Teaching Case

An elderly man with chronic obstructive pulmonary disease and ischemic cardiomyopathy was hospitalised in acute septic status (40°C body temperature) with dyspnoea, hypotension and oliguria. Vague abdominal tenderness was present. Laboratory disclosed anaemia, markedly raised WBC (90.000/mmc with 53% neutrophils and 32% monocytes) consistent with known haematologic disease; coagulation tests, platelets and fibrinogen within normal limits. Persistent negative results of multiple hemocultures were attributed to previous broad-spectrum antibiotic treatment.
Four years earlier he had been diagnosed with myelodysplastic syndrome (chronic myelomonocytic leukaemia) and was under oral treatment with hydroxiurea and prednisone.

Urgent abdominal CT disclosed, as the sole abnormality, splenomegaly with a large hypodense, mostly non-enhancing lesion with thin, slightly irregular margins and gas-fluid level, interpreted as abscess.
Echocardiogram excluded valvular endocarditic vegetations.
Bone marrow biopsy documented 30% blastic population consistent with acute leukemic transformation of chronic myelomonocytic leukaemia.
After transfusions and antibiotic therapy, splenectomy was performed. Pathology specimen was reported as a 2-kg spleen with large capsular discontinuity, subtotal infiltration of the red pulp by myeloid blasts (myeloperoxidase, CD68 and focally CD34-positive) consistent with progression of chronic myelomonocytic leukaemia, plus subcapsular necrotic – abscessual areas.
Despite intensive treatment, the patient did not recover postoperatively.

Infectious lesions involving the spleen are uncommonly encountered in clinical practice, and have been reported in less than 1% of autoptic studies. The majority of splenic abscesses (up to 75% of cases) result from haematogenous spread of infection, such as during endocarditis or septic conditions. Other predisposing factors include contiguous infections, intravenous drug abuse, immunodeficiency, steroids, chemotherapy, cancer, haematologic disorders, embolic disorders and trauma.
The usual clinical picture include fever, chills, upper quadrant pain and tenderness along with acute inflammation laboratory markers, but manifestations are often unspecific thus delaying diagnosis.
Splenic abscesses, unless promptly recognised and treated, are associated with a high mortality rate. Treatment consists in intensive antibiotic therapy and splenectomy.
Splenic abscess may be solitary or sometimes multiple, the latter more commonly found in immunocompromised patients and due to fungal infections such as Candida, Aspergillus and Cryptococcus.
Computed tomography (CT) represents the mainstay imaging modality for diagnosing splenic abscesses, since it is very sensitive although sometimes not specific. The typical CT appearance of a purulent splenic collection is that of a focal hypodense lesion (sometimes loculated with septations) with attenuation values ranging between 20 and 40 HU and absent internal enhancement; some peripheral “rim” enhancement may be observed but is less prominent than in liver abscesses. The spleen may be enlarged. The presence of gas, although uncommon, is considered diagnostic of splenic abscess.
Ultrasound, almost as sensitive as CT for assessing presence of splenic abnormalities, has limited specificity. Abscesses appear as hypo- or anechoic poorly defined lesions with irregular walls; high echogenicity with distal “dirty” shadowing corresponding to gas has been reported, but CT is by far more reliable in identifying even small amounts of gas; furthermore, at CT splenic infectious lesions typically appear more well-defined than with ultrasound.
In this uncommon case, emergency-setting CT allowed prompt detection and characterisation of splenic abscess as the disease underlying the patient’s critical condition, thanks to the pathognomonic finding of gaseous content. The patient’s medical history, the grossly trapezoidal shape of the lesion, and the pathologic report lead clinicians to speculate that this abscess was due to a splenic infarction with superimposed infection during bacteraemia. The disease proved fatal despite rapid diagnosis, surgery and intensive medical treatment.