A 56-year-old female with a history of pulmonary embolism, myotonic dystrophy, and complete heart block on pacemaker presented to the emergency department (ED) with sudden onset shortness of breath and substernal chest pain radiating to the back. There was no history of fever, chills, cough, sore throat, or chest trauma. Her history was negative for any gastrointestinal, musculoskeletal, or neurological symptoms. She was taking rivaroxaban 20 mg once daily for deep vein thrombosis of the left axillary vein diagnosed 7 weeks ago. There was no prior history of tuberculosis, chest irradiation, or chemotherapy. She had a history of pulmonary embolism in 2007 for which she was on coumadin for a year. She had a biventricular pacemaker placed in 2008 for complete heart block induced nonischemic cardiomyopathy. Complete heart block was diagnosed at the same time and was believed to be secondary to myotonic dystrophy. The pacemaker device reached elective replacement indicator and was replaced with a Medtronic Protecta D314TRG device in 3/2012. She was on Tylenol 500 mg as needed for back pain, levocetirizine 5 mg twice daily for seasonal allergies, and rivaroxaban and zolpidem 5 mg nightly as needed. The above-listed medications do not have p-glycoprotein altering activity or CYP3A4/5 or CYP2J2 inhibiting activity. The past surgical history and family history were unremarkable.
In the ED, her blood pressure was 78/48 mm Hg, pulse 106/minute, temperature 36.5 F, and respiratory rate 18/min with saturation of 87%. Her height and weight were 1.7 m and 180 lbs, respectively. Cardiac examination was normal. Chest examination was significant for bibasilar rales. Electrocardiogram revealed ventricular paced rhythm. There was no associated electrical alternans. Lab tests revealed negative troponin, INR of 1.3, and PTT of 28 s. Complete blood count and basic metabolic profile were unremarkable. Computed tomography (CT) on chest showed no pulmonary embolism but revealed a large hyperdense pericardial effusion (Figure 1). Echocardiogram showed moderate-sized circumferential effusion with a swinging heart consistent with pericardial effusion (prior echo 4 years ago showed no pericardial effusion) (Figure 2). Inferior vena cava was dilated with no respiratory collapse and right ventricle outflow tract collapsed in diastole. With the diagnosis of cardiac tamponade, emergency subxiphoid pericardial window was performed and a total of 300 mL of bloody pericardial fluid was drained. Hemostasis was achieved and was satisfactory. Transesophageal echocardiogram confirmed emptying of the collection as well as improved cardiac function. There was immediate improvement in her hemodynamic status. Postprocedure images showed complete resolution of the effusion. Further etiologic workup was unrevealing. Pericardial fluid culture was negative with normal cytology. Pericardial tissue biopsy was negative for malignancy. Thyroid and liver function tests were normal. ANA, rheumatoid factor, anti-saccharomyces cerevisae antibody, anti-mitochondrial antibody, C3, C4, and anti-liver-kidney-muscle antibody were negative making the autoimmune cause unlikely. Myotonic dystrophy was considered to be an unlikely cause of her hemopericardium as pericardial involvement has not been reported with it. In addition, her previous echo was negative for pericardial effusion. There was no temporal relation to the axillary vein DVT and the pacemaker lead implantation as CT scan done in 2013 and echocardiogram done in 2015 mentioned a normal pericardium with appropriately implanted leads. Intraoperatively, there was no mention of pacemaker lead induced pericardial perforation. Further hospital course, unfortunately, was complicated by healthcare associated pneumonia with septic shock and multiorgan failure. The autopsy was not done.