado Herráez A, et al; Study 309–KEYNOTE-775 Investigators. Lenvatinib plus Pembrolizumab for Advanced Endometrial Cancer. N Engl J Med. 2022 Feb 3;386(5):437-448. doi: 10.1056/NEJMoa2108330. Epub 2022 Jan 19. PMID: 35045221; PMCID: PMC11651366.3. Thompson JA, Schneider BJ, Brahmer J, et al; Management of Immune Checkpoint Inhibitor-Related Toxicities. NCCN Guidelines Version 1.2025. 2024 Dec 20.4. Durbin SM, Zubiri L, Perlman K, et al. Late-Onset Immune-Related Adverse Events After Immune Checkpoint Inhibitor Therapy. JAMA Netw Open. 2025;8(3):e252668. doi:10.1001/jamanetworkopen.2025.266taper. Immunotherapy with pembrolizumab and lenvatinib was discontinued indefinitely due to the prohibitive risk of recurrent ICI-related gastritis. Alternative lines of chemotherapy were considered once off prednisone. She received ten cycles of weekly paclitaxel and bevacizumab. Subsequent imaging showed progression of lung and liver metastases, while peritoneal and omental implants remained stable. She declined a clinical trial and instead started treatment with gemcitabine every fourteen days with ongoing follow-up with medical oncology.DISCUSSIONThe use of immune checkpoint inhibitors (ICIs) in the treatment of cancers, including recurrent and advanced endometrial cancer, has been expanding in recent years, and an increasing number of patients are becoming eligible candidates to receive ICIs as research on these medications continues. The Keynote-775 phase 3 trial found that lenvatinib and pembrolizumab led to significantly longer progression-free survival and overall survival than chemotherapy (paclitaxel or doxorubicin) among patients with advanced endometrial cancer.2 However, by increasing immune activity against both tumor cells and normal cells, ICIs have also been shown to cause irAEs in multiple organs with symptoms much akin to autoimmune diseases. ICI-associated hepatitis, colitis, and diarrhea are relatively common among irAEs, but gastritis is rarer and can be easily missed or misdiagnosed.While management of irAEs varies according to the organ system affected, intensity of treatment generally corresponds with the irAE’s degree of severity. According to the National Comprehensive Cancer Network’s guidelines for management of ICI-related toxicities, ICI-associated gastritis is classified into two groups: mild and moderate-to-severe.3 In mild ICI-associated gastritis, the patient’s functional status is not significantly affected (able to eat normally and maintain bodyweight), immunotherapy is continued, and treatment is supportive in nature. In moderate-to-severe cases, patients are much sicker, unable to eat normally or maintain bodyweight, and treatment is more aggressive, usually requir ing hospital ization for symptom management, gastroenterology consultation for upper endoscopy, corticosteroids (prednisone or IV methyl-prednisolone 1 mg/kg/day), and consideration of holding/discontinuing immunotherapy. Refractory cases may require more aggressive immunosuppressive therapy such as biologics (e.g. infliximab 5 mg/kg).Our patient was diagnosed with moderate-severe ICI-related gastritis, which resolved in a matter of days after initiation of corticosteroids. Her hospital course was complicated by acute blood loss anemia due to upper gastrointestinal bleeding, which could have been life-threatening, and could have been prevented if 61et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202562 | The Medicine Forum, Volume 26 Immune Thrombocytopenic Purpura in the Setting of Newly Diagnosed Colorectal Cancer: A Case ReportBeatriz Torre, MD1, Karlie Brasch, MD1, Christopher Henry, MD21. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Gastroenterology & Hepatology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAHEMATOLOGY & ONCOLOGYINTRODUCTIONImmune thrombocytopenic purpura (ITP) is an acquired thrombocytopenia caused by autoantibodies against platelet antigens. ITP is most often associated with infection or autoimmune disease, but it has also been linked to malignancy.1 In this case, we discuss the relationship between ITP and colon cancer.CASE PRESENTATIONA 62-year-old female with a past medical history of asthma, gastroesophageal reflux disease, and depression presented to the emergency department with hematochezia. She reported a three-month history of rectal bleeding associated with straining and constipation. She had never undergone upper endoscopy or colonoscopy, despite her father being diagnosed with colon cancer at age 60.On arrival, her hemoglobin was 5.2 g/dL with iron studies consistent with iron deficiency anemia, urine drug screen positive for cocaine, and the remainder of her labs unremarkable. She received two units of packed red blood cells (pRBC), with an appropriate hemoglobin response. She was admitted to the internal medicine service for a colonoscopy.The day after admission marked the onset of her platelet count declining from 249,000 K/μL to 131,000 K/μL, then 41,000 K/μL, and finally 17,000 K/μL. The colonoscopy was delayed due to the increased bleeding risk from new, severe thrombocytopenia. Although the differential diagnosis for acute severe thrombocy-topenia is broad, the hematology team believed ITP was the most likely etiology, as the timeline did not align with transfusion-related thrombocytopenia and the remainder of her workup was unremarkable.Her thrombocytopenia progressed, and she was treated for ITP with intravenous immunoglobulin (IVIG) and high-dose steroids for four days. After several days of treatment, her platelet count improved, and she was able to undergo colonoscopy. The procedure revealed a circumferential, ulcerated, bleeding mass with a malignant appearance in the sigmoid colon. Pathology confirmed moderately differentiated adenocarcinoma.DISCUSSIONITP is an autoimmune disorder characterized by isolated thrombocytopenia in the absence of other identifiable causes.1 While primary ITP is well described, secondary forms, such as those associated with solid tumors are far less common. This case adds to the limited body of literature documenting the rare association between ITP and colorectal cancer.2The pathophysiology linking ITP to solid tumors remains poorly understood.3 Proposed mechanisms include the generation of platelet autoantibodies triggered by tumor-induced immune dysregulation, molecular mimicry between tumor antigens and platelet surface proteins, and the direct production of antiplatelet antibodies by neoplastic cells. The temporal association between the onset of ITP and the detection of malignancy, and in some reports, resolution of thrombocytopenia following tumor resection supports a possible paraneoplastic phenomenon.4Although hematologic malignancies such as chronic lymphocytic leukemia and non-Hodgkin lymphoma are more commonly associated with ITP, associations with solid tumors including lung, breast, renal, and gastric cancers have been reported.5 Reports linking ITP to colorectal cancer are exceedingly rare. This rarity may contribute to under-recognition and diagnostic delays.6In our case, the diagnosis of ITP was made after excluding other common causes of thrombocytopenia, including disseminated intravascular coagulation, drug-induced thrombocytopenia, transfusion-related thrombocytopenia, and hematologic malignancy.This case reinforces the importance of maintaining a broad differential diagnosis when evaluating thrombo-cytopenia in patients with malignancy. Conversely, unexplained thrombocytopenia without an obvious cause may warrant investigation for an occult neoplasm, particularly in older adults. Clinician awareness of this rare association is essential for early diagnosis and effective multidisciplinary management.62The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 63 REFERENCES1. Neunert C, Terrell DR, Arnold DM, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia. Blood Advances. 2019;3(23):3829-3866. doi:https://doi.org/10.1182/bloodadvances.20190009662. Krauth MT, Puthenparambil J, Lechner K. Paraneoplastic autoimmune thrombocytopenia in solid tumors. Critical Reviews in Oncology/Hematology. 2012;81(1):75-81. doi:https://doi.org/10.1016/j.critrevonc.2011.02.0043. Ayesh Haj Yousef MH, Alawneh K, Zahran D, Aldaoud NH, Khader Y. Immune thrombocytopenia among patients with cancer and its response to treatment. European journal of haematology. Published online May 2018:10.1111/ejh.13091. doi:https://doi.org/10.1111/ejh.130914. Audia S, Mahévas M, Samson M, Godeau B, Bonnotte B. Pathogenesis of immune thrombocytopenia. Autoimmunity Reviews. 2017;16(6):620-632. doi:https://doi.org/10.1016/j.autrev.2017.04.0125. Yacob M, Raju R, Vyas F, Joseph P, Sitaram V. Management of colorectal cancer liver metastasis in a patient with immune thrombocytopaenia. Annals of The Royal College of Surgeons of England. 2013;95(2):e26-e27. doi:https://doi.org/10.1308/003588413x135116099574986. Schwartz KA, Slichter SJ, Harker LA. Immune-mediated platelet destruction and thrombocytopenia in patients with solid tumours. British journal of haematology. 1982;51(1):17-24. doi:https://doi.org/10.1111/j.1365-2141.1982.tb07285.63et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202564 | The Medicine Forum, Volume 26 An Unusual Complication of Metastatic Colorectal Cancer: Port-Site Hematoma as the First Sign of Bone Marrow Involvement and Disseminated Intravascular Coagulation Michael Predi, DO1, Julia Palecki, MD1, Jordan M. Isaacs, BA2, Ruben Rhoades, MD31. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 3. Division of Hematology, Cardeza Foundation for Hematologic Research, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA HEMATOLOGY & ONCOLOGYINTRODUCTIONDisseminated intravascular coagulation (DIC) is a life-threatening condition marked by a spectrum of thrombosis due to activation of procoagulant factors and bleeding due to eventual consumption of these factors. DIC invariably occurs secondary to an underlying condition, including infection, inflammatory conditions, trauma, and malignancies. Treatment of DIC primarily involves treatment of the underlying cause.1 Bone marrow invasion occurs when tumor cells infiltrate the hematopoietic marrow space, displacing progenitor cells and causing cytopenias. This process is distinct from bone metastases, where malignant cells spread to the cortical or trabecular bone, typically causing bone pain, pathologic fractures, or hypercalcemia. Disseminated carcinomatosis of the bone marrow (DCBM) is a particularly severe form of marrow involvement, characterized by widespread and uniform infiltration that can result in profound cytopenias, marrow failure, and DIC.2,3 Cancers most commonly associated with bone marrow invasion include prostate, lung, breast, and gastric malignancies. While gastric cancer rarely metastasizes to bone, it is frequently cited as a malignancy associated with marrow infiltration. In contrast, metastatic colorectal cancer rarely presents with DCBM leading to DIC.4,5We present a case of a patient with metastatic colon cancer who developed acute anemia due to a large port-site hematoma. Further investigation revealed DCBM, rising carcinoembryonic antigen (CEA) levels, and DIC. In this case report, we outline the clinical course and management of this patient. Additionally, we review published cases of this rare pathology, providing insights into its presentation and clinical implications. CASE PRESENTATIONA 62-year-old male with a history of type 2 diabetes mellitus, coronary artery disease, and metastatic colon cancer status-post hemicolectomy presented to the emergency department with a port-site hematoma. Six days prior to presentation, he underwent port placement in preparation for adjuvant folinic acid, 5-fluorouracil, and oxaliplatin (FOLFOX) chemotherapy. Two days prior to presentation, he developed a rapidly expanding hematoma at the port site, prompting his hospitalization. On admission, his vital signs were normal. His physical exam was notable for a hematoma at the port site (Figure 1A) and ecchymosis of bilateral flanks (Figure 1B). Labs on presentation were notable for hemoglobin 6.9 g/dL (baseline hemoglobin 8 g/dL), mean corpuscular volume 72 fL, platelets 288 B/L (baseline platelets 389 B/L), white blood cells 11.4 B/L, creatinine 1.19 mg/dL, prothrombin time 16.1 sec, international normalized ratio (INR) 1.43, partial thromboplastin time 46 sec, fibrinogen 88 mg/dL, D-dimer 8,567 ng/mL DDU, and CEA 82.6 ng/mL (prior CEA 22 ng/mL). Computed tomography (CT) of the abdomen and pelvis with contrast showed superior and inferior hematomas surrounding the right chest port. Repeat labs on hospital day 2 showed platelets 65 B/L, hemoglobin 5.7 g/dL, INR 1.45 sec, prothrombin time 15.4 sec, partial thromboplastin time 48 sec, lactate dehydrogenase 1539 IU/L, D-dimer 36,442 ng/mL D-dimer units (DDU), fibrinogen 42 mg/dL, and haptoglobin <10 mg/dL. The patient had a platelet nadir of less than 50 B/L. The International Society of Thrombosis and Hemostasis (ISTH) overt DIC score was eight. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) mixing studies corrected. Blood cultures were obtained and showed no evidence of growth. Peripheral blood smear showed normocytic, hypochromic red blood cells with anisopoi-kilocytosis, occasional schistocytes (1-2 per high power field), nucleated red blood cells, and decreased platelets. Bone marrow biopsy was performed and showed metastatic adenocarcinoma with carcinoma cells positive for cytokeratin-20 (CK20) and negative for cytokeratin-7 (CK7). Given the bone marrow findings, the patient was diagnosed with DCBM leading to DIC. The patient’s bleeding, severe lab abnormalities, and elevated ISTH DIC score (8/8) supported DIC. The hematoma was evacuated by interventional radiology. He was treated with supportive care including cryoprecipitate, packed red blood cell transfusions, and tranexamic acid. Antiplatelet therapy, which the patient was taking for coronary artery disease, was held. Despite supportive care, the patient’s condition continued to deteriorate. He 64The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 65 Table 1: Clinical Characteristics, Treatments, and Outcomes of Patients with Rectal or Colorectal Cancer, Diffuse Carcinomatosis of the Bone Marrow, and Disseminated Intravascular CoagulationAuthor Patient & CRC Characteristics Bleeding or ThrombosisFirst-Line Chemotherapy TreatmentResolution of DICSurvivalTakeyama et al (2017)465 MRecurrent moderately differentiated rectal adenocarcinoma of the rectumEpistaxis mFOLFOX6 Yes 263 daysEhara (2020)838 MPoorly differentiated adenocarcinoma of the rectumNoneCapecitabine + oxaliplatinYes 333 daysDesikan (2021)275 MRecurrent poorly differentiated mucinous adenocarcinoma of the colonDiffuse ecchymosisFOLFOX6 Yes 60 daysYoshida et al (2021)966 MModerately differentiated tubular adenocarcinoma and poorly differentiated adenocarcinoma of the rectumRectal bleedingmFOLFOX6 + panitumumabYes 333 daysPresent Case (2025)62 MModerate to poorly differentiated adenocarcinoma of the colonPort-site hematoma, ecchymosisNone No 0 daysFigure 1: (A) Hematoma at the port site. (B) Diffuse purpura of abdomen and flank. FOLFOX6= 5-Fluorouracil, mFOLFOX6 = Modified 5-Fluorouracilsignaling may facilitate tumor cell adhesion and implantation Once established in marrow, tumor proliferation causes bone destruction and hematologic complications.4 In DCBM, metastatic CRC disrupts hematopoiesis, damages endothelium, and releases procoagulants like tissue factor which can induce DIC and increase bleeding risk. The exact mechanism of DIC in DCBM is unclear but likely involves cancer cell-induced cytokine release (interleukin-1, interleukin-6, tumor necrosis factor), which impairs anticoagulant pathways was deemed to not be a candidate for chemotherapy due to severe anemia and thrombocytopenia. Ultimately, the patient was transitioned to hospice care and expired. DISCUSSIONColorectal cancer (CRC) will commonly metastasize to the liver and lungs via portal and systemic circulation. Although bone marrow involvement is uncommon with CRC, slow marrow blood flow and growth factor 65et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202566 | The Medicine Forum, Volume 26 REFERENCES1. Levi, M. & Scully, M. How I treat disseminated intravascular coagulation. Blood 131, 845-854 (2018).2. Desikan, S.P., McLaughlin, N., McClain, C. & Desikan, R. Recurrent Colon Cancer: Presentation With Disseminated Intravascular Coagulation From Disseminated Carcinomatosis of the Bone Marrow. J Investig Med High Impact Case Rep 9, 23247096211012224 (2021).3. van Bunderen, C.C., de Weger, V.A. & Griffioen-Keijzer, A. Disseminated intravascular coagulation as clinical manifestation of colorectal cancer: a case report and review of the literature. Neth J Med 72, 186-189 (2014).4. Takeyama, H. et al. Disseminated carcinomatosis of the bone marrow with disseminated intravascular coagulation as the first symptom of recurrent rectal cancer successfully treated with chemotherapy: A case report and review of the literature. Oncol Lett 13, 4290-4294 (2017).5. Nakashima, Y. et al. Rectal cancer with disseminated carcinomatosis of the bone marrow: report of a case. Int Surg 99, 518-522 (2014).6. Assi, R. et al. Metastatic colorectal cancer presenting with bone marrow metastasis: a case series and review of literature. Journal of Gastrointestinal Oncology 7, 284-297 (2015).7. Hanamura, F. et al. Favorable control of advanced colon adenocarcinoma with severe bone marrow metastasis: A case report. Mol Clin Oncol 5, 579-582 (2016).8. Ehara, T. et al. Treatment of Rectal Cancer-Induced Disseminated Carcinomatosis of the Bone Marrow with FOLFOX plus Cetuximab and Panitumumab. Case Rep Oncol 13, 145-152 (2020).9. Yoshida, K. et al. Disseminated carcinomatosis of the bone marrow from rectal cancer: A case report. Clin Case Rep 9, 1483-1489 (2021).10. Naito, M. et al. A Report of Disseminated Carcinomatosis of the Bone Marrow Originating from Transverse Colon Cancer Successfully Treated with Chemotherapy Using XELOX plus Bevacizumab. Case Rep Oncol 7, 426-434 (2014).by downregulating thrombomodulin, protein C, and protein S. Cancer cells and monocytes may also activate tissue factor, triggering the coagulation cascade. As procoagulant factors are consumed, bleeding ensues.5 Marrow involvement often leads to cytopenias and complications that may delay or preclude treatment.6 Overall DIC in CRC is a severe complication and portends poor prognosis.3 While CRC associated DCBM with DIC can be extremely challenging to treat, case reports show that chemotherapy can resolve acute hematologic issues like DIC.10 Table 1 highlights these instances. In most of these cases, hematologic complications of DCBM bleeding episodes include epistaxis, rectal bleeding, or diffuse ecchymosis. Classical adenocarcinoma is the most common CRC histology, and one patient had mucinous histology. Unlike our patient, most of the previously reported cases were treated with chemotherapy. Initial regimens included mFOLFOX6, capecitabine plus oxaliplatin, FOLFOX6, and mFOLFOX6 plus panitumumab. In all cases where chemotherapy was administered, DIC was successfully managed. However, long-term survival outcomes remained poor with no patient surviving beyond one year. CONCLUSIONBone marrow metastasis causing DIC is a rare but devastating complication of CRC. Patients can present with various manifestations including nonspecific back pain, thrombotic events, purpura, or major bleeding events. In this case, DIC manifested uniquely as a port-site hematoma. Ensuring the correct diagnosis hinges on obtaining laboratory markers and a bone marrow biopsy to confirm DIC and bone marrow infiltration. Treatment is a combination of supportive care, and if patients are deemed appropriate candidates, cytotoxic chemotherapy for the underlying malignancy. While chemotherapy has shown efficacy in the treatment of DIC in prior similar cases, the overall prognosis with confirmed DCMB associated with CRC remains poor. This case highlights the aggressive nature of metastatic CRC with bone marrow involvement and the challenges of treating DIC in this setting. 66The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 67 When the Cure Complicates: Ifosfamide, Methylene Blue, and A Life-Threatening DilemmaMichael Predi, DO1, Sarah Sulkowski, MD1, Anika Patel, BA2, Evan Nardone, MD31. