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Case Report |
1 Department of Radiology, National Naval Medical Center, 8901 Wisconsin Ave.,
Bethesda, MD 20889-5600.
2 Department of Radiology, F. Edward Hébert School of Medicine, Uniformed
Services University of the Health Sciences, Bethesda, MD 20814.
3 Radiology Imaging Associates, Ste. 250, 3900 S. Wadsworth Blvd., Lakewood, CO
80235.
Received October 16, 2002;
accepted after revision November 19, 2002.
Address correspondence to P. J. Pickhardt.
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A pelvic sonogram showed no evidence of ovarian torsion, adnexal lesions, or intraperitoneal pelvic fluid. Findings of contrast-enhanced abdominal multidetector CT performed primarily to evaluate for acute appendicitis showed soft-tissue fullness in the right adnexal region with ill-defined margins but no discernible cyst or mass (Fig. 1A). The appendix was normal. The CT scan also revealed right upper quadrant abnormalities, including diffuse gallbladder wall thickening, pericholecystic fluid, and segmental dynamic perfusion abnormality of the posterior right hepatic lobe (Figs. 1B and 1C). The geographic perfusion defect was transient because this segment became isoattenuating with the remainder of the hepatic parenchyma on delayed imaging. No space-occupying hepatic lesion or venous thrombosis was present to account for the transient hepatic attenuation difference. The portal vein showed normal enhancement without evidence of compromise. In conjunction with the findings of pericholecystic inflammation in the hepatorenal fossa, the dynamic perfusion abnormality was believed to be due to partial hepatic vein obstruction from the adjacent inflammatory process.
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Two weeks before the current visit, the patient had presented to the emergency department with isolated right lower quadrant abdominal pain and was given a provisional diagnosis of a symptomatic ovarian cyst. However, we discovered during the current visit that a cervical culture taken at the prior evaluation was positive for Chlamydia trachomatis, and the patient had not received antibiotic treatment. The findings of the gonococcal culture were negative.
By combining the CT findings and history of untreated pelvic inflammatory disease, a diagnosis of likely Fitz-Hugh–Curtis syndrome was made. The patient was admitted for IV antibiotic treatment and pain control and discharged 2 days later, taking oral antibiotics. She returned to the emergency department several days thereafter with recurrent right upper quadrant abdominal pain. She was evaluated by the general surgery department, given a provisional diagnosis of acute cholecystitis, and taken to the operating suite for laparoscopic cholecystectomy. Operative findings confirmed extensive pericholecystic inflammation in the hepatorenal fossa, compatible with Fitz-Hugh–Curtis syndrome. Cholecystectomy was made difficult by the inflammatory reaction and fibrotic-appearing adhesions in the gallbladder fossa. On pathologic examination, the degree of pericholecystic inflammation appeared out of proportion to any intrinsic gallbladder disease and further supported the diagnosis.
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Reports of cross-sectional imaging features in Fitz-Hugh–Curtis syndrome have largely focused on the anterior liver surface, corresponding to the classic surgical findings [3, 5, 6, 7]. Such findings include thickening and abnormal enhancement of the anterior liver capsule, with varying degrees of loculated perihepatic ascites and peritoneal septations. However, assuming intraperitoneal extension to be the primary mechanism for a spread of inflammation, we believe involvement in the hepatorenal fossa (Morison's pouch) is perhaps more likely, given its more dependent location in the supine position. In fact, one prior sonography study noted "increased width and echogenicity of the space between the liver and the kidney" in all nine cases of Fitz-Hugh–Curtis syndrome, yet incorrectly ascribed this finding to the anterior pararenal space of the retroperitoneum [4]. On CT, more confident differentiation between peritoneal and retroperitoneal spaces is possible.
Given the relatively dependent positioning of the gallbladder under the liver, we are surprised that peritoneal inflammation leading to secondary wall thickening seen on sonography and CT has not been previously reported in this syndrome. As in our patient, the clinical and imaging features can closely mimic typical acute cholecystitis, underscoring the importance of more detailed clinical correlation for untreated salpingitis. Although rare, Fitz-Hugh–Curtis syndrome should be added to the long list of causes for gallbladder wall thickening.
The peculiar CT finding of reversible perfusion defect in the posterior segment of the right hepatic lobe was believed to be due to partial hepatic venous outflow obstruction from the perihepatic inflammatory process. Transient hepatic attenuation differences are most often due to portal vein compression or occlusion, reflecting the underlying dual blood supply to the liver [8]. In this patient, however, the portal vein did not appear compromised. Less common causes include arterioportal shunting, steal phenomenon (siphoning) from hypervascular tumors, and local inflammation. Focal hepatitis is a less likely explanation for the right posterior defect because focal hepatitis would be expected to result in increased attenuation on the hepatic arterial phase and normal attenuation on the portal venous phase [8]. Right-sided heart failure and Budd-Chiari syndrome are the usual causes of hepatic vein out-flow obstruction and typically result in a global reticular or mosaic appearance. This patient could perhaps be considered to have a localized or limited Budd-Chiari phenomenon.
In summary, we describe the CT findings of gallbladder wall thickening, pericholecystic inflammation, and transient hepatic perfusion abnormality in a patient with Fitz-Hugh–Curtis syndrome. Intraperitoneal inflammation in the hepatorenal fossa likely accounted for these CT findings. Without knowledge of underlying salpingitis, the clinical presentation and imaging features of gallbladder wall thickening can mimic acute cholecystitis. In general, an imaging diagnosis of Fitz-Hugh–Curtis syndrome should be considered in any woman with findings suggestive of right upper quadrant peritonitis and pelvic inflammatory disease.
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