Case Report or Series Posters

Introduction/Background:

Lung cancer remains the leading cause of cancer death worldwide. Therefore, management decisions that follow nodule identification represent a crucial moment in patient care. Synchronous multiple primary lung cancer (SMPLC) refers to the simultaneous diagnosis of two or more distinct cancerous lesions rather than metastasis from a single primary site. This phenomenon is estimated to occur in approximately 2% of patients diagnosed with lung cancer. Although the underlying pathogenesis is incompletely understood, carcinogen exposure is able to create a large area of genetic alteration increasing the risk of dysplasia - a concept known as field cancerization.

Description:

A 71-year-old female presented to the emergency department (ED) for worsening dyspnea and chest pain in the setting of a 10-week nonproductive cough. Social history was significant for a 15-pack-year smoking history, and a family history of lung cancer. Three incidental pulmonary nodules were identified on computed tomography (CT): a 12.5 mm nodule in the left upper lobe (LUL), 10 mm nodule in the LUL, and a 17 mm nodule in the right lower lobe (RLL). Further workup in the ED was otherwise unremarkable. A positron emission tomography (PET)-CT scan revealed that all three nodules had mild avidity with standardized uptake values (SUVs) ranging between 1.75 and 2.24. Findings were discussed with the multidisciplinary tumor board, and biopsy was recommended after lack of interval improvement on a 6-week interval scan. Biopsies acquired via robot-assisted bronchoscopy identified three unique cancers: well-differentiated carcinoid tumor, well-differentiated adenocarcinoma with an acinar pattern, and poorly differentiated adenocarcinoma with a solid pattern. Surgical resection was performed and tolerated without complication.

Discussion:

Recognizing SMPLC is critical to ensuring an accurate diagnosis. Misclassifying unique primary lesions as metastatic disease can lead to missed opportunities for curative treatment. Clinicians should remain vigilant when evaluating patients with multiple pulmonary nodules, particularly those with risk factors. A multidisciplinary approach that incorporates advanced diagnostic technologies, such as robot-assisted bronchoscopy, enables a comprehensive and simultaneous biopsy of multiple nodules during a single procedure. Therefore, early involvement of lung nodule navigators and clinics may enhance patient outcomes in complex lung cancer presentations.

Introduction/Background:

Management of intermediate- to high-risk pulmonary embolism (PE) is complex when intracardiac shunting is present. A patent foramen ovale (PFO) increases the risk of paradoxical embolization and complicates decisions regarding thrombolysis, thrombectomy, and timing of definitive intervention. Limited guidance exists on optimal sequencing of therapies in patients with recurrent PE, right ventricular (RV) strain, and suspected malignancy. We present a case highlighting multidisciplinary management of submassive PE with large PFO requiring staged intervention.

Description:

A 65-year-old female with hypertension, chronic kidney disease, heart failure with preserved ejection fraction, and obesity presented with progressive dyspnea and presyncope. Imaging demonstrated a large saddle PE with RV strain and hypoxemic respiratory failure. Echocardiography revealed RV dilation, reduced systolic function, and atrial-level shunting consistent with PFO. She underwent catheter-directed thrombolysis with temporary clinical improvement and was discharged on anticoagulation. She re-presented within 24 hours with hypotension, persistent RV dysfunction, and residual bilateral PE despite a decreased clot burden. Given the large right-to-left shunt and concern for systemic embolization, a multidisciplinary team pursued staged intervention with percutaneous PFO closure followed by mechanical pulmonary thrombectomy, resulting in improved pulmonary pressures, oxygenation, and hemodynamic stability. Concurrent imaging revealed peritoneal carcinomatosis with markedly elevated CA-125, suspicious for advanced gynecologic malignancy. She was discharged stable on direct oral anticoagulation with plans for oncologic evaluation and neoadjuvant therapy.

Discussion:

This case illustrates the therapeutic challenge of managing submassive PE in the presence of a large PFO and suspected malignancy. Intracardiac shunting alters risk-benefit considerations for thrombolysis and thrombectomy due to potential paradoxical embolization. A staged strategy of PFO closure followed by thrombectomy enabled definitive clot removal while mitigating embolic risk and stabilizing RV function. Multidisciplinary coordination among cardiology, critical care, and oncology was essential. Further study is needed to clarify optimal sequencing of structural and pulmonary vascular interventions in similar high-risk patients.

Introduction/Background:

Traumatic cerebral venous sinus thrombosis (CVST) is an under-recognized complication of head trauma, particularly in skull fractures overlying dural venous sinuses. Among patients with skull fractures, venous sinus thrombosis is reported in up to 7% of cases and in 41–57% when fractures extend to a dural sinus or jugular bulb on dedicated imaging. We present a case of traumatic sigmoid sinus thrombosis associated with mastoid fracture involving the jugular bulb.

Description:

A previously healthy 15-year-old male presents after being thrown from the hood of a moving vehicle. He experienced a brief loss of consciousness followed by headache, dizziness, nausea, vomiting, amnesia, and right wrist pain. Examination reveals left hemotympanum and decreased hearing without additional focal neurologic deficits. Initial non-contrast CT head and cervical spine show no intracranial hemorrhage. CT temporal bone reveals a left mastoid fracture extending to the jugular bulb. Neurosurgery and otolaryngology are consulted. Given the fracture’s proximity to the sigmoid sinus and persistent headache and dizziness despite supportive management, dedicated venous imaging is obtained. MRI brain shows no hemorrhage or infarct. However, MR venography demonstrates a small nonocclusive thrombus extending from the distal left sigmoid sinus into the jugular bulb. Hematology is consulted, and anticoagulation is initiated following multidisciplinary clearance. The patient remains neurologically stable and transitions to outpatient therapy.

Discussion:

Diagnosis of CVST in the setting of skull fracture is challenging, as non-contrast head CT has limited sensitivity (approximately 30%) for detecting venous thrombosis, particularly in patients without additional focal neurologic deficits. In this case, initial CT head was negative, and the thrombus was identified only after targeted venous imaging prompted by the fracture’s proximity to the jugular bulb and persistent symptoms. This case highlights the need for high suspicion for venous injury in high-risk skull fractures despite reassuring initial imaging. Management is individualized given competing risks of anticoagulation and thrombus propagation, guided by multidisciplinary input. Future research is needed on the utility of detecting CVST in skull fracture, along with specific indications for dedicated venous imaging.

Introduction/Background:

Acromegaly is an endocrine disorder characterized by excess growth hormone secretion, typically from a pituitary adenoma, resulting in elevated insulin-like growth factor 1. It is associated with several cardiovascular complications, including hypertension, cardiomyopathy, and arrhythmias. While less commonly recognized, a prothrombotic state may also exist, possibly due to increased thrombin generation and elevated fibrinogen and factor VIII levels. Literature on the risk of venous thromboembolism (VTE) in acromegaly remains sparse, and documented cases of pulmonary embolism (PE) in this population are rare. This case highlights a massive PE in a patient with acromegaly and prior VTE following brief perioperative anticoagulation interruption.

Description:

A 64-year-old male with acromegaly secondary to pituitary adenoma s/p stereotactic radiosurgery, atrial fibrillation, obesity, and a history of recurrent DVT/PE presented for elective thyroidectomy and left parotidectomy. Due to his high thrombotic risk, hematology recommended holding rivaroxaban 24 hours preoperatively, followed by prophylactic enoxaparin postoperatively and resumption of full anticoagulation the next day. He remained intubated overnight due to ventilatory concerns. On postoperative day one, he was extubated and later collapsed while ambulating, suffering a pulseless electrical activity arrest. Return of spontaneous circulation was achieved after 3 minutes of CPR. Bedside ultrasound revealed right ventricular dysfunction, and CT pulmonary angiography confirmed bilateral PE. Systemic thrombolysis was deferred due to recent surgery. He was started on a heparin drip and inhaled nitric oxide and underwent catheter-directed thrombectomy. Post-procedure, he remained in right heart failure requiring vasopressors. He was transferred for evaluation of mechanical support, specifically ECMO, but ultimately improved with medical management. He was discharged on lifelong warfarin, with hematology advising IVC filter placement if anticoagulation interruption is again required.

Discussion:

This case illustrates the thrombotic risk in patients with acromegaly, particularly in the perioperative setting. Even short interruptions in anticoagulation may result in life-threatening PE. A heightened index of suspicion and proactive perioperative planning including interdisciplinary coordination and consideration of bridging or mechanical prophylaxis should be prioritized in high-risk patients with acromegaly and prior VTE.

Introduction/Background:

Although rare, cardiac myxomas can present with devastating symptoms including Raynaud's phenomena, stroke or even sudden death. It is important to rule out cardiac myxomas when evaluating a pediatric patient with vasooclusive symptoms. This case illustrates an example of a pediatric patient presenting with exercise induced Raynaud’s phenomena that was found to be due to a cardiac myxoma.

Description:

A 12-year-old female with a PMH of superficial angiomyxoma and subglottic infantile hemangioma presented to the ER for acutely worsening bilateral lower extremity pain in the setting of physical activity. She also endorsed episodic bilateral lower extremity pallor, paresthesia, and mild shortness of breath. She denied any chest pain, palpitations, or syncope. Prior to this presentation, she was found to have an elevated ESR and positive ANA. She recently had a CXR which showed no signs of cardiopulmonary pathology. She started oral steroids and was referred to as outpatient rheumatology. Prior to rheumatology consultation her symptoms continued to be more frequent with less activity which prompted her to present to the ED. Lower extremity vessel doppler imaging was reassuring with no signs of occlusion. However, during the initial evaluation, the patient was able to reproduce her symptoms with minimal activity, thus prompting more detailed vascular imaging. The patient underwent a CTA abdominal aorta with contrast which revealed a long segment of occlusion within the right anterior tibial artery. The patient was transferred to an OSH for urgent vascular surgery. During pre-op workup at the OSH, an echocardiogram was performed which revealed a large left atrial mass. To further delineate the mass, a cardiac MRI was performed which revealed a 4.9x.2.9x3.6 cm lobular mass. This was consistent with a cardiac myxoma. Given the size and location of the mass, emergency surgical resection was done. Pathology results are still pending.

