In order to understand cholelithiasis, choledocholithiasis and gastroenterology in general, you have to master pancreatitis. You have to have a good understanding of the pathology and prognosis of pancreatitis.
The two most common reasons people get pancreatitis are gallstones and ETOH abuse.
As you know, amylase is not specific. It’s like a confirmatory test. When we think about confirmatory tests, we have amylase lipase. When we really want lipase, we do troponins and CKs. Why CKs? It’s a confirmatory test. When we really want troponin, we do H and H, hemoglobin and hematocrits, where you’re either one or the other.
I think in terms of hematocrit; that’s the way I was trained. Most people think in terms of hemoglobin. You convey both of them.
Amylase is a non-specific test. You can get a bump in the amylase from a sialolith, a salivary gland. Lipase is where the money’s at. The degree of lipase elevation does not correlate with severity of the disease. I recently had a gallstone pancreatitis with a lipase in the 25,000 range. That set a record for me. It doesn’t mean they’re sicker than a guy with a lipase of 5,000. It’s the opposite of troponins; higher troponins mean more hearth damage.
Mnemonic: Ranson’s Criteria
Ranson’s criteria is a score that helps you look for prognosis. How sick are these people? When will you admit them? Do they need to be in the intensive care unit? This mnemonic to help with Ranson’s criteria is derived from the fact that most people with pancreatitis present with gallstones or ETOH abuse.
GALL, as in gallstones.
- Glucose: Is their glucose greater than 200?
- Age: Are they older than 65?
- Leukocytosis: Do they have a white count greater than 16,000?
- Liver function tests (AST and LDH): Are their AST and LDH elevated?
If you have three or more of these criteria, the prognosis is much worse. The chance that the patient will die is up 30%. Use these criteria in your note; say that the patient has high-risk factors for a poor prognosis. I have never had a patient die of pancreatitis, but I’ve talked to colleagues who have experienced it, and they say it’s a miserable death.
ETOH, as in ETOH abuse.
- Electrolytes: Is calcium dropping? The pancreas forms soap crystals, and that’s why, in chronic pancreatitis patients, you can see a calcified pancreas on a plain film radiograph.
- Third spacing of fluid, which causes an increased BUN. Remember that fluid rests in three compartments in the body: intracellular, intravascular or extracellular (in between the two). It stays there due to hydrostatic or oncotic pressure. When we get pancreatitis, our cells can’t keep fluid where they’re supposed to and it weeps into the third space. You can tell when a patient has fluid in the third space because they have pitting edema and there will be a difference between how much fluid went in to the patient’s body and what came out. People who are third spacing are going to have a rising BUN with a ratio typically greater than 20.
- O2: O2 will drop. I don’t know the exact reasoning for this, but I feel it has to do with the permeability of membranes.
- Hematocrit: Hematocrit will drop as well. Again, I’m not exactly sure of the mechanism.
Pancreatitis is not infectious. If they have a fever with pancreatitis, that’s a sinister finding. To treat, let the pancreas rest, make them NPO and give them pain control. Give IV fluids and pain control, remembering there’s no Dilaudid vs morphine debate anymore.
It used to be Dilaudid was preferred over morphine. It’s been disproven that Dilaudid keeps the sphincter or OD more open than morphine. They first did these studies on cat models, and they looked at the biliary tree of cat models and realized that morphine doesn’t work as well as Dilaudid and morphine causes more constriction at the sphincter or OD. That study was reproduced in possums (their biliary tree is more human-like) and they found both cause a little bit of constriction, so you don’t have to choose one over the other.