A 41-year-old man presented to the emergency department with substernal chest pain and was found to have ST elevations in the inferior leads on his electrocardiogram. An emergent cardiac catheterization did not identify significant coronary narrowing. Computed tomography of the thorax demonstrated a pneumopericardium and a hiatal hernia. The patient had a complicated past surgical history, including a Nissen fundoplication and three additional surgeries for postoperative complications. An esophagram later revealed an ulcer and possible fistula, and the patient underwent gastropericardial fistula resection after the fistula failed to close with fibrin sealant application. Enteropericardial fistulas occur infrequently but have high morbidity and mortality rates. This possibility is much more likely in patients with prior gastroesophageal surgery, including laparoscopic Nissen fundoplication. F istula formation between the gastrointestinal tract and the pericardium is very uncommon and usually occurs after esophagogastric surgical procedures (1-8). Laparoscopic Nissen fundoplication is the most common surgical treatment for gastroesophageal refl ux disease. Th e procedure off ers good long-term outcomes, but complications occur in 4.5% to 12.5% of patients and can cause substantial morbidity and mortality (1-4). We report a case of gastropericardial fi stula 16 years after a laparoscopic Nissen fundoplication associated with multiple postoperative complications. CASE DESCRIPTIONA 41-year-old man presented to our emergency department with complaints of constant substernal left chest pain radiating to his left shoulder that began a few hours prior to presentation. He rated the pain intensity at 8/10 and also noted shortness of breath. His initial vital signs included a blood pressure of 116/66 mm Hg, heart rate of 45 beats per minute, respiratory rate of 18 breaths per minute, temperature of 96.7°F, and oxygen saturation of 94%. He was immediately taken to the catheterization lab after an electrocardiogram showed a 2 mm ST elevation in leads II, III, and AVF (Figure 1a). Th e initial laboratory test results included a white blood cell count of 15.4 k/μL; hemoglobin, 14.6 g/dL; platelets, 240 k/μL; normal electrolytes; creatinine, 1.4 mg/dL; glucose 172 mg/dL; creatine kinase, 662 IU/L; troponin T, <0.01 ng/mL; and brain natriuretic peptide, 42 pg/mL. His past medical history included hypertension, asthma, anxiety, migraine headaches, posttraumatic stress disorder, postoperative pain syndrome, polysubstance abuse, and gastroesophageal refl ux disease. Previous surgical history included a laparoscopic Nissen fundoplication 16 years earlier complicated by a postoperative hiatal hernia. He had a revision with an open Nissen procedure 2 months later and then a diaphragmatic hernia repair with cortex mesh the following month. Two years later, the patient was diagnosed with a paraesophageal abscess, and cultures from the mesh grew a Haemophilus species. He underwent removal of the infected mesh, preservation of the latissim...

Historically, children evaluated for vomiting and diarrhea secondary to viral enteritis have symptoms lasting 2–4 days and respond to supportive care, including oral rehydration and anti-emetics if required. Recently, within a 14-day timespan, we encountered three children with severe diarrhea who rapidly became dehydrated and went into hypotensive shock. Although SARS-CoV-2 molecular tests were negative by nasopharyngeal swab, all were later found to have MIS-C. This small case series underscores features reported in previous larger studies and emphasizes the rapid clinical evolution of this condition. We highlight the importance of early recognition of cardinal laboratory findings characteristic of MIS-C (i.e., lymphopenia, markedly elevated acute phase reactants, and hypoalbuminemia). We also show serologic evidence that the pathophysiological mechanism of SARS-CoV-2 related diarrhea may differ from other causes of dehydrating vomiting and diarrhea, with no serologic evidence of villus cell injury.

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