Discussion:

Due to cardiac myxomas being rare within the pediatric population, a high degree of suspicion is required for accurate diagnosis. Outcomes of undiagnosed cardiac myxomas can result in significant life altering sequelae making prompt treatment imperative. Our patient had a PMH of vessel malformations with acutely worsening vasocclusive symptoms resulting in more detailed vascular imaging. As a result, a quick diagnosis was achieved, and the patient was able to receive proper treatment prior to any devastating outcomes.

Introduction/Background:

Endovascular stent-grafts are established treatments for hepatic artery stenosis and pseudoaneurysm. In rare cases there have been reports of migration/erosion, infection, and possibly serve as a persistent nidus for bacteremia. There have been reported cases of infected hepatic arterial stents and coils spontaneously excreted into the bowel and others requiring surgical intervention for removal including liver transplant. We report the first case in which percutaneous biliary access and internal– external drain placement coincided with endovascular stent migration with ultimate nonoperative removal/excretion of an infected proper hepatic artery stent-graft and resolution of recurrent cholangitis.

Description:

A patient with complex prior upper-abdominal surgery (distal gastrectomy Roux-en-Y for recurrent pediatric gastric leiomyosarcoma; tubulovillous adenoma requiring Whipple) had a 5 mm Gore Viabahn placed in the proper hepatic artery for post-Whipple arterial irregularity with subsequent stent occlusion and collateral hepatic perfusion. The patient also required chronic internal–external biliary drainage for radiation/anastomotic strictures and recurrent cholangitis. Now presenting with abdominal pain and Escherichia coli bacteremia which prompted CT showing extensive pneumobilia and intraluminal air within the hepatic artery stent. ERCP was determined to not be feasible as a result of post-surgical anatomy. Fluoroscopy demonstrated migration of the infected stent into the duodenum during percutaneous transhepatic cholangiography (PTC) and placement of a 10F internal– external biliary drain. Follow up CT showed progression of the device through the bowel and eventual radiographic absence consistent with excretion. The patient’s leukocytosis and LFT abnormalities normalized within 24 hours, and no further bacteremia was noted.

Discussion:

We present a novel case in which PTC and biliary instrumentation precipitated device migration into the GI tract, specifically in a patient with enteric communication and an infected hepatic arterial device. This case demonstrates that conservative nonoperative passage/excretion is possible with device migration into the bowel. Clinically it is important that this patient population remains physiologically stable with effective biliary drainage during this period to allow migration; multidisciplinary assessment and close follow-up were essential in management.

Introduction/Background:

Fever of unknown origin (FUO) is a common pediatric presentation with a broad infectious and noninfectious differential. Histiocytic necrotizing lymphadenitis (HNL), also known as Kikuchi-Fujimoto disease (KFD), is a rare, self-limited condition characterized by prolonged fever and cervical lymphadenopathy. Diagnosis is often delayed due to nonspecific findings, with definitive confirmation requiring histopathologic evaluation. We describe a case of FUO and cervical lymphadenopathy ultimately diagnosed as HNL.

Description:

A 14-year-old female presented with one month of neck pain, tender cervical lymphadenopathy, and fevers. Initial outpatient treatment with amoxicillin-clavulanate did not result in improvement. Reevaluation demonstrated leukopenia and neutropenia, prompting hospital admission. On admission, the patient was well appearing, with examination notable for cervical lymphadenopathy. Infectious Disease, ENT, Hematology/Oncology, and Rheumatology were consulted. Extensive infectious evaluation-including blood cultures and testing for EBV, CMV, Bartonella, toxoplasmosis, parvovirus, HHV-6, tuberculosis, and Lyme disease-was negative. Evaluation for oncologic and rheumatologic processes, including hemophagocytic lymphohistiocytosis, was unremarkable aside from an elevated ANA. Abdominal and cervical imaging demonstrated multiple enlarged supraclavicular lymph nodes without abscess. The patient experienced intermittent fevers managed symptomatically without further antibiotics. Given improvement in leukopenia and neutropenia and overall clinical stability, she was discharged with outpatient follow-up. An outpatient cervical excisional lymph node biopsy confirmed HNL. Total fever duration was 23 days. She continues to do well under rheumatology care.

Discussion:Although generally benign and self-limited, HNL can recur and be associated with the development of systemic lupus erythematosus, necessitating longitudinal care. This case highlights the diagnostic challenges of HNL due to nonspecific features and overlap with serious etiologies such as lymphoma. Increased recognition of HNL as a cause of FUO may reduce unnecessary testing and delays in diagnosis.

Introduction/Background:

Ornithine transcarbamylase deficiency (OTCD) is the most prevalent urea cycle disorder (UCD), affecting ~1 in 60,000 people. As an X-linked condition, it was historically associated with severe neonatal disease in males. However, newer data shows females often present postnatally with highly variable symptoms and age of onset, frequently causing mis- or delayed diagnosis.

Description:

We report a case of a 10-year-old female with cyclic vomiting syndrome, attention deficit/hyperactivity disorder, and recent orthopedic surgery who presented with acute onset altered mental status, lethargy, and visual hallucinations without focal neurologic deficits on exam. Initial labs were notable for normal glucose and liver function tests (LFTs) without metabolic acidosis. She was admitted to the PICU and underwent extensive neurologic, infectious, and autoimmune evaluation notable for EEG with diffuse slowing, normal CSF studies, hyperammonemia (116 mcmol/L), and non-specific signaling abnormality on brain MRI. Repeat ammonia levels remained mildly elevated, thought to be due to hemolysis. Her mental status improved, and she was transferred to the floor. There, she developed multiple acute episodes of agitation. She had persistently elevated ammonia on free-flowing samples (114-159 mcmol/L) and undetectable BUN levels. Further history revealed long standing self-restriction of protein, learning difficulties in school, and history of “cyclic vomiting syndrome” that improved with dextrose containing fluids. Metabolics was consulted due to concern for UCD. She was started on high dextrose containing fluids, IV lipids, IV arginine, and lactulose. Ammonia levels continued to rise prompting transfer to quaternary care center with metabolic specialists. Genetic testing confirmed late-onset OTCD. Patient improved and was discharged following targeted nutritional and medical directed therapies for OTCD.

Discussion:

Diagnosing late-onset OTCD requires a high index of suspicion due to variable presentation. This case highlights confirmation bias, as elevated ammonia was initially attributed to hemolyzed samples in the setting of normal LFTs. Key diagnostic points from this case include altered mental status after surgery, hyperammonemia, low BUN, protein self-restriction, history of “cyclic vomiting syndrome,” and newborn screen with low-normal citrulline despite being reported as normal. Early recognition of OTCD is critical, as delayed diagnosis carries high morbidity and mortality.

Introduction/Background:

Congenital extrahepatic portosystemic shunt, also termed Abernethy malformation, refers to abnormal drainage of the portal circulation into a systemic vein (e.g., inferior vena cava). Abernethy malformation remains a rare entity, with only a few hundred cases reported in the literature. Among many associated congenital malformations and acquired complications of Abernethy malformation, chronic encephalopathy may also develop as portal venous blood bypasses the liver and certain metabolites, namely ammonia, escape filtration. Vascular abnormalities are not often considered in the evaluation of chronic encephalopathy. However, we present here the case of a 31-year-old patient found to have Abernethy malformation and discuss the possible contribution of the vascular abnormality toward the patient’s longstanding developmental delay.

Description:

A 31-year-old female with history of developmental delay presented to the emergency department with several days of vague abdominal pain and hematemesis. Initial physical exam and vital signs were reassuring. Lab work was unremarkable, apart from elevated total bilirubin, AST, and alkaline phosphatase. An initial CT of the abdomen and pelvis was obtained, which demonstrated abnormal liver morphology with a poorly defined hepatic mass, sequelae of portal hypertension, and most notably a non-visualized portal vein. Over the course of the patient’s admission, robust imaging workup (including ultrasound, CT, and MRI) identified abnormal emptying of the portal venous system into the inferior vena cava, consistent with Abernethy malformation. The patient’s hematemesis was secondary to erosive portal hypertensive gastropathy diagnosed via EGD, which was subsequently treated. While admitted, Psychology was also consulted to further assess the possible contribution of newly diagnosed Abernethy malformation toward the patient’s developmental delay. The patient was discharged with Hepatology and Gastroenterology follow-up for further management of the identified vascular abnormality.

Discussion:

Through a multi-modal imaging approach, this patient was diagnosed with Abernethy malformation. Although rare, vascular anomalies should be considered as a potential cause of chronic encephalopathy and developmental delay, and imaging may play a role in their detection. Further understanding of the body’s adaptive mechanisms to congenital extrahepatic portosystemic shunt may lead to better recognition of chronic encephalopathy presenting as developmental delay.

Introduction/Background:

Post-bariatric hypoglycemia is a known complication of Roux-en-Y gastric bypass (RYGB), often due to dumping syndrome or, rarely, noninsulinoma pancreatogenous hypoglycemia syndrome (NIPHS), characterized by hyperinsulinemic postprandial hypoglycemia from pancreatic β-cell hyperplasia. Eating disorders, including anorexia, are prevalent in bariatric candidates (up to 17-19% with binge eating or depression per meta-analyses). Though anorexia nervosa relapse, post-surgery is uncommon and underreported. Current guidelines (AACE/TOS/ASMBS 2020) recommend preoperative mental health evaluation but do not view eating disorders as absolute contraindications unless active and untreated.

Description:

A 37-year-old transgender woman (MtF) with prior type 2 diabetes and morbid obesity (>270 lbs) underwent RYGB with paraesophageal hernia repair in November 2023. Preoperative management focused on diabetes control. Postoperatively, she initially felt well but developed dumping symptoms and blood glucose (BG) <90 mg>/dL by late November 2023. She identified trigger foods, leading to dietary restriction, nausea, vomiting, and stress. This progressed to suspected atypical anorexia relapses, requiring behavioral health admission. Hypoglycemia persisted (<60 mg>/dL regularly on CGM: 5% time low, 1% very low; average BG 95 mg/dL). Interventions included nasogastric feeding tube, then permanent gastrostomy tube with continuous feeds (~8 hours/day) alongside limited oral intake. She achieved >100 lbs. weight loss but experienced reduced quality of life, multiple admissions, and subspecialty evaluations.

