EMBRYOLOGIC DEVELOPMENT OF THE GALLBLADDER
The hepatic rudiment appears at approximately day 18 of gestation in the human embryo. By day 25, it can be recognized as an endodermal diverticulum, which projects into the mesenchymal septum transversum. By day 30, the hepatic diverticulum enlarges and divides into the pars hepatica cranially and the pars cystica caudally. The pars hepatica forms parenchymal liver components; the pars cystica differentiates into the gallbladder and cystic ducts (Figure 16.1). The gallbladder primordium is a solid structure that later in development becomes cystic, as found in the adult [1–3].
CONGENITAL ANOMALIES OF THE GALLBLADDER
A variety of structural anomalies of the gallbladder has been described (Table 16.1). Congenital absence of the gallbladder long has been recognized in humans; it was known to Aristotle. Overall, the incidence of agenesis of the gallbladder has been estimated at between 1 in 7500 and 1 in 10,000 among the general population [4, 5]. There are a number of mammalian species, including the horse, camel, deer, rat, and dolphin, lacking a gallbladder. Absence of the gallbladder may occur as an isolated anomaly or in association with other malformations. In the isolated form, absence of the gallbladder is of little clinical significance. It is believed to result from failed development of the pars cystica . Rarely, symptoms develop related to calculi formation in the biliary ductal system.
A number of anomalies have been described in association with congenital absence of the gallbladder.