MD Notes

creation date: 2025-12-24 23:50
tags: Pathologies

Chronic Pancreatitis

Background

Definitions

Chronic pancreatitis is a progressive inflammatory disease involving fibrosis and loss of acinar and islet cells manifesting as impaired pancreatic function.

Etiology and Risk Factors

Chronic pancreatitis generally involves multiple underlying etiology. The mnemonic “TIGAR-O” describes the causes.

Toxic metabolic factors

  • Excessive drinking over long period of time or frequent binge drinking
  • Smoking (25% of attributable risk)
  • Hypertriglyceridemia (fasting/postprandial triglyceride ≥11 mmol/L to precipitate)
  • Diabetes mellitus
    Idiopathic
  • Early onset: likely genetic
  • Late onset: likely pancreatic calcification or endocrine/exocrine insufficiency
    Genetic
  • Mutations to PRSS1 trypsinogen gene
  • Others: SPINK1, chymotrypsin C, and more
    Autoimmune
  • Type 1: IgG4-related disease; associated with extrapancreatic conditions
  • Type 2: idiopathic duct centric pancreatitis (isolated to pancreas)
    Recurrent and sever acute pancreatitis
  • Repeated acute pancreatitis progress to chronic
  • Strongest risk factor for progression
    Obstructive
  • Tumour, scars, ductal stones, duodenal wall cysts
  • Produce inflammation upstream of obstruction

Pathogenesis

The exact mechanism of chronic pancreatitis depends somewhat on the underlying etiology, genetic background, and environmental exposures. However, there appears to be a common pathway involving initial injury followed by an attempt at healing through fibrosis and regeneration.

The initial insult may be due to toxic metabolites (eg. alcohol), upregulation of apoptotic genes, or direct activation of pancreatic stellate cells which produces fibrosis.

As the injury progresses, acinar, islet, and ductal tissue are lost. Impairment to exocrine and endocrine function can result in steatorrhea and diabetes (type 3c), respectively. Additionally, dysplasia and malignancy and develop from chronic inflammation.

It should be noted the exocrine function is loss before endocrine function.

Clinical Presentation

Signs & Symptoms

Abdominal pain

  • Epigastric pain radiating to the back
  • Worse when recumbent and postprandial
  • Nausea, vomiting, anorexia associated with pain
  • Pattern may shift from episodic to continuous
  • Associated with alcohol, tobacco, and young-onset idiopathic pancreatitis

Steatorrhea

  • Usually associated with long-standing chronic pancreatitis (>5 years)
  • May manifest as maldigestion once 90% of exocrine function lost

Asymptomatic patients

  • Small subset of patients may be diagnosed by incidental CT scan showing pancreatic calcifications

History & Physical Exam

Diagnosis

Criteria

Diagnosis of chronic pancreatitis is made through high-quality CT or MRI with MRCP.

CT findings
Sensitivity: 80-90%, specificity: 85%; increases with duration of disease

  • Atrophy of pancreas
  • Ductal dilatation
  • Multiple parenchymal and intraductal calcifications

MRI may allow for earlier diagnosis (drop in T1-weighted sequences) and better details of pancreatic duct.

Work-up

Initial labs
Serum lipase and amylase may elevate initially due to acute pancreatitis but with subsequent attacks, lipase and amylase may normalize. In advanced cases, low serum levels may be seen.

Other lab findings may suggest underlying etiology:

  • Elevated triglycerides
  • Elevated IgG4

Imaging
The standard for diagnosis is CT or MRI. Other imaging modalities include:

  • Plain radiograph (diffuse pancreatic calcification)
  • Abdominal ultrasound (echogenicity, atrophy, dilated pancreatic duct, ductal stones may be present)

If diagnosis is ambiguous following CT/MRI, an endoscopic ultrasound or pancreatic function test with secretin may be considered.

Differential

Chronic pancreatitis may be mimicked by conditions that cause ductal obstruction:

  • Pancreatic ductal adenocarcinoma
  • Intraductal paillary mucinous neoplasms
  • Cystic neoplasms

Red Flags / Complications

Complications include those of acute pancreatitis known as acute on chronic pancreatitis. Additionally:

Splenic vein thrombosis
Obstruction of splenic drainage due to pancreatic inflammation manifests as:

  • Gastric varices
  • Splenomegaly
  • Upper GI bleeding

Pancreatic insufficiency
Loss of exocrine function manifests as:

  • Steatorrhea
  • Fat-soluble vitamin deficiencies
    Loss of endocrine function manifests as:
  • Diabetes (type 3c)

Management

General Measures

Alcohol and tobacco cessation may delay the progression of chronic pancreatitis and reduce risk of subsequent pancreatic carcinoma (in cases of smoking). Some patients may experience pain relief.

Diet and supplements

  • Consume low-to-moderate fat meals high in protein
  • Small meals and avoid dehydration
  • Avoid very low fat diets due to increased risk of fat-soluble vitamin deficiencies
  • Supplementations of vitamin D and calcium
  • Specific nutritional supplementation as needed

Pain Management

Due to the complex mechanisms of pain, management have limited efficacy. The stepwise choices are as follows:

  1. NSASIDs and acetaminophen
  2. Lower potency opioids (eg. tramadol) with an adjunctive agent (TCAs, SSrI, SNRI, gabapentoids)

It should be noted that opioids can affect sphincter of Oddi function which may worsen pancreatitis.

Subsequent invasive therapies may be available if pharmacologic management is insufficient:

  • Celiac plexus block
  • Surgical resection
  • Drainage of pancreatic duct if dilated

Management of Pancreatic Insufficiency

Exocrine insufficiency is treated with pancreatic enzyme replacement. This consist of lipase taken with the first bite of a meal.

Endocrine insufficiency may manifest as type 2 diabetes or type 3c diabetes. Treatment consist of:

  • Metformin (may also lower risk of secondary pancreatic carcinoma)
  • Insulin if needed

Note that GLP-1 and DDP4is are avoided due to risk of acute pancreatitis.

References

Tools / Guidelines

Additional Reading