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA3. Department of Medical Oncology, Sidney Kimmel Medical College, Philadelphia, PAINTRODUCTIONIfosfamide, an alkylating agent and a cyclophos-phamide analog, can be used alone or in combination with other agents as salvage therapy for metastatic soft tissue sarcoma. Neurotoxicity, often presenting as encephalopathy, is a common side effect of ifosfamide therapy, affecting up to 60% of patients.1 Symptoms can range in severity from mild cognitive disturbances to severe, potentially fatal neurological impairments, such as hallucinations, confusion, drowsiness, and coma, which may develop within 2 to 96 hours of drug administration.2 Treatment of neurotoxicity includes cessation of ifosfamide and initiation of methylene blue (MB), which is used as both a therapeutic and prophylactic agent in the management of ifosfamide-induced encepha-lopathy (IFE). It works by inhibiting monoamine oxidase (MAO), thereby preventing the accumulation of the neurotoxic metabolite chloroacetaldehyde.3 MB is known to increase the risk of serotonin syndrome (SS) when used alongside serotonergic medications due to its MAO inhibition, which leads to the buildup of 5-hydroxytryptamine (5-HT), potentiating SS.4 Treatment of SS includes discontinuing all serotonergic agents and administration of cyproheptadine, a serotonin 5-HT2 receptor antagonist and histamine H1 receptor antagonist. This report describes a patient on serotonergic agents who presented with rapidly progressing sarcoma, where the decision was made to initiate salvage ifosfamide therapy, highlighting the complex decision-making involved in managing such cases. While ifosfamide offers a potential option to extend survival, its use is associated with significant challenges, particularly due to the risk of neurotoxicity. In this case, the patient being on serotonergic agents complicates matters further, as ifosfamide neurotoxicity may necessitate the use of MB, a known monoamine oxidase inhibitor that can trigger serotonin syndrome. The interplay of these factors requires careful consideration, balancing the benefits of ifosfamide with the risk of life-threatening complications. CASE PRESENTATIONA 53-year-old woman with a history of hypertension, hyperlipidemia, and mood lability was diagnosed with a high-grade pleomorphic sarcoma of her left thigh. She had neoadjuvant radiation therapy (XRT) and underwent resection of the mass with negative margins. Imaging at the time of surgery showed interval development of multiple lung nodules with biopsy confirming metastatic disease, and she was started on doxorubicin. She presented to the emergency department with fever, worsening cough, and shortness of breath ten days after cycle 3 of doxorubicin. Infectious work up was negative, and chest imaging showed extensive progression of metastatic lung disease. Given the progression of disease despite 3 cycles of liposomal doxorubicin, a decision was made to change the chemotherapy regimen to ifosfamide, etoposide, and mesna with plans for inpatient infusion. Prior to initiation of therapy, psychiatry was consulted for guidance on reducing the risk of SS from the interaction of serotonergic medications (escitalopram, guaifenesin-codeine) with MB, if required for management of ifosfamide neurotoxicity. She had been taking escitalopram 10 mg daily for 20 years to manage mood lability. After consulting with psychiatry, the patient decided to discontinue escitalopram. Additionally, guaifenesin-codeine was stopped, and guaifenesin-dextromethorphan was ordered. After discussion of risks versus benefits of treatment with the patient, the decision was made to initiate the first dose of intravenous (IV) ifosfamide over 12 hours instead of over 8 hours. Ifosfamide was started hours after escitalopram was discontinued. On day 2 of infusion, she began to experience dizziness and lightheadedness and ifosfamide was withheld. Her symptoms resolved over the course of 24 hours and the ifosfamide infusion was restarted on day 3. About 10 hours after resuming the infusion, the patient became confused and oriented only to self. Based on the National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE), this patient had a grade 3 toxicity. During this period, she had a dose of IV hydromorphone ordered for abdominal pain. The infusion was held, and she was re-evaluated three hours after discontinuing ifosfamide. Her mental status did not improve, and treatment for HEMATOLOGY & ONCOLOGY67et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202568 | The Medicine Forum, Volume 26 suspected IFE was initiated with MB 50 mg every 4 hours. In addition to MB for management of IFE, IV albumin 50 g was ordered every 8 hours for a total of four doses and IV thiamine 250 mg daily. Despite 36 hours off ifosfamide and 24 hours of methylene blue, her mental and respiratory status worsened (CTCAE 4). On examination, the patient appeared flushed and tremulous with autonomic instability, dilated pupils, 2-3 up to 4-5 beats of ankle clonus, and hyperreflexia. Clinical presentation met Hunter criteria for SS. MB was discontinued. A rapid response team (RRT) was called overnight for respiratory distress, tachycardia, and worsening agitation. At the time of the RRT, the patient was ill-appearing, flushed, and tripoding with increased work of breathing with acidosis of pH 7.12 on arterial blood gas (ABG). Due to declining respiratory status, the patient was intubated and transferred to the medical intensive care unit (MICU) for further management. A nasogastric tube was placed, and she was started on cyproheptadine. The patient was extubated to 3 liters of oxygen by nasal cannula. A goals-of-care discussion was held to convey the severity of the patient’s condition with the primary team, medical oncology, and the patient’s family. Ultimately, the patient changed her code status to do-not-resuscitate/do-not-intubate (DNR/DNI) and decided to follow up closely with her outpatient oncologist to try pazopanib as an additional line of therapy. DISCUSSIONInitiating ifosfamide can result in downstream toxicities especially in combination with MB for patients receiving serotonergic drugs. Oncology patients are a vulnerable group for experiencing SS because many patients are receiving serotonergic drugs such selective serotonin reuptake inhibitors (SSRIs), tramadol, methadone, fentanyl, metoclopramide, and many other agents. Other case reports have reported SS developing secondary to salvage MB use for ifosfamide neurotoxicity in patients on serotonergic drugs.5,6 In these cases, patients experienced extended hospital stays involving intubation and ICU-level care for management of SS. Our study highlights a similar traumatic experience our patient endured requiring intubation, and an extended ICU stay secondary to treatment with MB. It should be noted that the evidence for the efficacy and safety of MB for ifosfamide therapy is based upon case reports and retrospective studies.5,6Most cases of IFE resolve within 48 hours after cessation of ifosfamide.6 Despite most cases of IFE self-resolving with discontinuation of ifosfamide, there have been reported fatalities in both IFE patients who received MB and those who did not.3,7 A study by Top et al. in 2014 reported the first published fatality of SS in a patient on an SSRI who developed SS while receiving MB during a parathyroid surgery. The lack of clarity surrounding the safety, efficacy, and implications of not using methylene blue for ifosfamide neurotoxicity suggests that further research must be done considering the significant toxicities that can occur with its use. Serotonin syndrome (SS) is a life-threatening adverse reaction that typically develops within 24 hours following a change in serotonergic therapy—such as the addition of another serotonergic agent, a dosage increase, or the introduction of a more potent serotonergic drug. It is often triggered by unintended drug interactions, underscoring the importance of recognizing potential precipitating agents. The Hunter Serotonin Toxicity Criteria is the most widely used diagnostic tool for identifying serotonin syndrome. This patient met Hunter criteria for SS by recent exposure to serotonergic agent, clonus, hyperreflexia, and tremor.8 One potential solution is to discontinue SSRIs at least five half-lives prior to administering methylene blue.9 Escitalopram has an elimination half-life of approximately 27 to 32 hours, meaning it generally takes about 5 to 7 days for the drug to be cleared from the body.10 However, the FDA recommends a more conservative washout period of 14 days to ensure safety. Drug clearance can vary significantly depending on several factors, including hepatic and renal function, age, and genetic variations—particularly in cytochrome P450 3A4 and cytochrome P450 2C19.10 Another intervention to help mitigate SS that was performed was cessation of serotonergic agents. When the patient was intubated, fentanyl was avoided given its serotonergic interactions. Also, stopping guaifenesin-codeine and guaifenesin-dextro-methorphan played a role in reducing potential harm. Early planning and discontinuation of serotonergic agents should be considered if planning to initiate MB as a potential salvage therapy for IFE. Additionally, for patients with rapidly progressive disease that are nearing end of life, extensive risk/benefit counseling needs to be done given the high rates of complications from both ifosfamide therapy and MB. Other patient factors, such as being on serotonergic agents, should be considered when considering ifosfamide as therapy in such patients. CONCLUSIONThis case presents a patient receiving escitalopram who experienced IFE that was treated with MB and who developed SS requiring intubation. Most cases involving the use of ifosfamide and subsequent MB require planning and preparation, especially in a patient on serotonergic agents. It is important to identify symptoms of IFE and SS early in their courses as well as identify risk factors for developing SS with administration of MB. More research is needed to determine the efficacy and safety of MB in IFE. 68The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 69 REFERENCES1. Lee Brink A, Bowe C, Dains JE. Risk factors for ifosfamide-related encephalopathy in adult cancer patients: an integrative review. J Adv Pract Oncol. 2020;11(4):368-380. doi:10.6004/jadpro.2020.11.4.42. Gangireddy M, Patel P, Nookala V. Ifosfamide [Internet]. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2025 Jan 9 [updated 2024 Jan 9; cited 2025 May 17]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519062/3. Shin YJ, Kim JY, Moon JW, You RM, Park JY, Nam JH. Fatal ifosfamide-induced metabolic encephalopathy in patients with recurrent epithelial ovarian cancer: report of two cases. Cancer Res Treat. 2011;43(4):260-263. doi:10.4143/crt.2011.43.4.2604. Ramsay RR, Dunford C, Gillman PK. Methylene blue and serotonin toxicity: inhibition of monoamine oxidase A (MAO A) confirms a theoretical prediction. Br J Pharmacol. 2007;152(6):946-951. doi:10.1038/sj.bjp.07074305. Snyder M, Gangadhara S, Brohl AS, Ludlow S, Nanjappa S. Serotonin syndrome complicating treatment of ifosfamide neurotoxicity with methylene blue. Cancer Control. 2017;24(5). doi:10.1177/10732748177290706. 6. Torchia A, Vari S, Onesti CE, et al. A narrative review on diagnosis and treatment of ifosfamide-induced encephalopathy, the perspective of a EURACAN reference center for sarcomas. Front Pharmacol. 2025;16:1512966. doi:10.3389/fphar.2025.15129667. Séjourné A, Noal S, Boone M, et al. Two cases of fatal encephalopathy related to ifosfamide: an adverse role of aprepitant. Case Rep Oncol. 2014;7(3):669-672. doi:10.1159/0003681848. Simon LV, Torrico TJ, Keenaghan M. Serotonin syndrome [Internet]. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2024 Mar 2 [cited 2025 May 17]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482232/9. Top WM, Gillman PK, de Langen CJ, Kooy A. Fatal methylene blue associated serotonin toxicity. Neth J Med. 2014;72(3):179-181. PMID: 2484693610. Landy K, Rosani A, Estevez R. Escitalopram [Internet]. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2023 Nov 10 [cited 2025 May 17]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK500548/69et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202570 | The Medicine Forum, Volume 26 "Three Sunrises at Miami Beach #1" – Gregary D. Marhefka, MD70The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 71 A Case of Varicella Zoster Virus Meningitis Presenting as Idiopathic Vocal Fold ParalysisDustin Sneed, MD1, M. Duncan Kilpatrick, MD1, Alicia Bao, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONThe typical presentation of a patient with herpes zoster, the reactivation of varicella zoster virus (VZV), involves a painful dermatomal vesicular rash known as shingles. However, as the following case demonstrates, VZV reactivation can present with atypical symptoms, sometimes without the characteristic rash. This presentation is known as zoster sine herpete. This case focuses on a patient presenting with dysphagia and dysphonia, who was diagnosed with VZV meningitis with suspected laryngeal involvement. We discuss workup and treatment for this disease, and the importance of a wide differential and multidisciplinary consultation to improve patient outcomes. CASE PRESENTATIONA 64-year-old female with a past medical history of hypertension, hyperlipidemia, pre-diabetes, peripheral artery disease, and migraines presented to the hospital for evaluation of rapid-onset dysphagia and dysphonia. She had upper respiratory symptoms, including cough, sore throat, and rhinorrhea in the five days prior to admission, but these symptoms rapidly progressed to dysphagia with inability to tolerate any solid food. She denied fevers, chills, chest pain, nausea, regurgitation, or vomiting. Her labs on presentation were significant for multiple electrolyte derangements including hypokalemia (2.4 mmol/L), hypocalcemia (5.9 mg/dL), hypomag-nesemia (1.2 mEq/L), hypophosphatemia (2.0 mEq/dL), and metabolic acidosis (bicarbonate 17 mmol/L) that were thought to be secondary to her inability to tolerate oral intake for multiple days beforehand. Initially, the gastroenterology (GI) team was consulted for consideration of esophagogastroduodenoscopy (EGD). Given the proximal nature of the patient’s dysphonia, GI recommended otolaryngology (ENT) evaluation first, with a plan to re-engage for possible EGD if clinically indicated. ENT was then consulted and performed a bedside laryngoscopy, which demonstrated left vocal cord paralysis in the paramedian position with no evidence of foreign body presence. Magnetic resonance imaging (MRI) of the skull base was performed, which demonstrated thickening and enhancement along the left oropharynx extending to the piriform sinus as well as medialized vocal cord without complete closure on the INFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE Table 1: Infectious Workup by Specimen SourceNasopharyngeal SwabSARS-CoV-2 RNA qualitative NAAT NegativeInfluenza A target RNA NegativeInfluenza B target RNA NegativeRSV target RNA NegativeRespiratory pathogen panel PCR NegativeSerumBlood culture No growthHIV-1 and HIV-2 antigen and antibody Non-reactiveVZV IgG PositiveNasopharyngeal SwabProtein 49 mg/dLGlucose 73 mg/dLTotal nucleated cell count 222/µLLymphocytes 135/µLMacrophages/monocytes 78/µLEosinophils 9/µLGram stain No organisms seenMeningitis/encephalitis CSF PCR PanelVZV detected, no other pathogens detectedVDRL Non-reactiveVZV quantitative PCR 63438 copies/mLHSV-1 and HSV-2 quantitative PCR Not detectedSARS-CoV-2 = Severe acute respiratory syndrome coronavirus 2RNA = Ribonucleic acidNAAT = Nucleic acid amplification testRSV = Respiratory syncytial virusPCR = Polymerase chain reactionHIV = Human immunodeficiency virusIgG = Immunoglobulin GCSF = Cerebrospinal fluidVDRL = Venereal Disease Research Laboratory testVZV = Varicella zoster virusHSV = Herpes simplex virus71et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202572 | The Medicine Forum, Volume 26 left. Additional imaging with computer tomography (CT) head and neck was consistent with these findings. She also underwent a fluoroscopic video swallow study per speech pathology (SLP) recommendations, which demonstrated continued aspiration. As such, she had a Dobhoff tube placed for enteral access, and tube feeds were started.On day 3, the patient developed a sore throat, headache, and neck stiffness with anterior flexion of the neck. Given that pain was primarily left-sided, this was initially attributed to her idiopathic vocal cord paralysis. She subsequently became febrile to 101.4° Fahrenheit (F) and was empirically started on meningitis treatment with vancomycin, cefepime, and amoxicillin. Lumbar puncture was performed on Day 4, with fluid studies demonstrating 222 white blood cells (WBCs)/uL (61% lymphocytes), 0 red blood cells (RBCs)/uL, protein 49mg/dL, and glucose 73mg/dL (Table 1). Multiplex polymerase chain reaction (PCR) of the cerebrospinal fluid (CSF) was positive for VZV. The infectious disease (ID) team was consulted and recommended discontinuing antibiotics and starting intravenous (IV) acyclovir 10 mg/kg every eight hours. After discussion with both the ENT and ID teams, she was also treated with dexamethasone 8 mg three times daily to treat any inflammatory contribution to vocal cord paralysis. The patient underwent repeat bedside laryngoscopy on hospital day 9 (six days after initiation of IV acyclovir and three days after steroids). This demonstrated continued lef t vocal cord paralysis; however, with better compensation from the contralateral vocal cord, resulting in improved glottic closure. She had a repeat fluoroscopic video swallow study on hospital day 10, which showed continued penetration of thin liquids as well as significant puree residue in the piriform sinuses but with no aspiration. The patient was discharged on hospital day 10 to complete a 14-day course of IV acyclovir and a 15-day prednisone taper. She was discharged with a Dobhoff tube in place with outpatient follow-up with SLP. She was seen in the ID clinic five days post-discharge. During her visit, she reported resolution of her sore throat, headache, and neck stiffness; however, she was still experiencing dysphagia and dysphonia with only minimal improvement since beginning treatment. She was seen in the ENT clinic two weeks later with mild improvement in phonation. Videostroboscopy, performed in the office, showed she was now achieving full glottic closure, but she had reduced abduction of the left vocal fold. She exhibited improved swallowing function at her outpatient SLP appointment with no evidence of aspiration during video swallow study. She was safely advanced to a pureed diet with plans for further advancement in the coming weeks.DISCUSSIONVZV is an alpha herpesvirus that establishes dormancy in latent infection in dorsal root ganglia, reactivating years later as herpes zoster, also known as shingles. Although VZV reactivation usually presents as dermatomal neurocutaneous lesions, reactivation can occur in the cranial nerve ganglia without the characteristic rash, known as zoster sine herpete.1 Here, we present a rare case of VZV meningitis presenting with vocal fold paralysis in an immunocompetent patient. Herpes zoster reactivation in the central nervous system is rare, accounting for roughly 7% of viral meningitis cases in a large observational study.2 Despite sharing many overlapping symptoms with bacterial meningitis (headache, neck stiffness, photophobia, and fever), viral meningitis tends to have a more benign presentation, often lacking high fevers, altered consciousness, focal neurologic findings, and shock.3 Viral meningitis is suggested by lumbar puncture findings showing lymphocytic pleocytosis, defined as WBC count > 5 cells/mm2, in the absence of a positive bacterial gram stain/culture. CSF obtained within the disease course may have a high percentage of polymorphonuclear leukocytes, but as the disease course progresses, there is a tendency towards lymphocytic predominance. Notably, in a case series comparing CSF findings between viral meningitides, the percentage of lymphocytes was higher in herpes simplex virus (HSV)/VZV cases compared to enteroviruses, the leading cause of aseptic meningitis.4 Other LP findings supportive of VZV meningitis include elevated protein and normal glucose. The CSF studies in the index case had primarily lymphocytic pleocytosis, consistent with expected findings for viral meningitis. The diagnosis can be confirmed with multiplex PCR studies, which are now available at many institutions, with the commercial meningitis/encephalitis panels having the ability to detect VZV deoxyribonucleic acid (DNA) in the CNS with exceedingly high positive predictive value, even if empiric antiviral therapy has already been started.5Although there is a recommended treatment for HSV meningitis, guidelines for the treatment of VZV meningitis are less clear. Most recommendations involve a similar approach, with the Infectious Diseases Society of America (IDSA) recommending IV acyclovir 10-15 mg/kg three times per day for a 10–14-day course.6 However, there is limited data to support the necessity of a particular antiviral regimen or duration of treatment. A recent retrospective cohort study of 123 patients with confirmed VZV meningitis showed no difference in outcomes for patients treated with standard IV acyclovir, short-course IV acyclovir, oral valacyclovir alone, or no antiviral treatment.7 In this study, IV antiviral administration was favored for patients who were older and immunosuppressed. Supportive care alone may be sufficient for milder cases in young, otherwise healthy patients. 