Infective endocarditis presenting as a splenic laceration.

To the Editor: Infective endocarditis is often a delayed diagnosis, many times secondary to difficulty in diagnostic modalities or lack of clinical consideration due to an atypical presentation. We present a case of viridans group streptococcus endocarditis that initially presented to a surgical trauma service as a splenic laceration.

An 80-year-old female presented to the emergency room with left upper quadrant pain after a fall, four days prior. She denied any fevers, chills, or night sweats. Her medical history was significant for coronary artery disease, diabetes, and diverticulitis. Medications included quinapril, furosemide, and simvastatin. She was afebrile with a blood pressure of 130/80. Heart sounds were distant with a soft systolic ejection murmur, and the abdominal examination was significant for left upper quadrant tenderness with guarding. Laboratory values revealed a white cell count of 19,700 cells/[mm.sup.3] with 74% neutrophils and 7% bands. Hemoglobin was 9.8 g/dL, platelets were 364,000/[mm.sup.3], and creatinine was 1.3 mg/dL. CT scan of the abdomen revealed a splenic laceration with pericapsular fluid.

While undergoing a repeat CT scan shortly after initial presentation, the patient experienced a cardiac arrest. She was resuscitated and rushed to the OR with concern for splenic rupture. Intraoperatively, purulent fluid was found in the left upper quadrant; however, the spleen was intact. Surgical pathology revealed multiple small abscesses and Gram positive cocci, consistent with septic emboli. Peritoneal cultures were positive for viridans group streptococcus. Blood cultures drawn after 72 hours of antibiotic therapy were negative. Transthoracic echocardiogram revealed 1.5 cm X 0.7 cm posterior leaflet mitral valve vegetation. Upon further questioning, the patient had undergone routine dental cleaning six weeks prior without receiving prophylactic antibiotic therapy. She was treated with two weeks of gentamicin and four weeks of ceftriaxone.

This case represents an unusual presentation of infectious endocarditis. The patient's clinical scenario was consistent with a splenic laceration or rupture, but operative findings and pathology implied an infectious etiology. While splenic injury occurs in approximately 30% of blunt abdominal trauma, spontaneous rupture has also been reported in the absence of injury. (1,2) Among these cases, infectious processes lead the list as culprits for such disease. (3) This case reminds us of the importance of following up on pathology specimens. A vigilant demeanor is necessary in pursuit of the underlying cause of apparent splenic injury as localized findings can be absent in 90% of splenic infarcts and abscesses. (4) It was retrospectively discovered that this patient's previous dental procedure had likely been the inciting event for hematologic bacterial dissemination and serves as a reminder not to overlook seemingly trivial historical data that can prove to be key clues to uncovering a difficult diagnosis.

Joseph R. Baber, DO, Capt, USAF, MC

Steven D. Burdette, MD

Department of Medicine

Boonshoft School of Medicine

Wright State University

Dayton, Ohio

References

1. Andreoli TE, Carpenter CCJ, Griggs RC, et al. Cecil Essentials of Medicine. 6th ed. Philadelphia, WB Saunders, 2004, pp 871-877.

2. Spelman D, Sexton DJ. Complications of infective endocarditis. UpToDate 2005.

3. Tartaria M, Dicker RA, Melcher M, et al. Spontaneous splenic rupture: the masquerade of minor trauma. J Trauma 2005;59:1228-1230.

4. Ting W, Silverman NA, Arzouman DA, et al. Splenic septic emboli in endocarditis. Circulation 1990;82:IV105-109.