• Clinical science

Acute pancreatitis

Abstract

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

  • Tests to confirm clinical diagnosis
    • ↑ Serum pancreatic enzymes
      • Lipase: if ≥ 3 x the upper reference range → highly indicative of acute pancreatitis
      • Amylase (nonspecific )
      • The enzyme levels are not directly proportional to severity or prognosis!
  • Tests to assess severity
    • Hematocrit (Hct)
      • Should be conducted at presentation as well as 12 and 24 hours after admissions
      • Hct (due to hemoconcentration) indicates third space fluid loss and inadequate fluid resuscitation
      • Hct indicates the rarer acute hemorrhagic pancreatitis
    • WBC count
    • Blood urea nitrogen
    • CRP and procalcitonin levels
    • ALT
  • Tests to determine etiology

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

Imaging

  • Ultrasound (most useful initial test): indicated in all patients with acute pancreatitis
    • Main purpose: detection of gallstones and/or dilatation of the biliary tract (indicating biliary origin)
    • Signs of pancreatitis
  • CT scan: not routinely indicated
    • Indications
      • At admission: only when the diagnosis is in doubt (e.g., not very highly elevated pancreatic enzymes, non-specific symptoms)
      • > 72 hours of symptom onset: if complications such as necrotizing pancreatitis or pancreatic abscess (e.g., persistent fever and leukocytosis, no clinical improvement or evidence of organ failure > 72 hours of therapy) are suspected
    • Findings
      • Enlargement of the pancreatic parenchyma with edema; indistinct pancreatic margins with surrounding fat stranding
      • Necrotizing pancreatitis: lack of parenchymal enhancement or presence of air in the pancreatic tissue
      • Pancreatic abscess: circumscribed fluid collection
  • MRCP and ERCP
    • Indications: suspected biliary or pancreatic duct obstructions
    • MRCP is noninvasive but less sensitive than ERCP
    • ERCP can be combined with sphincterotomy and stone extraction; but may worsen pancreatitis.
  • Conventional x-ray
    • Sentinel loop sign: dilatation of a loop of small intestine in the upper abdomen (duodenum/jejunum)
    • Colon cut off sign: gaseous distention of the ascending and transverse colon that abruptly terminates at the splenic flexure
    • Evidence of possible complications: pleural effusions, pancreatic calcium stones; helps rule out intestinal perforation with free air

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

Treatment

General measures

  • Admission to hospital and assessment of disease severity (consider ICU admission)
  • Fluid resuscitation: aggressive hydration with crystalloids (e.g., lactated Ringer's solution , normal saline)
  • Analgesia: IV opioids (e.g., fentanyl)
  • Bowel rest (NPO)and IV fluids are recommended until the pain subsides
  • Nasogastric tube insertion: not routinely recommended; indicated in patients with vomiting and/or significant abdominal distention
  • Nutrition
    • Begin enteral feeding (oral/nasogastric/nasojejunal) as soon as the pain subsides
    • Total parenteral nutrition: only in patients who cannot tolerate enteral feeds (e.g., those with persistent ileus and abdominal pain)
    • Jejunal feeding tube in severe forms with prolonged hospitalization

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!

  • Numerous scoring systems exist (e.g, Ranson criteria) for assessing the severity and predicting the prognosis of acute pancreatitis
    • Ranson criteria : consists of 11 parameters (five factors are assessed at admission and the other six during the next 48 hours) that are used to create a prognostic score
      • Mortality increases with an increasing score
      • Parameters:
        • On admission
        • After 48 hours
          • Hematocrit by ≥ 10%
          • Blood urea nitrogen by ≥ 5 mg/dL despite fluids
          • ↓ Calcium < 8 mg/dL
          • ↓ pO2 < 60 mmHg
          • Sequestration of fluids > 6 L
          • Base deficit > 4 mmol/L or mEq

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