Discussion:

RYGB achieved substantial weight loss and health improvement but triggered dumping, dietary restriction, and atypical anorexia relapse, culminating in severe, persistent hypoglycemia requiring invasive support. This case highlights a rare interplay: surgical anatomy exacerbating restriction in a patient with eating disorder vulnerability, potentially compounded by emerging NIPHS (typically presenting years post-RYGB). Key take-away: Bariatric surgery can precipitate or worsen eating disorders despite preoperative screening, leading to profound quality-of-life declines and complex hypoglycemia. Clinical relevance underscores the need for vigilant postoperative monitoring of mental health and glucose in high-risk patients. Future directions include refined preoperative risk stratification for eating disorder history and multidisciplinary management protocols to prevent such outcomes.

Introduction/Background:

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic disorder caused by fibroblast growth factor 23 (FGF23)–secreting phosphaturic mesenchymal tumors, leading to renal phosphate wasting, hypophosphatemia, and impaired bone mineralization. Patients commonly present with bone pain, weakness, and fractures, and diagnosis is frequently delayed due to nonspecific symptoms and difficulty localizing small tumors. 68Ga-DOTATATE PET/CT has the highest sensitivity for tumor detection; however, repeat imaging is often required. While complete surgical excision is curative in most cases, tumors in anatomically complex locations such as the sacrum may not be amenable to surgery. Image-guided ablation has emerged as a therapeutic alternative.

Description:

A 63-year-old man presented with severe bilateral lower extremity pain, reduced mobility, elevated alkaline phosphatase (257 IU/L), and hypophosphatemia (1.5 mg/dL). Laboratory evaluation showed low 1,25-dihydroxyvitamin D, elevated urinary phosphate excretion, reduced TmP/GFR (1.12 mg/dL), and markedly elevated FGF23 (285 RU/mL), confirming TIO. Initial PET/CT and 68Ga-DOTATATE imaging failed to localize a tumor. Over two years later, repeat PET/CT identified a 1.2 cm sclerotic lesion in the left sacrum. Biopsy demonstrated a bland mesenchymal proliferation, with expert review supporting phosphaturic mesenchymal tumor. Due to the lesion’s surgically challenging location, CTguided cryoablation was performed. One-month post-procedure, FGF23 normalized (39 RU/mL), phosphate supplementation and calcitriol were discontinued, and follow-up imaging demonstrated resolution of prior FDG avidity. Biochemical remission has been sustained for over four years.

Discussion:

This case highlights the diagnostic challenges of TIO, including delayed tumor localization and histopathologic ambiguity. Despite multiple negative functional imaging studies, persistent biochemical suspicion warranted repeat evaluation, ultimately leading to tumor identification. While surgery remains first-line therapy, sacral tumors may not be surgically accessible. Image-guided cryoablation offers advantages including precise visualization of the ablation zone and effectiveness in sclerotic bone. Sustained normalization of FGF23 and phosphate levels confirms durable remission in this anatomically complex case. Cryoablation should be considered a viable therapeutic alternative for TIO in surgically inaccessible locations.

Introduction/Background:

The combination of severe aortic stenosis and cardiogenic shock carries high morbidity and mortality. In patients who are not immediate candidates for emergent transthoracic aortic valve replacement (TAVR) or transfer to a tertiary center, balloon aortic valvuloplasty (BAV) may serve as a temporizing strategy to stabilize hemodynamics and improve end-organ perfusion.

Description:

A 78-year-old man with a past medical history of essential hypertension, hyperlipidemia, nonischemic cardiomyopathy and heart failure with reduced ejection fraction presented with acute decompensated heart failure. Transthoracic echocardiography demonstrated critical AS with an aortic valve area (AVA) of 0.26 cm2, peak velocity 6.2 m/s, mean gradient 77 mmHg, and stroke volume index 20.9 mL/m2, consistent with severe fixed outflow obstruction. Despite escalating intravenous diuretics and guideline-directed medical therapy, his condition deteriorated, progressing to cardiogenic shock with evidence of systemic hypoperfusion. Laboratory evaluation revealed lactic acidosis (7.5 mmol/L) and NT-proBNP >70,000 pg/mL. Given ongoing shock and lack of immediate TAVR availability, emergent BAV was performed using an 18-mm Z-Med II balloon. Invasive hemodynamics confirmed a pre-intervention LV-to-aortic gradient of 63 mmHg. Following balloon inflation, the patient developed pulseless electrical activity arrest secondary to transient severe aortic insufficiency. Return of spontaneous circulation was achieved, and an Impella CP device was placed for mechanical circulatory support. Over the next three days, hemodynamics improved, allowing successful device weaning and removal. Repeat echocardiography demonstrated improved AVA to 0.6 cm2 with mild-to-moderate aortic insufficiency. After clinical stabilization, the patient underwent successful TAVR one month later without complications.

Discussion:

BAV can serve as a bridge to definitive therapy in patients with both cardiogenic shock and severe aortic stenosis when an emergent TAVR or prompt transfer is not feasible. Although not a substitute for TAVR or surgical valve replacement, BAV can acutely reduce left ventricular outflow tract obstruction, improve cardiac output, and restore end-organ perfusion. This case highlights both the potential life-saving role of BAV and the importance of mechanical circulatory support in managing periprocedural instability.

Introduction/Background:

Orbital compartment syndrome is an ophthalmologic emergency characterized by intraorbital pressures exceeding ophthalmic arterial pressure with resultant ischemia to the retina and optic nerve and often irreversible vision loss. It is a clinical diagnosis in the setting of optic neuropathy and increased intraocular pressures and imaging is not required. Timely intervention is a hallmark of treatment with improved outcomes associated with decompression within two hours. The standard of care is lateral canthotomy with cantholysis to restore perfusion and preserve eyesight. While medical and pharmaceutical interventions and treatment play a supplemental role in treatment, their effectiveness has not been confirmed.

Description:

The patient is a 44-year-old male with a history of hypertension and an unspecified “brain palsy” reported by the family who presented after a mechanical fall. He tripped resulting in trauma to the right side of his face. On exam he had decreased visual acuity to the right eye, worse than 20/200, increased intraocular pressure (IOP) with right eye pressure of 45mmHg and left eye pressure of 15mmHg, as well as limited extraocular movements with inability to look up, down, or move his right eye in a lateral direction. CT imaging showed right orbital retrobulbar hemorrhage with proptosis. His right pupil was non-reactive to light. His presentation, exam, and imaging were concerning for orbital compartment syndrome. After extensive discussion, the patient and family decided against lateral canthotomy and left against medical advice. As possible salvage therapy, ophthalmology recommended high dose 100mg IV hydrocortisone and timolol, dorzolamide, and brimonidine drops BID. He returned three days later with a significantly improved exam where he was found to have acuity of 20/30 for both eyes, R IOP of 24, and near full range of extraocular movements.

Discussion:

Orbital compartment syndrome is a clinical diagnosis in which timely recognition and intervention is paramount. First line treatment is lateral canthotomy and cantholysis for decompression and reperfusion of the retina and optic nerve. The role of pharmaceutical interventions remains peripheral. It would be difficult to ethically develop a trial comparing pharmaceutical intervention to surgical decompression. However, in decisional patients adamant on not undergoing lateral canthotomy and cantholysis, this case shows there may be options for possible salvage therapy.

Introduction/Background:

Cholecystocolonic fistulas are rare, occurring in less than 0.5% of patients undergoing cholecystectomy. However, when they do develop, they can lead to complications such as colonic perforation, gallstone ileus, and infection. Here, we present a case of a patient who developed a cholecystocolonic fistula alongside gallstone-induced pancreatitis.

Description:

An 81-year-old woman with a history of hyperlipidemia and hypertension presented to the emergency department with acute onset abdominal pain. Laboratory results revealed a total bilirubin of 1.0 mg/dL, AST of 103 U/L, ALT of 119 U/L, ALP of 880 U/L, lipase of 6,421 U/L, and a WBC count of 11.8 K/mcL. Physical examination showed tenderness in the epigastric area, without guarding or rigidity. Gallbladder ultrasound revealed a 7mm common bile duct diameter and questionable pneumobilia. CT of the abdomen demonstrated an air-fluid level in the pancreatic head/uncinate process, along with small-volume pneumobilia. MRCP confirmed the presence of pneumobilia and suspected a communication between the gallbladder and the hepatic flexure of the colon, raising concern for a cholecystocolonic fistula. Several filling defects were also identified within the extrahepatic bile ducts, including a 1 cm dependent filling defect in the distal common bile duct. Given these findings, the patient underwent colonoscopy and ERCP. During ERCP, contrast was observed flowing from the gallbladder into the colon under fluoroscopy. Balloon sweep of the common bile duct revealed multiple small stones and one larger stone measuring approximately 12mm. Colonoscopy identified a fistulous connection between the gallbladder and right colon, which was marked with a tattoo. The following day, the patient underwent a successful right hemicolectomy, cholecystectomy, and takedown of the cholecystocolonic fistula using the previously placed tattoo as a guide. Postoperatively, liver chemistries improved in a stepwise fashion. The patient tolerated the procedure well with no complications and was discharged in stable condition.

Discussion:

Cholecystocolonic fistulas are rare complications of gallstone disease, typically presenting with large gallstones that compress the gallbladder and colon. This case highlights the clinical presentation, diagnostic evaluation, and surgical management of this unusual complication. Timely identification and appropriate management are crucial in preventing further complications such as gallstone ileus or bowel perforation.

Introduction/Background:

Lipomatous tumors span a spectrum from benign lipoma to atypical lipomatous tumor/well-differentiated liposarcoma (ALT/WDL) and dedifferentiated liposarcoma (DDLPS), with significant radiologic overlap. Because DDLPS carries higher morbidity and may coexist with additional malignancies, early recognition of malignant imaging features is essential. This case highlights the critical role of CT and MRI in distinguishing malignant from benign adipocytic tumors and in identifying dedifferentiation within a long-standing extremity mass.

Description:

A 77-year-old man presented with a posterior–medial thigh mass that had enlarged slowly over ~20 years before accelerating with new distal swelling. CT showed a 37-cm predominantly lipomatous mass with thick septations and two enhancing nonfatty nodules concerning malignancy. MRI demonstrated heterogeneous enhancement of a dominant 13-cm nodule, prominent septations, and low-fat regions suggesting hemorrhage, necrosis, or dedifferentiation. These findings guided biopsy of the enhancing nodule, which revealed lipoblasts, atypical multinucleated tumor cells, and myxoid stroma; MDM2 amplification confirmed at least ALT/WDL. Pre-operative CT chest/abdomen/pelvis performed to screen for additional malignancies showed a left adrenal nodule and a right thyroid nodule. Surgical resection demonstrated a focus of dedifferentiation within atypical lipomatous tumor, and external review confirmed DDLPS. Post-surgical PET/CT showed hypermetabolic activity in the adrenal nodule, prostate gland, and soft-tissue irregularity in the thigh surgical bed, guiding post-op management.