72The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 73 Cranial nerve (CN) reactivation of herpes zoster can cause a wide spectrum of symptoms depending on the involved nerve. The common syndromes are herpes zoster ophthalmicus, caused by involvement of the ophthalmic branch of CN V, and herpes zoster opticus (also known as Ramsay Hunt syndrome), caused by involvement of the geniculate branch of CN VII. There have been a handful of case reports describing laryngeal paralysis due to VZV reactivation without characteristic skin lesions. While certainly atypical in presentation, VZV reactivation can lead to vocal cord paralysis through involvement of the vagus nerve through which one subdivision (the recurrent laryngeal nerve) innervates the larynx. This can lead to decreased laryngeal sensation, vocal cord hypomobility, dysphonia, and dysphagia.8 The recurrent laryngeal nerve has been postulated to be the most susceptible branch of the vagus nerve due to the longer distance it must travel from the nerve root to the larynx.9 While mucosal lesions resolve with antiviral treatment, dysphonia and dysphagia can persist for months to years but generally exhibit a favorable outcome.10 In most cases, however, a mucosal lesion is seen on the affected larynx on laryngoscopy.8,9,11 The index case had no visible laryngeal lesions, which could suggest that this vocal cord paralysis was secondary to meningeal irritation of the nerve root instead of direct involvement. Further cases have found vocal fold paralysis related to inflammation of the medulla, which can be seen on MRI.12 An MRI brain without contrast was obtained in this patient, but well into her course of treatment, and no inflammatory lesions were noted. CONCLUSIONVZV reactivation can cause a spectrum of neurologic deficits depending on the location of the involved nerve. Here, we present a rare case of VZV meningitis initially presenting as idiopathic vocal fold paralysis. Diagnosis was confirmed with CSF studies once the patient began displaying typical symptoms of meningitis. Although rare, VZV reactivation in the vagus nerve can present with vocal cord dysfunction without characteristic skin or mucosal lesions. REFERENCES1. Kennedy PGE. The spectrum of neurological manifestations of varicella-zoster virus reactivation. Viruses. 2023;15(8):1163. doi:10.3390/v150816632. McGill F, Griffiths MJ, Bonnett LJ, et al. Incidence, aetiology, and sequelae of viral meningitis in UK adults: a multicentre prospective observational cohort study. Lancet Infect Dis. 2018;18(9):992-1003. doi:10.1016/S1473-3099(18)30245-73. Brivet FG, Ducuing S, Jacobs F, et al. Accuracy of clinical presentation for differentiating bacterial from viral meningitis in adults: a multivariate approach. Intensive Care Med. 2005;31(12):1654-1660. doi:10.1007/s00134-005-2811-14. Wright WF, Pinto CN, Palisoc K, Baghli S. Viral (aseptic) meningitis: a review. J Neurol Sci. 2019;398:176-183. doi:10.1016/j.jns.2019.01.0505. Liesman RM, Strasburg AP, Heitman AK, Theel ES, Patel R, Binnicker MJ. Evaluation of a commercial multiplex molecular panel for diagnosis of infectious meningitis and encephalitis. J Clin Microbiol. 2018;56(4):e01927-17. doi:10.1128/JCM.01927-176. Tunkel AR, Glaser CA, Bloch KC, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2008;47(3):303-327. doi:10.1086/5897477. Dulin M, Chevret S, Salmona M, et al. New insights into the therapeutic management of varicella zoster virus meningitis: a series of 123 polymerase chain reaction-confirmed cases. Open Forum Infect Dis. 2024;11(7):ofae340. doi:10.1093/ofid/ofae3408. Davis S, Thomas E, Lowery A, Kahue C, Gelbard A. Varicella zoster virus reactivation involving the vagus nerve. Ann Otol Rhinol Laryngol. 2023;132(7):818-824. doi:10.1177/000348942211112599. Chitose SI, Umeno H, Hamakawa S, Nakashima T, Shoji H. Unilateral associated laryngeal paralysis due to varicella-zoster virus: virus antibody testing and videofluoroscopic findings. J Laryngol Otol. 2008;122(2):170-176. doi:10.1017/S002221510700089810. Cheng L, Lin Y, Yang J, et al. Clinical characteristics and prognosis of herpes zoster laryngitis with vocal fold immobility. J Voice. Published online June 20, 2024. doi:10.1016/j.jvoice.2024.05.02011. Hosseini S, Zawawi F, Young J. Atypical presentation of a common disease: shingles of the larynx. J Voice. 2015;29(5):600-602. doi:10.1016/j.jvoice.2014.10.01012. Purbaugh MV, Pedavally S, Piccione E, Vuppala AD. Varicella zoster meningitis presenting with isolated dysphagia, dysarthria and dysphonia. Neurohospitalist. 2022;12(1):167-170. doi:10.1177/194187442097646973et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202574 | The Medicine Forum, Volume 26 A Patient with Recently Diagnosed HIV Found to have Cryptococcus Meningitis with Course Complicated by Pneumocystis Jirovecii Pneumonia, CMV Colitis, and Kaposi Sarcoma Benjamin Richter, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE INTRODUCTIONOpportunistic infections (OIs) remain a major cause of morbidity and mortality in individuals with advanced human immunodeficiency virus/acquired immunodefi-ciency syndrome (HIV/AIDS), particularly in those with severe immunosuppression. Among the most life-threatening OIs are cryptococcal meningitis, Pneumocystis jirovecii pneumonia (PJP), cytomegalovirus (CMV) colitis, and Kaposi sarcoma (KS), each of which poses significant diagnostic and therapeutic challenges.Here is a case of a man with recently diagnosed HIV who was admitted to the hospital with a chief complaint of headache and was found to have cryptococcal meningitis with a hospital course complicated by Pneumocystis jirovecii pneumonia (PJP), CMV colitis, and Kaposi sarcoma. This case highlights the complexity of managing multiple OIs in patients with advanced HIV and underscores the importance of screening for HIV in populations who are at higher risk for the disease. CASE PRESENTATIONA 57-year-old male with a history of recently diagnosed HIV presents to a hospital with a persistent headache for the past two weeks, which has been partially relieved with acetaminophen. He reported feeling generally unwell with a productive cough for the past month and was recently evaluated at an outpatient sick visit. At that visit, he noted unintentional weight loss for 5 months. Tuberculosis (TB), hepatitis, and HIV testing were completed, and he was given a course of amoxicillin-clavulanate and doxycycline to treat community-acquired pneumonia. HIV testing resulted with a viral load of 4,240,000 copies/mL and a cluster of differentiation 4 (CD4) count of 68 cells/mm3. His last HIV testing prior to this was in 2019 and was negative. He was seen by infectious disease as an outpatient and initiated on antiretroviral therapy (ART) as well as trimethoprim-sulfamethoxazole (TMP/SMX) for prophylaxis against opportunistic infections.The patient also noted the presence of three non-painful, non-pruritic lesions located on his right elbow and bilateral hips. He was initially prescribed amoxicillin-clavulanate for the presumed rash; however, he discontinued the medication due to headache and diarrhea. Subsequently, dermatology prescribed clindamycin, which has not resulted in improvement. Basic metabolic panel findings included a sodium level of 128 mmol/L, creatinine of 0.97 mg/dL, and albumin of 2.9 g/dL. Liver function tests showed an alkaline phosphatase of 55 U/L, aspartate aminotransferase (AST) of 23 U/L, alanine aminotransferase (ALT) of 25 U/L, and total bilirubin of 0.3 mg/dL. Hematologic studies demonstrated a white blood cell count of 7.2 ×10³/μL, hemoglobin of 10.4 g/dL, platelets of 249 ×10³/μL, and a mean corpuscular volume (MCV) of 85 fL. Chest x-ray (CXR) showed minimal left basilar atelectasis and was otherwise unremarkable. Computed tomography (CT) head did not show any acute intracranial hemorrhage, mass effect, or acute large territorial infarction. Because of his recent HIV diagnosis, infectious disease was consulted and recommended lumbar puncture due to the increased risk of opportunistic meningitis. Cerebrospinal fluid analysis from a lumbar puncture showed clear, colorless fluid with an opening pressure of 17 cm H₂O. The sample contained 124 red blood cells and 5 white blood cells (reference range: 0-5). Cerebrospinal fluid (CSF) glucose was measured at 55 mg/dL (reference: 40-70 mg/dL), while protein was slightly elevated at 56 mg/dL (reference: 15-45 mg/dL). Cryptococcal antigen serum testing was positive at a titer of 1:20, and Cryptococcus was isolated on culture. Blood cultures also returned positive for Cryptococcus, confirming systemic involvement. He was started on amphotericin and flucytosine.On day three of admission, the patient was found to be acutely hypotensive, hypoxic, tachycardic, altered, and diffusely erythematous with a fever of 103.5° Fahrenheit (F). Chest x-ray showed new infiltrates in the left lung. This acute change was thought to be in the setting of an allergic reaction to TMP/SMX due to the acuity and rash. The patient was given hydroxyzine, famotidine, and hydrocortisone. TMP/SMX was changed to clindamycin and primaquine, and he was started on vancomycin, cefepime, and prednisone. CT angiography of the chest was performed, which showed small bilateral pleural effusions in addition to diffuse regions of lung consolidation and ground glass opacities (Figure 1). Follow-up bronchoscopy revealed PJP.74The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 75 Figure 1: Diffuse consolidations and ground glass opacities as seen on coronal and transverse views of CT chest. Bronchoscopy specimens revealed Pneumocystis jirovecii pneumonia.Figure 3: Red and brown macules on the leg, trunk, arm, and thigh, consistent with Kaposi sarcoma.Figure 2: Ulcerative lesions and mucosal edema from terminal ileum to the rectum. Biopsy of lesions revealed CMV colitis.The patient’s diffuse erythematous rash resolved, but he was evaluated by dermatology in the setting of several non-pruritic and non-painful skin lesions reported on admission (Figure 3). He was diagnosed with Kaposi sarcoma based on clinical presentation.Several days following this event, the patient had maroon stool output. Clostridioides difficile testing and stool infectious panel were negative. CT of the abdomen showed diffuse enterocolitis. Follow-up colonoscopy (Figure 2) with biopsy was positive for CMV colitis, and he was started on ganciclovir. 75et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202576 | The Medicine Forum, Volume 26 DISCUSSIONColorectal cancer (CRC) will commonly metastasize to the liver and lungs via portal and systemic circulation. Although bone marrow involvement is uncommon with CRC, slow marrow blood flow and growth factor signaling may facilitate tumor cell adhesion and implantation Once established in marrow, tumor proliferation causes bone destruction and hematologic DISCUSSIONHIV/AIDS is associated with a range of opportunistic infections (OIs) due to progressive immune suppression, particularly in patients with CD4 counts below 200 cells/mm³. In this case, the patient presented with untreated, advanced HIV and was diagnosed with cryptococcal meningitis, Pneumocystis jirovecii pneumonia, CMV colitis, and Kaposi sarcoma all within one hospitalization and occurring within 30 days of HIV diagnosis. The individual incidence of these opportunistic infections is well-documented in the literature, but no reports have documented the concomitant incidence of three or four unique infections during one hospitalization. Cryptococcus neoformans typically enters the host via inhalation, leading to a latent pulmonary infection that can disseminate to the central nervous system. Cryptococcal meningitis remains a leading cause of morbidity and mortality in people with AIDS and requires prompt diagnosis and treatment with antifungal therapy, including liposomal amphotericin B and flucytosine, followed by long-term fluconazole maintenance.1 36% of patients present with cough,2 and 77% with headache,3 both of which were present in this patient. Delayed or inadequate treatment can lead to high intracranial pressure, neurological deficits, and death.4His cough also may have been the result of smoldering Pneumocystis jirovecii pneumonia, which is a common opportunistic pulmonary infection in patients with CD4 counts below 200 cells/mm³. The incidence is so high in this group that TMP/SMX is given prophylactically to prevent infection. Interestingly, the CXR on admission was relatively unremarkable, and the patient had no other respiratory symptoms until three days into hospital-ization, at which time his shortness of breath was thought to be from airway edema in the setting of an allergic reaction. The presence of ground-glass opacities on CT, in clinical context, made PJP infection more likely. The delay in TMP/SMX prophylaxis for this patient may have contributed to his development of infection. Cytomegalovirus (CMV) colitis is another life-threatening opportunistic infection in patients with profound immunosuppression, typically occurring at CD4 counts below 50 cells/mm³. CMV infection can affect multiple organ systems, with colitis presenting as abdominal pain, diarrhea, and mucosal ulcerations on endoscopy. Diagnosis is confirmed through tissue biopsy with immunohistochemical staining, and treatment consists of intravenous ganciclovir or oral valganciclovir.5 Early initiation of ART therapy may have prevented the immune deterioration that allowed CMV to proliferate. Kaposi sarcoma (KS), an AIDS-defining malignancy caused by human herpesvirus-8 (HHV-8), is frequently seen in patients with advanced HIV. It presents as violaceous skin lesions but can also involve visceral organs, including the lungs and gastrointestinal tract. Management of KS depends on disease burden, with localized lesions responding to initiation of antiretroviral therapy (ART), while extensive disease may require systemic chemotherapy.6CONCLUSION This case highlights the importance of early recognition and treatment of opportunistic infections in patients with untreated or advanced HIV. Moreover, the case is a reminder of the importance of regular HIV screening for individuals in high-risk categories, such as this patient. This screening should start by asking patients about their sexual habits during routine health maintenance exams. REFERENCES1. World Health Organization. Guidelines for Diagnosing, Preventing, and Managing Cryptococcal Disease Among Adults, Adolescents, and Children Living with HIV. World Health Organization; 2022. Accessed May 13, 2025. https://www.who.int/publications/i/item/97892400521782. Lee YC, Wang JT, Sun HY, Chen YC. Comparisons of clinical features and mortality of cryptococcal meningitis between patients with and without human immunodeficiency virus infection. J Microbiol Immunol Infect. 2011;44(5):338-345. doi:10.1016/j.jmii.2010.08.0113. Li Y, Zou M, Yin J, Liu Z, Lu B. Microbiological, epidemiological, and clinical characteristics of patients with cryptococcal meningitis at a tertiary hospital in China: a 6-year retrospective analysis. Front Microbiol. 2020;11:1837. doi:10.3389/fmicb.2020.018374. Centers for Disease Control and Prevention. Cryptococcosis: guidelines for the prevention and treatment of opportunistic infections in adults and adolescents with HIV. Accessed May 13, 2025. https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/cryptococcosis5. Centers for Disease Control and Prevention. Cytomegalovirus Disease: guidelines for the prevention and treatment of opportunistic infections in adults and adolescents with HIV. Accessed May 13, 2025. https://clinicalinfo.hiv.gov/sites/default/files/guidelines/documents/adult-adolescent-oi/cytomegalovirus-adult-adolescent-oi.pdf6. National Cancer Institute. Kaposi Sarcoma Treatment (PDQ®)–Patient Version. Updated February 9, 2024. Accessed May 13, 2025. https://www.cancer.gov/types/soft-tissue-sarcoma/patient/kaposi-treatment-pdq76The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 77 From Cure to Crisis: A Case of Severe Hypoxic Respiratory Failure Due to Daptomycin-Associated Eosinophilic Pneumonitis Muneeba Ali, MD1, Enad Haddad, MD1, Warda Naqvi, MD1, Conrad Reed, MD21. Division of Internal Medicine, Department of Medicine, Jefferson Abington Hospital, Abington, PA2. Division of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, Jefferson Abington Hospital, Abington, PAINTRODUCTIONDaptomycin is a cyclic lipopeptide antibiotic that commonly treats Gram-positive infections. Most frequently prescribed for osteoarticular infections.1 Daptomycin is associated with numerous side effects, including myopathy, rhabdo-myolysis, eosinophilic pneumonia, and anaphylactic hypersensitivity reactions.1 Daptomycin-induced eosinophilic pneumonitis (DIEP) is a rare but potentially life-threatening adverse effect associated with prolonged use.2 There are several established criteria for diagnosing this medical condition. However, the variation in its clinical presentation, coupled with the favorable outcomes of early diagnosis and the severe consequences of delayed diagnosis, emphasizes the need for further discussions. This case highlights the importance of monitoring patients on prolonged daptomycin therapy for this serious complication. Furthermore, it emphasizes the value and limitations of standardized scoring tools as clinical aids in decision-making, early diagnosis, and timely treatment. CASE PRESENTATIONA 64-year-old female presented to the emergency department with lethargy, hypoxia, non-productive cough, and chills four weeks after hospital discharge while being treated for Staphylococcus epidermidis discitis with a 7-week course of intravenous (IV) daptomycin. On examination, she was febrile (temperature 102°F). Laboratory findings included a white blood cell count of 13.0 cells/microliter (10⁹/L) (reference range: 4.0-11.0 × 10⁹/L), with 76.6% neutrophils (reference range: 40.0-73.0%) and 3.1% eosinophils (reference range: 0.0-7.0%), yielding an absolute eosinophil count of 0.40 × 10⁹/L (reference range: 0.0-0.70 × 10⁹/L). Chest radiography revealed moderate bilateral scattered infiltrates (Figure 1), and computed tomography demonstrated similar findings (Figure 2). She was admitted with a provisional diagnosis of multifocal pneumonia. Initial management included 2 liters/minute oxygen via nasal cannula, but progressive hypoxia necessitated a non-rebreather mask. Cefepime and vancomycin were started for suspected hospital-acquired pneumonia. Although prolonged daptomycin use was noted, daptomycin-induced eosinophilic pneumonitis (DIEP) was initially considered unlikely due to minimal peripheral eosinophilia. Within 48 hours, worsening respiratory distress required bilevel positive airway pressure support, followed by intubation. Mechanical ventilation began with assist-control volume control mode, later transitioning to INFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE Figure 1. Anteroposterior chest radiograph of a patient with daptomycin-induced eosinophilic pneumonitis demonstrating scattered infiltrates in the bilateral lung fields.Figure 2. Axial chest CT in the same patient showing multifocal pulmonary infiltrates.77et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202578 | The Medicine Forum, Volume 26 airway pressure release ventilation, due to refractory hypoxia. On the day of intubation, methylprednisolone 60 milligrams by intravenous route (IV) every 4 hours was started empirically for DIEP. Bronchoscopy with bronchoalveolar lavage (BAL) revealed 21% eosinophils, confirming the diagnosis. An extensive infectious workup—including respiratory pathogen panel, BAL Gram stain and culture, Streptococcus pneumoniae antigen, Legionella species deoxyribonucleic acid (DNA), and blood cultures—was negative. Within 48 hours of steroid initiation, the patient showed significant improvement. She was extubated, and three days post-intubation she was discharged home on an oral prednisone taper (2-week course). Her discitis treatment was completed with IV vancomycin. DISCUSSION Daptomycin is a cyclic lipopeptide antibiotic that exerts a bactericidal effect by disrupting multiple aspects of bacterial cell membrane function.1 It is only effective against Gram-positive bacteria and is used to treat skin and skin structure infections, Staphylococcus aureus bacteremia, osteomyelitis, septic arthritis, etc.1 Common side effects include myopathy, rhabdomyolysis, eosinophilic pneumonia, and anaphylactic hypersensi-tivity reactions.1 Eosinophilic pneumonia (EP) is a clinical syndrome that is further classified as acute or chronic, and character-istics include eosinophilic infiltration of lung parenchyma, peripheral eosinophilia, >25% eosinophils in bronchoal-veolar lavage, and clinical symptoms such as dry cough, dyspnea, chest pain, and fevers.3,4 It can also be classified into primary and secondary. The main causes of secondary EP are medications and toxins. Common medications contributing to EP include daptomycin, mesalamine, sulfasalazine, and minocycline.5 DIEP is a rare complication of daptomycin use, with a prospective cohort study reporting an incidence of 7 out of 1130 patients.2 The outcome of DIEP tends to be favorable, with one study reporting a recovery rate of 