 cellulitis, meningitis) for which ceftriaxone was started prior to peritoneal fluid collection.

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Conclusion
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Our study of ceftriaxone dosage for SBP yielded three core findings. First, there was a trend towards improved mortality with the 2 g dosage, however we did not detect a difference between the groups receiving either dose of ceftriaxone and the rate of in-hospital mortality or the rate of persistent renal injury. Second, a total ceftriaxone dose of 2 g daily over 1 g daily exhibited a non-significant reduction of intensive care utilization by cirrhotic patients with SBP, after adjusting for MELD score. Prospective studies in a larger cohort are indicated to explore the true significance of these results. While it could explain our results, whether the pharmacodynamics of intravenous ceftriaxone are such that the peritoneal drug concentration following a 1 g infusion results in slower control of infection is unclear from our study ^[@ref-19]^. Third, the number, duration and complexity of antibiotic regimens that cirrhotic patients experience is highly variable. The reasons for this finding are unclear and deserve further study in order to understand both the physician and patient factors that increase antibiotic regimen complexity as well as the effect on outcomes including mortality, morbidity and future infection with resistant organisms. Ultimately, we feel that the complexity of antibiotic regimens speaks to clinical uncertainty and the urgent need to improve the yield of ascitic cultures and tailor therapy for SBP with consideration of local microbiological data.

This study emphasizes the need for antibiotic stewardship and treatment standardization in the care of cirrhotic patients. We feel this can be easily achieved by computer programming. For centers that use electronic provider order entry, a preset dose of 2 g of ceftriaxone when prescribing for a diagnosis of SBP can ensure standardized and appropriate dosing. Beyond that, we have pro