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.