Pulmonary Embolus— Unusual Presentations and Diagnostic Dilemma
- Mon, 10/13/08 - 2:55pm
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Pages 25 - 28
Introduction
Pulmonary embolism (PE) is a common and often underdiagnosed clinical entity. It is one of the most common causes of unexpected death with over 300,000 deaths in the United States, most often diagnosed during autopsy.1 Despite advances in diagnostic technology, clinical presentation of PE is variable and nonspecific, making accurate diagnosis difficult for physicians. We present the case of an older patient with recurrent syncopal episodes treated initially with ablation for what was thought to be supraventricular tachycardia (SVT), subsequently diagnosed to have pulmonary embolus.
Case Presentation
Ms. T, an 84-year-old female with past medical history of heart failure (HF), coronary artery disease (CAD), and wheelchair-bound secondary to advanced osteoarthritis, presented to the Emergency Department with acute onset of left-sided chest pain, dyspnea, and syncope. Three months previously, she had presented from her daughter’s residence to the hospital with complaints of recurrent syncopal episodes. During that time, neurological examination was nonfocal, and magnetic resonance imaging (MRI) of brain and carotid Doppler ultrasounds were unremarkable. Stress test was negative for inducible ischemia, and 2D echocardiogram (echo) showed mild pulmonary hypertension (pulmonary artery [PA] systolic pressure = 43 mm Hg) with 50% ejection fraction. However, Ms. T then had several episodes of SVT on event monitor. Lab work including thyroid function was normal. The SVT morphology was consistent with atrioventricular nodal reentrant tachycardia (AVNRT). Although these episodes did not correlate with her symptoms, there were no other causes that better explained her recurrent syncopal episodes. In addition, the patient was not a reliable historian.
In light of her severe symptoms, she had radiofrequency ablation for AVNRT. Post-ablation, SVT was not inducible and she was subsequently discharged to a nursing facility on aspirin, furosemide, atenolol, valsartan, and simvastatin for CAD and HF. She was not on prophylactic anticoagulation or compression devices for deep vein thrombosis (DVT) prevention. Unfortunately, Ms. T continued to have isolated syncopal episodes in the nursing home. The patient and family elected to treat symptomatically with meclizine only.
During the patient’s current admission, she was admitted with dyspnea, syncope, and chest pain, with chest pain promptly relieved with sublingual nitroglycerin. Her oxygen saturation improved from 81% to 96% with 2 liters of nasal oxygen. Her vital signs were stabilized, and examination was unremarkable except for bilateral basal crepitations and pedal edema. A 12-lead electrocardiogram (EKG) showed sinus rhythm at 73 beats/minute with Q waves and new T wave inversions in leads III. Initial labs revealed mildly elevated troponin-I (0.52 ng/mL). The rest of her cardiac enzymes were negative. A 2D echo was ordered to assess her cardiac function and wall motion.
Interestingly, the echo showed a long tubular mobile thrombus (2.3 cm x 1 cm) attached to the interatrial septum near the tricuspid annulus (Figure 1). It was seen floating through the tricuspid valve during diastole causing severe (3+) tricuspid regurgitation. Ms. T also had mild right ventricular (RV) dilation and paradoxical septal motion. Her PA systolic pressure was elevated (62 mm Hg). Lower-extremity Dopplers revealed partially occlusive right popliteal vein thrombus. The patient and family declined any intervention for clot extraction. She was started immediately on intravenous heparin.








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