Background and Objecitves: Appendicitis is one of the most frequent surgical emergencies in pediatric surgery. Complicated appendicitis can evolve with appendicular peritonitis characterized by the diffusion of the pathological process to the peritoneal cavity, thus producing generalized or localized inflammation of the peritoneum. The capacity to anticipate the possibility of perforation in acute appendicitis can direct prompt management and lower morbidity. There is no specific symptom that could be used to anticipate complicated appendicitis, and diagnostic clues include a longer period of symptoms, diffuse peritoneal signs, high fever, elevated leukocytosis and CRP, hyponatremia, and high ESR. Imagistic methods, particularly US and CT, are useful but not sufficient. There are no traditional inflammation biomarkers able to predict the evolution of uncomplicated to complicated appendicitis alone, but the predictive capacity of novel biomarkers is being investigated. Materials and Methods: The present study represents a retrospective evaluation of children hospitalized between January 2021 and July 2022 in the Grigore Alexandrescu Clinical Emergency Hospital for Children with a diagnosis of acute appendicitis settled based on clinical characteristics, traditional and novel biomarkers, and ultrasonographic features. The children were subsequently grouped into two groups based on the existence of appendicular peritonitis on intraoperative inspection of the abdominal cavity. The aim of this report is to establish the predictors that may aid physicians in timely identifying pediatric patients diagnosed with acute appendicitis at risk for developing complicated appendicitis with evolution to appendicular peritonitis. Results: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte radio (PLR) are representative severity markers in infections. This report analyzes the benefit of these markers for distinguishing uncomplicated appendicitis from complicated appendicitis in pediatric patients. Conclusions: Our study suggests that a value of neutrophil-to-lymphocyte ratio greater than 8.39 is a reliable parameter to predict the evolution to appendicular peritonitis.

Background and Objectives: Choledocal cyst is a rare congenital disease of the biliary tree defined by dilatation of the extrahepatic and/or intrahepatic biliary ducts. Untreated, it leads to complications such as cholangitis, stone formation and malignant degeneration. The standard treatment for choledocal cyst is complete excision and subsequent biliary reconstruction via hepaticojejunostomy or hepatiocoduodenostomy. Materials and Methods: We report our experience with 16 pediatric cases of choledocal cyst over a 10-year period. Results: The predominant symptoms were nausea and jaundice, both at 62.5% (n = 10), followed by abdominal pain at 56.3% (n = 9). Ultrasonography was the diagnostic method used in all patients. Computed tomography was used in 75% (n = 12) and magnetic resonance imaging in 25% (n = 4) of cases. Age at the time of intervention ranged from 2 months to 17 years with a mean of 4 years and 5 months. The open approach was used in nine patients and the laparoscopic approach was used in seven patients, with one conversion to open surgery. Complete excision of the choledocal cyst was performed in 15 cases (93.7%), and partial excision with mucosectomy was performed in one case (6.2%). Eight patients (50%) underwent hepaticoduodenostomy and eight (50%) underwent hepaticojejunostomy, out of which one was attempted laparoscopically but was converted. We had a postoperative complication rate of 12.5% (n = 2) represented by anastomotic leak and pancreatitis. Conclusions: From our experience with these cases, we concluded that a wide hepaticoduodenostomy constitutes a favorable choice over the traditional hepaticojejunostomy, being more physiological and less time consuming.

Hypertriglyceridemia induced acute pancreatitis is a rare cause of pancreatitis in children. Hepatic lipase deficiency is an extremely rare cause of hypertriglyceridemia, reported in only a few families to date. Hepatic lipase is the enzyme involved in the hydrolysis of triglycerides and phospholipids in remnants of triglyceride-rich lipoproteins that have a role in the conversion of very low density lipoprotein remnants to low density lipoproteins. Hepatic lipase deficiency is inherited in an autosomal recessive pattern. Detection of heterozygous carriers of hepatic lipase mutations remains accidental at the population level, as affected persons with a heterozygous state of hepatic lipase mutation do not display specific lipoprotein abnormalities and also patients with complete hepatic lipase deficiency have inconstant phenotype. The proximal promoter of the LIPC gene consists of four polymorphic sites in complete linkage disequilibrium. Five missense mutations in encoding exons have been described and proved to be responsible for hepatic lipase deficiency to date: S267F, T383M, L334F, A174T, and R186H, affecting the activity and secretion of hepatic lipase. We identified a primary disorder of the lipid metabolism as the cause of the acute episode of pancreatitis in a four years old patient, consisting of hepatic lipase deficiency caused by a novel genetic variant of the LIPC gene, a gross deletion of the genomic region encompassing exon 1. This variant was not previously described in the literature in persons with LIPC-related disorders and its significance is currently uncertain, but in the presented clinical and paraclinical context, it has the characteristics of a pathological variant inducing a hepatic lipase deficiency phenotype.