Objectives: The aim of the study was to validate and optimize a severity prediction model for acute pancreatitis (AP) and to examine blood urea nitrogen (BUN) level changes from admission as a severity predictor. Study Design: Patients from 2 hospitals were included for the validation model (Children’s Hospital of the King’s Daughters and Children’s National Hospital). Children’s Hospital of the King’s Daughters and Cincinnati Children’s Hospital Medical Center data were used for analysis of BUN at 24 to 48 hours. Results: The validation cohort included 73 patients; 22 (30%) with either severe or moderately severe AP, combined into the all severe AP (SAP) group. Patients with SAP had higher BUN ( P = 0.002) and lower albumin ( P = 0.005). Admission BUN was confirmed as a significant predictor ( P = 0.005) of SAP (area under the receiver operating characteristic [AUROC] 0.73, 95% confidence interval [CI] 0.60–0.86). Combining BUN ( P = 0.005) and albumin ( P = 0.004) resulted in better prediction for SAP (AUROC 0.83, 95% CI 0.72–0.94). A total of 176 AP patients were analyzed at 24–48 hours; 39 (22%) met criteria for SAP. Patients who developed SAP had a significantly higher BUN ( P < 0.001) after 24 hours. Elevated BUN levels within 24 to 48 hours were independently predictive of developing SAP (AUROC: 0.76, 95% CI: 0.66–0.85). Patients who developed SAP had a significantly smaller percentage decrease in BUN from admission to 24 to 48 hours ( P = 0.002). Conclusion: We externally validated the prior model with admission BUN levels and further optimized it by incorporating albumin. We also found that persistent elevation of BUN is associated with development of SAP. Our model can be used to risk stratify patients with AP on admission and again at 24 to 48 hours.

We describe the case of a 6-year-old boy who presented to a tertiary care emergency department after a motor vehicle accident with facial trauma and bradycardia. The patient was found to have an orbital floor fracture and inferior rectus muscle entrapment with resulting bradycardia secondary to the oculocardiac reflex. The oculocardiac reflex is an uncommon cause of bradycardia in the setting of trauma but should be considered because it can necessitate surgical intervention.

FV is primarily produced in the liver, and congenital FV deficiency is a disorder with an incidence of one in 1 million. Standard care is to treat severe bleeding phenotypes with FFP as there is no recombinant or plasma-derived FV concentrate. We present a case of a neonate with known severe FV deficiency diagnosed after prolonged bleeding after circumcision who represented at age 2 months with a large left intraparenchymal hemorrhage. His bleed was treated with FFP, platelet transfusion, recombinant VIIa, and emergent evacuation. He was maintained on plasma infusions but was unable to space his infusions beyond 48 hours. Liver transplantation was considered as a definitive treatment for this condition. While awaiting a suitable liver, his FV trough levels occasionally dropped below 5%, and he suffered from a second acute intracranial bleed. He received an orthotopic liver transplant at age 5 months, resulting in correction of his FV levels. He has not required any plasma infusions post-transplantation and has had no further bleeding episodes. Liver transplantation should be considered as definitive treatment early in the course for patients with severe FV deficiency and first time life-threatening bleed.

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