20
Severe Infections in Asplenic Patients
in Critical Care
Mohammed S. Ahmed
Infectious Diseases Fellow, Southern Illinois University School of Medicine, Springfield, Illinois, U.S.A.Nancy Khardori
Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, Illinois, U.S.A.INTRODUCTION
The spleen is the largest lymphoid organ in the body, at a crossroads between arterial blood
supply and venous return. It acts as a mechanical filter for particulate antigens and
microorganisms. As a part of the immune system, the spleen is involved in production of
immune mediators like opsonins. A decrease in the level of factors responsible for
opsonization, such as properdin and tuftsin, occurs in splenectomized patients (1,2).
Complement levels are generally normal after splenectomy, but defective activation of
alternate pathway has been reported. In addition, neutrophil and natural killer cell function
and cytokine production are impaired (3). The ability of the spleen to remove encapsulated
bacteria is especially significant, because these organisms evade antibody and complement
binding (4). The antibody response to capsular polysaccharide (in encapsulated bacteria) in
normal adults consists of IgM and IgG 2. In patients with asplenia, IgM production is impaired,
recognition of carbohydrate antigens and removal of opsonized particles containing
encapsulated organisms are defective. There is no compensatory mechanism within the
immune system to overcome these defects in patients with asplenia or suboptimal splenic
function. Consequently asplenic and hyposplenic patients are susceptible to fulminant
infections, e.g., overwhelming postsplenectomy infections (OPSIs) (4,5).
An extensive review concluded that the incidence of sepsis in adult asplenics is equal to
that of the general population, but the mortality rate from sepsis is 58-fold higher (6). A meta-
analysis showed that incidence of sepsis after splenectomy done for hematologic disorders,
such as thalassemia, hereditary spherocytosis, congenitally acquired anemia, and lymphomas,
is as high as 25% (7,8). Most of the infectious complications (50% to 70%) occur within two
years of splenectomy (6–10). However the risk of overwhelming infection is lifelong, and
postsplenectomy sepsis has been reported more than 40 years after surgery (10–14).
The precise incidence of postsplenectomy infections remains controversial. In one
retrospective review of 5902 postsplenectomy patients studied between 1952 and 1987, the
incidence of infection was 4.4% in children<16 years and 0.9% in adults (7). A Danish study
found that the incidence of pneumococcal infection in splenectomized children decreased
dramatically following the introduction of the pneumococcal vaccine and the promotion of
early penicillin therapy (15). In another study the overall rate of first, second, and third severe
infections in postsplenectomy patients were reported as 7, 45, and 109 per 100 person-years
respectively. Second (42% to 76%) and third (61% to 84%) episodes of severe infections
occurred within 6 months after the first severe infection. The susceptibility to severe infection
was highest in older age groups (5.5 per 100 person-years in those aged >50 years) and in
patients splenectomized for hematologic malignancy (9.2 per 100 person-years). Between 50%
and 80% of all severe infections or deaths occurred within one to three years after splenectomy;
males had a shorter survival compared with females after splenectomy (16).
MECHANISM OF SEPSIS SYNDROME
In brief, endotoxins released from the breakdown of lipopolysaccharides in the bacterial cell
wall initiate the cytokine cascade leading to sepsis syndrome. The host macrophages, plasma
cells, endothelial cells, and neutrophils produce reactive products such as tumor necrosis