Neonatal sepsis presenting as a choledochal cyst

Shaoul, Ron; Sukhotnik, Igor; Toubi, Aurora

doi:10.1111/j.1651-2227.2007.00609.x

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…Sludge formation may also be associated with sepsis, parenteral nutrition, severe hemolytic diseases, metabolic disease, some drugs and pyloric stenosis. 13, 14, 15, 16, 17 We confirmed hypothyroidism in our patient after excluding other causes of sludge formation. Sludge disappeared after L-thyroxine treatment.…”

Section: Discussionsupporting

confidence: 72%

Neonatal Sludge: A finding of congenital hypothyroidism - Case Report

Kurtoğlu¹,

Çoban²,

Akın³

et al. 2009

Jcrpe

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Congenital hypothyroidism is one of the most urgent diseases of the neonate. When diagnosed and treated at an early stage, its most important complication, mental retardation, is preventable. The signs of congenital hypothyroidism are nonspecific in neonates. Only 5% of the cases have characteristic clinical findings. One of the most important and earliest signs is prolonged jaundice during the neonatal period. We report herein a case of congenital hypothyroidism, who presented with icterus accompanied with sludge formation into the gallbladder, which disappeared after treatment with L-thyroxine.Conflict of interest:None declared.

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Section: Discussionsupporting

confidence: 72%

Neonatal Sludge: A finding of congenital hypothyroidism - Case Report

Kurtoğlu¹,

Çoban²,

Akın³

et al. 2009

Jcrpe

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“…It is well known that gallbladder storage of a compound is influenced by the gallbladder motor functions that regulate gallbladder volume and its concentration capacity; therefore, in sepsis the concentration of a cytokine in the gallbladder bile is influenced by reduced hepatic bile secretion and impaired gallbladder motility (22). It is also influenced by possibly altered gallbladder mucosal concentration capacity.…”

Section: Discussionmentioning

confidence: 99%

Bile high-mobility group box 1 contributes to gut barrier dysfunction in experimental endotoxemia

Yang¹,

Kushima²,

Oksala³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Lipopolysaccharide (LPS) is an important factor in sepsis. LPS given by intraperitoneal injection induces intestinal hyperpermeability and bacterial translocation in animals and stimulates hepatic Kupffer cells to release TNF-alpha into the bile. This study aims to test the hypothesis that in response to LPS stimulation, hepatic Kupffer cells and extrahepatic macrophages release a large amount of the inflammatory cytokine high-mobility group box 1 (HMGB1) into the bile and that bile containing HMGB1 contributes to gut barrier dysfunction in experimental endotoxemia. To test this, rat common bile ducts were catheterized and bile flow rate was monitored before and during the LPS administration. Eight hours after LPS challenge, anti-HMGB1 neutralizing antibody or nonimmune (sham) IgG was injected into the duodenal lumen of endotoxemic rats; normal mice were also gavaged with normal or endotoxemic rat bile (bile collected from LPS-treated rats). We found that after LPS challenge, the bile flow rate in rats was significantly decreased at the 4- to 12-h time points, TNF-alpha concentration in the bile was markedly elevated at the 3- to 4-h time points, and bile HMGB1 levels were significantly increased at the 8- to 12-h time points. Duodenal injection with anti-HMGB1 antibody reversed LPS-induced gut barrier dysfunction in rats. In addition, feeding endotoxemic rat bile to normal mice significantly increased both mucosal permeability and bacterial translocation. The increase in permeability and bacterial translocation was reversible following removal of HMGB1 from the endotoxemic rat bile. These findings document that bile HMGB1 mediates gut barrier dysfunction in experimental endotoxemia.

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“…This case highlights the challenge in management of asymptomatic patients with progressive CC growth. Indolent growth without any overt symptoms may mask the potential severity of the disease and patients may present in extremis [ 10 ] . Liver dysfunction is not always apparent and requires laboratory confirmation [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Prenatal diagnosis of rapidly enlarging choledochal cyst with gastric outlet obstruction

Scalise

Yang

Neumeyer

et al. 2021

Journal of Surgical Case Reports

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Choledochal cysts are congenital malformations of the biliary tract that involve aberrant configurations of the pancreaticobiliary ductal system. The pathology exists on a spectrum from fusiform dilation of the common bile duct to multiple dilations involving the intra- and extrahepatic bile ducts with potential risks of malignant transformation and hepatic fibrosis. Advancements in ultrasound technology have increased the incidence of prenatal diagnosis of choledochal cysts. Here, we present the case of a prenatally diagnosed initially asymptomatic Type I choledochal cyst with rapid progression in the neonatal period to a complete gastric outlet obstruction within the first month of life. We demonstrate the feasibility of cyst resection and reconstruction with Roux-en-Y hepaticojejunostomy in the neonatal age group. Finally, we discuss management of the case based on evolving imaging findings and laboratory evidence of impending liver dysfunction.

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Neonatal sepsis presenting as a choledochal cyst

Abstract: we suggest that in any case of sepsis presenting as a choledochal cyst, it is essential to repeat the ultrasound after complete recovery before a surgery is planned.

Cited by 5 publications

References 25 publications

Neonatal Sludge: A finding of congenital hypothyroidism - Case Report

Neonatal Sludge: A finding of congenital hypothyroidism - Case Report

Bile high-mobility group box 1 contributes to gut barrier dysfunction in experimental endotoxemia

Prenatal diagnosis of rapidly enlarging choledochal cyst with gastric outlet obstruction

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