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Requests for reprints should be addressed to Gbolahan Ogunbayo, MD, Department of Internal Medicine, Rochester General Hospital, 1425 Portland Avenue, Rochester, NY 14621.
A 76-year-old man presented with shortness of breath and cough productive of clear sputum that progressively worsened over 1 day. He denied chest pain, sick contacts, fever, chills, or rigors. On examination, he was anxious and in respiratory distress. His temperature was 96.5°C; respiratory rate was 34 breaths per minute with an oxygen saturation of 76% on a nonrebreather mask; blood pressure was 93/56 mm Hg, and heart rate was 124 beats per minute. Auscultation revealed right-sided rales and a normal cardiac examination.
His laboratory values were significant for a white blood cell count of 22,700/μL with neutrophilic predominance and no bands, lactate of 2.4 mg/dL, creatinine of 1.2 mg/dL, and elevated transaminases. His troponin was 0.13 ng/mL and his brain natriuretic peptide titer was 369 pg/mL. His electrocardiogram was notable for sinus tachycardia with no ischemic changes. His blood gas analysis revealed a pH of 7.00, partial pressure of oxygen (PO2) of 42 mm Hg, partial pressure of carbon dioxide (PCO2) of 26 mm Hg, and a chest radiograph revealed extensive right-sided infiltrate compatible with pneumonia (Figure 1).
Figure 1Chest radiograph (AP view) at presentation.
He was immediately started on vancomycin, ceftriaxone, and azithromycin. Unfortunately, his condition worsened quickly and he was transferred to the intensive care unit, where he was intubated due to worsening hypoxia. He also required 5 vasopressors for blood pressure support. Due to the refractory nature of his shock as well as a rapid decline in his clinical state, a transthoracic echocardiogram was done to rule out a cardiac cause of his hypoxia. This revealed a flail mitral valve leaflet with severe mitral regurgitation (Figures 2 and 3; Video). He underwent emergent mitral valve replacement, had an uneventful recovery, and was discharged 2 weeks later.
Figure 2Two chamber view of transesophageal echocardiogram Showing the Flail posterior leaflet (pMV) the normal anterior leaflet (aMV) and the Ruptured chordae. The Atrial appendage (AA) is shown.
Figure 3Color Doppler (Long axis view) of transesophageal Echocardiogram showing the flail posterior leaflet (pMV), normal anterior leaflet (aMV) and the direction of the regurgitant jet (RJ).
Disease entities and factors that could mimic or cause unilateral pulmonary edema include pneumonia (including aspiration), patient positioning, bronchial or pulmonary vein obstruction, pulmonary contusion or infarction, alveolar hemorrhage, or malignancy.
Predilection for the right pulmonary vein is due to a higher susceptibility of the thinner posterior leaflet to rupture, directing the regurgitant jet toward the right pulmonary vein.
It is especially important to distinguish this entity from shock caused by pneumonia, as the treatment for both conditions are different.
Acknowledgments
I would like to acknowledge Tunji Sangoleye, PsychD, who helped with augmenting the pictures to meet the journals specification as well as Sara Catalano, LMSW, who helped proof-reading the manuscript.
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