Abstract Introduction Acute pancreatitis (AP) is one of the most common causes of gastrointestinal hospitalization in the United States. While overall mortality is approximately 1%, it rises to 30-40% in cases complicated by organ failure or necrosis. Pancreaticopleural fistula (PPF) is an uncommon sequela, accounting for less than 1% of pleural effusions and 0.4-7% of chronic pancreatitis cases. Pancreatorenal fistula (PRF) is even rarer, with only isolated reports in the literature. We present a rare case of necrotizing pancreatitis complicated by both PPF and PRF, along with splenic vein thrombosis, managed successfully with endoscopic therapy. Case Presentation A 30-year-old male with alcohol use disorder presented with severe epigastric pain radiating to the back, nausea, and persistent non-bloody emesis. Imaging confirmed acute pancreatitis despite serum lipase not exceeding three times the upper limit of normal, fulfilling two of three diagnostic criteria. He was managed with intravenous fluids and opioid analgesia. Within 48 hours, the patient developed worsening abdominal pain, hypoxemia requiring high-flow oxygen, and stage-2 acute kidney injury. His Modified Marshall Score >2 confirmed severe pancreatitis. Repeat CT demonstrated peripancreatic collections extending into the left anterior pararenal space, consistent with evolving PRF. Empiric Meropenem was initiated for suspected secondary infection. Progressive dyspnea prompted thoracentesis, which yielded >1 L of exudative pleural fluid with low glucose (38 mg/dL), elevated LDH (650 U/L), and markedly increased amylase (>10,000 U/L), confirming PPF. Imaging later showed walled-off pancreatic necrosis (WON). Despite supportive care, pleural effusions recurred, prompting ERCP, which revealed pancreatic duct disruption. Endoscopic sphincterotomy with transpapillary stenting achieved rapid reduction of pleural drainage and clinical stabilization. The patient was discharged with new-onset diabetes on insulin therapy and close outpatient follow-up. Discussion This case illustrates the systemic and local complications of necrotizing pancreatitis, including PPF, PRF, WON, and splenic vein thrombosis. PPF typically presents with recurrent large pleural effusions and pleural fluid amylase >10,000 U/L. PRF, a rarer entity, signifies retroperitoneal extension of necrosis. Early recognition and a step-up approach, are critical. In this case, ERCP-guided ductal stenting diverted pancreatic secretions, allowing fistula closure and recovery. Conclusion This case underscores the severity of necrotizing pancreatitis, which can swiftly progress to multiorgan failure with complex fistulization. Despite walled-off necrosis and multiple fistulae, timely endoscopic stenting led to recovery. Persistent symptoms despite normalized enzymes warrant evaluation for complications, and pleural fluid analysis in recurrent effusions is essential. Early multidisciplinary collaboration and step-up management are key to improving survival. This abstract is funded by: None
Abstract Introduction Fungal empyema thoracis is an uncommon but life-threatening condition, accounting for less than 5% of all empyema cases and occurring primarily in immunocompromised hosts, such as post-organ transplant recipients. Its occurrence as a complication of hepatic hydrothorax in the absence of overt ascites is exceptionally rare and diagnostically challenging. We present a case of hepatic hydrothorax complicated by fungal empyema in a post-liver transplant patient. Case Description A 43-year-old man with cryptogenic cirrhosis status post orthotopic liver transplantation in 2023, prior aortic valve replacement, and on maintenance immunosuppression presented with subacute progressive dyspnea worsened by exertion and orthopnea. Examination revealed bilateral decreased breath sounds. Laboratory studies showed WBC 8.4 × 109/L, hemoglobin 10.3 g/dL, platelets 114 × 109/L, and creatinine 2.1 mg/dL. Chest radiograph demonstrated bilateral pleural effusions without significant ascites. Echocardiogram revealed left ventricular ejection fraction of 42% with grade II diastolic dysfunction. Diagnostic thoracentesis yielded exudative fluid that grew Candida albicans. Despite antifungal therapy and bilateral chest-tube drainage with intrapleural tPA/DNase for three days, the effusions reaccumulated, progressing to bilateral pneumothoraces and trapped-lung physiology. Repeated pleural cultures identified Candida famata and Trichosporon beigelii complex. Given persistent infection refractory to medical and fibrinolytic therapy, the patient underwent sequential bilateral thoracotomies with lung decortication. Postoperatively, he remained hemodynamically stable with re-expanded lungs, decreased chest-tube output, and preserved graft function. Discussion This case represents a rare occurrence of bilateral fungal empyema in an immunosuppressed liver-transplant recipient, likely originating from an infected hepatic hydrothorax, possibly via microscopic diaphragmatic defects, even in the absence of overt ascites. Blood cultures have a diagnostic yield below 20% in fungal empyema, underscoring the need for direct pleural fluid analysis. Failure of medical and fibrinolytic therapy highlights that organized fungal empyemas may require surgical decortication for definitive source control. Conclusion Hepatic hydrothorax, even without overt ascites, can progress to fungal empyema in post-transplant patients. Given the low yield of blood cultures, early pleural sampling, targeted antifungal therapy, and timely multidisciplinary escalation to surgical management are essential for survival. This abstract is funded by: None