Discussion:

This case emphasizes the essential role of multimodality imaging in raising suspicion for malignancy and detecting dedifferentiation in large lipomatous tumors. Thick septations, large enhancing nonfatty nodules, and heterogeneous MRI signal significantly increased the likelihood of malignancy and enabled targeted biopsy of the highest-risk area. Imaging also supported screening for associated malignancies, an important consideration in DDLPS. Although current evidence is limited, systematic analyses consistently support these imaging characteristics as reliable indicators of ALT/WDL and DDLPS. Radiomics, supported by large datasets such as the NETSARC+ registry, represents a promising direction for improving diagnostic accuracy and risk stratification in the evaluation of lipomatous tumors even before biopsy results.

Introduction/Background:

Iatrogenic Kaposi Sarcoma (KS) is a human herpesvirus-8 (HHV-8)-driven angioproliferative neoplasm that can occur after solid-organ transplantation. Post-transplant KS often involves lymph nodes and viscera and is managed primarily by reducing or modifying immunosuppression. Conversion from calcineurin inhibitors (CNI) to mechanistic target of rapamycin (mTOR) inhibitors is frequently employed given potential antitumor and antiangiogenic effects. This report details a unique case of disseminated, predominantly extracutaneous KS, initially concerning for post-transplant lymphoproliferative disorder (PTLD), which achieved complete radiographic response after CNI-tosirolimus conversion alone.

Description:

A woman with end-stage renal disease from congenital renal hypoplasia underwent deceased-donor kidney transplant at age 40 and was maintained on Tacrolimus, Mycophenolate Mofetil, and Prednisone. Three years later, she presented with months of fatigue and night sweats and one day of abdominal pain, nausea, and emesis. Laboratory studies were notable only for mild leukocytosis of 11.5 (reference range 4.2-11 K/mcL). Examination revealed 1-2 cm cervical and supraclavicular lymphadenopathy. CT imaging demonstrated new anterior mediastinal, left para-aortic, and right aortocaval lymphadenopathy, 6-8 mm pulmonary nodules, and multiple hypodense hepatic lesions. Given concern for lymphoma or PTLD, peripheral blood flow cytometry, tumor lysis studies, and Epstein-Barr virus PCR were obtained and results were unrevealing. An IR-guided retroperitoneal lymph node biopsy confirmed KS, with HHV-8-positive lesional cells. After multidisciplinary discussion with the transplant team, Tacrolimus was replaced with Sirolimus. CT at six weeks showed minimal interval change. By four months, mediastinal adenopathy had markedly decreased. By months 6-7, CT and MRI demonstrated complete radiographic resolution of adenopathy, pulmonary nodules, and hepatic lesions with preserved allograft function.

Discussion:

Disseminated iatrogenic KS may lack cutaneous lesions and can mimic PTLD, yet management differs substantially. Early histopathologic confirmation and immunosuppression modifications are essential. In this case, CNI-to-sirolimus conversion led to complete regression without evidence of rejection, supporting mTOR-based strategies as a first-line approach for post-transplant KS.

Introduction/Background:

Structural complications following prosthetic valve endocarditis (PVE) may progress subtly over time, with early imaging abnormalities often underestimated. Delayed recognition can result in abrupt hemodynamic collapse. This case highlights the importance of maintaining suspicion for evolving prosthetic valve pathology despite initially reassuring studies.

Description:

A 57-year-old male with prior surgical bioprosthetic aortic valve and ascending aortic root replacement developed progressive dyspnea resulting in acute hypoxic respiratory failure and cardiogenic shock (CS). Three months earlier, a transthoracic echocardiogram (TTE) demonstrated mild aortic insufficiency (AI), leaflet thickening, and a small hypodensity, deemed nonspecific given negative transesophageal echocardiogram (TEE). Repeat TTE during clinical decompensation revealed severe AI, aneurysmal dilation of the sinus of Valsalva with rupture, and possible prosthetic dehiscence, representing a dramatic interval change. Subsequent TEE confirmed excessive prosthetic motion, global thickening of the bioprosthesis, a mobile echodensity attached to the bioprosthetic aortic valve, and an aortic root pseudoaneurysm. Computed tomography angiography demonstrated multiple aortic root outpouchings with marked root dilation. Hemodynamic assessment showed markedly elevated right- and left-sided filling pressures with reduced cardiac index, confirming valvular failure as the primary driver of CS. Despite persistently negative blood cultures, the index of suspicion remained high for culture-negative PVE due to rapid structural deterioration. Surgical intervention was initially contraindicated due to multifocal embolic cerebral infarcts with intracranial hemorrhage. The patient was medically stabilized with inotropic support, afterload reduction, and aggressive diuresis. Following neurologic stabilization, he underwent complex redo aortic root replacement with concomitant cardiac repair. Postoperative course required VA-ECMO support prior to final recovery.

Discussion:

This case illustrates how subtle echocardiographic abnormalities may represent early manifestations of progressive prosthetic valve failure, even in the absence of definitive infection or positive cultures. In patients with prosthetic valves and new or worsening symptoms, index of suspicion for prosthetic complications should be high. Evaluation should include careful reassessment of prior imaging findings, early repeat multimodality imaging, and close surveillance.

Introduction/Background:

Pediatric Pulmonary Emboli (PE) are rare but have a high mortality rate. Evidence based guidelines for PE management in children are limited, and most recommendations stem from adult populations. Decisions regarding pursuing systemic thrombolysis, surgical embolectomy, catheter-based interventions, or medical management are often made on a case-by-case basis by a multidisciplinary team after careful consideration of the risks and benefits. We present a case of a 17-year-old female who was successfully treated with mechanical thrombectomy for bilateral PE after recent initiation of oral contraceptives.

Description:

Patient presented to the ED with dyspnea. Vital signs showed tachycardia, hypoxia, and hypotension. Labs revealed significantly elevated NT-pro-BNP, Troponin, and 4.36 mg/L D-Dimer. TTE showed a severely dilated Right Ventricle (RV) with reduced systolic function, interventricular septal bowing, and tricuspid regurgitation. CTA PE revealed prominent bilateral pulmonary emboli involving all lobes of the lungs. Patient was admitted to Pediatric Intensive Care Unit on HFNC, milrinone, and heparin infusions. A multidisciplinary discussion amongst Pediatric Cardiology, Hematology, and Adult Interventional Cardiology determined she would benefit from thrombectomy given her severe symptoms. Patient’s family elected to proceed, and emergent bilateral thrombectomy was successfully performed. Post-thrombectomy the mean Pulmonary Artery Pressure improved from 36 to 20 mmHg, with complete resolution of tachycardia, hypotension, and hypoxia. Repeat TTE showed normal RV size and function, and resolution of tricuspid regurgitation.

Discussion:

Mechanical thrombectomy was performed on our patient because of the extent of the PE, the severity of right heart strain, and concerns for right heart failure from persistent pulmonary hypertension. Guidelines for PE management in children are limited to case reports and small retrospective randomized trials, thus current recommendations are based on data from adult populations. Mechanical thrombectomy has been growing in popularity as an intervention for sub-massive PE because of its benefits regarding length of hospital stay and reduction in ICU admissions. This case highlights the effective use of mechanical thrombectomy as an emergent intervention for PE in a pediatric patient. Mortality from PE is high in pediatric populations underscoring the importance of early recognition and effective intervention.

Introduction/Background:

Pericardial effusion as the initial manifestation of diffuse large B-cell lymphoma (DLBCL) is a rare, extranodal presentation that upstages the disease to stage IV, per Lugano classification. In patients with underlying cirrhosis or volume overload, such effusions can be misattributed, delaying oncologic evaluation. We present a case of new pericardial effusion found to be DLBCL in the setting of alcoholic cirrhosis.

Description:

A 79-year-old male with alcoholic cirrhosis presented with bilateral lower extremity edema, abdominal edema, and hypotension that was unresponsive to outpatient diuresis. On admission, day 0, imaging showed cardiomegaly concerning pericardial effusion and left pleural effusion. Echocardiography revealed a fibrinous circumferential pericardial effusion and preserved ejection fraction (65%). Pericardiocentesis removed 650mL of serosanguinous fluid. Fluid studies showed elevated LDH and protein. Further cytology and flow cytometry confirmed DLBCL, activated B-cell subtype (CD10-, CD5-). The patient continued to have accumulation of effusion on repeat echocardiograms, despite consistent drainage. The patient was evaluated by oncology and cardiothoracic surgery, with chemotherapy chosen over surgical intervention. Rituximab with dose-reduced cyclophosphamide, doxorubicin, vincristine, and prednisone (R-miniCHOP) was initiated on day 8 with filgrastim support. Following initiation of chemotherapy, the patient struggled with pancytopenia, renal injury, and hepatic encephalopathy. The patient’s continued decline in the setting of his severe illness led to election of hospice and passing away on hospital day 21.

Discussion:

This case demonstrates DLBCL presenting as an isolated pericardial effusion in a patient with overlapping cirrhosis, confounding the cause of his hypervolemia. Diagnosis was achieved through pericardial fluid cytology, enabling early initiation of chemotherapy- though underlying comorbidities limited tolerance and aggression of treatment. This is noted by the usage of R-miniCHOP as opposed to the standard R-CHOP. This case expands the literature regarding extranodal, pericardial DLBCL and elucidates the importance of oncologic vigilance in complex presentations to ensure early intervention. In individuals like above, pericardial fluid should undergo cytologic and cytometric analysis to exclude malignancy as well as early multidisciplinary involvement for prompt intervention.

Background/Significance:

Acute respiratory distress in infancy is commonly attributed to viral bronchiolitis; however, children with trisomy 21 represent a high-risk population in whom alternative diagnoses must be considered. In these patients, respiratory symptoms may reflect congenital heart disease, pulmonary hypertension, airway anomalies, reactive airway disease, and many more pathologies. In the setting of subtle bleeding manifestations, it is important to include hematologic and oncologic diseases in the initial diagnostic approach.

