I was called to the ER to see a 28 YO male-insulin dependent diabetic- patient who presented with RUQ pain, chills and high fever. He gave a history of a laparoscopic cholecystectomy a year ago- elsewhere; during the year which followed he was admitted 7 times with RUQ pain and temperature, each episode responding to a short course of IV antibiotics; CT- guided percutaneous drainage of “something” was performed on 2 occasions.
On examination the patient was febrile; his RUQ was tender and guarding with percussion tenderness over the liver and right loin; the rest of the abdomen was innocent. White cell count was elevated; absence of clinical jaundice and normal LFT excluded more or less ascending cholangitis. We admitted him and started IV antibiotics. We went then to study his obese hospital chart- learning the following:
The lap chole was performed for “acute cholecystitits” and “multiple gallstones”. The pathology report- “acute cholecystitits- no stones submitted”. (the patient and family denies receiving any gallstones). On the subsequent re-admissions- CT was done -reporting an “effusion in the Morrison pouch (hepatorenal fossa) and a soft tissue phlegmon at that region. On all admissions the patient responded to a brief IV antibiotic course. A month ago, a PC drainage was performed, obtaining clear fluid which grew S.fecalis (?).
We CT scanned the patient again- some fluid in the Morrison pouch and a large, soft tissue density just below (the same as at the time of the previous PC drainage). Liver and bile ducts-normal. My initial diagnosis was “lost” or “dropped” gallstones-forming a chronic abscess. The radiologist did not know that gallstones may be “dropped” during 85. I booked the patient for a laparotomy pn Saturday morning- telling the PGY -IV to start writing another case report -level 5- paper.
We explored him through a 12 cm’ transverse RUQ incision; dissecting dense adhesions between the transverse colon and liver, the LC clips at the porta-hepatic were identified- nothing there. Nothing at the right gutter or on the kidney; the retroperitoneal overlying the duodenum-shining and healthy. The tissue plans exposed above the colon were hard and inflamed; we dissected the colon from above, exposing the base of the mesocolon- and found -stuck on the retroperitoneum just below the portal hepatis, a 2 X3 cm’ inflamed tip of a chronically perforated appendicitis – very long retrocolic APPENDIX. Appendectomy was uneventful.
So the acute cholecystitis was in fact perforated appendicitis “treated” with LC – the histological changes on the GB were caused by the nearby appendicitis. Further re-activation of the resulting- partially treated by antibiotics appendicular abscess- were again masked by more antibiotics.
Ten years ago all the above would have never occured- as during the open cholecystectomy for “acute cholecystitis ” the surgeon would have identified the real problem. And then there is the issue of over-reliance on modern imaging methods and non-invasive therapies.