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Possible Infectious Causes of Spontaneous Splenic Rupture

Possible Infectious Causes of Spontaneous Splenic Rupture

Case Presentation


A previously healthy 52-year-old Caucasian woman was rushed to the emergency department after experiencing sudden acute left-sided chest pain. The pain was rated as 9 out of 10 in intensity, radiating bilaterally to her shoulders as well as in a band-like pattern across her upper abdomen and into her flanks. There was no history of preceding trauma but there was history of recent upper respiratory tract infection symptoms including fever, chills, coryza, mild pharyngitis, non-productive cough and shortness of breath 3 weeks prior, that had mostly resolved a few days before presentation.

She is employed as a communications director. She visited a local animal adoption agency 5 weeks prior to her presentation and was bitten by a stray cat. She did not receive medical attention for this bite. She has no history of immune-compromising conditions, recent travels, past travels to Africa or sick contacts. She denies any high-risk sexual or social behaviors. She does not drink alcohol but has a 30-pack year smoking history. She had no personal or family history of leukemia, lymphoma, autoimmune diseases or coagulopathies.

While in the emergency department, she was found to be alert and orientated but in significant pain. She was afebrile, heart rate of 94 beats per minute and blood pressure of 98/45mmHg. She did not have any rashes or dermatological findings. No lymphadenopathy was found but significant abdominal discomfort on light palpation and hepatosplenomegaly were noted. No rigidity or guarding or peritoneal signs were elicited. There was no rebound tenderness. CT imaging showed hepatosplenomegaly (liver span: 19.4cm; spleen length: 14.5cm) with subcapsular hematoma in the spleen and hematoma in the left subphrenic perisplenic regions, consistent with grade III splenic rupture with associated mild abdominal and pelvic ascites (Figure 1). Her liver enzymes were as follows: aspartate aminotransferase 146U/L, alkaline phosphatase 67U/L, alanine aminotransferase 166U/L and total bilirubin 6.0μmol/L. Her hemoglobin was 102g/L, white blood cells 6.8 × 10 cells/L and platelets of 131 × 10 cells/L. A blood smear showed no atypical lymphocytes and the differential was otherwise normal. The rest of her routine biochemical investigations were unremarkable. She received immediate hemodynamic stabilization in the ICU and was followed closely by General Surgery. During this time, she received a full infectious diseases workup. She had negative blood cultures and negative serologies for viral hepatitis, human immunodeficiency virus, cytomegalovirus, parvovirus, toxoplasmosis, and syphilis. She had negative Legionella urinary antigen. Her Monospot test was negative, but Epstein–Barr virus (EBV) serology showed EBV viral-capsid antigen (VCA) immunoglobulin (Ig) G reactivity and early antigen (EA) IgG reactivity but Epstein–Barr virus nuclear antigen (EBNA) IgG and EBV VCA IgM non-reactivity. Finally her Bartonella serology showed IgG reactivity (titers 1:128). Her transthoracic echocardiogram was negative for signs of bacterial endocarditis. She remained hemodynamically stable in the ICU and was discharged without need for any surgical interventions. One week after discharge, she returned to the Infectious Disease clinic with ongoing complaints of fatigue and improving abdominal pain. She was started on a 2-week course of azithromycin and rifampin and improved symptomatically (decreased pain and improved energy) and biochemically (normalization of her liver enzymes) over a 2-week period. She was seen back in follow up 3 months later. She remained well clinically with normal liver enzymes. Repeat Bartonella serological titers remained at 1:128 with conversion of EBNA IgG to reactive.



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Figure 1.



Computed tomography images of atraumatic splenic rupture. Representative sagittal (left) and axial (right) computed tomography images of the patient's abdomen taken on the day she presented to the hospital. Grade 3 splenic injury (crescent-shaped subcapsular hematoma measuring up to 3cm in thickness along the lateral border of the spleen with lobulated regions of hemorrhage along the superior and medial border of the spleen and left subdiaphragmatic region, and linear densities in the spleen) and marked splenomegaly can be seen.







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