Acute pancreatitis K85.90

Acute pancreatitis is a sudden inflammation of the pancreas that is not primarily infectious.

Incidence: 10-20/100,000 inhabitants/year; in USA and Finland higher incidences; m>w;

Acute pancreatitis can have multiple causes:

Biliary tract diseases (approx. 55 %) such as choledochal stones, stenoses of the papilla Vateri

Alcohol abuse (about 35%)

Medications (about 10%) such as: beta blockers, diuretics, ACE inhibitors, methyldopa, estrogens, glucocorticosteroids, antibiotics - erythromycin, rifampicin, tetracyclines, antivirals, anticonvulsants, NSAIDs, melsalazine, ciclosporin, cytostatics and immunosuppressants (e.g. Imurek).

Other less common causes include:

Heredity: hereditary pancreatitis (rare, autosomal dominant inheritance with mutations in the trypsinogen gene PRSS1 and the SPINK1 gene); Note: both mutations can also lead to chronic pancreatitis.

Infections: Viral infections (mumps, AIDS, viral hepatitis)

Other:

• Duodenal diverticulum
• Hypertrigyceridemia
• Autoimmune pancreatitis
• worm infestation with ascarids in the bile ducts
• Pancreas divisum.

Prominent symptoms of acute pancreatitis are upper abdominal pain associated with an increase in pancreatic enzymes. Other symptoms include nausea and vomiting, meteorism, ascites, fever, hypotension, jaundice, facial flushing.

As follows is classified:

• Acute interstitial (edematous) pancreatitis, most common form with 85% (lethality = 0%).
• Acute necrotizing pancreatitis, with partial necrosis, 10-15% (lethality approx. 15%)
• Acute necrotizing pancreatitis, with total necrosis (lethality > 50%)

Less frequent are bluish periumbilical spots (Cullen's sign) or bluish spots in the flank area (Grey-Turner's sign).

To diagnose acute pancreatitis, a medical history, clinic, sonography and clarification of the lipase level are performed.

The following diseases must be diagnosed differentially: An acute abdomen, including ureteral and/or renal colic, biliary colic, perforations of the stomach, intestine and gall bladder, mechanical ileus, acute appendicitis, mesenteric ischemia, an incarcerated abdominal wall hernia. Other diseases are myocardial infarction, pulmonary embolism and aneurysm dissecans.

Acute pancreatitis can lead to bacterial infections, acute renal failure, circulatory shock, a pancreatic abscess, thrombosis and post-acute pancreatic pseudocysts.

Conservative therapy is carried out on an in-patient basis with close monitoring, parenteral volume, electrolyte and glucose substitution, thromboembolism prophylaxis, administration of analgesics and antibiotics as required, and treatment of any complications that arise.
The minimally invasive therapy removes choledochocytes, pancreatic pseudocytes and necroses and pancreatic abscesses. Surgical therapy is used after an unsuccessful application of minimally invasive therapy.

The first stage of pancreatitis is pancreatic edema or necrosis. This results in an increase in pancreatic enzymes, CRP and leucocytes. In the second stage they heal. In the third stage there is an inflammation of the necroses including sepsis and abscess with a renewed increase in CRP and leukocytes.

The course of acute pancreatitis is difficult to predict. However, it is important to have a close, in-patient control in order to be able to detect and treat necrotizing pancreatitis early enough.