78.4%, an improvement rate of 18.9%, and a mortality rate of 2.7% among 74 cases.6 It is reported mostly in patients who are being treated for bone and joint infections, due to the use of higher dosages and longer courses of treatment for this particular indication.2 Proposed mechanisms for DIEP include drug uptake by alveolar macrophages, followed by antigen presentation to T helper cells. This process stimulates the release of interleukin-5 and eotaxin, leading to the recruitment of eosinophils into the alveolar spaces. The resulting inflammatory cascade leads to acute epithelial damage.6,7 Risk factors for the development of DIEP include higher cumulative doses, longer treatment courses, and impaired renal function.2 Symptoms typically appear after a mean of 21.75 days of daptomycin treatment.8 Reported symptoms include fever, dyspnea, dry cough, and acute respiratory failure.9 It is more common in males.8 Radiological findings often include bilateral opacities, ground-glass opacities, patchy infiltrates, consolidation, and peripheral predominance of infiltrates.6,9 It is characterized by significant eosinophilia in peripheral blood and bronchoalveolar lavage.9 Treatment strategies involve discontinuation of daptomycin, respiratory support, and corticosteroid therapy, though some patients recover without added interventions once daptomycin is stopped.6 Numerous diagnostic criteria have been proposed for DIEP, including the Food and Drug Administration (FDA) criteria, Kim’s criteria, Philip’s criteria, and Lyon’s algorithm.10 The primary concern about DIEP is improving diagnostic accuracy. Our case would be classified as "probable" according to the FDA criteria and Kim’s criteria and "definite" according to Philip’s criteria and Lyon’s algorithm. The "probable" classification in the first two cases is due to the absence of peripheral eosinophilia and fewer than 25% eosinophils on bronchoalveolar lavage. Many cases of DIEP do not fully meet these earlier criteria, leading to the development of Kim’s criteria and Lyon’s algorithm. These criteria are particularly important as they view DIEP as a “syndrome,” thereby charac-terizing it as a definite, probable, or possible case of DIEP. In the Lyon algorithm's case, it does not require bronchoscopy to establish the diagnosis. Given the rare incidence of DIEP, an integrated and comprehensive set of criteria that encompasses these differences has yet to be established. Most of the studies that led to the development of existing criteria have been single-center studies or studies with small sample sizes, which negatively impact the predictive value of these criteria. CONCLUSION This case is unique as it is the uncommon presentation of an uncommon condition. It emphasizes the importance of monitoring patients prescribed prolonged daptomycin therapy for pneumonitis development. Our case highlights the importance of considering these newer diagnostic criteria (i.e. Kim’s criteria and Lyon’s algorithm) and highlights the need for ongoing refinement of these tools to improve diagnostic accuracy for this unique clinical syndrome.78The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 79 REFERENCES1. Patel S, Saw S. Daptomycin. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2024. http://www.ncbi.nlm.nih.gov/books/NBK470407/.2. Garreau R, Pham TT, Bourguignon L, et al. Daptomycin exposure as a risk factor for daptomycin-induced eosinophilic pneumonia and muscular toxicity. Clin Infect Dis. 2023;77(10):1372-1380. doi:10.1093/cid/ciad3863. Katz U, Shoenfeld Y. Pulmonary eosinophilia. Clin Rev Allergy Immunol. 2008;34(3):367-371. doi:10.1007/s12016-007-8053-y4. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med. 1994;150(5 Pt 1):1423-1438. doi:10.1164/ajrccm.150.5.79525715. Bartal C, Sagy I, Barski L. Drug-induced eosinophilic pneumonia. Medicine (Baltimore). 2018;97(4):e9688. doi:10.1097/MD.00000000000096886. Gidari A, Pallotto C, Francisci D. Daptomycin eosinophilic pneumonia, a systematic review of the literature and case series. Infection. Published online July 19, 2024. doi:10.1007/s15010-024-02349-z7. Daptomycin-induced acute eosinophilic pneumonia. Cureus. Accessed December 4, 2024. https://www.cureus.com/articles/12995-daptomycin-induced-acute-eosinophilic-pneumonia#!/8. Di Lorenzo A, Rindi LV, Campogiani L, et al. Daptomycin-induced eosinophilic pneumonia: a case report and systematic review. Chemotherapy. 2024;69(2):85-99. doi:10.1159/0005351909. Wu C, Li Z, Wang C, Deng Z. Clinical characteristics, management, and outcome of eosinophilic pneumonia associated with daptomycin. Med Clin (Barc). 2023;160(1):17-22. doi:10.1016/j.medcli.2022.03.01710. Pham TT, Garreau R, Craighero F, et al. Seventeen cases of daptomycin-induced eosinophilic pneumonia in a cohort of patients treated for bone and joint infections: proposal for a new algorithm. Open Forum Infect Dis. 2022;9(11):ofac577. doi:10.1093/ofid/ofac57779et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202580 | The Medicine Forum, Volume 26 Negative Urine Nucleic Acid Amplification Testing in a Case of Disseminated Gonococcal Infection Presenting as Migratory ArthritisBenjamin Richter, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE INTRODUCTIONDisseminated gonococcal infection (DGI) is a well-documented complication of Neisseria gonorrhoeae infection, most characteristically presenting as migratory arthritis, tenosynovitis, and dermatitis. Although modern nucleic acid amplification tests (NAATs) and cultures from mucosal sites have significantly improved diagnostic capabilities, discrepancies between clinical manifes-tations and laboratory findings still occur.1 One such challenge arises when the urine gonorrhea test returns negative despite strong clinical evidence pointing toward gonococcal involvement.Migratory arthritis—a transient, shifting pattern of joint inflammation—has long been recognized as a hallmark of DGI.2 Typically, the pathogen is detected in blood, synovial fluid, or from mucosal specimens; however, negative urine testing can complicate the clinical picture and delay definitive diagnosis.CASE PRESENTATIONA 52 year-old male with a past medical history of type 2 diabetes and hyperlipidemia was transferred from a community hospital to an academic hospital for rheumatology evaluation in the setting of joint pain and swelling for 10 days. The patient was in his usual state of health when he swerved to avoid hitting a raccoon. Later that day, he noticed increasing pain and swelling in his bilateral wrists which was more predominant in the left wrist (Figure 1). He presented to a local emergency room, where x-rays of the wrists were negative for fractures. He was diagnosed with a wrist sprain and advised to follow up with orthopedics, who prescribed a methylprednisone taper at an outpatient visit four days later. He completed one dose but then that evening the patient fell from his bed due to joint pain and swelling, which had now started to affect his lower extremities (Figure 2). He was unable to lift himself back into bed so he called emergency medical services, who took him to the local emergency department (ED). In the ED, laboratory testing was notable for hyperglycemia and leukocytosis (22.7 M/L), suspected to be secondary to the corticosteroid he had taken. Hemoglobin was 15.8 g/dL, with platelets of 247 K/uL. He was admitted to the hospital with infectious disease consultation. He reported no recent travel, no time spent in wooded areas, and no known tick or insect bites. He had a cat at home but he had noted no scratches or bites. Laboratory findings revealed an elevated rheumatoid factor (RF) (15.5 IU/ml), elevated C-reactive protein (CRP) (419 mg/L), increased ferritin levels (979 ng/ml), and a positive antinuclear antibody (ANA) titer of 1:320. He was started on vancomycin for coverage of skin and soft tissue infection, and urine gonorrhea and chlamydia NAAT was negative that same day. Human immunodeficiency virus (HIV) testing and Treponema pallidum antibody enzyme immunoassay were also negative. Additional infectious workup, including blood cultures and urinalysis, were unremarkable. A computed tomography (CT) scan of the chest, abdomen and pelvis showed hepatomegaly but no lymphadenopathy and no evidence of pneumonia. A small area of fluctuance on the left wrist was noted on physical exam, for which follow-up magnetic resonance imaging (MRI) revealed a 1.5 x 0.8 x 3.4 cm abscess overlying the dorsum of the third metacarpal base in addition to ill-defined mild enhancement and T2 hyperintense signals of the capitate, hamate, trapezium, trapezoid, and bases of the second through fourth metacarpals, thought to be consistent with a diffuse myositis of the intrinsic hand musculature. He underwent incision and drainage (I&D) of the abscess, which showed purulence but initial drainage cultures were without growth. Vancomycin was discontinued and infectious disease signed off. Their service suspected his symptoms were likely rheumatologic in nature. The patient was then transferred to a large academic hospital for rheumatologic evaluation. On evaluation, rheumatology suspected reactive, inflammatory arthritis and noted while ANA and RF were positive, his history was inconsistent with a rheumatologic diagnosis such as systemic lupus erythematosus. The rash was noted to have spontaneously improved (Figure 3). He was started on prednisone 10 mg daily for inflammatory arthritis. Autoimmune antibody testing, complement levels, and repeat RF were sent, all of which were negative. ANA was thought to be elevated in the setting of inflammation. Two days after I&D, the patient was contacted by the outside hospital and notified of cultures growing Neisseria gonorrhoeae. He was treated with 14 days of intravenous ceftriaxone and seven days of oral doxycycline to cover for Chlamydia 80The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 81 CONCLUSION While NAAT testing for Neisseria gonorrhoeae is reported to have high sensitivity and specificity, there is still a risk for false negative testing. While not typically used as a diagnostic tool, bacterial cultures of I&D specimens offer additional laboratory information that, when combined with clinical evidence, can assist in making a diagnosis. REFERENCES1. Li R, Hatcher JD. Gonococcal Arthritis. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK470439/2. Lutro O, Lillebø K, Schrama JC, Dale H, Sjursen H. A man with fever and joint pain. Tidsskr Nor Laegeforen. 2016 Dec;136(23-24):1999-2001.3. Workowski KA, Bolan GA; Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64(RR-03):1-137.4. Whiley DM, Tapsall JW, Sloots TP. Nucleic acid amplification testing for Neisseria gonorrhoeae: an ongoing challenge. J Mol Diagn. 2006;8(1):3-15. doi:10.2353/jmoldx.2006.050045co-infection. He completed a steroid taper to reduce inflammation associated with his infective arthritis. On physical therapy evaluation he was noted to be making progress in ambulation and functional mobility and recommended for continued rehabilitation. He was discharged to an acute rehabilitation facility. DISCUSSIONUrine NAAT for Neisseria gonorrhoeae is highly sensitive and specific with sensitivity of approximately 90-95% and specificity of 99-100%.3 This patient’s NAAT for N. gonorrhoeae was negative but biopsy cultures from I&D revealed gonococcal infection. A falsely negative NAAT may be seen in cases where patients have initiated antibiotics prior to testing, thus reducing detectable bacterial load.4 However, this patient’s only antibiotic was vancomycin that was started on the day of NAAT collection. While offering coverage for common skin and soft tissue infections such as Staphylococcus aureus and Streptococcus pyogenes, vancomycin does not offer coverage for N. gonorrhoeae. The patient also received a dose of methylprednisone prior to NAAT, but steroids are unlikely to cause false negatives on NAAT testing as they do not directly affect bacterial load. Due to a false negative test, the patient received a broad rheumatologic workup that may have been avoided if the NAAT had resulted positive for Neisseria, as his migratory polyarthritis is a well-documented complication of infection. Because I&D is typically performed for clinical management and symptom relief rather than as a screening or diagnostic tool, it does not have established sensitivity and specificity values applicable to the detection of Neisseria gonorrhoeae infection.Figure 1. Erythema and edema of the patient's left wrist. MRI detected an underlying abscess in addition to diffuse synovitis.Figure 2. Erythematous rash developed on the patient's bilateral lower extremities.Figure 3. Improvement of rash. This occurred prior to initiation of antimicrobial therapy.81et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202582 | The Medicine Forum, Volume 26 String Theory - A Case of Hypermucoviscous Klebsiella Pneumoniae Causing Distant Necrotizing InfectionsNatasa Kostic, MD1* and Marina Gonzalez, MD1*1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA* These authors contributed equally to this workINFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE INTRODUCTIONKlebsiella pneumoniae is a Gram-negative, encapsulated bacterium belonging to the Enterobacteriaceae family. It is more frequently associated with nosocomial infections and is one of several bacteria developing high rates of antibiotic resistance.1 Since the mid-1980s, there have been reported cases of Klebsiella pneumoniae causing life-threatening, invasive infections acquired in the community by otherwise healthy individuals. The propensity to form metastatic foci of infection in immunocompetent hosts is unusual for an enteric, Gram-negative pathogen.2 This hypervirulent variant of K. pneumoniae was originally noted only in Asian-Pacific countries but is now being identified globally.3 The variant has unique mucoid characteristics and is also often referred to as hypermucoviscous. We discuss a case of a young male who presented with severe sepsis secondary to hypervirulent K. pneumoniae (hvKP) causing distant concomitant abscesses and necrotizing fasciitis. CASE PRESENTATIONA 40-year-old male with no known past medical history presented to the emergency room with two weeks of right neck swelling and pain as well as four days of left calf pain. The symptoms occurred suddenly without known inciting factors. The patient denied trauma, sick contacts, intravenous drug use, dental work, or pet exposures. He had an episode of tonsillitis about two months prior, which was treated with oral antibiotics. On further review of systems, he endorsed worsening odynophagia but denied fevers, chills, dyspnea, cough, nasal congestion, and dysphagia.He was a former 25 pack-year smoker who had quit three years ago. He took no daily medications. He was born in Vietnam and moved to the United States at the age of one. He worked at a salon. He traveled to Vietnam in the past year. On presentation, his temperature was 100.9 degrees Fahrenheit, heart rate 130 beats per minute, blood pressure 176/104 mmHg, respiratory rate 20 breaths per minute, and he was saturating 97% on room air. His physical exam was notable for a 7x5 cm area of induration without fluctuance over the right sternocleidomastoid (SCM) muscle with blanching erythema. Labs were notable for hyponatremia (sodium 126 mmol/L), hyperglycemia (glucose 370 mg/dL), leukocytosis (white blood cell count 18.8 B/L), and lactic acidosis (lactate 2.1 mmol/L). A computed tomography (CT) scan of the neck demonstrated a 7 centimeter rim-enhancing, loculated fluid collection involving the right SCM muscle with mild retropharyngeal edema and lymphadenopathy consistent with SCM pyomyositis. An ultrasound of his left calf was read as a ruptured popliteal cyst.He was fluid resuscitated and blood cultures were collected prior to starting empiric antibiotics which included intravenous (IV) vancomycin and piperacillin/tazobactam (pip/tazo). He was evaluated by otolaryn-gology and started on IV dexamethasone to reduce the risk of airway inflammation. He underwent incision and drainage of the right neck abscess, which revealed pus and necrotic lymph node material. Direct laryngoscopy showed normal, cryptic-appearing tonsils. Cultures of the purulent material grew Klebsiella pneumoniae, resistant only to trimethoprim/sulfamethoxazole (TMP-SMX), and Staphylococcus capitis. No phenotyping was performed.On day five of admission, the patient endorsed worsening left posterior calf pain. Examination was now notable for an indurated posterior calf, increased erythema up to the posterior thigh, and severe pain on palpation. He was taken urgently to the operating room (OR), where debridement and fasciotomy of the left calf and thigh were performed. Findings were consistent with necrotizing fasciitis. Cultures obtained in the OR grew K. pneumoniae, again, resistant only to TMP-SMX.Clindamycin was added to his antibiotic regimen and there was concern for dose-dependent susceptibility to pip/tazo, so he was switched to cefepime and metronidazole. Three sets of repeat blood cultures during his hospital-ization remained negative. An echocardiogram showed no vegetations.He required two additional debridements of the neck abscess where progression of necrosis was noted. Additional intraoperative cultures again yielded K. pneumoniae, now noted to have intermediate suscep-tibility to ciprofloxacin. The wound was managed with a wound vacuum and ultimately closed.82The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 83 Similar to the hvKP isolated in this patient, the majority of reported cases of hvKP have been susceptible to most antimicrobial agents. Recently though, there has been growing concern for the development of multi-drug resistance in this already hypervirulent pathogen. These include extended-spectrum beta lactamases and carbapenemases.3 This combination of hypervirulence and multi-drug resistance could lead to a significant public health threat. Selection of antimicrobials should be guided by in-vitro susceptibility testing, and the recommended treatment course depends on specific site of infection and adequate source control.Several risk factors for hvKP have been identified, including Asian ethnicity and type 2 diabetes mellitus, both of which were seen in this patient. The propensity for infection in those of Asian descent has not been explained, and it remains unclear if this predisposition is due to genetic susceptibility, endemic gastrointestinal colonization, or geographic exposure.3,9 In this case, it was an Asian male who had recently traveled to Vietnam.He required four additional washouts for his left leg, followed by management with a wound vacuum. The thigh and calf wounds were ultimately closed with skin grafts.He developed a drug rash which progressed even after switching his antibiotics to ertapenem only. He was switched to oral ciprofloxacin due to concern for beta-lactam allergy, and he ultimately completed a 22-day course of antibiotics after no additional infection was noted in the OR.Laboratory testing during his admission revealed a new diagnosis of diabetes with a hemoglobin A1c of 13%. He was briefly treated for diabetic ketoacidosis with an insulin continuous infusion after his initial operation. He transitioned to insulin glargine and lispro and ultimately had significant improvement of his hemoglobin A1c to 6.3% within the next 6 months. Outpatient follow up was arranged for monitoring. DISCUSSIONWhile hvKP was initially noted in Asian countries, it is being reported with increasing frequency in the United States and worldwide among patients of diverse ethnicity.4-6 Classical K. pneumoniae is known to colonize primarily the gastrointestinal tract, and limited studies of hvKP colonization in Asian patients also demonstrates the GI tract as a source, and less commonly the oropharynx and skin.3,7,8 In this patient’s case, his recent tonsillitis suggests the oropharynx may have been the source of infection. This pathogen most frequently causes pyogenic liver abscess but has been noted to spread to multiple organ systems.9,10 Other reported infections include splenic abscess, spontaneous bacterial peritonitis, pneumonia, empyema, endophthalmitis, meningitis, soft tissue abscess, necrotizing fasciitis, bacteremia, and endocarditis.3,9 Interestingly, in this individual, there were two distant sites of infection caused by the same organism, but blood cultures remained negative. The pathogen has a unique mucoid nature allowing for adherence to epithelial barriers and avoidance of phagocytosis resulting in direct tissue invasion, thus metastatic infection.11 This is thought to be due to either overexpression of a gene encoding the mucoid phenotype or to overproduction of capsular polysaccharide compared to other K. pneumoniae strains.10,11 These traits allow colonies to form a viscous string greater than 5 millimeters in length (Figure 1). Other mechanisms of virulence that have been theorized are its ability to acquire iron more readily than other strains, lipopolysaccharide production, adhesion, and biofilm production.3,11 This patient’s case of monomicrobial necrotizing fasciitis also highlights the pathogen’s increased iron acquisition, allowing it to progress rapidly in iron-limited environments.9,12,13Figure 1. “String test” performed on K. pneumoniae isolated from this patient’s OR cultures. In this qualitative test, the hypermucoviscous phenotype creates a string of greater than 5 mm when a colony is stretched with an inoculation loop.83et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202584 | The Medicine Forum, Volume 26 CONCLUSION This case illustrates the severe morbidity associated with hvKP infection, emphasizing its unique pathogenic traits that enable metastatic infection and monomicrobial necrotizing fasciitis. Prompt identification of the pathogen is crucial and should trigger vigilant monitoring for secondary infection sites. Early and aggressive surgical intervention to manage identified abscesses is vital, considering hvKP's propensity for rapid disease progression. While patients with compromised immune systems or diabetes, as in this case, are intuitively at greater risk of hvKP infection, the observed prevalence in Asian populations remains intriguing and not yet fully understood. REFERENCES1. Ashurst JV, Dawson A. Klebsiella Pneumonia. Nih.gov. Published 2023. https://www.ncbi.nlm.nih.gov/books/NBK519004/2. Sriskandan S, Cohen J. Gram-Positive Sepsis. Infectious Disease Clinics of North America. 