Description:

An 11-month-old male with trisomy 21, bicuspid aortic valve with aortic root dilation, laryngomalacia, and dysphagia presented to the emergency department for three days of congestion, increased work of breathing, diarrhea, and decreased oral intake. On physical exams, he was in respiratory distress with notable petechiae on the forehead, which was attributed to excessive coughing and crying at the time. He was presumed to have viral bronchiolitis, placed on supplemental oxygen, and admitted to the inpatient floor for supportive care. On hospital day two, he developed high fevers and significant bruising at an intravenous site. A complete blood count was obtained and revealed marked leukocytosis, anemia, and thrombocytopenia. Peripheral smear showed circulating blasts, and cytologic evaluation confirmed acute myeloid leukemia. Due to concern for coagulopathy and tumor lysis syndrome, he was transferred to the pediatric intensive care unit for monitoring and initiation of leukemia-directed therapy.

Discussion:

Trisomy 21 confers a 10-to-20-fold greater likelihood of acute leukemia, with myeloid leukemia of Down syndrome (ML-DS) occurring in 1–2% of affected children. Transient abnormal myelopoiesis develops in up to 10% of neonates with trisomy 21 and progresses to acute myeloid leukemia in 20– 30% of cases within the first four years of life. In these patients, leukemogenesis results from genetic–associated perturbations in fetal hematopoiesis and acquired GATA1 mutations, producing a biologically distinct leukemia that has increased chemosensitivity but heightened treatment-related toxicity. Prompt recognition is critical, as ML-DS demonstrates favorable survival with the appropriate chemotherapy. Because early presentations may be clinically indistinct, this case highlights the need to avoid diagnostic anchoring and maintain a broad differential to ensure timely recognition and improved outcomes for high-risk pediatric populations.

Background/Significance:

Myxedema coma (MC) is an endocrine emergency precipitated by physiological stress and characterized by hypothermia, bradycardia, hypoglycemia, and altered mental status. Diagnosis is primarily clinical but is typically associated with low Free T4/T3 and elevated TSH, although cases with normal or minimally abnormal thyroid tests have been reported. There is a paucity of literature on the benefit of thyroid hormone replacement therapies and steroids in critically ill patients with features of MC with nondiagnostic labs.

Description:

An 81-year-old female with a history type two diabetes and chronic kidney disease presented with altered mental status and weakness. She was bradycardic (HR 30’s), hypotensive (69/31) and hypothermic (79.3 F). EKG revealed a third-degree AV block. On exam she was lethargic, with bilateral pitting edema and pulmonary crackles. Warming and vasopressors had minimal hemodynamic response prompting emergent transvenous pacing. Imaging demonstrated pulmonary edema with bilateral lower lobe consolidations, and broad-spectrum antibiotics were initiated. While in the intensive care unit (ICU), worsening lethargy, hypercapnia, and persistent anuria prompted intubation and CRRT. Stress-dose steroids were initiated given persistently high vasopressor requirements. Echocardiography showed preserved ventricular function and her blood cultures were negative. Despite some clinical improvement, she remained lethargic and vasopressor dependent. Thyroid studies showed a mildly low-free T4 (0.7), free T3 (0.8), and a normal TSH (2.1). Due to persistent concern for MC, IV levothyroxine was initiated on day 5. By day 7, vasopressors were discontinued, and steroids were tapered. She was discharged on day 14 on oral levothyroxine.

Discussion:

Undifferentiated shock remains difficult given limited early diagnostic clarity. The patient’s AV block was likely secondary to profound hypothermia. Concern for septic shock remained high despite negative cultures, which occur in up to half of cases. Several case reports document MC with normal biomarkers, associated with subclinical hypothyroidism, central hypothyroidism, or non-thyroidal illness. Evidence suggests that there is a poor correlation between thyroid biomarkers and disease severity. Therefore, patients with strong clinical suspicion for MC may benefit from empiric thyroid hormone therapy.

Background/Significance:

Gestational Trophoblastic Disease (GTD) are tumors originating from trophoblastic cells of the placenta including premalignant hydatidiform moles and malignant gestational trophoblastic neoplasia. Incidence in the United States is from 1.1 to 1.2 per 1000 pregnancies. Rarer is pregnancy with a complete hydatidiform mole and coexisting fetus (CHMCF), from 1/22,000 to 1/100,000 pregnancies. GTD causes hyperthyroidism by cross-reactivity between the ɑ subunit of human Chorionic Gonadotropin (hCG) and Thyroid Stimulating Hormone (TSH), potentially resulting in devastating consequences.

Description:

A 23-year-old White Hispanic female presented with vaginal bleeding. hCG level was >248,400 mU/mL and an abdominal ultrasound (US) revealed a single, live intrauterine pregnancy of 15 weeks with a heterogeneous 11.7 cm echogenic mass. Week 18 US showed an area of mixed echogenicity with internal cystic structures up to 12.8 cm, possibly a partial mole. At 22 weeks, she developed palpitations. Beta-hCG exceeded 400,000 mU/mL; TSH was <0.008 mU/mL (0.4–5.5), and free T4 was 2.8 ng/dL (0.8–1.9). Hyperthyroidism was diagnosed, and methimazole and labetalol were initiated. At 26 weeks, she presented with chest pain, tremors, blood pressure of 197/101, uterine contractions with worsening labs. Magnetic Resonance Imaging confirmed CHMCF without invasion of adjacent structures. We started propylthiouracil, super-saturated potassium iodide, propranolol and cholestyramine. Two days later, she developed dyspnea with pulmonary edema, concerning for impending thyroid storm. She delivered a live female with normal anatomy via an urgent C-section. The mole was completely evacuated without complication. Labs began normalizing and anti-thyroid therapy was discontinued. At two weeks of post-partum, labs continued to normalize. The baby had a low TSH and normal fT4 at birth.

Discussion:

Molar pregnancies hypersecrete hCG, however, being 4000 times less potent than TSH, hyperthyroidism is rare with an incidence of 16% in those with complete molar pregnancy, with levels >400,000 IU/L posing greater risk. This case presented a unique challenge in its complexity due to comorbid pre-eclampsia. Prompt multimodal management prevents poor outcomes like neonatal hyperthyroidism, thyroid storm, eclampsia, maternal or fetal death or disability. We averted catastrophic consequences by aggressive management via a combination of synergistic thyroid hormone lowering strategies, culminating in an uncomplicated delivery.

Background/Significance:

Lynch syndrome, caused by pathogenic variants in DNA mismatch repair (MMR) genes, increases risk for colorectal, small-bowel, and periampullary cancers. In MSH6-associated disease, tumors may appear proficient on immunohistochemistry (pMMR) despite underlying germline dysfunction, complicating surveillance. Because lesions often arise beyond routine endoscopic reach, cross-sectional imaging plays a critical role in early detection and treatment planning.

Description:

Patient with Lynch syndrome (germline MSH6 c.3694del3, likely pathogenic, and an additional MSH6 p.S998F variant of uncertain significance in trans) developed invasive colon adenocarcinoma at age 38 with pMMR by immunohistochemistry. Years later, endoscopy suggested a duodenal lesion with high-grade dysplasia; contrast-enhanced computed tomography (CT) and magnetic resonance enterography (MRE) clarified lesion extent, transmural invasion, and lack of nodal disease, guiding resection of a poorly differentiated adenocarcinoma (pT3N0). A subsequent periampullary recurrence was localized using pancreas-protocol multiphase CT, targeted esophagogastroduodenoscopy (EGD), and capsule endoscopy. Biopsy demonstrated invasive adenocarcinoma with deficient MMR (dMMR) due to loss of MSH6 expression. Given close margins and the morbidity of pancreaticoduodenectomy, the multidisciplinary team pursued programmed cell death-1 (PD-1) inhibitor therapy (pembrolizumab) for one year. Serial CT, MRE, and capsule endoscopy showed no radiologic evidence of recurrence on follow-up.

Discussion:

This case highlights the importance of multimodality imaging in MSH6-associated Lynch syndrome, where malignancies may be subtle, multifocal, or obscured by postoperative anatomy. Teaching points include: Combined MRE, multiphase CT, and capsule endoscopy to evaluate the proximal small bowel and periampullary region; Use of cross-sectional imaging to distinguish recurrence from postsurgical change; Low threshold for advanced imaging when discordant MMR results or equivocal endoscopic findings are present. These findings support incorporating scheduled cross-sectional imaging into surveillance for MSH6 carriers when endoscopy is negative or indeterminate. Multimodality imaging directly influenced diagnosis, staging, and management in this patient with MSH6-associated Lynch syndrome and recurrent gastrointestinal malignancy. Radiologic surveillance is essential for early detection and informed treatment decisions in this high-risk population.

Background/Significance:

Blunt traumatic diaphragmatic rupture is an uncommon but potentially life-threatening injury frequently associated with intra-abdominal trauma. Operative exploration is typically required to evaluate associated injuries and perform repair. While delayed or chronic cases often favor a transthoracic approach, minimally invasive strategies for early postoperative failure of primary repair are not well described.

Description:

A 40-year-old male presented after a motor vehicle collision. Computed tomography revealed a left-sided diaphragmatic rupture with gastric herniation into the thoracic cavity. Associated pelvic and sacral fractures were managed non-operatively. He underwent exploratory laparotomy with reduction of the herniated stomach and primary two-layer repair using running 0 Prolene suture. A left-sided chest tube was placed. On postoperative day three, he developed recurrent chest pain and intolerance of oral intake. Imaging demonstrated recurrent gastric herniation consistent with repair failure. Given the short interval from the index operation and anticipated minimal adhesions, a robotic-assisted transabdominal re-repair was performed. Intraoperative esophagogastroduodenoscopy confirmed gastric viability and allowed decompression. Using a four-port robotic technique, prior suture material was removed and minimal adhesions were encountered. The defect was closed with interrupted, pledgeted 0 Ethibond horizontal mattress sutures, reinforced with a running 2-0 Stratafix layer. Mesh was not used, and the defect was closed without tension. The patient tolerated the procedure well without perioperative complications. No hernia recurrence was noted on follow-up.

Discussion:

Traumatic diaphragmatic rupture requires prompt repair to prevent visceral strangulation and respiratory compromise. Early failure of primary repair is uncommon but challenging. Reoperation is often performed via a transthoracic approach in delayed cases with dense adhesions. In this case, early recognition allowed minimally invasive reintervention before significant adhesion formation. The robotic-assisted transabdominal approach provided excellent visualization and precise suturing, enabling durable two-layer closure without mesh. Robotic repair is a feasible option for early postoperative diaphragmatic repair failure in selected patients and may reduce morbidity associated with thoracotomy while maintaining sound reconstructive principles.

