Gallstone ileus is a rare form of small bowel obstruction caused by an impaction of a gallstone within the lumen of the small intestine. Such a gallstone enters the bowel via a cholecysto-enteric fistula. The presence of large stones, >2.5 cm in diameter, within the gallbladder are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus. Once a fistula has formed, a stone may travel from the gallbladder into the bowel and become lodged almost anywhere along the gastrointestinal tract. Obstruction occurs most commonly at the near the distal ileum, within 60 cm proximally to the ileocecal valve. Rarely, gallstone ileus may recur if the underlying fistula is not treated.First described by Thomas Bartholin in 1654, the name "gallstone ileus" is a misnomer because an ileus is, by definition, a non-mechanical bowel motility failure  (as opposed to a mechanical obstruction by a stone). Diagnosis
Diagnosis of gallstone ileus requires radiographic studies. Classic radiographic findings are known as Riglers triad:
pneumobilia (air within the biliary tree)
evidence of small bowel obstruction
radiopaque gallstone on abdominal radiograph

Treatment
Initial management involves fluid resuscitation and potentially nasogastric suctioning. Since gallstone ileus constitutes a form of mechanical small bowel obstruction, it can be a surgical emergency and requires open or laparoscopic surgery to remove an impacted stone. The different strategies for surgical management are either enterolithotomy alone, allowing a delayed cholecystectomy after an inflammation-free period of 4–6 weeks (and therefore two-stage surgery) or enterolithotomy in combination with a cholecystectomy and fistula division (one-stage surgery).
Side effects
Sodium and water retention
Swelling due to fluid retention (edema)
High blood pressure (hypertension)
Headache
Low blood potassium level (hypokalemia)
Muscle weakness
Fatigue
Increased susceptibility to infection
Impaired wound healing
Increased sweating
Increased hair growth (hirsutism)
Thinning of skin and stretch marks
Disturbances of the gut such as indigestion (dyspepsia), distention of the abdomen and ulceration (peptic ulcer)
Decreased bone density and increased risk of fractures of the bones
Difficulty in sleeping (insomnia)
Depression
Weight gain
Raised blood sugar level
Changes to the menstrual cycle
Partial loss of vision due to opacity in the lens of the eye (cataracts)
Raised pressure in the eye (glaucoma)
Increased pressure in the skull (intracranial pressure)

Pharmacology
Fludrocortisone is a corticosteroid and acts as a powerful mineralocorticoid, along with some additional but comparatively very weak glucocorticoid activity. Relative to cortisol, it is said to have 10 times the glucocorticoid potency but 250 to 800 times the mineralocorticoid potency. Fludrocortisone acetate is a prodrug of fludrocortisone, which is the active form of the drug.Plasma renin, sodium, and potassium are checked through blood tests to verify that the correct dosage is reached. Chemistry
Fludrocortisone, also known as 9α-fluorocortisol (9α-fluorohydrocortisone) or as 9α-fluoro-11β,17α,21-trihydroxypregn-4-ene-3,20-dione, is a synthetic pregnane steroid and a halogenated derivative of cortisol (11β,17α,21-trihydroxypregn-4-ene-3,20-dione). Specifically, it is a modification of cortisol with a fluorine atom substituted in place of one hydrogen atom at the C9α position. Fluorine is a good bioisostere for hydrogen because it is similar in size, with the major difference being in its electronegativity. The acetate form of fludrocortisone, fludrocortisone acetate, is the C21 acetate ester of fludrocortisone, and is hydrolyzed into fludrocortisone in the body.