Abstract Introduction Cardiogenic syncope from transient asystole can resemble epileptic seizures in critically ill patients, often leading to misdiagnosis and unnecessary antiseizure therapy. Recognition is essential in postoperative transplant patients, where autonomic dysregulation and hemodynamic instability predispose to arrhythmia-related cerebral hypoperfusion. Stokes-Adams attacks are an uncommon but important cause of syncope, representing up to 8% of unexplained cases, typically occurring in patients with intermittent high-grade atrioventricular block or sinus node dysfunction.Similar physiology may transiently emerge in the post-transplant setting due to autonomic instability, critical illness, or medication effects. Case Presentation A 56-year-old man with Budd-Chiari syndrome and hepatocellular carcinoma underwent orthotopic liver transplantation. His postoperative course was complicated by hemorrhagic shock, multiple re-explorations, and respiratory failure requiring tracheostomy. During ICU recovery following extubation, he developed recurrent tonic episodes of unresponsiveness despite escalating antiseizure therapy. Each event lasted 20-30 seconds, with generalized stiffening, loss of consciousness, and rapid recovery with mild confusion. Continuous EEG-ECG monitoring revealed sinus arrest lasting up to 10.4 seconds without epileptiform activity, confirming a cardiogenic mechanism. Laboratory studies—including electrolytes, thyroid function, troponin, and QTc—were normal, and no AV-nodal-blocking or vagotonic drugs were used. Echocardiography showed preserved biventricular function. Electrophysiologic evaluation confirmed sinus node dysfunction as the cause of syncope. A permanent pacemaker was implanted, leading to complete resolution of episodes and full neurologic recovery. Discussion Cardiogenic syncope secondary to sinus arrest can present with convulsive movements due to transient cerebral hypoperfusion, mimicking seizures. These episodes represent a Stokes-Adams-type convulsive syncope—a modern manifestation of the classic syndrome in which sinus node dysfunction replaces complete heart block as the precipitating rhythm disturbance. The combination of stereotyped convulsive episodes, normal EEG, documented sinus arrest, and resolution after pacing is diagnostic of Stokes-Adams-type syncope rather than true epilepsy. Misdiagnosis can lead to prolonged antiseizure therapy, avoidable morbidity, and delayed pacing. In this patient without prior cardiac or neurologic disease, post-transplant autonomic dysfunction or immunosuppressant-related bradyarrhythmia likely contributed to sinus node suppression. Conclusion Sinus node dysfunction should be suspected in post-transplant or critically ill patients presenting with seizure-like episodes lacking EEG correlation. Integrated EEG-ECG monitoring and early multidisciplinary evaluation are essential for timely pacing and prevention of recurrent syncope or sudden cardiac death. This abstract is funded by: None
Abstract Tuberculosis (TB) is an uncommon cause of acute respiratory distress syndrome (ARDS), accounting for 1-5% of pulmonary TB cases, with mortality rates exceeding 50-70%, most often in immunocompromised hosts. We report a case of a 40-year-old HIV-negative Puerto Rican woman with a history of crack cocaine and heavy alcohol use who presented with two months of fatigue, dizziness, productive cough, and significant weight loss. On admission, she was cachectic with severe microcytic hypochromic anemia, marked lymphopenia, and hypoalbuminemia. Chest computed tomography revealed bilateral consolidations, a left upper-lobe cavitation, and right-sided tree-in-bud opacities. She was admitted under airborne precautions and started on empiric antibiotics for community-acquired and opportunistic pneumonia. By the third hospital day, she developed severe hypoxemia meeting Berlin criteria for ARDS, requiring intubation, lung-protective ventilation, and prone positioning with transient improvement in oxygenation. Induced sputum nucleic acid amplification testing confirmed Mycobacterium tuberculosis, and four-drug antituberculous therapy was initiated. Despite aggressive intensive care management, her course was complicated by septic shock requiring vasopressors, refractory hypoxemia, and multi-organ failure, resulting in death on day 16 of hospitalization. This case highlights the aggressive course and high mortality of TB-associated ARDS (TB-ARDS) even in immunocompetent, HIV-negative patients. It underscores the importance of early recognition and consideration of TB in patients presenting with ARDS and CT findings suggestive of TB, particularly in high-risk populations. Prompt diagnosis and initiation of therapy remain crucial, yet outcomes are often poor despite timely treatment and advanced supportive care. This abstract is funded by: None