Background/Significance:

Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents approximately 6– 8% of all myocardial infarctions and is more common in younger patients and women.

Description:

A 20-year-old woman taking adderall and combined oral contraceptives presented with her second episode of sudden-onset central chest pain at rest. Troponin was elevated, and EKG showed nonspecific ST-T wave changes. Transthoracic echocardiogram demonstrated an ejection fraction of 63% with a small area of hypokinesis in the mid-anterolateral and inferolateral walls. Cardiac MRI suggested a recent myocardial infarction in a diagonal branch territory with active inflammation. Left heart catheterization revealed normal coronary arteries. She was treated with aspirin, clopidogrel, and rosuvastatin. Three months later, repeat MRI showed persistent basal anterior wall hypokinesis with ongoing inflammatory changes. Her repeat echocardiogram demonstrated resolution of wall motion abnormalities. It was recommended she discontinue her combined oral contraception and switch to progesterone only.

Discussion:MINOCA may be triggered by stimulants and hormonal contraceptives, with recurrent chest pain suggesting coronary vasospasm. In this case, coronary angiography demonstrated normal epicardial vessels, while cardiac MRI revealed transmural late gadolinium enhancement in a diagonal branch distribution, supporting an ischemic cause rather than myocarditis. Given the absence of obstructive coronary disease, coronary vasospasm or transient thrombotic occlusion were considered as likely mechanisms of MINOCA. After exploring her medications, two potential triggers emerged. Amphetamine-based stimulants, including adderall, raise catecholamine levels which promotes coronary vasoconstriction and endothelial dysfunction. Additionally, combined estrogen-progestin oral contraceptives are independently associated with increased arterial and venous thrombotic risk. Careful assessment, multimodality imaging, and individualized risk modification—including adjustment of potentially contributory medications—are essential components of management.

Background/Significance:

Tumor-induced osteomalacia (TIO) is an ultra-rare paraneoplastic syndrome caused by excessive fibroblast growth factor 23 (FGF23) secretion from phosphaturic mesenchymal tumors, resulting in hypophosphatemia and osteomalacia. Diagnosis is frequently delayed due to nonspecific symptoms and difficulty localizing small tumors.

Description:

A 55-year-old male presented with 16 months of progressive muscle weakness, multiple bilateral metatarsal fractures, and chronic bone pain. Laboratory evaluation revealed profound hypophosphatemia (1.6 mg/dL), markedly elevated FGF23 (455 RU/mL), and evidence of renal phosphate wasting (TRP 35%, TmP/GFR 1.04 mg/dL). Initial FDG-PET/CT was non-localizing. Upon referral, specialized re-interpretation at a tertiary referral center identified faint focal uptake in the right third metacarpal, subsequently confirmed by technetium-99m sestamibi scanning and MRI, which demonstrated a 1.9 × 1.8 × 1.2 cm soft-tissue mass in the palmar tissues. Surgical excision confirmed a phosphaturic mesenchymal tumor with positive FGF23 in situ hybridization. Serum phosphorus normalized postoperatively, confirming cure.

Discussion:

This case highlights the diagnostic challenges of TIO, particularly the difficulty in localizing the tumor and the critical importance of expert imaging interpretation. Complete surgical resection remains the definitive treatment, with rapid biochemical normalization and symptom improvement. The unusual hand location and initially non-localizing imaging underscore the need for systematic diagnostic approaches and multidisciplinary management in this rare but treatable condition.

Background/Significance:

Chronic constipation is one of the most common pediatric complaints and accounts for 1/4 of pediatric GI consults. It affects approximately 12-18% of individuals between 0 to 18 years of age. Although outcomes are generally positive with appropriate management including dietary changes, laxatives, and medications such as linaclotide, undiagnosed or inadequately treated constipation could have detrimental results. Abdominal compartment syndrome (ACS) due to fecal impaction is a considerably rare complication of constipation. We present the exceptional case of an adolescent who developed ACS secondary to severe constipation and required prolonged intensive care admission.

Description:

A 17-year-old male with a history of constipation was brought to the ED due to severe abdominal pain and non-bilious, non-bloody vomiting for 1 day. He had been followed by GI six years prior but was lost to follow-up. At admission, he was found to have severe hyperkalemia due to acute kidney injury. He subsequently developed bradyarrhythmia and cardiac arrest, requiring 90 minutes of resuscitation. Bedside laparotomy revealed a massively dilated colon filled with stool. Fecal disimpaction and temporary abdominal closure were performed. Progressive ischemia in the following days prompted total colectomy with end ileostomy. Pathology showed no Hirschsprung disease or structural abnormalities. Testing for celiac disease and inflammatory bowel disease was negative. His course was complicated by acute heart failure, acute kidney injury, pleural effusions, ascites, and femoral deep vein thrombosis. He later developed recurrent abdominal pain with pneumatosis. After months of recovery and improved oral intake and weight gain, he was ultimately ready for discharge with multidisciplinary care and close follow up.

Discussion:

This case highlights ACS as a catastrophic but preventable complication of pediatric constipation. Timely surgical intervention saved the patient’s life, while gastroenterology played a critical role in nutritional rehabilitation and evaluation for the etiology of his constipation. Constipation is often treated conservatively with minimal intervention. However, this case demonstrates that constipation can have life-threatening consequences if not addressed appropriately. For this reason, constipation must be followed closely, and management should be escalated as indicated. The cause of his constipation remains unknown, emphasizing the need for thorough evaluation of this condition.

Background/Significance:

Coronary artery aneurysms associated with coronary fistulae are rare and may cause shunt physiology, ischemia, and heart failure. Multimodality imaging and invasive hemodynamics are essential for diagnosis and management planning.

Description:

A 78-year-old man with hypertension and hyperlipidemia presented with new-onset decompensated heart failure. Transthoracic echocardiography revealed severe biventricular dysfunction (LVEF 10%) with severe aortic and mitral regurgitation. Coronary angiography demonstrated severe multivessel coronary artery disease and a markedly aneurysmal right coronary artery (RCA) with suspected fistulous communication. Right-heart catheterization revealed elevated filling pressures, a reduced cardiac index, and a right atrial oximetry step-up, indicating a left-to-right shunt. Coronary CTA identified a giant RCA aneurysm, while cardiac MRI confirmed an RCA–coronary sinus fistula with Qp/Qs of 1.27. Following medical optimization, the patient underwent bioprosthetic aortic valve replacement, coronary artery bypass grafting, RCA aneurysm exclusion, and fistula ligation with a good clinical outcome

Discussion:

This case illustrates a high-risk, multifactorial substrate for new-onset severe HFrEF involving severe calcific multivessel coronary artery disease, severe multivalvular disease, and a giant RCA aneurysm with an RCA–coronary sinus fistula. Although coronary CTA did not clearly define a discrete fistulous tract, invasive oximetry showed a marked step-up from the superior vena cava to the right atrium, and cardiac MRI confirmed physiologically significant left-to-right shunting (Qp/Qs 1.27), underscoring the value of multimodality imaging integrated with invasive hemodynamics to characterize the heart failure drivers. The markedly dilated RCA (≈10–15 mm) met accepted criteria for a giant coronary artery aneurysm, a lesion associated with thrombosis, embolization, ischemia, rupture, and progressive heart failure risks amplified by concomitant fistula and coronary steal physiology. Given the coexistence of multiple lesions independently capable of worsening heart failure (ischemic burden, severe aortic regurgitation–related LV volume overload, and aneurysm-fistula shunt/steal), a multidisciplinary heart-team approach favored single-stage surgery with CABG ×3, surgical aortic valve replacement, and multi-level RCA ligation to exclude the aneurysm and fistula while preserving distal perfusion via bypass grafting.

Introduction/Background:

Patient is a 54-year-old male with a history of 5 prior inguinal hernia repairs with multiple layers of mesh who presented to our office with discomfort in his right groin, seeking elective repair. During our procedure multiple meshes were encountered, including a portion of Marlex mesh encompassing the appendix. A decision was made at the time to perform an appendectomy. Our case reviews the decision to place mesh for hernia repair, after performing appendectomy, and measures taken to limit infection. We have shown in this case that it is safe to place mesh even if the bowel is transected.

Description:

Given the patient’s complex abdominal history decision was made to repair hernia in a transabdominal approach to allow us to lyse adhesions and prevent bowel obstruction. Upon entering the abdomen, it was noted that there were many adhesions in the right lower quadrant tethering the colon and appendix to the anterior abdominal wall. On closer inspection it was found that the appendix was completely encased in previously placed Marlex mesh. We performed a no touch appendectomy, deploying a stapler at the base of the appendix. Given the number of adhesions and the multiple layers of mesh, the mesh was explained, and peritoneum was sacrificed.

Discussion:

After multiple months of observation, no signs of mesh infection have been noted. We believe our precautions intraoperatively with mesh choice, post-operative antibiotics and omental flap all led to successful mesh placement after transected bowels in an elective hernia repair.

Introduction/Background:

Meningiomas are the most common primary central nervous system (CNS) tumors arising from the meninges. Although typically benign, extracranial metastasis is rare, occurring in less than 1% of cases, most often involving the lungs, bones, or liver. We present a case of recurrent meningioma with malignant transformation and pulmonary metastases in an elderly patient following multiple resections and radiation treatments.

Description:

An 86-year-old male was diagnosed in 2013 with a WHO grade I meningioma treated with bifrontal craniotomy and resection. In 2020, he developed progression along the superior sagittal sinus and received radiation therapy. Imaging in 2024–2025 revealed recurrent right frontal convexity and parasagittal lesions invading the superior sagittal sinus and sphenoid wing. In May 2025, he underwent embolization and gross total resection. Pathology demonstrated transformation to anaplastic (WHO grade III) meningioma with skeletal muscle invasion. Postoperative proton radiation therapy was administered for progression. Systemic therapy with abemaciclib was initiated in October 2025. In November 2025, computed tomography obtained during hospitalization for abdominal pain and anemia revealed a left lower-lobe pulmonary mass with multiple bilateral pulmonary nodules. Biopsy confirmed metastatic malignant meningioma.

