hematologic diseases. Many of the symptoms of SLE are nonspecific and are very similar to symptoms of Cocciodiodomycosis infection, as in this case. While there are an estimated 150,000 cases of Coccidiodal infections in the U.S annually, 60% of patients remain asymptomatic. Symptomatic patients experience symptoms similar to SLE, which can obfuscate and further delay an already difficult to diagnose rare disease, as in the case of the patient below. Case: A 33-year-old male presented with a 3-week history of cough, dyspnea, hemoptysis, fevers, chills, fatigue, myalgias, and loss of appetite. He had recently traveled to Arizona where he initially experienced symptoms and was given a course of antibiotics without improvement. During his admission, the patient tested positive for Coccidioides Ab IgM, Coccidioides titer of <1:2, and Coccidioides immitis Ab <1:2. The respiratory sputum fungal culture grew 2 colonies of Coccidioides immitis/ posadasii. The patient also tested positive for anti- dsDNA, anti-RNP, anti-SM, anti-smRNP, and anti- chromatin, but these results were attributed to acute infection rather than SLE. He was discharged on a 3-month course of fluconazole and outpatient follow-up with rheumatology. He was subsequently
lost to follow-up and presented back 9 months later with worsening dyspnea, cough, fatigue, rash and weight loss. It was unclear if the patient completed the fluconazole treatment, so there was high concern for recurrent or disseminated Coccidioidosis. He subsequently underwent a battery of tests including imaging studies, lab studies (hepatitis, HIV, fungal and bacterial studies) and biopsies (renal, lymph nodes, bone marrow, skin and gastrointestinal). After ruling out infectious and malignancy as sources, attention turned to SLE with the patient being positive again for SLE markers and positive for dsDNA Crithidia (1:160). He was started on steroids and hydroxychloroquine with symptom improvement. Discussion: In this case of a patient with concomitant Coccidioides and SLE, it is still difficult to delineate if the patient’s already existing SLE resulted in an immunocompromised state that allowed the Coccidioides infection to become symptomatic, or if it was the Coccidioides that triggered or unmasked the SLE. Because of the non-specific presentation and inconsistent follow-up, the patient’s final diagnosis was not reached until over 1 year after symptom onset and potentially longer given the uncertainty of when symptoms actually began.
SYSTEMIC LUPUS ERYTHEMATOUS FLARE PRESENTING WITH PERICARDIAL TAMPONADE Edwards Leonard MD, Mehnaz Rahman MD, David Beyer MD, Jacob Dubuc MD, Fernanda Correa MD; Department of Medicine, LSU Health New Orleans, New Orleans, LA.
Introduction: Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disorder with widespread effects including on the cardiovascular system. Case: A 24-year-old female with SLE presented with acute shortness of breath associated with a few days of lethargy, loss of appetite and a syncopal episode. She had been admitted to the intensive care unit for pneumonia at an outside facility 4-5 days prior to presentation with initiation of oral antibiotics and an interruption in her home lupus regimen of hydroxychloroquine, mycophenolate, and prednisone. On the morning of presentation, she reported feeling progressively short of breath and with sudden loss of consciousness from a standing position. Clinically, she was hypotensive at 84/64 mmHg and tachycardic to 118 bpm. Crackles were present at the bilateral lung bases, without jugular venous
distension, and her heart sounds were difficult to auscultate. Laboratory evaluation was significant of lactic acidosis and elevated inflammatory markers. A Computed Tomography scan of her chest was significant for a pericardial effusion. A transthoracic echocardiogram showed a large pericardial effusion with cardiac tamponade physiology, namely diastolic right ventricular collapse, plethoric inferior vena cava and marked respiratory variation in her mitral inflow velocities by doppler. Biventricular systolic function was preserved, and she did not have any hemodynamically significant valvulopathy. Her overall clinical picture was consistent with obstructive shock secondary to tamponade. She was taken urgently for pericardiocentesis which yielded 350 cc of yellow, cloudy pericardial fluid, with a pericardial drain left in place for close monitoring of output in the cardiac critical care unit.
Discussion: Cardiac Tamponade is a severe possible
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