1999;13(2):397-412. doi:https://doi.org/10.1016/s0891-5520(05)70082-93. Shon AS, Bajwa RPS, Russo TA. Hypervirulent (hypermucoviscous)Klebsiella pneumoniae. Virulence. 2013;4(2):107-118. doi:https://doi.org/10.4161/viru.227184. Pomakova DK, Hsiao C-B, Beanan JM, et al. Clinical and phenotypic differences between classic and hypervirulent Klebsiella pneumonia: an emerging and under-recognized pathogenic variant. European Journal of Clinical Microbiology & Infectious Diseases. 2011;31(6):981-989. doi:https://doi.org/10.1007/s10096-011-1396-65. Spaite DW, Stiell IG, Bobrow BJ, et al. Effect of Transport Interval on Out-of-Hospital Cardiac Arrest Survival in the OPALS Study: Implications for Triaging Patients to Specialized Cardiac Arrest Centers. Annals of Emergency Medicine. 2009;54(2):248-255. doi:https://doi.org/10.1016/j.annemergmed.2008.11.0206. Decré D, Verdet C, Aurélie Emirian, et al. Emerging Severe and Fatal Infections Due to Klebsiella pneumoniae in Two University Hospitals in France. Journal of Clinical Microbiology. 2011;49(8):3012-3014. doi:https://doi.org/10.1128/jcm.00676-117. Fung CP, Lin YT, Lin JC, et al. Klebsiella pneumoniaein Gastrointestinal Tract and Pyogenic Liver Abscess. Emerging Infectious Diseases. 2012;18(8). doi:https://doi.org/10.3201/eid1808.1110538. Lin YT, Siu LK, Lin JC, et al. Seroepidemiology of Klebsiella pneumoniae colonizing the intestinal tract of healthy chinese and overseas chinese adults in Asian countries. BMC Microbiology. 2012;12(1). doi:https://doi.org/10.1186/1471-2180-12-139. Choby JE, Howard-Anderson J, Weiss DS. Hypervirulent Klebsiella pneumoniae – clinical and molecular perspectives. Journal of Internal Medicine. 2019;287(3):283-300. doi:https://doi.org/10.1111/joim.1300710. Siu LK, Yeh KM, Lin JC, Fung CP, Chang FY. Klebsiella pneumoniae liver abscess: a new invasive syndrome. The Lancet Infectious Diseases. 2012;12(11):881-887. doi:https://doi.org/10.1016/s1473-3099(12)70205-011. Xu Q, Yang X, Chan EWC, Chen S. The hypermucoviscosity of hypervirulent K. pneumoniae confers the ability to evade neutrophil-mediated phagocytosis. Virulence. 2021;12(1):2050-2059. doi:https://doi.org/10.1080/21505594.2021.196010112. Hsieh PF, Lin TL, Lee CZ, Tsai SF, Wang JT. Serum-induced iron-acquisition systems and TonB contribute to virulence in Klebsiella pneumoniae causing primary pyogenic liver abscess. The Journal of Infectious Diseases. 2008;197(12):1717-1727. doi:https://doi.org/10.1086/58838313. Russo TA, Olson R, MacDonald U, et al. Aerobactin Mediates Virulence and Accounts for Increased Siderophore Production under Iron-Limiting Conditions by Hypervirulent (Hypermucoviscous) Klebsiella pneumoniae. Infection and Immunity. 2014;82(6):2356-2367. doi: https://doi.org/10.1128/iai.01667-1384The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 85 From ER to Mortality in 48 Hours: A Fatal Case of Overwhelming Post-Splenectomy InfectionMiriam Stern, BA1, Blaise O’Malley, BS1, Amry Majeed, MD2, Michael Grodsky, MD31. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA2. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Hospital Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONOverwhelming post-splenectomy infection (OPSI) is a known complication of asplenia.1,2 While the precise rates of morbidity and mortality are unknown, estimates range from 38% to as high as 70%.2 Because the spleen plays an important role in protecting against infections with encapsulated microorganisms, OPSI is most commonly caused by infection with encapsulated bacteria, specifically Streptococcus pneumoniae.1–3 While pneumococcal vaccines have been shown to improve immunogenicity in asplenic people, OPSI remains a danger to both vaccinated and unvaccinated patients.4,5 Additional measures to protect asplenic patients from overwhelming infection have been proposed, but the evidence remains mixed.6–8 Prophylactic antimicrobial therapy has been recommended for certain populations, specifically children under five years old or adults during the first year post-splenectomy, but to our knowledge, no evidence-based guidelines currently exist.7,9 Studies have also considered intravenous immunoglobulin (IVIG) for the acute treatment of pneumococcal infection in asplenic patients. However, while IVIG has shown promise in mouse models and some preliminary human studies, it has not been conclusively studied.8,10,11 We describe a rapidly progressive and ultimately fatal case of overwhelming pneumococcal infection in an asplenic patient, with a discussion of presentation and management. CASE PRESENTATIONA 61-year-old man presented to the emergency department for 3 days of shortness of breath, headache, vomiting, and generalized weakness. He had a past medical history of splenectomy and left nephrectomy following a gunshot wound in 1994, which had been complicated by a chronic abdominal abscess in the left upper quadrant. Over the past 2 years, he had been hospitalized several times for pain and ongoing complications of the abscess and was treated with several rounds of antibiotics and drainage. During his most recent admission six months prior, aspiration of the abscess grew Bacteroides fragilis. Recently, the patient had been experiencing ongoing drainage from the abscess, and reported feeling increasingly ill prior to presentation.On arrival to the emergency department, the patient had a heart rate of 98 beats/minute, blood pressure of 149/105 mmHg, and respiratory rate of 41 breaths/minute. He was febrile at 101.6° Fahrenheit (F) with an oxygen saturation of 94% on room air. Laboratory assessment revealed a lactic acidosis with pH of 7.32 and a lactate of 8.0 mmol/L that improved to 7.5 mmol/L with 2 liters of normal saline. He had acute kidney injury with blood urea nitrogen (BUN) of 27 mg/dL and creatinine of 3.16 mg/dL. He had signs of liver damage with alkaline phosphatase of 201 U/L and alanine transaminase of 55 U/L. He also had marked derangements in his coagulation labs, with a prothrombin time (PT) of 31s, international normalized ratio (INR) of 2.82, partial thromboplastin time (PTT) of 101s, D-dimer greater than 69,000 ng/mL, fibrinogen of 66 mg/dL, and platelets of 27,000 cells/mm3. Outpatient labs drawn just three days prior were all within normal limits. He was found to be COVID-19 positive, and blood cultures were positive for Streptococcus pneumoniae. On physical exam, the patient was initially alert and oriented but in clear discomfort with diffuse purpura fulminans and increased work of breathing. Based on the clinical presentation, physical exam, and laboratory findings, the patient was diagnosed with septic shock complicated by multi -organ failure and disseminated intravascular coagulation (DIC), likely secondary to Streptococcus pneumoniae bacteremia. He was started on broad-spectrum antibiotics with Streptococcus pneumoniae coverage; within 3 hours, his breathing decompensated further—he was intubated, given a central line, and admitted to the ICU. Over the next day, he was resuscitated with intravenous fluids; blood transfusions; and maximum doses of norepi-nephrine, epinephrine, vasopressin, and phenylephrine. He was also given intravenous immunoglobulin (IVIG). His blood pressure was maintained until the evening when his QRS widened and his mean arterial pressure decreased. He lost pulses; resuscitation efforts were unsuccessful at reviving him. He died approximately thirty-eight hours after initial presentation. INFECTIOUS DISEASES & ENVIRONMENTAL MEDICINE 85et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202586 | The Medicine Forum, Volume 26 DISCUSSIONThis case illustrates the risk of overwhelming pneumococcal infection and sepsis in asplenic patients, even decades after splenectomy. The spleen is the largest secondary lymphatic organ in the body and has several important functions in the immune system. Macrophages in the spleen filter blood of defective or old red blood cells, as well as infectious pathogens.12 Additionally, the spleen is the site of production for many immunoglobulins, opsonins, and complements that are responsible for clearing encapsulated bacteria. Without a spleen, the body is left particularly vulnerable to infection with encapsulated organisms. The most common pathogens include Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis with Streptococcus pneumoniae alone accounting for up to 50-90% of severe infection in asplenic patients.2,12–14 Because the body lacks a mechanism for clearing encapsulated pathogens, patients with asplenia can very quickly succumb to overwhelming infection and sepsis. Asplenic patients remain at increased risk of infections with non-encapsulated bacter ia as well , including Staphylococcus aureus, Salmonella, Escherichia coli, and Pseudomonas aeruginosa.15 However, the risk of overwhelming sepsis is lower. Because of the significantly increased risk of infection with encapsulated organisms, vaccination against the most common pathogens is strongly recommended for all patients with asplenia. In particular, asplenic patients should receive pneumococcal, meningococcal, and Haemophilus influenzae type b vaccines. While the patient in this case had an unknown vaccination status, vaccination is not entirely preventative of pneumococcal infection, including overwhelming sepsis.1,5 Despite prompt antibiotic administration with coverage for Streptococcus pneumoniae, this patient’s disease course progressed rapidly to multi-organ failure. Given his body’s inability to clear the bacteria on its own, it is possible that the infection had progressed too far for the antibiotic to overcome it.Furthermore, while the patient did receive IVIG, there are not currently evidence-based recommendations for the use of IVIG in asplenic patients with pneumococcal infections.7,9 The theory behind giving IVIG to these patients is to replenish some of the immunoglobulins needed for opsonizing encapsulated bacteria that the spleen normally produces. However, in patients with functioning spleens, this immunoglobulin defense is normally part of the immediate response to infiltrating pathogens. While IVIG remains a promising therapy for septic asplenic patients, more research is needed to determine when and how to administer the therapy to maximize the chances of tamping down overwhelming infections. CONCLUSION We present a case of a 61-year-old man with asplenia, presenting to the emergency department for shortness of breath, vomiting, and weakness, found to have Streptococcus pneumoniae bacteremia that rapidly progressed to fatal septic shock with DIC. This case underscores the need for updated, evidence-based strategies for acute OPSI management. Further research should focus on acute treatment protocols and evaluating the efficacy of IVIG to improve outcomes in asplenic patients with overwhelming pneumococcal sepsis. REFERENCES1. Styrt B. Infection associated with asplenia: risks, mechanisms, and prevention. Am J Med. 1990;88(5N):33N-42N.2. Sinwar PD. Overwhelming post splenectomy infection syndrome: review study. Int J Surg. 2014;12(12):1314-1316. doi:10.1016/j.ijsu.2014.11.0053. Ashorobi D, Fernandez R. Asplenia. In: StatPearls. StatPearls Publishing; 2025. Accessed March 1, 2025. http://www.ncbi.nlm.nih.gov/books/NBK538171/4. Bonanni P, Grazzini M, Niccolai G, et al. Recommended vaccinations for asplenic and hyposplenic adult patients. Hum Vaccin Immunother. 2016;13(2):359-368. doi:10.1080/21645515.2017.12647975. Forstner C, Plefka S, Tobudic S, Winkler HM, Burgmann K, Burgmann H. Effectiveness and immunogenicity of pneumococcal vaccination in splenec-tomized and functionally asplenic patients. Vaccine. 2012;30(37):5449-5452. doi:10.1016/j.vaccine.2012.06.0486. Chironna M, Sallustio A, De Robertis M, Quarto M, Germinario C. Fulminant pneumococcal sepsis in an unvaccinated asplenic patient in Italy: case report. Euro Surveill. 2010;15(23):19585. doi:10.2807/ese.15.23.19585-en7. Rubin LG, Schaffner W. Care of the asplenic patient. N Engl J Med. 2014;371(4):349-356. doi:10.1056/NEJMcp13142918. Shankar-Hari M, Spencer J, Sewell WA, Rowan KM, Singer M. Bench-to-bedside review: immunoglobulin therapy for sepsis—biological plausibility from a critical care perspective. Crit Care. 2012;16(2):206. doi:10.1186/cc105979. Brigden ML. Detection, education, and management of the asplenic or hyposplenic patient. Am Fam Physician. 2001;63(3):499-508.10. Nakamura K, Takahashi Y, Sonoo T, Hashimoto H. Intravenous immuno-globulin for overwhelming postsplenectomy infection. J Glob Infect Dis. 2021;13(1):44-51. doi:10.4103/jgid.jgid_93_1911. Nakamura K, Doi K, Okamoto K, et al. Specific antibody in IV immuno-globulin for postsplenectomy sepsis. Crit Care Med. 2013;41(8):e163. doi:10.1097/CCM.0b013e318287f1de12. Kapila V, Wehrle CJ, Tuma F. Physiology, spleen. In: StatPearls. StatPearls Publishing; 2025. Accessed May 6, 2025. http://www.ncbi.nlm.nih.gov/books/NBK537307/13. Sawmiller CJ, Dudrick SJ, Hamzi M. Postsplenectomy Capnocytophaga canimorsus sepsis presenting as an acute abdomen. Arch Surg. 1998;133(12):1362-1365. doi:10.1001/archsurg.133.12.136214. Lee GM. Preventing infections in children and adults with asplenia. Hematology Am Soc Hematol Educ Program. 2020;2020(1):328-335. doi:10.1182/hematology.202000011715. Davidson RN, Wall RA. Prevention and management of infections in patients without a spleen. Clin Microbiol Infect. 2001;7(12):657-660. doi:10.1046/j.1198-743x.2001.00355.x86The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 87 "Stasis" – Jasmine Lee, MD87et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202588 | The Medicine Forum, Volume 26 Enhancing Community Health Center Safety Through Participatory Co-DesignArman Afifi, BS1, Kelsey Smith, BS1, Megan Reed, PhD, MPH2, Lara Weinstein, MD, MPH31. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA2. Department of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, PA 3. Department of Family & Community Medicine, Thomas Jefferson University Hospital, Philadelphia, PAMEDICAL EDUCATION & HEALTH SYSTEMS SCIENCE INTRODUCTIONHealth and social service programs are often designed from the top down, with people in power making decisions that affect others. Integrating all staff and clients in the co-design process ensures that interventions are culturally competent and tailored to the unique challenges faced by the community. Participants bring firsthand knowledge, allowing for a more accurate assessment of needs and preferences. Additionally, involving marginalized individuals helps build trust between service providers and the community, creating a foundation for sustained collaboration and positive outcomes. Overall, participant inclusion is not only a practical necessity but an ethical imperative in delivering effective and equitable quality improvements. Co-design typically employs creative and participatory methods, and has been implemented in a variety of health care settings. For example, co-design has been utilized to prototype successful models of youth opioid use treatment services, to improve transitions for patients with complex health needs in hospital and home settings, and to develop a user-friendly application that allows patients to access remote services.1-3As part of a larger community partnership to increase access to treatment for people with opioid use disorder (OUD), the project team worked with a permanent supportive housing program (PSHP) with a mission to end homelessness for people with serious mental illness and substance use disorders. This urban-based program serves approximately 500 people and has an on-site integrated healthcare clinic. The PSHP offices temporarily closed in October of 2020 after a serious onsite safety event. The primary care services during this time continued to be offered at an affiliated clinical site. In preparation for reopening, the PSHP community sought to cultivate a safer space through utilizing co-design as a vehicle to solicit feedback from program participants and staff. CO-DESIGN PROCESS Co-design research embodies a collaborative method in which researchers, practitioners, and end-users collaborate to devise solutions for intricate problems. Co-design does more than merely consult stakeholders using materials and processes defined by the researchers; it gives stakeholders shared ownership of the design process and outcomes. Beyond expanding the efficacy of research outcomes, this participatory model cultivates a feeling of ownership and empowerment among stakeholders, ultimately advancing sustainable and meaningful results.4 Participants in this endeavor included both participants and staff at PSHP. Staff at PSHP reached out to engaged participants to invite them to join in the co-design discussions. Ten participants were identified and contacted by staff, who then explained the purpose of the co-design project. Participants were compensated with $20 and a lunch per 1-hour focus group, as per the PSHP standard approach to soliciting participant input. All staff members at PSHP were invited to participate in the co-design discussions. Staff were provided with lunch during the 1-hour focus groups taking place during business hours. This project focused on exploring processes and values that contribute to a safe and secure environment at PSHP. The intent of the project was not to contribute to generalizable knowledge as it was in response to a specific incident in a unique setting and therefore is not considered research and did not require IRB review. CO-DESIGN MEETING PROCEDURES There were four one-hour co-design sessions in total, occurring twice per week over two weeks in April 2022. During each session, a facilitator would record what was being said on a large piece of paper that everyone could track and edit. The first co-design meeting (n=3) included only participants, the second only staff (n=8), the third only participants (n=5) again, and the final meeting included both staff and participants together (n=10; 7 staff, 3 participants). Three of the program participants attended both participant meetings and the final community meeting. Two participants only attended the second participant meeting. Five staff members were present for both the staff meeting and the final community meeting. Three staff members only participated in the all-staff meeting, and two staff members only participated in the final all-community meeting. In total, the co-design process involved 5 different participants and 10 different staff members. 