acute onset depressed systolic function (EF 30%), and subsequent catheterization revealed normal coronaries. It was deduced that a recent viral illness was the mostly likely cause of her non-ischemic cardiomyopathy (diagnosed as Takotsubo) and the patient was instructed to continue her home medications. Her symptoms had largely resolved at time of discharge from the neighboring facility. She presented to this facility after re-initiation of etanercept. Upon further interviewing the patient, she stated she had only recently (3-weeks prior) restarted the etanercept which caused her presenting complaints. A CT-scan was ordered which incidentally revealed a pericardial effusion. A formal echocardiogram was then ordered which identified a moderate-sized pericardial effusion without tamponade physiology and with recovered systolic function (ejection fraction of 55-60%). Examination findings included orthopnea as well as respiratory improvement with forward-leaning, but no jugular venous distention. Laboratory findings indicated elevated inflammatory c-reactive protein and elevated creatinine. EKG showed electrical alternans. No infectious etiology was identified on
labs. At this point, the differential of autoimmune versus medication-induced pericardial effusion was considered and thus the patient was administered steroids in place of NSAIDs (due to AKI on labs) as well as intravenous fluids. Auto-immune work up was ordered and resulted negative (ANA, anti- Histone, anti-DNA, anti-Smith). The patient began to experience symptomatic improvement. Here, it was presumed that the initiation of the TNF-a inhibitor was the primary cause of the development of the pericardial effusion. The patient was closely followed and approximately three months later, with continued cessation of etanercept, a repeat echocardiogram revealed resolution of the pericardial effusion and stability of the systolic function. Discussion: This case demonstrates the potential of TNF-a inhibitors to cause spontaneous pericardial effusions. While there are few cases illustrating such an association, usage of TNF-a inhibitors and new complaints should prompt evaluation for cardiac dysfunction and/or the presence of extra-cardiac manifestations.
KILLIAN-JAMIESON DIVERTICULUM PRESENTING SIMULTANEOUSLY WITH ZENKER’S DIVERTICULUM Samantha Wu, Vance Hartke, Benjamin Alfred Guider, Jr; Department of Medicine, Tulane Health Sciences Center, New Orleans, LA.
Introduction: Patients with cervical esophageal diverticulum often present with dysphagia, which can cause cough, regurgitation, and affect quality of life. Zenker’s diverticula affect women more than men and are more common in the elderly. They occur when increased pressure during swallowing leads to esophageal mucosal herniation into Killian’s triangle. Case: A 94-year-old woman with a history of stroke with residual intermittent dysphagia, atrial fibrillation, hypertension and recent critical limb ischemia with above-the-knee amputation one week prior presented with several days of new dysphagia to both solids and liquids and regurgitation with associated 20-pound weight loss for the last couple months. She described a globus sensation, but denied abdominal pain, nausea, or vomiting. She denied history of neck surgeries. She was a former smoker but quit 40-50 years ago and denied alcohol/illicit drug use. On exam, there was no oropharyngeal swelling, erythema, and exudates nor were there palpable neck masses or lymph nodes. Labs were
significant for leukocytosis 16.6 and potassium 2.6. CT scan and barium esophagram both showed 4.5cm and 2.0cm proximal esophageal diverticula, one likely a Zenker and the other a Killian-Jamieson, as the likely causes of her progressive dysphagia. There was normal swallowing mechanism, and no aspiration was seen. Given her age and comorbidities, she was a poor procedural and surgical candidate. She opted for conservative management, pureed diet, and was discharged with home hospice. Discussion: Killian-Jamieson diverticulum is a rare diagnosis resulting from herniation of the esophageal mucosa in the Killian-Jamieson space below the cricopharyngeal muscle and should also be considered in the evaluation of dysphagia. As with Zenker’s, patients are typically elderly and female. The definitive management for symptomatic
patients is surgery, including transcervical diverticulectomy and esophagomyotomy, or endoscopic interventions. Instead of endoscopic correction, percutaneous endoscopic gastrostomy 38
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