The incidence of acute pancreatitis is increasing in children. Imaging plays an important role in the diagnosis of acute pancreatitis because imaging findings can be used to establish the cause of acute pancreatitis, evaluate for complications of acute pancreatitis, and possibly predict the course of the disease.

Data were collected of children admitted with ALF to 16 US pediatric liver transplant centers from 2008 to 2013 using the PHIS for a retrospective analysis of PALF trends. Patient data linked to the principal diagnosis code for acute necrosis of the liver (570.00) were analyzed for the following: demographics, regional differences, changes over time, pharmaceutical trends, procedural trends, associated diagnoses, and patient outcomes. In 52.5% of 583 patients who met the selection criteria for PALF, the etiology remained undetermined. Acetaminophen toxicity (18.7%) was the most common identifiable etiology, and hepatic encephalopathy (38.6%) was the most common complication. Mortality was lower than previously reported; 95.4% survived and 73.2% survived without a liver transplant. Acute respiratory failure (OR = 3.4, p = 0.035), acute kidney injury (OR = 3.6, p = 0.003), and cerebral edema (OR = 3.6, p = 0.02) were independently associated with increased risk of mortality. The use of N-acetylcysteine in non-acetaminophen-related ALF, the use of intracranial pressure monitoring, and the proportion of sepsis decreased significantly during the study period. The PHIS database can be a useful tool to study the future trends of PALF patients.

Early recognition of this complication, prompt diagnosis with US of liver and timely treatment can lead to better outcome in newborns with hepatic collections secondary to inadvertent parenteral nutrition infusion via malposition of UVC.

All serious liver injuries alter metabolism and initiate hepatic regeneration. Recent studies using partial hepatectomy (PH) and other experimental models of liver regeneration implicate the metabolic response to hepatic insufficiency as an important source of signals that promote regeneration. Based on these considerations, the analyses reported here were undertaken to assess the impact of interrupting the hypoglycemic response to PH on liver regeneration in mice. A regimen of parenteral dextrose infusion that delays PH-induced hypoglycemia for 14 hours after surgery was identified, and the hepatic regenerative response to PH was compared between dextrose-treated and control mice. The results showed that regenerative recovery of the liver was postponed in dextrose-infused mice (versus vehicle control) by an interval of time comparable to the delay in onset of PH-induced hypoglycemia. The regulation of specific liver regeneration-promoting signals, including hepatic induction of cyclin D1 and S-phase kinase-associated protein 2 expression and suppression of peroxisome proliferator-activated receptor γ and p27 expression, was also disrupted by dextrose infusion. These data support the hypothesis that alterations in metabolism that occur in response to hepatic insufficiency promote liver regeneration, and they define specific pro- and antiregenerative molecular targets whose regenerative regulation is postponed when PH-induced hypoglycemia is delayed.

Background: While prior adult studies have shown that approximately 20%-38% of subjects undergoing solid-organ transplant develop neutropenia, similar analyses in pediatric subjects are scarce. Methods:We conducted a retrospective chart review of liver transplant (LT) and kidney transplant (KT) recipients at our center during the period 2008-2018. All of the KT and none of the LT subjects during this time period had induction with either anti-thymocyte globulin (ATG) or basiliximab at time of transplant. Neutropenia was defined as absolute neutrophil count (ANC) value ≤1000/mm 3 .Results: One hundred subjects with LT and 82 subjects with KT were included. The incidence of neutropenia within the first year of transplant in KT was higher compared to LT (54.8% vs 39%, p = .01). The median number of hospitalizations (p = .001) and infectious complications (p = .04) was significantly higher only in the KT subjects who developed neutropenia (compared to those who did not). Multivariate analysis identified factors associated with severity of liver disease at transplant, namely h/o upper gastrointestinal bleeding (p = .02), weight deficit (p = .01), and pre-LT ANC (p = .01), along with high or moderate risk cytomegalovirus status (p = .05) as predictors of neutropenia in LT subjects. Female gender (p = .03) predicted neutropenia, while BK virus infection was protective for neutropenia (p = .04) in KT subjects. Conclusions:The incidence of and morbidity associated with neutropenia within 1 year post-transplant is higher in KT subjects compared to LT subjects. The likely reason for this is the use of induction therapy (ATG, basiliximab) at the time of transplant in KT subjects.