At the Focal Point

occurs in association with other malformations, especially cerebrotendinous xanthomatosis and Opitz’s syndrome(hypertelorism-hypospadias), but also with trisomy 18, the Klippel-Feil syndrome (congenital fusion of cervical vertebrae), andwith congenital malformations caused by thalidomide. AGb has been attributed to abnormal development of the bloodvessels on each side of the gallbladder bud (sinus venosus, omphaloenteric, and umbilical veins). AGb is almost always afortuitous finding during abdominal surgery or at autopsy, but about 25% of patients with AGb will become symptomatic, withright upper abdominal pain, nausea or vomiting, and fatty food intolerance; 25% to 50% will have common bile duct (CBD)stones. The frequency of CBD stones in AGb is much greater than is seen after cholecystectomy (about 5%). So, remember thatAGb predisposes to calculus formation when you see a dilated, stone-containing CBD and no GB in a patient who cannot givea good history (and on whom you have neglected to perform a good physical examination!). There also may be a higherincidence of associated biliary dyskinesia. Diagnosis of AGb is difficult, and regardless of whether by hepatobiliary scintigra-phy, US, or ERCP, the diagnosis made is almost always cystic duct obstruction (because the GB is not seen) or a small contractedGB. However, because magnetic resonance cholangiography does not require contrast and is not compromised by biliarystasis, it may be the optimal diagnostic test. While there are no specific guidelines for management of AGb, conservativetreatment with smooth muscle relaxants has been recommended; sphincterotomy also has been reported in severe cases.AGb is a challenge for the surgeon because biliary or portal structures can be injured during the search for a GB that does notexist. The take-home message: remember AGb and don’t rush into the diagnosis of cystic duct or CBD obstruction if you seeCBD dilatation and gallstones, but no gallbladder. A quote about “absence” that I like is by Ouida (pseudonym of the Englishnovelist Maria Louise Ramé), who said, “The longest absence is less perilous to love than the terrible trials of incessantproximity.” At least without the GB you’ll never get cholecystitis.

Lawrence J. Brandt, MD

Associate Editor for Focal Points

Lipoma mimicking a perforation

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A 72-year-old man presented to our hospital for a screen-ing colonoscopy, during which a pedunculated, 4-cm polypwas found in the ascending colon (A). Before removing thepolyp by snare cautery, we secured an endoloop at its base.On removal of the polyp, there appeared to be an openingfrom which fat protruded (B). Multiple unsuccessful attemptswere made to close the defect with clips. The area wastattooed, and further attempts to close the defect wereaborted. The surgical team was then consulted because ofour high suspicion for perforation, and it was decided to takethe patient emergently to surgery. In surgery, the tattooedarea was located, and it was noted that there were no signs

the authors were sure there was a perforation, they probably tho

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attooed area (C), and a right hemicolectomy was performedD). The pathology specimen confirmed the presence of aubmucosal lipoma that focally involved the mucosa at theite of the polyp, thereby mimicking a perforation.

ISCLOSURE

All authors disclosed no financial relationships relevanto this publication.

ason Yip, MD, Moises Guelrud, MD, Adult Gastroenterology/epatology, Tufts Medical Center, Boston, Massachusetts, USA

of perforation. A 5 � 5 cm, rubbery mass was felt at the http://dx.doi.org/10.1016/j.gie.2012.07.023

CommentaryColon lipomas are uncommonly seen in clinical practice but nonetheless are easily diagnosed by their yellow color, smoothsurface, and soft, pliable nature; the endoscopic “pillow sign” (a surface indentation observed upon pushing the mass withclosed biopsy forceps) and the “naked fat sign” (fat prolapsing through the biopsy site) are two endoscopic signs characteristicof lipoma. Most colon lipomas are asymptomatic and found incidentally during colonoscopy, although lesions larger than 2cm may cause symptoms such as abdominal pain from obstruction or perforation and rectal bleeding from surface ulcerationor ischemic colitis associated with prolapse and intussusception. Fear of such occurrences has prompted endoscopists andsurgeons to remove the larger lesions, and I think this was reasonable in the present case. Endoscopic removal of large, sessileadenomas may be difficult to ensnare, because the snare wire tends to slip during closure. In addition, the low water contentof fat makes it a poor conductor of electrosurgical current, and the prolonged cautery required for cutting may result inthermal damage to deep tissues, with resultant perforation. In this case, the resection was done well, although the appearanceof the site was misinterpreted and led to unnecessary surgery. I am surprised that a CT scan was not done, although because

ught it not needed. Placing myself in the role of consulting

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surgeon who was one step removed from the authors’ emotional and personal investment in the patient’s iatric injury,however, I would like to think I would have found it strange that a patient with a diagnosed perforation did not have abdominalpain, tenderness, or signs of peritonitis. But, to be fair, it is neither productive nor helpful to be an “armchair quarterback.” Solet’s all learn from these authors’ observations, and when you see fat at the base of a lesion you just removed, consider thepossibility of the lesion being a lipoma and that nothing bad happened.

Lawrence J. Brandt, MDAssociate Editor for Focal Points

1250 GASTROINTESTINAL ENDOSCOPY Volume 76, No. 6 : 2012 www.giejournal.org