The CBD is hard to see on the ultrasound because the common bile duct itself seems infiltrated, squeezing the lumen from the walls of the duct itself. There is no apparent obstruction, which would actually dilate the lumen. Are they discussing cholangiocarcinoma?

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Note added at 1 hr (2006-06-26 20:45:15 GMT)
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By obstruction, I mean an occlusion at the distal end of the CBD. The process may well result in bile obstruction, but by a different mechanism than that, of say, a stone in the CBD.

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Note added at 2 hrs (2006-06-26 22:06:23 GMT)
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OK, here is the translation:
The CBD is poorly visualized. It is not dilated, in fact it appears infiltrated, with the lumen virtually indistinguishable.

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Note added at 9 hrs (2006-06-27 05:05:08 GMT)
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Hi Wendy.
I am adding this information now because at the time I entered the answer I was in the midst of a busy office and I didn't have the time to properly address the questions.

The ultrasonographer is painting a classic picture for cholangiocarcinoma.

The first translation issue is that "choledochus" is virtually never called that in English. It is the "common bile duct". The second issue is that the picture is not one of obstruction as caused by the typical scenario - a gall stone stuck in the the CBD. That would cause the CBD to become dilated. Neither is it a "partial obstruction" as suggested by another contributor. Rather, the lumen of the CBD is obscured because the walls of the structure have become thckened (with cancer) to the point that virtually nothing is left of the lumen. These are not metastases or polyps blocking the lumen - that would produce a picture similar to a gall stone. It is a difffuse infiltration of the tube's wall which is responsible.

See: Pathophysiology of cholangiocarcinoma:

Pathophysiology: Cholangiocarcinoma is a tumor that arises from the intrahepatic or extrahepatic biliary epithelium. More than 90% are adenocarcinomas, and the remainder are squamous cell tumors. The etiology of most bile duct cancers remains undetermined. Long-standing inflammation, as with primary sclerosing cholangitis (PSC) or chronic parasitic infection, has been suggested to play a role by inducing hyperplasia, cellular proliferation, and, ultimately, malignant transformation. Cholangiocarcinomas tend to grow slowly and to infiltrate the walls of the ducts, dissecting along tissue planes. Local extension occurs into the liver, porta hepatis, and regional lymph nodes of the celiac and pancreaticoduodenal chains. Life-threatening infection (cholangitis) may occur that requires immediate antibiotic intervention and aggressive biliary drainage.

Thus it is seen that the radiologist is painting a picture for the clinician which is quite distinctive. Once it is understood what he is getting at, it is easy to translate.