88The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 89 them, distribute the five stickers evenly across five values, or anything in between. After the dots were placed and tallied, there was discussion on trends of which values were more and less prioritized. The remainder of the session was spent brainstorming how to implement and honor the two values that received the most stickers. Notes were written by a facilitator during the meeting and were available for everyone in the room to see. CO-DESIGN MEETING VALUES AND VOTES Outcomes of the dot activity are shown in Figure 1. Of the values identified by the co-design facilitators based on prior conversations between staff and participants, the two most prioritized in the final session were adequate staffing and trust between staf and participants. Staff highlighted their investment in providing the best care possible. Providing excellent care includes many of the values above: active listening, communication, trust, and cultivating a judgment-free zone. Staff unanimously cited inadequate staffing as the primary barrier to providing excellent care. Staff clarified that they do not lack confidence about being able to provide excellent care, however, when the program is not fully staffed, they feel stretched too thin, making them feel like they cannot provide the level of In the first focus group, program participants were asked to reflect on their experience at PSHP, and then identify a list of values conducive to promoting a safe environment at PSHP. After the list was generated, participants discussed which values felt particularly important to the group. This was followed by a staff focus group discussion in which staff discussed their experience at PSHP and then identified a list of values conducive to promoting a safe environment at PSHP. Staff then discussed the participant-specific list of values generated in the first session, comparing similarities and differences between the staff and participant-specific lists. In the third meeting, participants reviewed the previous staff discussion and then reevaluated their original list of values in light of staff findings. In preparation of the final combined community meeting the co-design facilitators consolidated the values generated by staff and participants into a single all encompassing list. The combined co-design session started by summarizing the consolidated list, and then asked attendees to select which values were most salient. Through a "dot activity," attendees were asked to select their preferred values according to importance, rather than the feasibility of the value. Attendees were given five stickers and were asked to distribute those stickers according to item importance. They could place all five stickers on one value that felt especially important to Brief Explanations of the Value Listed: Guards/De Escalation – De-escalation trainings for guards could reduce conflict. Physical Safety – A participant voiced initial concern when PTHPA reopened with no additional perceived physical security measures (e.g. metal detectors). Cleanliness – How frequently PTHPA is cleaned and sanitized, especially in regard to the larger COVID-19 pandemic.Less Crowded/Chaotic Space – There is one common waiting room for multiple departments (e.g. medical, housing, social services). Frustration and long wait times from one department affected the staff and participants in other departments. Figure 1. Outcomes of the “Dot Activity”Communication – Staff and participants speaking the same language, both literally (e.g. Spanish) and culturally. Judgement Free Zone – A client expressed that staff have always treated him the same, irrespective of his substance use status.Finding Common Ground – Having staff with similar life experiences to the participants they are working with. Adequate Staffing – Staff feel fully comfortable providing their highest level of care.# of Votes89et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202590 | The Medicine Forum, Volume 26 care that they aspire to. Part of adequate staffing means the person has the soft skills (empathy, speaking the client's language) and the hard skills to do their job. DISCUSSIONThe co-design sessions at the PSHP sought to clarify which values felt most fundamental to feelings of safety amongst PSHP participants and staff. The two most commonly shared values were trust between staff and participants and adequate staffing. Trust is bidirectional, which means staff understand when to give participants the benefit of the doubt and when to hold them accountable, but it also involves participants trusting that staff have their best interests in mind. Interestingly, every single staff member selected adequate staffing as a top priority; however, no participants selected this as a top priority. Although staff members expressed that they occasionally feel they cannot provide the level of care that PSHP participants deserve due to inadequate staffing, participants across sessions reiterated the excellent care that they receive at PSHP. However, sometimes participants could tell that staff were "stressed," which staff link directly back to staffing needs. LIMITATIONS In the final all community meeting, participants were notably quieter than in the previous client only meetings. This dynamic may be inevitable due to the power dynamic between staff and participants. However, if future meetings are held with both participants and staff, we recommend initially breaking into smaller groups for more discussion. As this particular co-design project was highly specific to population and setting, the findings should not be considered generalizable. A search of existing literature on PubMed and Scopus on the use of participatory design methods to address a safety concern in a healthcare setting yielded no results.CONCLUSION This co-design project started as preparation for re-opening of healthcare services. A range of safety enhancements were under consideration. The co-design discussions indicated that physical safety concerns–such as metal detectors, wands, and de-escalation training for guards–were not the highest priority. For PSHP staff and participants, rebuilding after a crisis means valuing relationships and ensuring there is adequate staffing. We hope this descriptive paper can serve as one model for undertaking this process. ACKNOWLEDGEMENTS We sincerely thank the PSHP staff and participants for their invaluable contributions and the Foundation for Opioid Response Efforts for their generous funding support in making this project possible. REFERENCES1. Marchand K, Tallon C, Katan C, et al. Improving Treatment Together: a protocol for a multi-phase, community-based participatory, and co-design project to improve youth opioid treatment service experiences in British Columbia. Addict Sci Clin Pract. 2021;16(1):53. doi:10.1186/s13722-021-00261-72. Gray C, Tang T, Armas A, et al. Building a digital bridge to support patient-centered care transitions from hospital to home for older adults with complex care needs: protocol for a co-design, implementation, and evaluation study. JMIR Res Protoc. 2020;9(11):e20220. doi:10.2196/202203. Bird M, McGillion M, Chambers EM, et al. A generative co-design framework for healthcare innovation: development and application of an end-user engagement framework. Res Involv Engagem. 2021;7(1):12. doi:10.1186/s40900-021-00252-74. Green T, Bonner A, Teleni L, et al. Use and reporting of experience-based codesign studies in the healthcare setting: a systematic review. BMJ Qual Saf. 2020;29(1):64-76. doi:10.1136/bmjqs-2019-00957090The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 91 The Factor VIII Debate: An Auto-Cancelled Lab Near MissAvish Patel, MD1, Daniel Elchediak, MD1, Zachary Pang, MD1, Charlotte Shields, MD1, Bethanne Venkatesan, MD1, Ananya Venkatesh, MD1, Michael J. Alessandro, BSN2, Jeffrey Riggio, MD, MS3, Alexis Wickersham, MD31. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Thomas Jefferson University Hospital, Philadelphia, PA3. Division of Hospital Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAINTRODUCTIONNear misses, medical errors with no appreciable resultant harm, often go undetected and underreported despite great emphasis on patient safety event reporting over the past two decades.1 Additionally, near misses are often not triggers for proactive institutional corrective action due to the widespread retroactive safety culture following more harmful or catastrophic safety events.2 At Thomas Jefferson University Hospital, all internal medicine first-year residents (PGY1s) participate in an immersive safety event review curriculum of near miss or low-harm safety events, previously described in the literature.3 The following details the event review findings and implemented health-system level changes following a trainee-led apparent cause analysis involving post-transfusion labs auto-cancelled by the electronic medical record without physician knowledge in a patient admitted to the hospital with active bleeding related to von Willebrand disease (vWD) requiring von Willebrand factor/factor VIII replacement therapy (Humate-P®). METHODSA near miss of an auto-cancelled factor VIII lab was directly referred for review by an involved night-coverage resident tasked to follow up on post-Humate-P® transfusion labs overnight. The event review team, consisting of six PGY1 internal medicine resident physicians, one registered nurse, one faculty health informatics expert, and one faculty facilitator, performed an apparent cause analysis over a two-week period during protected resident ambulatory education time. An event story map was created, causal threads and causal statements were identified, and action items for improvement, including implementation plans, were developed. Following the event review, factor VIII lab draws were added to an exception list in the electronic medical record (EMR) to prevent further auto-cancellation of identical lab orders in close proximity. Additionally, a health system-wide EMR order-set was created to easily time pre- and post-Humate-P® transfusion factor VIII labs for ordering clinicians and to safely track factor VIII levels for repeat dosing. MEDICAL EDUCATION & HEALTH SYSTEMS SCIENCE Problem Statement: Necessary post treatment (Humate®) infusion lab not collectedKey Contributing Factors: Day team appropriately ordered labs but did not notice labs ordered did not show up in EMR to be collected at ordered timesCaused By: Ease of putting multiple ordersin at once. Assume orders entered are present. "Shopping Cart" tendency for order entry of multiple ordersCaused By: EMR auto-cancellation of same labs ordered at same time or same labs within a certain time periodCaused By: Lack of auto-cancellation notifications upon ordering duplicate labs increased likelihood of team not noticing Key Contributing Factors: Multiple labs are required to adequately dose Humate®Caused By: Confusion regarding timing of duplicate ordersCaused By: Inadequate physician to nursing hand-off led to poor communication about necessity and timing of lab draw increasing likelihood of lab not being collected Caused By: Scheduling factors, communication difficulty between physicians and nursesCaused By: Lack of system to review and monitor ordersCaused By: No alert for lab monitoring for infrequently used medications. Lack of clinical and electronic guidance for Humate® monitoring protocol increasing likelihood of lab overnight leading to possibility of not being collectedCaused By: No discontinuation alerts by EMR for auto-cancelled or personnel cancelled ordersFigure 1: Event Causal Thread Diagram91et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202592 | The Medicine Forum, Volume 26 RESULTSAn institution-wide creation and go-live of the EMR factor VIII order-set started in April 2024 and has increased in utilization over the months, with goals to prevent near-miss errors described above by preventing auto-cancellation of labs and increasing provider awareness of appropriate humate monitoring. Figure 1 is an event causal thread diagram illustrating the process of problem identification that led to this successful intervention. DISCUSSIONFollowing an apparent cause analysis of a near miss safety event involving an auto-cancelled factor VIII level in a patient with active bleeding from vWD, health system-wide EMR interventions were implemented to prevent further safety events in high-risk patient populations requiring frequent lab monitoring for safe and effective factor VIII level dosing. By creation of an exception rule to the EMR lab-auto cancellation list, we have ensured that identical lab orders placed in the same ordering encounter and in close proximity to one another (pre- and post-transfusion timing) are not auto-cancelled by the EMR. This ensures orders at the times written for are available to nurses and phlebotomists to collect at the appropriate timing related to Humate-P transfusion. Following the creation of a health system-wide factor VIII order-set, there has been increasing use by clinicians to utilize pre- and post-transfusion factor levels. We are hopeful order-set usage rate will continue to increase as more clinicians become familiar with the order-set through ongoing improvement initiatives. This near miss apparent cause analysis led by PGY1s with interprofessional involvement showcases the systems-level impact trainees can have on patient care when patient safety culture and education are embedded into the clinical learning environment. Additionally, it demonstrates how implementing a high- leverage risk-reduction strategy via EMR systems-level interventions can lead to proactive risk-reduction strategies when near misses are identified. REFERENCES1. Hamilton EC, Pham DH, Minzenmayer AN, et al. Are we missing the near misses in the OR? Underreporting of safety incidents in pediatric surgery. J Surg Res. 2018;221:336-342. doi:10.1016/j.jss.2017.08.0052. Panagioti M, Khan K, Keers RN, et al. Prevalence, severity, and nature of preventable patient harm across medical care settings: systematic review and meta-analysis. BMJ. 2019;366:l4185. doi:10.1136/bmj.l41853. Perkons M, Wickersham A, Bharel S, Kuchera T, Jaffe R. Early immersion in team-based event review: experiential patient safety education for PGY-1 internal medicine residents. MedEdPORTAL. 2024;20:11376. doi:10.15766/mep_2374-8265.1137692The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 93 HEART CORE: A Framework for Leading with Empathy in Medical EducationAkash Patel, DO1* and Mark Liotta, MD1*1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA* These authors contributed equally to this workIn medical training, much of what defines leadership happens outside of clinical decision-making. It happens at 2 a.m. when a resident breaks down from burnout. It happens when a team is navigating interpersonal conflict or when a trainee is overwhelmed by grief, imposter syndrome, or failure. While these moments are deeply impactful, many of us are never taught how to lead through them.This gap inspired us to create HEART CORE, a framework designed to help residents, faculty, and administrators approach complex, emotional, or high-stakes situations with clarity and compassion. Although it was originally built for chief residents handling difficult calls and conversations, we quickly realized that HEART CORE can be used in many contexts. It is a tool that can support managing learners, mentoring trainees, guiding faculty, navigating conflict, and even engaging patients and families during emotionally charged encounters.Here is how it works:H – Hear them outLet the resident fully express themselves. Do not interrupt. Sometimes they just need a safe space to vent.This makes them feel seen and heard, which is the foundation of psychological safety.E – EmpathizeAcknowledge the emotion. “That sounds really tough,” or “I can see why that would be frustrating.” This builds trust.This helps the learner feel less alone and validates their emotional experience.A – Assess the situationWhat is the actual issue? Is it clinical, interpersonal, burnout, or systems-based? Get the full picture before reacting.This makes the learner feel like their concern is being taken seriously and handled thoughtfully.R – Reflect before respondingPause to think. Stay calm even if the learner is not. Your tone sets the tone for the rest of the conversation.This models emotional regulation and helps the learner feel grounded and respected.T – Triage your responseDecide what level of action is needed. Does it require escalation? Can it wait? Be firm when necessary, and supportive when possible.This gives the learner a realistic plan and reassures them that they are not alone in addressing the problem.C – Coach, don’t just fixGuide them toward a solution rather than solving it for them. This builds independence and confidence.This helps the learner grow into a capable problem-solver rather than staying dependent.O – Offer perspectiveHelp reframe. “This sounds like it’s part of the learning curve,” or “You handled that better than you think.”This combats self-doubt and builds resilience and insight.R – Reconnect laterFollow up. A quick “How are you doing after the other night?” shows that you care and builds long-term mentorship.This reinforces that they matter beyond the moment and strengthens the relationship.E – Establish boundariesYou are here to support them, not absorb all of their stress. Lead with kindness while protecting your own well-being.This models sustainable leadership and reminds them that self-care is not selfish.MEDICAL EDUCATION & HEALTH SYSTEMS SCIENCE 93et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202594 | The Medicine Forum, Volume 26 We introduced HEART CORE at a national conference of internal medicine chief residents and received overwhelmingly positive feedback. Over 70 rising chiefs across the country engaged with the framework. Many reflected that it gave structure and language to respon-sibilities they had long sensed but had never named. Others said they wished they had been taught this approach earlier in residency or medical school.HEART CORE is not a script. It is a mindset. It reminds us that effective leadership requires presence and not just problem-solving. It invites us to listen deeply; respond intentionally; and lead with empathy, clarity, and humility.We are now incorporating HEART CORE into our chief resident onboarding and working on a toolkit to bring it into faculty development and graduate medical education leadership programs. Because at the end of the day, the culture of medicine is not just built through protocols and procedures. It is shaped by how we show up for one another in moments of uncertainty, stress, and growth.94The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 95 "Resplendent Quetzal" – Bret McCarty, MD 95et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202596 | The Medicine Forum, Volume 26 A Complex Case of Multifactorial Hypoxemia from Metastatic Testicular CancerSusanna Betti, MD1 1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAPULMONARY, ALLERGY & CRITICAL CARE MEDICINECASE PRESENTATIONA 27-year-old male with no known past medical history presented for evaluation of a 14.1 cm testicular mass (Figure A). He was found to have severe anemia (Hgb 2.8 g/dL), and biopsy demonstrated a non-seminomatous mixed germ cell tumor of testicular origin with imaging demonstrating widespread metastases to the brain, lungs, and liver. The patient received multiple blood transfusions and one dose of bleomycin, etoposide, and cisplatin followed by the development of acute respiratory failure. Computed tomography angiography (CTA) chest was negative for pulmonary thromboem-bolism but demonstrated diffuse ground-glass opacities (Figure B, arrows) and metastatic pulmonary masses containing dilated vessels suspicious for arteriovenous malformations (Figure C, arrows). It was theorized that this decompensation could be a result of volume overload after receiving 15 units packed red blood cells (pRBCs), transfusion-related acute lung injury (TRALI), infection, cytokine release, and/or chemotherapy toxicity. The patient was intubated and started on high dose steroids, antibiotics, sedatives, paralyzing agents, and epoprostenol. Workup for infection was negative, and bronchoscopy was without alveolar hemorrhage. The patient was unable to receive further rounds of chemotherapy given the high risk for oxidative toxicity and degree of acute illness. Due to lack of improvement, the patient required extracorporeal membrane oxygenation (ECMO) cannulation and continuous veno-venous hemodialysis (CVVHD). Unfortunately, due to continued deterioration, he was transitioned to comfort measures and expired. This case highlights the likely combined effects and complex interactions of chemotherapy toxicity, metastatic disease, and circulatory overload contributing to respiratory failure. 96The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 97 A Case of Streptococcus Pneumoniae Necrotizing Pneumonia with Pneumothorax and Abscess FormationSusanna Betti, MD1 1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAPULMONARY, ALLERGY & CRITICAL CARE MEDICINECASE PRESENTATIONA 63-year-old female with a past medical history of left breast ductal carcinoma in situ, now post-left-sided lumpectomy and radiation in 2005, presented to an outside hospital with chest pain and a cough productive of green sputum. Computed tomography (CT) chest demonstrated patchy ground-glass opacities and dense consolidations in the right middle and lower lobe. Blood cultures and bronchoalveolar lavage culture were positive for Streptococcus pneumoniae, and she was started on antibiotics for community-acquired pneumonia. Her respiratory status rapidly worsened and she required intubation. She developed a large right-sided pneumothorax and had a chest tube placed for a right pleural effusion in the setting of a new lung abscess. Repeat CT chest showed necrotizing right lower lobe pneumonia. The patient was transferred to Thomas Jefferson University Hospital for further management. Throughout the patient’s hospital course, her respiratory status continued to worsen despite antibiotics, inhaled epoprostenol, paralytics, and sedatives. She required tracheostomy placement and a repeat chest tube placement. Repeat CT chest showed a persistent large right-sided pneumothorax (blue arrows), worsening multifocal consolidations (red arrows), areas of cavitation (white arrows), and ground-glass opacities. The patient was transitioned to comfort care and expired. This case serves to highlight an aggressive case of necrotizing Streptococcus pneumoniae pneumonia.97et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 202598 | The Medicine Forum, Volume 26 McConnell’s Sign in the Absence of Pulmonary EmbolismAlicia Bao, MD1* and Tendai Marume, MD1*1. