Discussion
Splenic abscesses are commonly caused by septic emboli from complications of infective endocarditis in about 5% of these patients, with the pathogens being streptococcus or staphylococcus[1]. It carries a very high mortality of greater than 70% if the diagnosis is missed, but with appropriate treatment the mortality can be reduced to less than 1% . With the availability of CT scan today the condition is rapidly diagnosed in addition to a potential treatment by aspiration [1-3]. The second common cause is a secondary infection of an infarcted spleen following trauma, interventional radiological embolization of splenic artery pseudoaneurysm complicating acute pancreatitis or a haemoglobinopathy such as sickle cell disease [1, 3, 5]. Other risk factors include immunocompromised states with 80% mortality, diabetes mellitus, illicit intravenous drug use in which splenic abscesses occur from a contiguous focus of infection. In these cases, the organisms commonly associated are polymicrobial (>50%), aerobes, anaerobes, fungi (usually candida) [1-4]. Salmonella typhosa has been a well- documented cause in the sickling disorders [6]. Splenic abscesses can also be associated with parasitic infection of the spleen and miscellaneous rare organisms such as Burkholderia . Mycobacterium andActinomycetes [3]. Spontaneous rupture has been reported in a number of conditions in which the spleen is enlarged which includes typhoid, malaria, leukaemia, Gaucher’s disease, and polycythemia. These may be restricted to a subcapsular haematoma or there may be rupture into the peritoneal cavity which would be suggested by the symptoms of shock, left upper quadrant guarding and tenderness, pain referred to the left shoulder, and clinical and radiological evidence of bleeding [7]. The common symptoms and signs of splenic abscess include the triad of fever, left upper quadrant tenderness and leukocytosis as seen in this case [1, 3, 7, 8]. Just as with splenic cysts the definitive treatment is splenectomy as most of the spleen is affected (fig 2) [9, 10]. In addition, pneumococcal, haemophilus influenza type b and meningococcal conjugate vaccinations against the life-time risk (0.1-0.5%) but 50% mortality from a subsequent OPSI is required [10]. Percutaneous drainage is less likely to be successful in patients with multilocular abscesses, ill-defined cavities with necrotic debris and thick viscous fluid. Mortality rates of greater than 50% is reported in patients managed with antibiotics only [1, 3]. Unfortunately, microbiological culture and sensitivity of a pus sample was not available to this patient which may have given a clue to its aetiology.