• Clinical science

Acute pancreatitis

Summary

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by biliary tract disease or alcohol abuse. Damage to the pancreas causes local release of digestive proteolytic enzymes that autodigest pancreatic tissue. Acute pancreatitis usually presents with epigastric pain radiating to the back, nausea and vomiting, and epigastric tenderness on palpation. The diagnosis is made based on the clinical presentation, elevated serum pancreatic enzymes, and findings on imaging (CT, MRI, ultrasound) that suggest acute pancreatitis. Treatment is mostly supportive and includes bowel rest, fluid resuscitation, and pain medication. Enteral feeding is usually quickly resumed once the pain and inflammatory markers begin to subside. Interventional procedures may be indicated for the treatment of underlying conditions, such as ERCP or cholecystectomy in gallstone pancreatitis. Localized complications of pancreatitis include necrosis, pancreatic pseudocysts, and abscesses. Systemic complications involve sepsis, ARDS, organ failure, and shock and are associated with a considerable rise in mortality.

Etiology

"I GET SMASHED": I = Idiopathic, G = Gall stones, E = Ethanol, T = Trauma, S = Steroids, M = Mumps, A = Autoimmune, S = Scorpion poison, H = Hypercalcemia, Hypertriglyceridemia, E = ERCP, D = Drugs.

References:[1][2][3][4]

Pathophysiology

Sequence of events leading to pancreatitis:

  1. Intrapancreatic activation of pancreatic enzymes: secondary to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
  2. Enzymatic autodigestion of pancreatic parenchyma
  3. Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokinespancreatic inflammation (pancreatitis)

Sequelae of pancreatitis (depending on the severity of pancreatitis)

  1. Capillary leakage: Release of inflammatory cytokines and vascular injury by pancreatic enzymesvasodilation and increased vascular permeability → shift of fluid from the intravascular space into the interstitial space (third space loss) → hypotension, tachycardiadistributive shock
  2. Pancreatic necrosis: Uncorrected hypotension and third space loss → decreased organ perfusion → multiorgan dysfunction (mainly renal) and pancreatic necrosis
  3. Hypocalcemia: Lipase breaks down peripancreatic and mesenteric fat → release of free fatty acids that bind calcium → hypocalcemia

Disease progression

References:[5][6][7]

Clinical features

References:[1][8][9]

Diagnostics

Acute pancreatitis is diagnosed based on a typical clinical presentation, with abdominal pain radiating to the back, and either detection of highly elevated pancreatic enzymes or characteristic findings on imaging. Serum hematocrit is an easy test that should be conducted to help quickly predict disease severity.

Laboratory tests

Determining calcium values is very important: Hypercalcemia may cause pancreatitis, which may then, in turn, cause hypocalcemia!

Imaging

References:[1][8][5][9][10][11][12][13][14][15][16][17][18]

Treatment

General measures

Drug therapy

Procedures/surgery

The most important therapeutic measure is adequate fluid replacement (minimum of 3–4 liters of crystalloids per day)!

"PANCREAS" - Perfusion (fluid replacement), Analgesia, Nutrition, Clinical (observation), Radiology (imaging), ERC (endoscopic stone extraction), Antibiotics, Surgery (surgical intervention, if necessary).

References:[19][20][21][22][23][24][25]

Complications

Localized

Systemic

References:[9][19][15][26]

We list the most important complications. The selection is not exhaustive.

Prognosis

Amylase and lipase, which are used for the diagnosis of pancreatitis, cannot be used to predict the prognosis!

References:[5][27][28][29][30]