DIAGNOSTIC DILEMMA

Aimee K. Zaas, MD, Section Editor

Unusual Enhancing Foci

Abhishek Agarwal, MD,a Meghana Bansal, MD,a Rebecca E. Martin, MDb
a

Department of Internal Medicine, bDivision of Infectious Diseases, University of Arkansas for Medical Sciences, Little Rock.

PRESENTATION
Pressure to treat can discourage physicians from carrying out the careful investigations needed for correct diagnosis. Here, we describe a case in which the correct diagnosis took several years, and became apparent only after a review of patient records revealed a decade-old surgical history of laparoscopic cholecystectomy performed for acute calculous cholecystitis. The patient, a hypertensive 78-year-old man, presented with fevers and increased abdominal pain 4 weeks after beginning chemotherapy for the presumed recurrence of a gastrointestinal stromal tumor. Three years previous to this presentation, he had undergone endoscopy during an evaluation for melena; the procedure had revealed a 1-cm submucosal abdominal mass that was identied by pathologic analysis as a low-grade gastrointestinal stromal tumor. The tumor had been removed by a partial gastrectomy without any further imaging studies, and because it was small and low-grade, with non-malignant surgical margins, no chemotherapy had been prescribed. The management plan had been to follow the patient by periodic abdominal imaging with computed tomography (CT). The rst follow-up CT, recorded 3 months after the gastrectomy, had revealed a soft-tissue density with some enhancing foci inferolateral to the right lobe of the liver and a right pleural effusion (Figure 1). These ndings were considered unusual for a recurrence of a gastrointestinal stromal tumor, which tends to recur locally. The pleural uid was exudative and contained 1600 white blood cells/L (21% neutrophils, 46% lymphocytes, and 23% macrophages), but cultures and cytology studies were negative for infection and malignancy. A tuberculin skin test was negative. A workup for malignancy, including upper
Funding: None. Conict of Interest: None. Authorship: All authors had access to the data and were involved in the conception and drafting of this article. Requests for reprints should be addressed to Abhishek Agarwal, MD, Division of General Internal Medicine, Department of Medicine, University of Arkansas for Medical Sciences, Slot 641, 4301 W. Markham Street, Little Rock, AR 72205. E-mail address: aagarwal@uams.edu

and lower gastrointestinal endoscopies, a bone scan, and serum analysis for tumor markers, was negative. Over the course of the next 3 years, follow-up CT scans had shown slow enlargement of the mass. Four weeks prior to the current visit, the patient had presented with subjective fevers, anorexia, and right upperquadrant abdominal pain of 3 months duration, as well as a gradual weight loss of 40 pounds over the preceding 2 years. He had no chest pain, cough, melena, hematochezia, or change in bowel habits. He used chewing tobacco and had family history (brother) of lung cancer. An abdominal CT scan during that visit had shown a further increase in the size of the mass. A positron emission tomography (PET) scan showed increased glucose uptake in the mass inferolateral to the right lobe of the liver, as well as in the ascending colon, bilateral hilar lymph nodes, and anterior abdominal wall, consistent with peritoneal metastases (Figure 2). Fine-needle aspiration cytology of the mass had shown only non-specic inammatory cells, but the night sweats, anorexia, weight loss, and slow tumor enlargement seemed to suggest a recurrence of the gastrointestinal stromal tumor, and imatinib chemotherapy had been initiated.

ASSESSMENT
On examination, the patient was febrile at 38.3C. He had a large (10-cm) palpable mass over the right anterior chest and abdominal wall and decreased air entry over the right lower-lung eld, prompting hospital admission. Pertinent laboratory results were as follows: hemoglobin, 12 mg/dL; white blood cell count, 13,000/L (82% neutrophils, 14% lymphocytes); serum bilirubin, 1.1 mg/dL; aspartate aminotransferase, 32 IU/L; and alkaline phosphatase, 170 IU/L. The CT scan showed marked enlargement of the mass with invasion of the anterolateral chest and abdominal wall (Figures 3 and 4). An attempt at ne-needle aspiration returned gross pus. Cytology on the uid was negative, but cultures grew Klebsiella pneumoniae. An examination of patients records from his cholecystectomy performed 10 years previously revealed that the gallbladder had ruptured during surgery, spilling bile and pigment stones into the abdominal cavity, and that the

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The American Journal of Medicine, Vol 125, No 1, January 2012

Figure 1 CT image showing a mass with 2 gallstones (arrow) inferolateral to the liver.

Figure 3 CT image showing enlargement of the abscess with an embedded gallstone (arrow).

gallbladder specimen had grown K. pneumonia. His most recent treating physicians had been unaware of this surgical complication. A review of the CT scans in light of the new information suggested that the enhancing foci within the mass might be gallstones (arrows in Figures 1 and 3).

DIAGNOSIS
The mass that had been followed as a suspect tumor for 3 years was diagnosed as an intra-abdominal bacterial abscess resulting from gallstone spillage during the patients laparoscopic cholecystectomy 10 years ago. Laparoscopic cho-

lecystectomy is associated with a fairly high rate of gallbladder perforation (5-40%), but the incidence of resultant complications is low (0.08-0.3%), and most patients remain asymptomatic.1,2 The length of time between gallstone spillage and the reported complications ranges widely, from a few days to as long as 20 years.3 Because the symptoms are nonspecic, mimicking several more common pathologies, the correct diagnosis is often delayed considerably. Abscesses, the most frequent complication of spilled gallstones, are often confused for a malignancy. They occur predominantly in the liver or hepatic area4 but also can occur at more distant sites, such as the abdomen and retro-

Figure 2 nodes.

