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Volume 44, Issue 11, Pages 2088-2091 (November 2009)


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Partial splenectomy prevents splenic sequestration crises in sickle cell disease

Laura R. Vicka, John R. Goscheb, Saleem IslamcCorresponding Author Informationemail address

Received 11 February 2009; received in revised form 27 May 2009; accepted 1 June 2009.

Abstract 

Purpose

Acute splenic sequestrations (SSs) are potentially fatal complications in sickle cell disease (SCD). Total splenectomies in young patients may predispose them to a higher risk of overwhelming infections, whereas partial splenectomy may maintain immunocompetence. We present our series of partial splenectomies in patients with multiple SS episodes.

Methods

We retrospectively reviewed the records of 6 patients who underwent open partial splenectomies for SS. Data on their clinical courses were collected and analyzed.

Results

None of the 6 patients had SS postprocedure, down from 2.1 ± 1.0 (P = .003) sequestrations per year and 3.5 ± 1.4 (P = .002) total sequestrations per patient. The transfusion requirements were significantly reduced postoperatively (10.2 ± 5.6 vs 2.0 ± 3.1 per year; P = .002). There was no increase in the infection-related hospital admissions during the period of follow-up (1.5 ± 1.8 vs 0.8 ± 0.8 per year after partial splenectomy; P = .363). The upper pole was preserved in all cases with blood supply off the main splenic artery.

Conclusions

Partial splenectomy decreases the risk of SS in SCD and reduces the need for blood transfusions. Infection rates did not increase after the procedure during the follow-up period. Partial splenectomy should be considered for patients who experience multiple acute SS crises or have long-term transfusion requirements.

a Division of Pediatric Surgery, Department of Surgery, University of Mississippi Medical Center, Jackson, MS 39216, USA

b Division of Pediatric Surgery, Department of Surgery, University of Nevada, Las Vegas, NV 89102, USA

c Division of Pediatric Surgery, Department of Surgery, University of Florida, Gainesville, FL, 32610, USA

Corresponding Author InformationCorresponding author. Tel.: +1 352 392 3718; fax: +1 352 392 9081.

PII: S0022-3468(09)00464-3

doi:10.1016/j.jpedsurg.2009.06.007


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