Presentation
A relic from a previously undiagnosed event was a persistent source of infection in a 50-year-old man. The patient presented to his primary care provider’s office with a 3-week history of fevers, dyspnea on exertion, nonproductive cough, and left shoulder pain. He was sent to the Emergency Department to exclude an acute pulmonary embolism after initial blood work revealed an elevated D-dimer level. Ciprofloxacin had been prescribed for a urinary tract infection 14 days earlier, after he was evaluated in the emergency department of another hospital. At that time, urine cultures grew methicillin-sensitive Staphylococcus aureus.
Assessment
Upon admission, the patient’s pulse was 145 beats per minute, and his blood pressure was 170/100 mm Hg. After receiving intravenous crystalloid boluses for presumed sepsis, his heart rate improved to the 80s. His admission blood work was notable for a white blood cell count of 15.4 × 103 cells/mm3 and a lactic acid level of 5.9 mEq/L (normal, 0.5-2.2 mEq/L). Subsequently, his blood pressure dropped to 68/38 mm Hg, and vasopressor support with intravenous norepinephrine was initiated. Empiric antibiotic coverage with vancomycin and piperacillin/tazobactam was begun as well.
An electrocardiogram showed sinus tachycardia with T-wave inversions in leads V5 and V6 with no ST-segment changes. Inferior Q waves were consistent with an age-indeterminate inferior infarction. Computed tomography (CT) angiography excluded pulmonary embolism but was remarkable for a large calcified ventricular aneurysm. As with the patient’s previous urine cultures, admission blood cultures grew methicillin-sensitive Staphylococcus aureus.
His hypotension and tachycardia resolved with intravenous fluids and antibiotic therapy. Vancomycin and piperacillin/tazobactam were stopped and cefazolin was started. A chest x-ray study demonstrated no infiltrate, and a urinalysis did not show signs of infection. Inferolateral wall motion abnormalities, an inferior aneurysm containing a thrombus, and an ejection fraction of 40% were evident on a transthoracic echocardiogram, but no valvular vegetations were seen. CT of the abdomen and pelvis also failed to demonstrate a clear source of infection. An indium-tagged white blood cell scan showed possible increased uptake in the lungs, but no other explicit evidence of infection was revealed. The patient remained very ill, with altered mental status, and he had persistent bacteremia despite appropriate antibiotics.
Diagnosis
Cardiac CT revealed an infected thrombus. A large posterior left ventricular aneurysm with a heavily calcified wall contained a sizable thrombus, and multiple surrounding gas pockets extended outside of the aneurysm. Ventricular aneurysms can form with abnormal remodeling of the left ventricular wall after acute transmural myocardial infarction. Complications include congestive heart failure, ventricular tachycardia, and thrombus formation with cerebral or peripheral embolization. Infection of a thrombus is much less common. The time interval from the initial myocardial infarction to infection varies widely and has been reported to be anywhere from a few weeks to several years. Our patient most likely suffered a silent infarction, as he had no previous history of a cardiac event.
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-Elizabeth Hubbard, BA, Eric Wise, MD, PhD, Bradley Hubbard, MD, Steven Girard, MD, PhD, Bobby Kong, MD, Varsha Moudgal, MD
This article originally appeared in the June 2016 issue of The American Journal of Medicine.
