2.5 cm esophago-pleural fistula. Video-assisted thorascopy was performed and the patient was treated with intravenous fluconazole, pantoprazole, and jejunostomy tube placement. A repeat EGD with transoral esophageal stent was placed. His clinical course improved, and he was discharged with plans to have stent retrieval in 8 weeks. Discussion: This case represents the rare discovery of an esophago-pleural fistula in a hospitalized patient who was being treated for DKA and a diabetic foot wound infection. Upon further
examination of outside hospital records, the patient was previously followed by gastroenterology and received multiple EGDs. Approximately one year prior to this presentation, the patient had an EGD which revealed grade D reflux esophagitis with an esophageal stricture. The patient was lost to follow up and had not been adherent with proton pump inhibitor therapy. Though it is not well described, we propose this patient’s chronic, untreated esophagitis with stricture ultimately led to the formation of this esophagoplerual fistula.
PRESENTATION OF BIVENTRICULAR STRESS INDUCED CARDIOMYOPATHY AS POTENTIAL SEVERE PATHOLOGY MIMIC Alex Fixler MD, Keyur Patel MD; Department of Medicine, LSU Health New Orleans, New Orleans, LA.
Introduction: Biventricular stress induced cardiomyopathy is an uncommon variant of stress induced cardiomyopathy and comprises 20-40% of cases.
was high clinical suspicion for an acute coronary syndrome (ACS) versus a pulmonary embolism (PE). The patient was given 325 mg aspirin and started on a heparin drip. She deferred computed tomography angiogram and venous doppler of extremities were negative for VTE, making PE less likely despite the clinical picture. Transthoracic echocardiogram was performed that revealed an ejection fraction of 30-35% with biventricular akinetic apex and biventricular hyperkinetic basilar segments consistent with stress induced cardiomyopathy versus ischemic cardiomyopathy. Cardiology performed a right and left coronary angiography that did not reveal significant coronary artery disease. The presumed diagnosis was stress induced cardiomyopathy with a reduced ejection fraction and the patient was started on goal directed medical therapy in addition to dual antiplatelet therapy. The patient improved clinically over two days and was discharged with close cardiology follow- up with recommendations for outpatient cardiac MRI and repeat transthoracic echocardiogram. Discussion: With a clinical picture of hypoxia, chest pain, tachycardia, hypotension, Q-waves on EKG, up-trending troponin with right ventricular wall motion abnormalities on bedside echo, there is high clinical suspicion for severe pathology such as a massive or sub-massive PE or ACS. This case is significant because right ventricular involvement in stress induced cardiomyopathy is a rare variant of an already rare pathology.
Case: A 59-year-old female with COPD and hypertension was admitted for acute hypoxemic respiratory failure. The patient presented with a complaint of shortness of breath and intermittent chest pain for 4 hours. The patient’s dyspnea was refractory to home albuterol which prompted the presentation. Her chest pain was substernal, sharp, intermittent and non-radiating. EMS reported an oxygen saturation of 70% and she was placed on CPAP which was transitioned to BiPAP. She was given methylprednisolone, continuous ipratropium bromide/albuterol, azithromycin, and ceftriaxone for initial concern of a COPD exacerbation. Following initial management, the patient was quickly weaned from the BiPAP to a non-rebreather and then to 2 liters nasal cannula. The patient was noted to be tachycardic and hypotensive with an oxygen saturation of 90% on 2 liters nasal cannula. She was anxious but not in acute respiratory distress. Lungs were clear to auscultation bilaterally. No lower extremity edema or jugular venous distension noted. A bedside echo showed a hyperdynamic RV with initial concern for diastolic collapse with decreased left ventricular function. An EKG was notable for Q waves in the inferior and anterolateral leads. The patients’ high sensitivity troponin increased from 20 ng/L to 900 ng/L. At this juncture, there
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