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA* These authors contributed equally to this workPULMONARY, ALLERGY & CRITICAL CARE MEDICINEINTRODUCTIONMcConnell ’s sign is an echocardiographic finding characterized by hyperdynamic motion of the right ventricular (RV) apex with akinesis of the RV free wall. It is widely known as an indicator of RV strain in acute pulmonary embolism (PE) but has been described in other conditions such as sepsis-induced RV dysfunction, acute cor pulmonale, and right-sided heart failure. In critically ill patients, RV dysfunction is a major contributor to hemodynamic instability, respiratory failure, and poor outcomes. Given the overlapping signs of various underlying conditions, McConnell’s sign serves as a useful marker for assessing RV involvement but can be challenging to interpret as an initial imaging finding. Here, we present a rare case of McConnell’s sign seen in a patient in the absence of a PE.CASE PRESENTATIONAn 80-year-old male with a past medical history of coronary artery disease status-post percutaneous coronary intervention in 2005, heart failure with preserved ejection fraction (HFpEF), esophageal cancer status-post esophagectomy, hypertension, atrial fibrillation on apixaban, sick sinus syndrome, chronic kidney disease stage 3b, gastroesophageal reflux disease, and arthritis status-post left total knee arthroplasty initially presented to a regional hospital with altered mental status, fever, and left knee erythema. He had undergone left total knee arthroplasty three months prior. Laboratory tests revealed leukocytosis and elevated inflammatory markers (erythrocyte sedimentation rate of 119 mm/hr, C-reactive protein 223 mg/dL). Blood cultures returned positive for methicillin-resistant Staphylococcus aureus (MRSA). Synovial fluid analysis of the left knee returned with a white blood cell (WBC) count of 122,175 cells/mm3 with Gram-positive cocci on Gram stain, confirming prosthetic joint infection as the source of bacteremia. Due to worsening hemodynamic instability, he was transferred to Thomas Jefferson University Hospital's medical intensive care unit where he required vasopressor support with norepinephrine. On hospital day 2, the patient underwent left knee revision surgery, including irrigation, debridement, and hardware exchange. Postoperatively, he was unable to be extubated due to irregular respiratory patterns and failure to follow commands, requiring continued ventilatory support for another day. He was extubated on day 3 but exhibited increasing volume overload despite aggressive diuresis due to an oliguric acute kidney injury (AKI). On day 5, the patient continued to exhibit clinical deterioration, going into rapid atrial fibrillation with worsening tachypnea, hypothermia, and signs of pulmonary congestion. Laboratory tests showed a blood urea nitrogen of 103 mg/dL, creatinine of 3.96 mg/dL (baseline 1.5 mg/dL), and elevated cardiac biomarkers of troponin of 116 ng/L and pro-B-type-natriuretic peptide (pro-BNP) of >35,000 pg/nL. His oxygen requirements rapidly increased from 2 L/min to 10 L/min nasal cannula. Chest x-ray demonstrated low lung volumes, patchy opacities, and bilateral pleural effusions, raising concern for asymmetric pulmonary edema or pneumonia. A transthoracic echocardiogram (TTE) revealed a dilated right ventricle with hyperdynamic apex consistent with McConnell ’s sign (Figure 1). Additional findings included impaired tricuspid annular plane systolic excursion (TAPSE) and mild pulmonary hypertension. In response to these findings, a computed tomography angiogram (CTA) of the chest was performed to evaluate for PE. Surprisingly, the CTA was negative for acute PE and instead showed a dilated gastric pull-up with a dilated intrathoracic stomach and intrathoracic herniation of the transverse colon, causing complete atelectasis of the right lung (Figure 2). Despite aggressive diuresis, the patient’s respiratory status continued to worsen, requiring high flow nasal cannula of 40 L/min by day 6. A goals-of-care discussion was had with family, who determined it was not within the patient’s goals to be re-intubated. The patient passed away peacefully that evening. Although the family declined autopsy, suspected cause of death was hypoxic respiratory failure from a combination of a large intrathoracic hernia, atelectasis, and volume overload. DISCUSSIONMcConnell’s sign is an echocardiographic ultrasound finding of right ventricular free wall hypokinesis with apical sparing, described most often as an indicator of right heart strain in pulmonary embolism (PE).1 The proposed mechanism for the development of this particular contraction pattern includes a combination of right ventricular ballooning to accommodate for increased afterload, but tethering to the hyperdynamic left ventricle (LV) which leads to preservation of RV wall motion at the apex. The initial proposed specificity of 98The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 99 orrhages and sickled erythrocyte-rich thrombi in small tertiary branches. These patients had basal pulmonary hypertension from chronic hypoxia and microthrom-boembolic disease that was exacerbated by a vaso-occlusive crisis. Further cases have demonstrated McConnell’s sign seen in cases of cor pulmonale from chronic obstructive pulmonary disease (COPD) and systemic lupus erythematosus (SLE),6 acute hypoxemia due to multifocal pneumonia,7 pulmonary contusion,8 or pulmonary vascular occlusion from leukostasis due to hematologic malignancy.9 All cases appear to be linked by pulmonary vascular vasoconstriction and acute hypoxia, leading to an acute rise in pulmonary artery pressures. Another case report demonstrated McConnell’s sign as the finding that led to diagnosis of a lung carcinoma, which was physically compressing smaller branches of the pulmonary arteries.10In the index case, the development of RV dysfunction may be attributable to multiple concurrent factors. First, the patient’s large intrathoracic herniation was large enough to cause complete atelectasis of the right lung, and thus also likely causing extrinsic compression of small pulmonary artery branches. Although the right main pulmonary artery appeared largely patent on the CTA study, the segmental and subsegmental branches were not visualized due to the hernia, which may have predisposed the patient to RV dysfunction. Notably, the hernia was not a new finding for the patient—due to his prior history of esophageal cancer, he had an esophagectomy with gastric pull-through. Computed tomography (CT) scans in the two years prior noted marked herniation; however, these scans were done at other hospitals and were unable to be directly compared to evaluate the extent of herniation. Secondly, the patient was grossly volume overloaded due to acute renal failure, contributing to RV pressure overload. McConnell’s sign was as high as 94% compared to patients with chronic pulmonary hypertension of other etiologies, with the theory that chronic pulmonary hypertension causes compensatory RV hypertrophy that limits the degree of dilation.1 Although most studies maintain a high degree of specificity and positive predictive value of McConnell ’s sign, there are increasing reports of other pathologies leading to the ultrasonographic sign. Here we present a case of McConnell ’s sign on echocardiography that led to detection of a large intrathoracic colonic hernia. Given the proposed mechanism, it is unsurprising that McConnell’s sign has been an increasingly common echocardiographic finding in cases of early RV ischemia. In a retrospective study, McConnell’s sign was detected in 70% of cases of pulmonary embolism and 67% of cases of right ventricular myocardial infarction when echocardiograms were read by two independently blinded cardiologists, meaning the finding alone should not be considered pathognomonic for the presence of PE.2 A second retrospective study also showed similar incidence of McConnell ’s sign in patients with PE compared to RV myocardial infarction.3 Further case series have similarly found McConnell ’s sign in RV ischemia, particularly in cases where a wrap-around left anterior descending (LAD) artery may supply the apex.4 Although McConnell’s initial study showed a distinct ultrasonographic difference, there are increasing reports of similar patterns in even chronic pulmonary hypertension. A case series published in 2018 showed three cases of McConnell’s sign associated with acute chest syndrome in sickle cell disease.5 Post-mortem autopsies in all three cases did not find pulmonary emboli, but they instead found presence of microhem-Figure 1. Apical four chamber view demonstrating a dilated right ventricle and hyperkinesis of the RV apex during systole (arrow)Figure 2. Intrathoracic herniation of the stomach and transverse colon, causing compression of the right lung.99et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025100 | The Medicine Forum, Volume 26 Third, the patient may have had a prior unrecognized coronary event affecting the RV, despite stable troponin levels during the admission. Lastly, the patient had evidence of mild pulmonary hypertension on TTE, so an acute pulmonary vasoconstrictive response to hypoxia may have caused an exacerbation of his existing pulmonary hypertension. Regardless of the mechanism, severe RV dysfunction portends a poor prognosis and was likely a contributor in his eventual passing. CONCLUSION Although McConnell’s sign maintains high specificity for acute PE, there are increasing reports of other causes of RV dysfunction leading to the distinctive ultrasono-graphic RV strain pattern. Ultrasonography is an exceedingly useful tool, but as its utilization is increased, it is important to recognize the clinical context of interpreting ultrasound signs and to understand the underlying pathophysiology. Here, we present a case of McConnell’s sign in the absence of a PE that was instead caused by a large, intrathoracic colon hernia and volume overload. Most other non-PE cases involve either RV ischemia from myocardial infarction or acute worsening of pulmonary hypertension in patients with a pre-existing insult, as was in the index case. As such, patients with the McConnell ’s sign finding who are stable should undergo CTA imaging to confirm the diagnosis prior to initiating empiric treatment for PE. REFERENCES1. McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996;78(4):469-473. doi:10.1016/s0002-9149(96)00339-62. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr. 2005;6(1):11-14. doi:10.1016/j.euje.2004.06.0023. Mazur ES, Mazur VV, Rabinovich RM, Myasnikov KS. Right ventricular longitudinal strain in acute pulmonary embolism and right ventricular myocardial infarction in patients with McConnell's sign. Kardiologiia. 2020;60(7):20-27. doi:10.18087/cardio.2020.7.n11514. Rafie N, Foley DA, Ripoll JG, et al. McConnell's sign is not always pulmonary embolism: the importance of right ventricular ischemia. JACC Case Rep. 2022;4(13):802-807. doi:10.1016/j.jaccas.2022.05.0075. McCutcheon JB, Schaffer P, Lyon M, Gordon R. The McConnell sign is seen in patients with acute chest syndrome. J Ultrasound Med. 2018;37(10):2433-2437. doi:10.1002/jum.145856. Walsh BM, Moore CL. McConnell's sign is not specific for pulmonary embolism: case report and review of the literature. J Emerg Med. 2015;49(3):301-304. doi:10.1016/j.jemermed.2014.12.0897. Jackson P, Ranches G. 1903: An unusual case of McConnell sign. Crit Care Med. 2016;44(12):551. doi:10.1097/01.ccm.0000510576.64778.ce8. Hook CJV, Shapiro R, Warner B. McConnell's sign in the setting of pulmonary contusion. Am J Respir Crit Care Med. 2022;205:A2828. Abstract presented at: American Thoracic Society International Conference; May 2022; San Francisco, CA.9. Rozenbaum D, Lebold KM, Lee D, Salmi D, Htet NN. Cardiovascular collapse and McConnell's sign as early manifestations of leucostasis. BMJ Case Rep. 2024;17(2):e257330. doi:10.1136/bcr-2023-25733010. Antoine S, Oye M. McConnell's sign in invasive small cell lung cancer. Eur Heart J Case Rep. 2020;4(6):1-2. doi:10.1093/ehjcr/ytaa302100The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 101 "Three Sunrises at Miami Beach #2" – Gregary D. Marhefka, MD01et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025102 | The Medicine Forum, Volume 26 Recurrent Post-Viral Rhabdomyolysis in a 36-Year-Old Male: A Case ReportWarda Naqvi, MD1, David J. Walz, MD1, Lucy Checchio, DO11. Division of Internal Medicine, Department of Medicine, Jefferson Abington Hospital, Abington, PARHEUMATOLOGYINTRODUCTIONRhabdomyolysis is a syndrome of skeletal muscle breakdown, releasing intracellular contents such as creatine kinase (CK) and myoglobin into the bloodstream, which can precipitate acute kidney injury (AKI).1 While trauma, extreme exertion, and toxins are frequent culprits, infections, particularly viral illnesses, represent a less common but significant trigger.2 Influenza and other respiratory viruses have been implicated in sporadic cases of rhabdomyolysis, often presenting with acute myalgias and elevated CK levels following a viral prodrome.3 In contrast, recurrent rhabdomyolysis is typically associated with inherited metabolic myopathies (e.g., McArdle disease) or autoimmune myositis, conditions often marked by distinct genetic or inflammatory character-istics.4,5 The intersection of viral infections with recurrent muscle breakdown, however, remains poorly explained, posing diagnostic and therapeutic challenges. Here, we report a case of an African American male with a decade-long history of recurrent rhabdomyolysis linked to viral infections, lacking a clear genetic or autoimmune etiology, offering insight into this rare clinical phenomenon.CASE PRESENTATIONA 36-year-old African American male with a history of asthma and a decades-long pattern of recurrent rhabdo-myolysis triggered by viral infections. His first episode occurred in childhood during a hospitalization for an asthma exacerbation secondary to an upper respiratory infection, marked by severe generalized muscle pain and dark urine. Since then, he experienced multiple similar episodes associated with both upper respiratory and gastrointestinal infections, consistently presenting with significant myalgias, dark urine due to myoglobinuria, and markedly elevated creatine kinase (CK) levels. He reported self-recognizing early symptoms in milder cases and often aborted them with aggressive oral hydration at home. However, three severe episodes necessitated hospitalization, including the most recent admission at age 29 when CK exceeded the maximum recordable range of 42,600 U/L, and he tested positive for influenza. Extensive workup included a muscle biopsy revealing myopathic changes (variation in fiber size, scattered atrophic fibers, and numerous ring fibers) without inf lammation, negative autoimmune serologies (antinuclear antibody, anti-Jo-1, and comprehensive panel of both myositis-associated antibodies and myositis-specific antibodies), and normal electromyography. He denied any family history of neuromuscular disorders, and specialists, including rheumatology, diagnosed this as viral-triggered rhabdomyolysis.He presented to our emergency department—his fourth hospitalization—with generalized myalgias starting one week after an upper respiratory infection, with resolving respiratory symptoms. The pain began in the bilateral shoulders and upper back and later involved the calves. He endorsed moderate exercise (2-3 times weekly) but denied excessive exertion, alcohol use, or illicit drug use. Examination showed tenderness in the bilateral posterior upper arms and calves with no edema, erythema, or weakness (strength 5/5 in all muscle groups). Laboratory findings included a CK level exceeding the recordable range of 22,000 U/L (reference range: 38-174 U/L), aspartate aminotransferase (AST) of 803 U/L (10-40 U/L), and alanine aminotransferase (ALT) of 116 U/L (7-56 U/L). Urinalysis was consistent with myoglobinuria. SARS-CoV-2 testing, influenza testing, and respiratory pathogen panel were negative.Aggressive intravenous hydration with isotonic saline was initiated on admission to prevent kidney injury. Repeat autoimmune and viral hepatitis panels were negative. Abdominal ultrasound showed mild hepatic steatosis without structural abnormalities. Nephrology and rheumatology consultations supported a post-viral etiology. Over seven days, CK decreased only to 18,000 U/L despite aggressive hydration. AST and ALT improved, and myalgias resolved. He was discharged on hospital day 8 with plans for outpatient follow-up with primary care, rheumatology, and neuromuscular specialists.DISCUSSIONThis case is distinguished by recurrent rhabdomyolysis consistently precipitated by viral infections, including upper respiratory and gastrointestinal illnesses, in an African American male. The patient’s history of multiple episodes with dark urine, significant myalgias, and extreme CK elevations strongly implicates a post-viral etiology. Viral infections are established triggers of rhabdomyolysis, with influenza notably linked to severe muscle breakdown in both pediatric and adult populations.2,3,6 The temporal pattern—symptoms 102The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 103 CONCLUSION This case highlights a rare pattern of recurrent rhabdo-myolysis in an African American male, consistently triggered by viral infections. Extensive evaluation failed to identify common genetic or autoimmune etiologies, thereby supporting a diagnosis of post-viral rhabdomy-olysis; however, the possibility of an exceedingly rare genetic cause cannot be entirely excluded. These observations encourage clinicians to consider viral causes in cases of unexplained recurrent muscle breakdown, especially in patients who may have elevated CK responses. Additional research into viral mechanisms and possible racial factors could improve diagnostic precision and treatment strategies for this underrec-ognized condition. REFERENCES1. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. doi:10.1056/NEJMra08013272. Crum-Cianflone NF. Bacterial, fungal, parasitic, and viral myositis. Clin Microbiol Rev. 2008;21(3):473-494. doi:10.1128/CMR.00001-083. Hu JJ, Kao CL, Lee PI, et al. Clinical features of influenza-associated rhabdomyolysis in children. J Formos Med Assoc. 2008;107(8):617-623. doi:10.1016/S0929-6646(08)60179-84. Scalco RS, Gardiner AR, Pitceathly RD, et al. Rhabdomyolysis: a genetic perspective. Orphanet J Rare Dis. 2015;10:51. doi:10.1186/s13023-015-0264-35. Mammen AL. Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis. Nat Rev Neurol. 2011;7(6):343-354. doi:10.1038/nrneurol.2011.636. Ayala E, Kagawa FT, Wehner JH, Tam J, Updike G, Kass J. Rhabdomyolysis associated with 2009 influenza A(H1N1). JAMA. 2009;302(17):1863-1864. doi:10.1001/jama.2009.15327. Kenney K, Landau ME, Gonzalez RS, Hundertmark J, O’Brien K, Campbell WW. Serum creatine kinase levels in African-American and Caucasian men: a comparative study. Muscle Nerve. 2010;41(6):856-859. doi:10.1002/mus.216248. Nance JR, Mammen AL. Diagnostic evaluation of rhabdomyolysis. Muscle Nerve. 2015;51(6):793-810. doi:10.1002/mus.246069. Zutt R, van der Kooi AJ, Linthorst GE, Wanders RJ, de Visser M. Rhabdomyolysis: review of the literature. Neuromuscul Disord. 2014;24(8):651-659. doi:10.1016/j.nmd.2014.05.00510. Lillian MJ, Quinlivan R. Metabolic myopathies: a clinical approach. Pract Neurol. 