Clinical Presentation of Pancreatitis (Necrotizing, Acute and Chronic) Flashcards
What are the 3 types of pancreatitis?
- acute, which can become:
- chronic -OR-
- necrotizing
How does acute pancreatitis present, clinically?
- epigastric pain= dull, boring, steady, usually suden onset, and gradually becomes a constant intense ache (pain improves when sitting forward).
- pain radiation to back
- nausea and vomiting
- diarrhea
What key histories should we seek on H&P, if suspicious of acute pancreatitis?
- PSHx (past surgical Hx) of recent operative or invasive procedures (especially ERCP) -OR-
- FMHx of hypertriglyceridemia -OR-
- PMHx of BILIARY DISEASE (those with gallstones), CHRONIC ALCOHOL ABUSE, cystic fibrosis, inflammatory bowel disease -OR-
- recent Hx of BINGE DRINKING, trauma, use of certain prescription meds (furosemide, sulfa drugs…).
Why can high triglyceride levels cause pancreatitis?
bc when they are transported on large chylomicrons, they can become wedged in the pancreatic capillaries, which will activate LIPASE, causing self-digestion of the pancreas.
What are the physical exam findings on H&P for acute pancreatitis (in order of likelihood)?
- FEVER (remember this is a marker of inflammation)
- abdominal tenderness/guarding
- TACHYCARDIA
- HYPOTENSION (due to pancreatic enzymes entering the blood causing damage to vascualr walls, allowing fluid to leak into the extravascular space).
- ABDOMINAL DISTENSION
- DECREASED OR ABSENT BOWEL SOUNDS
- PALLOR
- DIAPHORESIS
What causes abdominal distention in acute pancreatitis?
edema of Pancreas +/- gaseous distention of colon, secondary to narrowing of colonic splenic flexure from inflammation +/- sympathetically-induced ileus
What is a sentinel loop?
- sign seen on a radiograph that indicates localized ileus (painful obstruction) from nearby inflammation. Aka, it is the dilatation of a segment of small intestine, and an inability to move things forward.
What are some less likely findings you will find with acute pancreatitis?
- jaundice (due to possible blocking of bile duct).
- dyspnea (due to enzymes released into the blood stream affecting the lungs).
- hemodynamic instability
- hematemesis or melena
- Purtscher retinopathy= delivery of fat emboli with destroyed tissue of the pancreas to the retinal vessels causing loss of vission.
- muscle spasms of extremities= due to lowering of serum calcium levels. As lipase is digesting fats to 3 fatty acids and glycerol, the fatty acids are amphipathic, and will avidly bind calcium with one end bc it is charged. This is essentially soap!
What are some diagnostic tests for acute pancreatitis?
LABS are a must!
- amylase and lipase (bc they are made by the pancreas).
- alkaline phsphatase, AST, ALT, total bilirubin (to see if there is an effect on the liver).
- BUN, creatinine, and electrolytes (to see effects on kidney).
- glucose (bc pancreatic islet cells make insulin, and if these are affected, you will have hyperglycemia).
- cholesterol and triglycerides (bc if these are high it will make the situation worse)
- CBC (for WBC count; this is almost always elevated bc this is a marker for inflammation) and hematocrit (to show how volume depleted the patient is; if it is high then you have more RBCs relative to water, since you are losing plasma).
- CRP (marker for inflammation)
- +/- ABG (to see if lungs are effected)
LDH (shows anaerobic respiration) and bicarb (drops since we see a metabolic acidosis).
- +/- IgG4 (elevation will indicate autoimmune pancreatitis).
Is imaging necessary?
only if Dx in doubt
What are some imaging considerations?
- abdominal ultrasound= test of choice for suspected biliary disease; not a test to test “for” pancreatitis
- MRCP (Magnetic Resonance Cholangiopancreatography)= provides non-invasive image of biliary and pancreatic ducts; done if choledocholithisasis is suspected.
- Abdominal CT= ALWAYS done if disease is severe.
What are the 2 classifications of acute pancreatitis?
- Mild= interstitial edema + inflammatory infiltrate (admitted to med-surg floor, lower mortality).
- sever= sever inflammatory infiltrate, necrosis, +/- severe gland dysfunction, +/- multi-organ failure (admitted to ICU, higher mortality rate, complications).
How do we stage acute pancreatitis? (aka what is their risk for death)
- RANSON criteria= only able to provide assessment for 1st 48 hours, but easier; thresholds are only met with EtOH or gallstone induced pancreatitis.
- APACHE (acute physiology and chronic health evaluation) II= able to assess pt at any time of illness, but very cumbersome; provides a better mortality predictions, and is useful despite the cause of the pancreatitis.
*** What are the RANSON criteria? (She said to memorize)
On admission:
- Pt > 55
- WBC > 16,000
- Blood glucose > 200 gm/dL
- serum LDH >350 IU/L
- AST > 250 IU/L
Within 48 hours:
-Hct drops >10% (bc this could mean hemolysis of RBCs is occurring due to excessive pancreatic enzymes).
- BUN increases by 5 mg/dL
- serum Ca2+ 4 mEqu/L (this means metabolic acidosis).
- Estimated fluid sequestration > 6 L (fluid that is not in the vessels).
*You get one point for each of these that is met.
0-2= minimal mortality
3-4= 15% mortality rate
> 5 mortality rate > 40%
How does chronic pancreatitis present?
- epigastric pain= constant/chronic OR recurring severe attacks that last for hours.
- weight loss
- +/- diarrhea, steatorrhea (fatty stools)
- insulin-dependent DM (late)
