factor (TNF), interleukins (IL) 1,2,6, and 8, platelet-activating factor (PAF), endorphins, and
endothelial-derived relaxin factor. Other reactants in the cascade are arachidonic acid
metabolites, prostaglandins, cyclooxygenase lipoxygenase, complement C5a, leukotrienes,
bradykinins, and kinins. The bacterial products bind to CD14 molecules on leukocytes,
endothelial cells, and other cells leading to release of inflammatory mediators like
interleukins, TNF nitric oxide, leading to fever and production of acute-phase reactants.
Later during the course it causes vasodilatation and thrombosis with tissue injury. If the
cascade is not interrupted, it leads to DIC (disseminated intravascular coagulation), decreased
myocardial function, adult respiratory distress syndrome, acute renal failure, shock,
multiorgan failure, and ultimately death (17,18). Waterhouse–Friderichsen syndrome and
bilateral adrenal hemorrhage may be found at autopsy (19). The mechanism of sepsis
syndrome in asplenic patients is the same as in the general population. However, the course is
rapid and fulminant.
CAUSES OF ASPLENIA
There are various conditions that require surgical removal of spleen, but also there are
nonsurgical equivalents of splenectomy like congenital asplenia and functional hyposplenism,
i.e., anatomically present but poorly performing organ. Functional hyposplenism is associated
with various disorders. Although most severe infections are seen in splenectomized patients,
they may also occur in functional hyposplenism as well. Functional hyposplenism is associated
with the following:hematologic diseasessuch as sickle cell hemoglobinopathies, hemophilia;
neoplasmssuch as chronic myeloid leukemia, non-Hodgkin’s lymphoma, and following bone
marrow transplantation;gastrointestinal disorderssuch as Crohn’s disease, ulcerative colitis, and
Whipple’s disease, the degree of hyposplenism appears to be less in Crohn’s disease than
ulcerative colitis;autoimmune disorderssuch as chronic active hepatitis, rheumatoid arthritis,
Sjogren’s syndrome, and systemic lupus erythematosus;infiltrative diseasessuch as amyloidosis
and sarcoidosis. Alcoholism and splenic irradiation can also lead to hyposplenism (20).
Epidemiology
The significance of postsplenectomy infections is in its excessive morbidity and mortality
despite low incidence. The indications for splenectomy have been reevaluated and there is
more conservative approach to splenic resection. Overall numbers are decreasing as well as the
percentage of cases for particular indications. This has been the case primarily in two areas:
splenic trauma and hematologic malignancies. The growing awareness of potential long-term
complications continues to lead to more caution in the use of splenectomy with greater effort in
surgery to preserve some splenic tissue (21–26).
Microbiology
Infections in asplenic or hyposplenic patients can occur with any organism, be it bacteria,
virus, fungus, or protozoan. Acute and short-term complications in the perioperative period,
such as subphrenic abscess, are high when multiple other procedures are performed. The
etiology of these infections is primarily staphylococci and enteric gram-negative bacilli, not the
conventional bacteria involved in OPSIs. Delayed and long-term major risks include recurrent
bacterial infections with encapsulated bacteria (10). The three most common encapsulated
organisms that cause OPSIs areStreptococcus pneumoniae, Haemophilus influenzae,andNeisseria
meningitides(6,10).
Streptococcus pneumoniae
S. pneumoniaeis the most common organism involved in postsplenectomy sepsis, it is the
causative agent in 50% to 90% of cases (6,10). Age appears to be an important factor; the
percentage of pneumococcal OPSIs tends to increase with age (27). There is neither a
predominant pneumococcal capsular serotype nor anything to suggest that the distribution of
pneumococcal serotypes involved in OPSI is different than in the general population.
Severe Infections in Asplenic Patients in Critical Care 351