Discussion:

Extracranial metastasis from meningioma is uncommon but more frequently reported in high-grade tumors. The lungs are the most common site of distant spread. Proposed mechanisms include hematogenous dissemination through venous sinuses, particularly in tumors involving the superior sagittal sinus, vascular invasion, and possible surgical seeding. In this patient, recurrent disease, sinus invasion, malignant transformation, and multiple surgical interventions likely contributed to systemic dissemination. Management of anaplastic meningioma remains challenging. Surgical resection followed by adjuvant radiation therapy is standard; however, recurrence is common. No established systemic therapy exists for metastatic disease, and treatment decisions rely on limited evidence. Targeted agents such as CDK inhibitors are under investigation. Prognosis for metastatic grade III meningioma remains poor despite multimodal therapy. This case illustrates the aggressive clinical course of recurrent meningioma with malignant transformation and pulmonary metastasis, underscoring persistent challenges in surveillance, risk stratification, and therapeutic management of metastatic meningioma.

Introduction/Background:

Cardiac involvement in systemic lupus erythematosus (SLE) has variable manifestations. Pericarditis is the most common cardiac manifestation (20%), whereas myocarditis is rare, occurring in approximately 1–2% of cases. Cardiac tamponade is also rare, but possible in lupus pericarditis. Heart failure develops in 2-3% of patients. While stress cardiomyopathy can occur, sustained heart failure with reduced ejection fraction (HFrEF) due to inflammatory myocarditis is uncommon.

Description:

A 40-year-old woman with SLE complicated by lupus nephritis induced end-stage renal disease had multiple admissions for renal failure and progressive cardiac decline. Chest x-ray initially showed new, sudden onset cardiomegaly. Transthoracic ECHO (TTE) showed a large pericardial effusion with tamponade physiology and newly reduced ejection fraction (26%). Despite worsening ECHO features, she declined pericardiocentesis. Later admissions were marked by recurrent uremia, persistent large pericardial effusion, and worsening biventricular dysfunction despite intermittent hemodialysis, steroids, colchicine, and plasmapheresis. Later, she presented with fever, confusion, and severe cardiomegaly; echocardiography demonstrated LVEF of 18–19% with persistent effusion. Right and left heart catheterization revealed normal coronaries, elevated filling pressures, and low cardiac output. The patient was later amenable to pericardiocentesis; however, it was cancelled after interval reduction in effusion size following consistent dialysis. Cardiac MRI demonstrated extensive myocardial fibrosis, consistent with autoimmune myocarditis and acute pericarditis in SLE, confirming inflammatory lupus cardiomyopathy causing sustained HFrEF. She transitioned to guideline directed heart failure therapy.

Discussion:

This case shows rare cardiac manifestations of SLE: recurrent large pericardial effusion with tamponade physiology and persistent HFrEF. Although the patient’s tamponade can be attributed to either uremia or lupus pericarditis, her heart failure is due to autoimmune inflammatory myocarditis. New cardiomegaly in SLE should prompt timely evaluation of pericardial effusion and tamponade. Early rheumatologic management and initiation of dialysis are essential in patients with lupus nephritis and uremia. Cardiac MRI was critical in diagnosing autoimmune myocarditis over stress cardiomyopathy. Early recognition and multidisciplinary care are essential to improve outcomes in rare, high-risk cardiac complications of SLE.

Introduction/Background:

Spinal cord infarction is a rare type of stroke that occurs within the spinal cord or the arteries that supply it. The etiology of spinal cord infarction is commonly a result of atherosclerosis and related complications. The outcome of this condition often results in severe disabilities and functional impairment. The focus of long-term management is on rehabilitation to optimize function and quality of life. This case report highlights how a chiropractor functioned within an interdisciplinary healthcare team to manage low back pain in a patient with a history of spinal cord infarction.

Description:

A 46-year-old male with a history of spinal cord infarction was referred by pain management for chiropractic evaluation and treatment of chronic low back and bilateral lower extremity pain. Orthopedic testing provoked pain in the lumbosacral region, and hypertonicity of the pelvic musculature was noted bilaterally. Lumbar range of motion was globally decreased and painful. A Visual Analog Scale (VAS) pain score of 10/10 and Defense and Veterans Affairs (DoD/VA) Pain Supplemental Questions score of 40/40 were reported. The patient's condition was managed with comprehensive, interdisciplinary care that involved neurology, pain management, physical therapy, behavioral health, and chiropractic services. This integrated approach aims to reduce pain, improve quality of life, and enhance overall well-being. Chiropractic care involved a multimodal treatment plan of 12 visits over 6 weeks consisting of low-velocity, low-amplitude manipulation, Cox distraction technique, and soft tissue mobilization. After 12 visits, the patient reported a score of 0/10 on the VAS and 20/40 on the DoD/VA Pain Supplemental Questions. The patient had increased function, decreased pain, and no adverse reactions.

Discussion:

Spinal cord injuries present complex challenges that often require coordinated care across multiple disciplines. This case report emphasizes the inclusion of chiropractic treatment in an interdisciplinary clinical approach without adverse events for a patient with low back pain and multiple comorbidities including spinal cord infarction. The findings suggest that there is a need for additional research on this topic to further develop management strategies and best practices within the chiropractic field.

Introduction/Background:

Ewing sarcoma is an aggressive small round blue cell tumor most commonly arising from bone in children and adolescents. Primary renal Ewing sarcoma is exceedingly rare and is frequently misidentified as more common renal neoplasms. Although metastatic disease is present in 20–25% of cases at diagnosis, multifocal noncontiguous epidural spinal metastases causing acute cord compression are uncommon. We present a rare case of Ewing sarcoma presenting with disseminated disease and multifocal thoracic epidural spinal cord compression.

Description:

Patient is a 23-year-old female who presented with one week of bilateral low back pain. She was treated with NSAIDs and muscle relaxants with temporary relief. Two weeks later, she returned with flank pain and fever. Imaging revealed renal mass presumed to be nephroma, and patient was treated with steroids, antibiotics, and outpatient urology follow-up. Patient returned with fever to 104°F. MRI demonstrated a 5.2 cm renal neoplasm with suspected osseous metastases and a possible liver lesion. Labs showed anemia and thrombocytopenia. During hospitalization, she developed progressive lower extremity weakness. Emergent spinal imaging showed diffuse abnormal thoracic marrow signal and epidural masses at T5 and T9 causing severe circumferential cord compression and edema, with an additional lesion at T11. Findings suggested disseminated metastatic or marrow-infiltrative malignancy. She underwent emergent T4–T6 and T8–T10 laminectomies with resection of two separate epidural tumors through distinct incisions. Pathology confirmed Ewing sarcoma with EWSR1 gene rearrangement. She was transferred to a tertiary center and is currently receiving treatment with Cytoxan, Adriamycin, vincristine, alternating with ifosfamide and etopside.

Discussion:

This case highlights a rare presentation of Ewing sarcoma with extensive metastatic disease and multifocal epidural spinal cord compression at diagnosis. Nonspecific back pain, transient steroid exposure, and initial mischaracterization of the renal mass contributed to delayed recognition. Cytopenias and diffuse marrow abnormalities further complicated the differential diagnosis. It is unclear if renal mass was primary Ewing sarcoma due to lack of pathology; however, this was the initial mass identified. Persistent back pain accompanied by systemic symptoms and an atypical renal mass should prompt early imaging and biopsy. Timely recognition is essential to prevent irreversible neurologic injury and to initiate appropriate management.

Introduction/Background:

Merkel cell carcinoma (MCC) is an aggressive, rare neuroendocrine tumor, typically arising in the skin. However, there are few documented cases of neuroendocrine tumors of breast parenchyma with Merkel cell differentiation. This accounts for less than 0.1% of all breast cancers with almost all cases being described in females.

Description:

We present here a 62-year-old, immunocompetent, Hispanic male with a palpable and painful right sided breast mass, present for three to four months. On the exam, a four-centimeter mass was palpated in the 9 o’clock region of the right breast without associated skin nodularity or dermal attachment. Diagnostic mammography revealed a large irregular mass, with follow up ultrasound-guided core needle biopsy resulting in a high-grade carcinoma with neuroendocrine differentiation and immunostaining favoring Merkel cell carcinoma. Staging work-up with PET CT showed no metastatic disease. The patient underwent a right breast wide-local excision with a sentinel lymph node procedure.

Discussion:

Final pathology revealed a 4.5-centimeter primary breast Merkel cell carcinoma without skin involvement, and all four sentinel lymph nodes were negative for carcinoma. For his Stage IIA (T2N0M0) disease, he will be undergoing adjuvant radiotherapy. Not only is current literature regarding Merkel cell carcinoma of the breast parenchyma extremely limited, but it is also incredibly rare to be found in the male gender. There has only been two other reported case of a male patient developing primary breast parenchymal Merkel cell carcinoma. Awareness of this rare pathology, especially in an atypical population, is important to prevent misleading or delayed diagnosis and treatment.

Introduction/Background:

An 84-year-old woman with CAD, cardiomyopathy, hypertension, and diabetes presented with recurrent embolic strokes despite dual antiplatelet therapy. Initial TEE showed severe MAC without thrombus. No atrial fibrillation was detected. After another stroke, repeat TEE revealed a new mobile mass on the posterior mitral annulus. Deemed high-risk for surgery, she underwent transseptal AngioVac aspiration. At one-month follow-up, she remained neurologically intact and functional. Angiography and/or Other Diagnostic Tests: MRI showed multifocal embolic strokes. TTE showed severe MAC with mobile echodensity. TEE showed a 1.8 x 0.8 cm mobile posterior mitral annular mass, likely caseous MAC. CT consistent with severe MAC, imaging limited by calcification and motion artifact. Rhythm monitoring showed no atrial fibrillation. Blood cultures were negative.

Description:

Under general anesthesia, right radial arterial and bilateral femoral venous access were obtained. A Sentinel cerebral protection device was deployed into bilateral carotid arteries. Using TEE and fluoroscopic guidance, transseptal puncture was performed, followed by balloon dilation of the septum. An 18 Fr AngioVac cannula was advanced via the right femoral vein, carefully navigated across the septum into the left atrium, and positioned adjacent to the posterior mitral annular mass. Under continuous TEE visualization, controlled aspiration dislodged and removed the mass completely. Postprocedural TEE confirmed full extraction with mild residual mitral regurgitation. Hemostasis was achieved using Perclose ProGlide and figure-of-eight sutures. The patient was transferred to CICU and discharged home on postoperative day two without complications.

