The most frequent mechanism of appearance is represented by the migration of a gallstone through a gallbladder–duodenal fistula (68%, 96,5% Japanese patients–8), but gallbladder–jejunal fistula, gallbladder–colonic fistula (5–25%–9,20), gallbladder–duodenal–colonic(2,5%), gallbladder–gastric (Clavien, Rodriguez Sanjuan, Glenn in [21
]), common billiary duct–duodenal, duodeno–left hepatic billiary duct [1
], have also been reported. The classic gallstone ileus is preceded by an acute cholecystitis episode, inflammation and gallbladder–bowel adhesions (usually at the level of the fundus of the gallbladder), which, associated with the ischemic effect and local pressure exercised by the gallstone, facilitates the creation of a bilio–enteral fistula (the decrease in the arterial, venous and lymphatic flow associated with the increase in the intravesicular pressure). Sometimes the cystic obstruction can be realized as well [16
]. The gallbladder becomes scleroatrophic, not functional in most cases.
The size of the gallstone plays an important part in the appearance of the bowel obstruction, the majority of the authors saying that gallstones of over 2,5 cm realize the bowel impaction (in the absence of a digestive pathology which can determine stenosis–spasm, adhesions, Crohn disease).
Usually, the gallstone impaction is realized in the terminal ileum (65%) and the ileocecal valve (the most narrow part of the small bowel, with lower peristaltic movement–[9
]). The potential reactive substances in the bile can interact with the epithelium cells of the bowel and can induce the impaction of the gallstone associated with lesions of the mucosa (Chipman in [8
The duodenal obstruction appears in rare cases (3–10%), being described by Bouveret in 1896; seldom, the gallstone can block the entrance of a Meckel diverticulum (Nakamoto–24
. Emparan), the sigmoid colon (Mastin–[6
]) or the appendix (Mehrotra in [11
]). The sigmoid colon is the most frequent location of the colon obstruction (due to the stenosis produced by diverticulitis), being described by Reisner [14
] in only 4% of the cases.
In rare occasions, the gallstone can create a fistula between the common billiary duct and the gastro–intestinal tract.
There have been cases of bowel obstruction caused by gallstones, without the intraoperatory finding of a bilio–enteral fistula [26
]. The explanation resides in the migration of a gallstone through the Vater papilla followed by the ‘in situ’ growth. This may happen in the event of a stenosis of the small bowel. Yoshida and co. published a case of gallstone ileus determined by the migration through the Vater papilla.
] Lindsey and Warner [28
] presented the gallstone ileus postcholecystectomy, the gallstone passing through the CBD (after sphyncterotomy) or from a duodenal diverticulum. Saedon [29
] presents a case that appeared after 24 years of postcholecystectomy, in a patient with jejuno–ileal diverticulosis.
] and Dittrich [30
] published two cases of bowel obstruction, which describe the migration of a gallstone through the jejunal wall after being lost intraoperatorily, due to a difficult laparoscopic cholecystectomy. These are the first cases produced by this mechanism. There is just one more case published, of a subocclusion resolved in a conservative manner (Wills –[31
]). Later, other authors presented cases produced by the same mechanism [32
]. Habib [33
] published a case of a gallstone ileus after 8 years of postcholecystectomy, as a result of a gallstone lost intraoperatorily, that migrated transepiplooicly, and eroded the apex of a Meckel diverticulum. Afterwards, the gallstone moved in the bowel determining obstruction. The gallstone was mobilized cranially and removed through the large base of the Meckel diverticulum.
The association of the Mirizzi syndrome with the cholecysto–enteric fistula was first suggested by Beltran [34
]. Subsequently, cases of gallstone ileus of type Ⅳ Mirizzi syndrome, associated with a cholecysto–colic fistula were cited in the medical literature.
Iatrogenous gallstone ileus can appear after ERCP with sphyncterotomy (Allen [16
]) and in the absence of the gallbladder.
Patients with a prolonged evolution of the Crohn disease present a particular risk of developing gallstones, because of the overall modification in the entero–hepatic circuit of the bile salts (secondary of terminal ileitis) and the solubility of the cholesterol [35
] especially after an ileum resection. The modified peristalsis and the high content of the bile in the bilirubine levels, also contribute to this.
The average size of an obstructive gallstone in patients with Crohn disease is lower than the ones in ‘classic’ described cases: 2.5 cm (1,5–3cm) opposed to 4,5 cm(2–9 cm). This can be explained by the enteral fibrous stenosis [5
Colonic gallstone ileus is the most frequent in the case of a stone passed through a gallbladder–colon fistula. The colonic gallstone ileus has also been described in a gallbladder–duodenal fistula (Moller 1913, Harris, McNamara and Dardinsky 1947, Buetow, Glaubitz and Crampton 1963 [13
]) or a CBD–duodenal fistula (Shore, Jacob and Cannon 1953). Holm-Nielsen and Linnet–Jepson think that it occurs when many small gallstones come together to form a bigger one, and Haffner, Semb and Aakhus describe the growth of the gallstone due to the accumulation of faeces around it, as a possible cause [13