PET-CT images showing glucose uptake in the liver, inferolateral to the liver, in the ascending colon, and in the hilar lymph

Agarwal et al

Abscess from Spilled Gallstones

33 was drained percutaneously, and the patient was treated for several months with ciprooxacin (for the Klebsiella) and metronidazole (for possible concomitant infection with anaerobes). He gained weight, the fevers resolved, and the abscess shrank signicantly. Even though imatinib is associated with low toxicity, its empiric use for treatment of a presumed gastrointestinal tumor is not the usual practice. A better approach would be to pursue open biopsy for mass lesions that remain suspicious for malignancy despite negative cytology. In our patient, imaging studies performed prior to the gastrectomy could have revealed the enhancing foci and prevented the subsequent misdiagnosis of a tumor recurrence. Radiologists and other physicians should be alert to the possibility of spilled gallstones in patients with a history of laparoscopic cholecystectomy, and a meticulous surgical history and access to operative reports are helpful in the diagnosis.

Figure 4 CT image showing invasion of the right chest and abdominal wall.

References
peritoneum. Cultures from these abscesses usually grow bacteria typically associated with acute cholecystitis, such as E. coli, Klebsiella, or Enterococcus species.2 Other reported complications include non-healing stulas and sinus formation,6 intestinal obstruction,7 appendicitis,8 incarcerated hernias,9 obstructive cholangitis,10 thoracic abscesses, and empyema.11 Pelvic migration of the stones can cause a granulomatous peritonitis mimicking endometriosis12 and sometimes resulting in dyspareunia and tenesmus. In one reported case, the spilled gallstones had been seeded with Staphylococcus aureus from a septic knee, resulting in recurrent episodes of staphylococcal bacteremia until the stones were identied and removed.13 Most pigment stones harbor bacterial microcolonies that produce stone-promoting -glucuronidase, slime, and phospholipase.14 In our patient, the pigmented stones and bile that spilled into the peritoneum during surgery were infected with K. pneumonia. The weakening of the host immunity by chemotherapy allowed the bacteria to multiply in an aggressive fashion, leading to a marked enlargement of the abscess and the eventual diagnosis. CT, magnetic resonance, and ultrasound imaging can play important roles in the radiologic diagnosis of these abscesses. In particular, CT scans can reveal calcications consistent with gallstones and can provide guidance in percutaneous drainage. However, the stones can be missed on imaging studies, as occurred for several years in this case.
5

MANAGEMENT
Spilled gallstones behave as a foreign body, and a failure to identify and remove them can lead to multiple surgeries that fail to resolve patient symptoms.3 If the stones are not retrieved for reason of high surgical risk or patient preference, prolonged antibiotic treatment may be needed. Our patient refused surgery to retrieve the stones. The abscess

1. Schafer M, Suter C, Klaiber C, et al. Spilled gallstones after laparoscopic cholecystectomy: a relevant problem? A retrospective analysis of 10,174 laparoscopic cholecystectomies. Surg Endosc. 1998;12:305309. 2. Horton M, Florence MG. Unusual abscess patterns following dropped gallstones during laparoscopic cholecystectomy. Am J Surg. 1998; 175(5):375-379. 3. Rothlin MA, Schob O, Schlumpf R, Largiader F. Stones spilled during cholecystectomy: a long-term liability for the patient. Surg Laparosc Endosc. 1997;7(5):432-434. 4. Van Brunt PH, Lanzafame RJ. Subhepatic inammatory mass after laparoscopic cholecystectomy: a delayed complication of spilled gallstones. Arch Surg. 1994;129(8):882-883. 5. Jacob H, Rubin KP, Cohen MC, et al. Gallstones in a retroperitoneal abscess: a late complication of perforation of the gallbladder. Dig Dis Sci. 1979;24 (12):964-966. 6. Pavlidis TE, Papaziogas BT, Koutelidakis IM, Papaziogas TB. Abdominal wall sinus due to impacting gallstone during laparoscopic cholecystectomy: an unusual complication. Surg Endos. 2002;16(2): 360. 7. Tekin A. Mechanical small bowel obstruction secondary to spilled stones. J Laparoendosc Adv Surg Tech A. 1998;8(3):157-159. 8. Yamamuro M, Okamoto B, Owens B. Unusual presentations of spilled gallstones. Surg Endosc. 2003;17:1498. 9. Bebawi M, Wassef S, Ramcharan A, Bapat K. Incarcerated indirect inguinal hernia: a complication of spilled gallstones. JSLS. 2000;4: 267-269. 10. Petit F, Vons C, Tahrat M, et al. Jaundice following laparoscopic cholecystectomy: an unusual complication of spilled stones. Surg Endosc. 1998;12(5):450-451. 11. Barnard SP, Pallister I, Hendrick DJ, et al. Cholelithoptysis and empyema formation after laparoscopic cholecystectomy. Ann Thorac Surg. 1995;60:1100-1102. 12. Merchant SH, Haghir S, Gordon GB. Granulomatous peritonitis after laparoscopic cholecystectomy mimicking pelvic endometriosis. Obstet Gynecol. 2000;96(5 Pt 2): 830-831. 13. Van Mierlo PJ, De Boer SY, Van Dissel JT, Arend SM. Recurrent staphylococcal bacteraemia and subhepatic abscess associated with gallstones spilled during laparoscopic cholecystectomy two years earlier. Neth J Med. 2002;60(4):177-180. 14. Stewart L, Ponce R, Oesterle AL, et al. Pigment gallstone pathogenesis: slime production by biliary bacteria is more important than -glucuronidase production. J Gastrointest Surg. 2000;4(5):547-553.