Discussion:

This case demonstrates the feasibility, safety, and efficacy of transseptal AngioVac aspiration of a mobile mitral annular mass causing recurrent embolic strokes. It highlights a minimally invasive alternative for high-risk, surgically ineligible patients.

Introduction/Background:

Cervical radiculopathy occurs when a spinal nerve root becomes mechanically compressed or chemically inflamed. This can cause an array of symptoms along the dermatomal distribution of the affected nerve including neck stiffness, pain in the shoulder, reduced range of motion, impaired deep tendon reflexes, upper extremity weakness, numbness, paresthesia, and loss of fine motor control. This case illustrates a collective approach among healthcare professionals to restore a patient's fine motor skills by treating cervical radiculopathy with chiropractic care.

Description:

A 59-year-old female patient presented with right shoulder pain associated with radiculopathy into her 2nd-4th digits. She endorsed weakness in her right hand that affected her daily living, specifically, her fine motor skills. Electromyography and nerve conduction studies revealed moderate cervical radiculopathy involving C7-8 distributions. MRI evaluation demonstrated C5-6 severe foraminal narrowing, C6-C7 minimal disc bulge, and C7-T1 mild bilateral facet arthropathy. After completing physical therapy, the patient’s symptoms remained unchanged. A neurosurgeon and pain specialist then collaborated with a chiropractor in their integrated system to curate a treatment plan that included low amplitude chiropractic manipulation techniques, long Y-axis traction, Active Release Techniques, and interferential current therapy. After 12 treatments, subsequent dynamometer evaluation revealed that the patient had doubled her right-hand grip strength and regained the ability to perform all interrupted activities. The patient remained symptom-free for over four weeks and transitioned to an as-needed basis.

Discussion:

The interprofessional collaboration within this integrated healthcare system facilitated an effective course of treatment for a patient with cervical radiculopathy. The providers' ability to review and exchange documentation across their shared electronic health records streamlined the management of the patient's condition while reducing redundancy of prior unsuccessful interventions. This patient-centered approach allowed the subsequent care teams to formulate a novel chiropractic treatment plan that would ultimately restore the patient’s quality of life, strength, and dexterity.

Introduction/Background:

The incidence of pulmonary embolism (PE) in hospitalized children is rare, with only 56 per 100,000 patients affected, predominantly females. Although rare, the use of hormonal contraceptives (HC) in adolescent females is linked to 79% of all venous thromboembolism (VTE) and PE cases. This risk is further doubled when using transdermal HC compared to oral. This case highlights the importance of recognizing the life-threatening hypercoagulable side effects of HC in adolescent women, particularly when symptoms may mistakenly be attributed to benign causes.

Description:

A 17-year-old female with no medical history presented with a two-week history of pleuritic chest pain and severe dyspnea with minimal exertion after initial outpatient treatment for presumed muscle strain. She had started transdermal HC two months before presentation. On admission, she was tachycardic to 130 bpm but otherwise hemodynamically stable, saturating well on ambient air. Laboratory evaluation revealed normal troponin and NT-proBNP levels, with a markedly elevated D-dimer of 11.62 mg/dL (normal 0.0–0.5 mg/dL). Bilateral lower extremity venous duplex ultrasonography showed no evidence of VTE. Computed tomography pulmonary angiography demonstrated extensive bilateral pulmonary emboli, with significant clot burden near the left pulmonary artery bifurcation and evidence of pulmonary infarction at the lung bases. Transthoracic echocardiography showed no evidence of right heart strain. The patient was admitted to the pediatric intensive care unit and started a heparin infusion. Despite relative hemodynamic stability, a multidisciplinary team of hematology, critical care, and interventional cardiology elected to proceed with a hypercoagulable workup and mechanical thrombectomy. Bilateral pulmonary artery thrombi were successfully removed using the Inari FlowTriever device, resulting in rapid symptomatic improvement.

Discussion:

This case illustrates the importance of maintaining a high clinical index of suspicion for uncommon, yet serious thromboembolic complications associated with HC use in adolescents. Although the patient lacked right heart strain and biomarker elevation, the degree of clot burden, pulmonary infarction, and severe exertional symptoms supported advanced intervention. This case highlights the value of timely multidisciplinary decision-making, enabling an often-missed extensive hematologic workup, and supports the need to establish a PE response team to improve efficiency and outcomes.

Introduction/Background:

Pediatric autoimmune encephalitis is a rare condition with high morbidity. Diagnosis requires a high index of suspicion. Earlier initiation of treatment, particularly in refractory cases, improves long-term outcomes. We describe a case of anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis in a child whose diagnosis and treatment were hastened due to a history of the same in her sibling, a previously described but rare occurrence.

Description:

A 4-year-old female presented with acute onset of fever, truncal ataxia, and altered speech. Her parents noted that their older daughter had similar symptoms two years ago and was diagnosed with autoimmune encephalitis. In our patient, head CT and MRI brain/spine with and without contrast were normal. Her nasal swab was positive for rhino/enterovirus, suggesting viral/postviral encephalitis, though cerebrospinal fluid (CSF) rapid meningitis viral panel was negative. On hospital day (HD) 4, she developed episodes of agitation and unresponsiveness which prompted repeat neuroimaging (normal), lumbar puncture (second negative CSF rapid meningitis viral panel), and sedation. EEG showed encephalopathy without seizures. Her serum NMDAR titer was negative but due to a high clinical suspicion, first-line treatment of anti-NMDAR encephalitis – intravenous immunoglobulin and steroids – was started on HD6. On HD8, it was confirmed with a neurologist in Missouri that her sister had anti-NMDAR encephalitis treated with rituximab. On HD10, her CSF NMDAR IgG returned positive with a titer of 1:320. After confirming the absence of latent infections, rituximab was started on HD12. Over the next 4 weeks, her symptoms improved, allowing sedation medications to be titrated off. She was initially fed by nasogastric tube, then gastrostomy tube due to involuntary oral movements and poor secretion management. Because she remained far from baseline in terms of speech, motor, and feeding capabilities, she was transferred to a long-term rehabilitation center for intensive multimodal rehabilitation.

Discussion:

This case highlights the importance of family history when diagnosing rare conditions. We were able to quickly initiate both first line and second-line treatments for our patient due to cross-hospital collaboration. Three months after discharge, she remains admitted at the long-term rehabilitation center with little cognitive recovery, but it is known that outcomes continue to improve up to 18 months after presentation.

Introduction/Background:

Left atrial (LA) masses in patients with new onset atrial fibrillation (AF) are uncommon but clinically consequential findings. Differentiating between LA thrombus and myxoma is critical in determining proper management, which may include anticoagulation, cardioversion, and/or surgery. While cardiac magnetic resonance imaging (cMRI) is considered the gold standard for tissue characterization, overlap in imaging features may limit diagnostic certainty in select cases. This case highlights management options when the gold standard fails to provide a definitive diagnosis.

Description:

A 74-year-old woman with HFpEF presented with chest pain and dyspnea and was admitted with new onset atrial fibrillation with RVR. TTE and TEE demonstrated mild mitral stenosis, severe left atrial enlargement, and a large, mobile, pedunculated LA mass arising from the LAA, raising concern for myxoma vs organized thrombus. Cardioversion was subsequently deferred, and the patient was managed with rate control and apixaban for anticoagulation. cMRI was performed for definitive clarification; however, despite contrast-enhanced imaging, the findings were unable to distinguish myxoma from organized thrombus. Several days later, she developed acute limb ischemia requiring thrombectomy, a small ischemic stroke, and renal infarcts. Anticoagulation was maintained with a heparin drip perioperatively and later transitioned to apixaban. Shortly after thrombectomy, a repeat TTE showed near resolution of the mass with only a thin stalk, and follow-up TEE revealed a small residual thrombus with dense spontaneous echo contrast.

Discussion:

This case highlights the diagnostic limitations of cMRI in differentiating LA myxoma from thrombus, even when classic tumor features such as pedunculated stalk are present. Although cMRI is regarded as the gold standard for intracardiac mass evaluation, clinical behavior and serial imaging proved more informative than morphology alone. Massive left atrial enlargement and mild mitral stenosis likely predisposed the patient to thrombus formation despite short AF duration, ultimately resulting in sequalae of shower emboli. When imaging findings are discordant or indeterminate, proper management may include minimizing embolic risk with anticoagulation and monitoring response to therapy with surveillance imaging.

Introduction/Background:

Pacemaker deactivation at the end of life presents complex ethical and logistical challenges. While Heart Rhythm Society affirms a patient’s right to withdraw life-sustaining treatments, clinicians often experience moral distress when patients are pacemaker-dependent. Unlike defibrillators, pacemakers are perceived as integral to the body rather than external interventions, leading to concerns regarding hastening of death with pacemaker deactivation. In this case, we highlight how device manufacturer procedural requirements can also create obstacles to deactivation, resulting in unintended prolonged suffering and increased distress for the patient and family.

Description:

A 74-year-old male with metastatic renal cell carcinoma developed third-degree heart block, necessitating a permanent pacemaker. Over the subsequent four weeks, the patient experienced progressive functional decline, becoming unable to participate in rehabilitation. Due to poor quality of life with profound dysphagia, anorexia, pain, and dyspnea—the patient requested deactivation of the device to align with comfort-focused goals. While the hospital ethics committee confirmed the patient’s capacity and affirmed that deactivation was ethically equivalent to withdrawing other life-sustaining treatments, the treating cardiologists declined to perform the procedure based on personal ethical objections. The patient was transferred to hospice care, where such device deactivation had been performed within the preceding 12 months. Upon transfer, however, the device manufacturer declined to provide programming support, citing changes in liability policy. The patient died eight hours later with the device still functioning, resulting in significant distress to the family.

Discussion:

Ethical principles of autonomy, beneficence, justice, and non-maleficence were all at play in this case. We identified a need to create a protocol to address requests for pacemaker deactivation. Following this case, an interdisciplinary framework involving cardiology, ethics, risk management, and palliative care was established. This provides clear clinical pathways for deactivation, identifies "willing providers" to ensure timely access, and includes pre-negotiated agreements with manufacturers for technical support. This can be formalized into an institutional policy for future requests and provide a scalable model for ensuring patient-centered end-of-life care across the health system.