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“PHYSIOLOGIC” LEUKOCYTOSIS IS NOT PHYSIOLOGIC FOLLOWING NON-TRAUMA SPLENECTOMY
Kathleen S Romanowski, MD, Alaine Kamm, APN, Alex Bailey, BS, Kevin K Roggin, MD, Jeffery B Matthews, MD, University of Chicago

Background: According to classical teaching, splenectomy is associated with a postoperative increase in platelet count (PC) and white blood cell count (WBC). The “physiologic” leukocytosis (above 15 x 10/?L) following splenectomy is thought to complicate interpretation of the WBC as an indicator of early postoperative infection. In trauma patients, a persistently elevated WBC (above 15 x 10/?L) or a ratio of PC/WBC< 20, has been proposed as markers of infection. This concept has not been validated outside of the trauma population. We hypothesize that there is no “physiologic” leukocytosis following non-trauma splenectomy and that the PC/WBC ratio is not applicable to the non-trauma patient.

Methods: With approval by the Institutional Review Board, we completed a retrospective chart review of the clinical course of all patients who underwent non-trauma splenectomy from January 2000 to January 2009. As most of the included patients underwent splenectomy associated with distal pancreatectomy, patients who underwent distal pancreatectomy alone served a control group. All relevant clinical information was collected. PC, WBC, and PC/WBC ratios were collected and calculated daily until post-operative day 20. Infectious complications were defined using the 2008 CDC guidelines. ANOVA analysis of the data for statistical significance (p<0.05) was conducted with SPSS software.

Results: Chart review identified 183 eligible patients. Non-trauma, non-hematologic splenectomy was performed in 171 patients (splenectomy +/- other organ resection) while 12 patients underwent a spleen preserving distal pancreatectomy. Forty-eight patients (28.4%) had a total of 70 surgical infections (23 intra-abdominal abscess, 15 bacteremia, 12 UTI, 11 wound infection-superficial, 7 wound infection-deep and 2 pneumonia). In the absence of infection, there was no difference in the postoperative WBC for patients under going splenectomy or splenic preservation. In patients with a documented infection, a leukocytosis was significant when observed in POD 3-7 (p<0.05). Postoperative thrombocytosis (PC > 500) was evident in all patients who underwent splenectomy irregardless of their infection status. In patients who underwent spleen-preserving distal pancreatectomy, postoperative thrombocytosis developed only in patients with infection. PC/WBC ratio did not predict infection in non-trauma splenectomy patients on any post-operative day.

Conclusion: Postoperative elevation of WBC should raise suspicion of infection and not be attributed to a “physiologic” response to splenectomy. We found no evidence of non-infectious postoperative leukocytosis in non-trauma splenectomy patients. The post-splenectomy thrombocytotic response is not different between patients with or without infection, and the postoperative PC/WBC does not reliably predict infection in non-trauma splenectomy patients.


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