Now compare your patient's pancreas to the pancreas of the boy with hemolytic uremic syndrome from lab 2.

How would you characterize the differences?

Is there inflammation in the boy's pancreas? If so, why?

Could the changes seen in the boy's pancreas have occurred post-mortem?

If you would like to see a CT of the boy's abdomen. Click here.

The patient from lab 2 had HUS. In addition to the microthrombi found in the kidney, another complication of this disease is microthrombotic infarction of the pancreas leading to acute pancreatitis. There are many other causes of acute pancreatitis -- alcohol and gallstone being chief among them -- which be addressed next year. The common result of each is autolytic destruction (digestion) of the pancreas and surrounding fat, which induces an acute inflammatory response.

Although any tissue can undergo post-mortem autolysis, the pancreas, kidney, gallbladder, and intestines are the most frequently observed. Remember acute tubular necrosis from Lab 1? It can be very difficult to distinguish from post-mortem autolysis, unless you see an inflammatory response.