2020;20(1):31-39. doi:10.1136/practneurol-2019-002349emerging post-infection, as seen with the current upper respiratory infection and prior documented influenza—aligns with reports of viral myositis, where muscle damage follows viral clearance.3 The absence of trauma, excessive exertion, or toxins in this patient’s history further solidifies the viral trigger as the primary driver.The recurrence of episodes, with three prior severe events requiring hospitalization and milder episodes aborted by self-administered hydration, suggests a heightened susceptibility to post-viral muscle injury. Viral myositis may involve direct viral invasion or immune-mediated damage, mechanisms plausible here given the lack of inflammatory infiltrate on biopsy.5 Influenza-associated rhabdomyolysis with CK levels exceeding 10,000 U/L has been reported, akin to this patient’s severe elevations, though recurrence is less documented.3 The patient’s African American background may be relevant, as studies suggest racial differences in CK response to muscle stress, potentially amplifying post-viral effects.7 The nonspecific biopsy findings (fiber size variation, ring fibers) likely reflect cumulative damage from repeated viral insults rather than a primary myopathy, supported by normal electromyography, which excludes chronic neuromuscular disease.8,9Alternative diagnoses, such as inherited metabolic myopathies (e.g., carnitine palmitoyltransferase II deficiency or McArdle disease), are improbable given the lack of exertional triggers, family history, or enzymatic abnormalities.4,10 While occult metabolic defects unmasked by infection are conceivable, the consistent viral prodrome across various infections and a confirmed influenza episode strongly favors a post-viral mechanism.9 Hepatic steatosis, though present, is mild and uncorrelated with rhabdomyolysis timing, reducing its significance. Mitochondrial myopathies, suggested by ring fibers, are unlikely without multisystem involvement or electromyographic abnormalities.10 Additionally, autoimmune etiology was deemed unlikely in this case, as there was no evidence of proximal muscle weakness, which is a key characteristic of autoimmune myopathies.5The patient’s ability to abort milder episodes with hydration and the rapid response to intravenous fluids underscore the acute, reversible nature of these post-viral events.1 Future evaluation during an acute episode, including viral serologies or polymerase chain reaction testing, could confirm specific pathogens, while muscle histochemistry might reveal post-viral changes.8 This case reinforces recurrent post-viral rhabdomyolysis as the most likely diagnosis, driven by a unique suscepti-bility to infection-induced muscle breakdown.103et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025104 | The Medicine Forum, Volume 26 Unmasking the DVT Mimic: A Rare Case of Diabetic Myonecrosis in a Young PatientAvish Patel, MD1, Paul Endres, MD1, Alexander Marchese, MD2, Dianna Cheney-Peters, MD31. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA2. Division of Diagnostic Radiology, Department of Radiology, Thomas Jefferson University Hospital, Philadelphia, PA3. Division of Hospital Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PARHEUMATOLOGYINTRODUCTIONDiabetic myonecrosis is an uncommon complication of diabetes mellitus, often falsely believed to be a deep vein thrombosis (DVT). Patients present with similar presentations of edema and focal tenderness that are most often unilateral in a proximal lower extremity.1 When venous ultrasound is negative, magnetic resonance imaging (MRI) is the preferred diagnostic modality over muscle biopsy, given the potential complications.2,3 Treatment includes rest, analgesia, and improved glycemic control.4 Given the rise of metabolic disorders and insulin resistance, it is important to be aware of this diagnosis to prevent overutilization of healthcare resources.5CASE PRESENTATIONThis is a 26-year-old male with a past medical history of type 1 diabetes mellitus, deep vein thrombosis of the right lower extremity, chronic kidney disease (CKD), hypertension, diabetic retinopathy, and ambulatory dysfunction who presented due to worsening right thigh pain and swelling for two weeks. The patient had a recent hospitalization weeks prior to admission for hypertensive emergency, and he was diagnosed with an acute kidney injury (AKI) on CKD, proteinuria, and nephrotic syndrome. His lower extremity edema was thought to be due to nephrotic syndrome with a right greater than left distribution in the setting of prior right lower extremity DVT. The patient was also treated with antibiotics for cellulitis and bacteremia, which were completed. The chronic significant pain of the right lower extremity and ambulatory dysfunction were felt to be due to diabetic lumbosacral plexopathy treated with pregabalin.He presented again to the hospital with worsening right lower extremity pain, edema, and tightness in his groin and lateral aspect of the right thigh for several weeks, limiting mobility or movement of his thigh even more than his minimal baseline mobility. Initial labs included an unremarkable lactate level; no leukocytosis; platelets of 507,000 B/L; creatinine of 1.43 mg/dL; no electrolyte abnormalities; prothrombin time (PT) of 13.8 seconds; international normalized ratio (INR) of 1.24; partial thromboplastin time (PTT) of 41 seconds; creatine kinase (CK) of 351 IU/L; normal lactate dehydrogenase (LDH); and haptoglobin of 736 mg/dL. Thyroid-stimulating hormone (TSH) was 4.78 uIU/mL on recent outpatient labs. The hemoglobin A1c (HbA1c) level was greater than 14% a few months before admission but did trend down to 9.5% and then 6.6% with better glucose control during admission. He was influenza-positive on admission. Bilateral venous ultrasound did not demonstrate any acute DVT in the right or left femoro-popliteal veins, although calf veins were poorly seen. Computed tomography (CT) of the right femur demonstrated diffuse right lower extremity thickening and subcutaneous edema without drainable fluid collections and with asymmetric enlargement of the right thigh musculature with heterogeneous enhancement, notably within the vastus muscles and adductor magnus and longus muscles. Subsequent MRI of the right femur was remarkable for asymmetric edema and enlargement involving a majority of the right thigh musculature, most notably in the vastus muscles and adductor muscles.The initial examination by surgery was remarkable for a soft right thigh with minimal medial thigh tenderness to palpation and soft compartments; Therefore, no acute surgical intervention was indicated. The initial differential diagnosis included diabetic myonecrosis, inflammatory myopathy, and infectious myositis. Another consideration was statin-induced myositis, which was lower on the differential due to chronic use.The initial plan was for pain control, physical therapy, and rheumatology consult. Rheumatology recommended additional testing, including a myositis panel; aldolase level; muscle biopsy; and testing for antinuclear antibody (ANA), anti-double-stranded DNA antibody (anti-dsDNA), and anti-neutrophil cytoplasmic antibodies (ANCA). While awaiting the rheumatologic results, neurology was also consulted and recommended an MRI of the lumbar spine for evaluation of diabetic plexopathy. MRI lumbar spine demonstrated no significant degenerative changes in the lumbar spine but showed bilateral, right-greater-than-left posterior paraspinal muscle edema with sagittal post-contrast enhancement that extends from T11-S2, 104The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 105 Figure X: Axial contrast-enhanced CT of the proximal right thigh on initial presentation demonstrates heterogeneous enhancement and enlargement of the adductor longus muscle (arrow), with overall increased caliber of the medial compartment musculature compared to the partially imaged contralateral thigh.Figure Y: Large field-of-view coronal short tau inversion recovery (STIR) sequence (left) demonstrates diffuse subcutaneous edema and asymmetric enlargement of the right thigh compared to the left thigh. Axial T2-weighted sequence of the right thigh (right) shows extensive intramuscular edema involving the anterior and medial compartments, most notably affecting the vastus musculature and the adductor magnus (double-sided arrow), with relative sparing of the posterior compartment.Figure Z: Follow-up contrast-enhanced CT of the right femur two weeks after presentation. Axial image through the proximal right t h i g h ( l e f t ) d e m o n s t r a t e s heterogeneous enhancement of the gluteus medius and gluteus m i n i m u s m u s c le s (c u r ve d double-sided arrow). Axial image through the mid thigh (right) shows further interval enlargement of the thigh musculature with diffusely decreased intramuscular enhancement.105et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025106 | The Medicine Forum, Volume 26 control. Limited case studies have shown a high rate of recurrence of diabetic myonecrosis in up to 50% of patients.9 Recurrence may occur in the same or different muscle groups, highlighting the importance of proper recognition and management of this disease process.CONCLUSION Diabetic myonecrosis, while uncommon, is a known and notable mimic of DVT in patients with uncontrolled diabetes of all ages. It most frequently presents as unilateral proximal lower extremity edema and tenderness but can present bilaterally, distally, or in the upper extremities. This is an important diagnosis to have in the differential for this presentation, given increases in insulin resistance and metabolic disorders. Proper management of diabetes can prevent the initial incidence of diabetic necrosis and further recurrence of this pathology. Recognition and proper treatment with rest, analgesia, and glycemic control are important given the high recurrence rates and high insulin resistance rates to prevent improper diagnostic tests, which strain healthcare resources. REFERENCES1. Storandt M, Thondapi C, Matta A. Diabetic myonecrosis: an uncommon complication of a common condition. Eur J Case Rep Intern Med. 2020;7(3):001389. doi:10.12890/2020_0013892. Chason DP, Fleckenstein JL, Burns DK, Rojas G. Diabetic muscle infarction: radiologic evaluation. Skeletal Radiol. 1996;25(2):127-132. doi:10.1007/s0025600500483. Rabczyński M, Fenc M, Kuźnik E, Lubieniecki P, Hałoń A. Diabetic muscle infarction—a rare diabetic complication: literature review and case report. Int J Environ Res Public Health. 2023;20(4):3390. doi:10.3390/ijerph200433904. Umpierrez GE, Stiles RG, Kleinbart J, Krendel DA, Watts NB. Diabetic muscle infarction. Am J Med. 1996;101(3):245-250. doi:10.1016/S0002-9343(96)00156-85. Mazoch MJ, Bajaj G, Nicholas R, et al. Diabetic myonecrosis: likely an underrecognized entity. Orthopedics. 2014;37(10):e936-e939. doi:10.3928/01477447-20140924-916. Solankee J, Zaki T, Hoff E, Chowdhury S. Novel case of diabetic myonecrosis in a teenage patient with type 2 diabetes mellitus. BMJ Case Rep. 2022;15(3):e246173. doi:10.1136/bcr-2021-2461737. Khanna HK, Stevens AC. Diabetic myonecrosis: a rare complication of diabetes mellitus mimicking deep vein thrombosis. Am J Case Rep. 2017;18:38-41. doi:10.12659/AJCR.9009038. Grigoriadis E, Fam AG, Starok M, Ang LC. Skeletal muscle infarction in diabetes mellitus. J Rheumatol. 2000;27(4):1063-1068.9. Nadeem D, Furqan S, Ram N. Diabetic myonecrosis: a vascular complication. J Coll Physicians Surg Pak. 2022;32(12)(Suppl 1):SS162-SS164. doi:10.29271/jcpsp.2022.Supp0.SS162most consistent with myositis. In review of this imaging, neurology had a low suspicion for primary neurologic etiology of pain and deemed weakness likely due to pain. Right thigh skeletal muscle biopsy pathology returned with some lymphocyte inflammation and very few necrotic and regenerating muscle fibers. It showed the presence of fiber type grouping in the skeletal muscle compatible with neurogenic change. These features are known to be seen in inflammatory myopathies. However, skeletal muscle fibers that have undergone chronic denervation for an extended period can exhibit histologic features known as secondary myopathic degeneration that can share histologic features of inflammatory myopathy. We therefore present that the skeletal muscle pathologic changes presented in this case are consistent with diabetic myonecrosis. DISCUSSIONDiabetic myonecrosis is an uncommon complication of diabetes mellitus. Given the rise of metabolic disorders and insulin resistance, this diagnosis is important to have on the differential for patients coming in with similar presentations as found in our patient. It can be found in patients with type 1 or type 2 diabetes.1,6 A case similar to ours was published in which a 16-year-old female with newly diagnosed type 2 diabetes presented with acute-onset, bilateral lower extremity pain and tenderness concerning for bilateral gastrocnemius myonecrosis in the setting of poorly controlled type 2 diabetes for at least 4-5 years.6 Another reported case was of a 54-year-old man with poorly controlled diabetes presenting with 2 weeks of unilateral lower extremity swelling and pain.7 These cases highlight that diabetic myonecrosis frequently presents similarly to a deep vein thrombosis and can occur in patients of any age. Most frequently, it presents in the proximal muscles of the lower extremities and less commonly presents bilaterally in the distal muscles of any extremity. Clinicians taking care of patients with uncontrolled diabetes mellitus should be mindful of this diagnosis for any patients presenting with limb swelling and tenderness with a negative venous ultrasound. MRI is the preferred diagnostic modality as it is non-invasive and can identify the characteristic findings of muscle edema and necrosis.2,3 MRI findings of diabetic myonecrosis include high signal intensity on T2-weighted images and muscle enlargement with diffuse edema. This can be helpful to distinguish from similar conditions of painful edema, such as cellulitis, abscess, necrotizing fasciitis, and deep vein thrombosis. Muscle biopsy is helpful to confirm the diagnosis; however, if there is enough clinical suspicion with the proper MRI findings, it is preferred to be avoided, given the potential complications.6,8 The treatment for diabetic myonecrosis is rest, pain control, and glycemic 106The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 107 "Hoatzin" – Bret McCarty, MD 107et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025108 | The Medicine Forum, Volume 26 The microscope is held aloft in a sea of darkness,Illuminating the gyri and sulci of the exposed brain below.Its harsh, sterile light creates a veritable barrierSo hot, so intense, it threatens to explode forth at any moment.The screens scattered across the room provide companionship to this lonely machineAnd I, residing amidst the sea of shadows,Bear witness to its solitudeTo the silence of the light.I have seen vessels tied and aneurysms clipped,And an eon has gone by…There’s an air of anticipation,An expectation of something more.But, solace and quietude prevailThe light remains resoluteThe microscope remains afloat in the same placeFor eternity and evermore…Eternal LightAnurag Modak, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAHUMANITIES & REFLECTIONS108The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 109 A new type of painNever covered in a lectureNot neuropathic, visceral, post-procedural, cancer, phantom pains,But existential.She didn’t want pain medsAnd she had her reasons -We didn’t push.What she wanted was to talkTo be heardFor us to be silent and stopAsking her every secondIf she’d moved bowels, vomited, slept…What she wanted was to talk.What other medication is there for pain of the soul?Existential PainKian Waddell11. Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PAHUMANITIES & REFLECTIONS109et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025110 | The Medicine Forum, Volume 26 There is only one of the loved one you know.Often it can be hard to let go.Five years old the world became cold.Lost my mother to breast cancer.A cold wound that can’t be answeredFather raised you in a foreign land.Drove you to school, combed your hair, gave you a life you could have never planned.Taught me that I would catch a cold from the wind.No arguing about modern medicine, my dad was thick skinned,Here comes college, first generation, what an exciting time.Get to medical school so exciting; here comes the climb.Up so high then you fell and broke your hip.I am not well equipped.At eighty years old,The world is cold,Unable to walk,dementia wrought,Not eating, not talking and confused,Father this is not good news.Your hip replaced,Foreign place,you lost all your social cues,Navigating Care and Loss Through Aging, Disease, and Decision-Making in The Covid EraMichael Predi, DO11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAHUMANITIES & REFLECTIONS110The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 111 Your malnutrition grows worse.Sitting isolated in the “covid-verse”.Decisions, decisions; nutritional status is declining.Michael, your father is not dining.Do you want a feeding tube, he is withering away?We never discussed his goals of care, but sir, I need an answer by today,Pursued the tube, started the tube feeds.Covid19 MRNA vaccine trending on the newsfeeds.Six feet social distancing in the nursing facility.Being unable to hug my dad was killing me.Vaccine administered, time passed pandemic better under control,Now I am loading up my dad in a wheelchair and we are taking a stroll,Driving you to restaurants, combing your hair, and watching the game.The tables had turned but now life without you is not the same.There is only one of you in my world.You are experiencing reoccurring pneumonias,Worsening of dementia,Losing your ability to swallow,is not something that I follow.I can understand the pathophysiology, but I cannot comprehend that you are sick,No more labs, no more unnecessary sticks,Hospice gave you comfort you with comfort in your final days,Glad I could be near.I love you dad, the time was dear.111et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025112 | The Medicine Forum, Volume 26 Small Gifts, Big Questions: The Ethical Dilemma in Accepting Gifts in MedicineMeiqi Luo, MD11. Division of Internal Medicine, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PAHUMANITIES & REFLECTIONSI remember discussing the topic of gift-giving by patients in a small group session in medical school. When asked whether it’s ethical for medical professionals to accept gifts from patients, I responded, “It depends on the value of the gifts.” If the gifts were of appropriate value and given purely out of appreciation, they serve to strengthen the physician-patient relationship. However, what I failed to realize was the difficulty in determining the value and intention of a gift. My personal experience of receiving gifts from a patient made me aware of such ethical ambiguities.At the community clinic where I volunteer, I took care of an undocumented immigrant who did not speak English and was unable to work due to a disability. Because of his complicated medical and social needs, he had been a frequent visitor. He was one of the most appreciative people I had ever met – he remembered the names of everyone who had helped him and said thank you to them on his way out. As his primary provider, I wasn’t surprised when I received a text message from him stating that he wanted to give me something in return. Despite my repeated refusals, he brought the gifts to the hospital one day, asking if I could meet him briefly during my lunch break. The gifts, consisting of food donated to him by the community, were packaged neatly in grocery bags, with plastic rope wrapped around them for ease of carrying. Knowing it wasn’t easy for him to carry these bags all the way there with his disability, I accepted them with deep gratitude.He reached out a few more times trying to hand me similar gifts. I felt conflicted about accepting them but struggled to decline more sternly, fearing it would damage our relationship. The American Medical Association Code of Medical Ethics suggests that one should be sensitive to the gift’s value relative to the patient’s or physician’s means and not allow the gift or offer of a gift to influence the patient’s medical care.1 On one hand, these gifts weren’t of excessive value. On the other hand, the patient has no income, making these community donations his only source of food security. Is it justifiable to believe that they are of the same value to me as they are to him? While I could assume that these gifts were well-intended as a sign of gratitude, would he have the same expectations for our patient-physician relationship? Furthermore, accepting them would create a slippery slope situation where it could be more difficult for me to reject them in the future. Among the numerous considerations, I couldn’t decide on the appropriateness of accepting these gifts.I eventually donated the nonperishable items to local food drives. And thankfully, my patient expressed understanding and agreed not to bring any more gifts after my clinic supervisor offered to speak to him on my behalf. The experience of ethical uncertainty reminds me to always approach these situations with ethical scrutiny, as the social power of a gift to influence decisions can often be underappreciated. While ethical guidelines should be consulted, accepting gifts from patients should be steered by one’s internal moral compass built with professionalism and humanity.REFERENCE1. OPINION 1.2.8, AMA Code of Medical Ethics. American Medical Association, 2016, https://code-medical-ethics.ama-assn.org/sites/amacoedb/files/2022-08/1.2.8.pdf Accessed 27 Feb. 2024.112The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.j fferson. du/t f/vol26/iss1/1 The Medicine Forum, Volume 26 | 113 "Three Sunrises at Miami Beach #3" – Gregary D. Marhefka, MD113et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025114The Medicine Forum, Vol. 26 [2025], Art. 1https://jdc.jefferson.edu/tmf/vol26/iss1/1©Thomas Jefferson University Photography Services115et al.: The Medicine Forum: Volume 26Published by Jefferson Digital Commons, 2025

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