Pediatr Blood Cancer 2006;47:740741

Post-Splenectomy Antibiotic ProphylaxisUnnished Story: To Treat or Not to Treat?

Chaim Kaplinsky,
MD
1

* and Zvi Spirer,

MD

Overwhelming infection in asplenic patients is a well documented occurrence in the literature. The introduction of immunization with polyvalent pneumococcal, Hemophilus Inuenza and meningococcal vaccines signicantly cut down the incidence of postsplenectomy sepsis and mortality. However, the issue of prophylactic antibiotic therapy in these patients remains inconclusive. There are contradictory reports bouncing between life-long treatment to no

treatment. There are also more exible approaches emerging from patient difculties complying with a prolonged therapy. This debate calls for developing a better predictive approach based on genetic proling of patients with different susceptibility to infectious pathogens, host-pathogens interactions as well as to identify the impact of factors such as age, on immunological competence. Pediatr Blood Cancer 2006;47:740741. 2006 Wiley-Liss, Inc.

Key words:

antibiotic prophylaxis; post-splenectomy sepsis; ITP

Prophylactic antibiotic treatment post-splenectomy was a practice used by most medical treating physicians. A systematic review of the literature revealed discrepancies among the different schools of thought and policy making. However, potentially life threatening infection is a major long-term risk in asplenic or hyposplenic patients. Published data suggest an incidence of overwhelming postsplenectomy infection varying from 0.18 to 0.42 cases/ 100 person years [1,2]. Most of these infections are caused by encapsulated organisms such as streptococcus pneumonia, Hemophilus Inuenzae and meningococci, but also by intraerythrocytic organisms [3,4]. The highest incidence of infection is mostly within the rst year post-splenectomy in children less than 5 years of age. Children under 2 years of age are especially susceptible to encapsulated bacteria because they have an inherently reduced ability to mount antibody response to polysaccharide antigens. The lower incidence of infection under 1 year of age in splenectomized infants is not completely understood. It is apparent that in elective splenectomy for hemoglobinopathies there is a higher risk for infection than in post-trauma splenectomy, possibly due to intra-abdominal residual splenic tissue leading to splenosis [5]. There are few reports on late onset infection in advanced age, even 40 years post-splenectomy, with most cases (60%) occurring 1030 years after splenectomy [6,7]. There is a consensus among the various guidelines regarding immunization prior to elective splenectomy and post-trauma. The British Committee for Standards in Hematology guideline update, based on Medline, BID Embase and Cochrane Library concluded that triple vaccination with Pneumoccocal, Hemophilus Inuenazae and meningococcal vaccines is essential [8]. However, data are insufcient regarding the actual decrease in infection rate and severity of morbidity. The role of antibiotic prophylaxis in these patients remains unsolved. Recommendations vary from treatment
2006 Wiley-Liss, Inc. DOI 10.1002/pbc.21014

to a need only basis to life-long prophylaxis [9]. Waghorn [10] recommend antibiotics for 25 years post-splenectomy for all splenectomized patients and at least 5 years for sickle cell disease patients [11,12]. The Working Party of the British Committee for Standards in Clinical Hematology Task Force recommends life-long prophylaxis in all cases, especially in the rst 2 years after splenectomy, for all children aged up to 16 years [13]. A more exible approach has been suggested for those patients who nd it too difcult to comply with a long-life regimen. The dilemma of performing splenectomy or using a nonsurgical, conservative therapy has been discussed at length and raises many questions. It seems that fewer discrepancies exist between clinicians in this respect. From a recent guideline [14] it has been concluded that the best preventive measure would be avoidance of splenectomy in most patients, especially children, when possible, and to use decision analysis in order to achieve a best management strategy. Better laboratory assessment of platelet function and vascular integrity, and a better clinical assessment of bleeding tendency may contribute to a physicians decision. As we do not yet know what is the minimal volume of splenic tissue required for maintenance of active bactericidal effect [15], it may be reasonable to consider minimal residual splenic tissue in elective splenectomy (articial splenosis). However, in post-trauma splenectomy, most probably residual microscopic splenic tissue is scattered in the splenic bed site and in the abdominal cavity [16].
1
Department of pediatric hematology oncology, Edmond and Lily Safra Childrens Hospital, Tel Hasomer, Israel; 2Department of pediatrics, Edmond and Lily Safra Childrens Hospital, Tel Hasomer, Israel *Correspondence to: Chaim Kaplinsky, The Chaim Sheba Medical Center, Sackler School of Medicine Tel Aviv University, Israel. E-mail: chaim.kaplinsky@sheba.health.gov.il Received 10 July 2006; Accepted 10 July 2006

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Several questions should be addressed: from where do these extreme variations stem? Why some investigators claim that prophylaxis for 2 years is as good as life long treatment? What is the physiological or immunological basis for either decision? Can we really assume that there is an age dependent immunological or a genetic prole that render some children extremely susceptible for sudden onset of post-splenectomy sepsis? Will future molecular array analysis and proteinomics help sorting out this issue? Scientists have long known that some people have a genetic predisposition to bacterial infection. The Human Genome Project, which recently completed a map of the entire human genome, increased our ability to locate specic genes related to infectious disease susceptibility. Ultimately, investigators hope to use genetic testing to identify people who are at increased risk of infectious diseases, then design drug therapies that target specic genetic defects that are expressed in conjunction with diseases [17,18]. Microarrays and single nucleotide polymorphic site analysis (SNPs) have been used to investigate the genetic polymorphism of pathogens, host-pathogen interactions and whole genome expression proles of pathogens. Microarrays have also been used to identify virulent genes that promote colonization and subsequently endanger the host, and identify the regulatory elements that control the expression of the network. In the last few years a large amount of data accumulated, suggesting that identication of individuals susceptible to specic pathogens is feasible and applicable in daily practice [19]. In an historical review, Imbach et al. [20] expressed their hope that decision making will shift from opinion-based to evidence-based clinical policies, but the up-to-date methodologies have not yet provided answers. REFERENCES
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Pediatr Blood Cancer DOI 10.1002/pbc