Acute and Chronic Pancreatitis¶
Chapter 359 | Part 10: Disorders of the Gastrointestinal System
KEY CLINICAL POINTS¶
- Acute pancreatitis is the most common gastrointestinal admission, with gallstones (70%) and alcohol (20%) as leading causes.
- The Revised Atlanta Criteria classify acute pancreatitis into interstitial, necrotizing, and fluid collections (pseudocysts, necrosis).
- Chronic pancreatitis is characterized by irreversible damage, with key features including abdominal pain, exocrine insufficiency, and diabetes.
- Management of acute pancreatitis prioritizes fluid resuscitation, nutritional support, and early intervention for complications like necrosis.
- Autoimmune pancreatitis (AIP) is a distinct entity with IgG4 elevation, lymphoplasmacytic infiltration, and response to steroids.
1. DEFINITION & OVERVIEW¶
Acute pancreatitis is an inflammatory condition of the pancreas, while chronic pancreatitis involves progressive, irreversible damage. Both are classified by severity and etiology. The Revised Atlanta Criteria define morphologic features on imaging.
Table 359-1: Causes of Acute Pancreatitis¶
| Common Causes | Uncommon Causes | Causes to Consider |
|---|---|---|
| Gallstones | Drugs (azathioprine, valproic acid) | Occult biliary disease |
| Heavy alcohol use | Connective tissue disorders | Hereditary pancreatitis |
| Severe hypertriglyceridemia | Pancreatic cancer | Cystic fibrosis |
| ERCP | Hypercalcemia | Idiopathic |
Table 359-2: Revised Atlanta Definitions¶
| Definition | CT Features |
|---|---|
| Interstitial Pancreatitis | Pancreatic parenchyma enhancement without necrosis |
| Necrotizing Pancreatitis | Lack of contrast enhancement with peripancreatic necrosis |
| Acute Pancreatic Fluid Collection | Homogeneous fluid without wall |
| Walled-Off Necrosis | Encapsulated necrosis with inflammatory wall |
1.1 Acute Pancreatitis¶
Defined by inflammation of the pancreatic parenchyma, often with systemic complications. Common causes include gallstones, alcohol, hypertriglyceridemia, and ERCP.
1.2 Chronic Pancreatitis¶
Characterized by fibrosis, calcification, and loss of exocrine/endocrine function. Etiologies include alcohol, hereditary factors, and autoimmune conditions.
2. EPIDEMIOLOGY¶
Acute pancreatitis affects ~300,000 annually in the U.S., with incidence 15–45/100,000. Chronic pancreatitis prevalence is 1–2/100,000. Risk factors include alcohol, gallstones, hypertriglyceridemia, and genetic predispositions.
2.1 Demographics¶
Age >60, obesity, and African American ethnicity correlate with higher incidence. Mortality ~1% for acute cases.
2.2 Risk Factors¶
Alcohol (15–30% of cases), gallstones (70%), hypertriglyceridemia (1–4%), and iatrogenic causes (ERCP).
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Pathogenesis involves premature activation of pancreatic enzymes, leading to autodigestion. Genetic factors (PRSS1, SPINK1, CFTR) and environmental triggers (alcohol, biliary obstruction) contribute.
Table 359-5: TIGAR-O Classification of Chronic Pancreatitis¶
| Category | Examples |
|---|---|
| Toxic-Metabolic | Alcohol, hypercalcemia, hypertriglyceridemia |
| Idiopathic | Early/late onset, tropical pancreatitis |
| Genetic | PRSS1, CFTR, SPINK1 mutations |
| Autoimmune | Type 1/2 AIP |
| Obstructive | Pancreas divisum, duct stones |
3.1 Acute Pancreatitis¶
Triggers include gallstones (70%), alcohol (20%), and hypertriglyceridemia. Inflammation leads to necrosis and systemic complications.
3.2 Chronic Pancreatitis¶
Progressive fibrosis from repeated injury. Genetic mutations (PRSS1, CFTR) and autoimmune mechanisms (AIP) are key drivers.
4. CLINICAL FEATURES¶
Acute presents with severe epigastric pain radiating to back, nausea, vomiting. Chronic features include persistent abdominal pain, steatorrhea, and diabetes.
4.1 Acute Pancreatitis¶
Epigastric pain, fever, leukocytosis. Complications: necrosis, pseudocysts, systemic inflammation (SIRS).
4.2 Chronic Pancreatitis¶
Persistent pain, exocrine insufficiency (steatorrhea), diabetes, and calcifications. May present with pseudocysts or biliary obstruction.
5. DIFFERENTIAL DIAGNOSIS¶
Acute: cholecystitis, perforated viscus, myocardial infarction. Chronic: peptic ulcer, gallstones, biliary disease.
5.1 Acute Pancreatitis¶
Differentiate from cholecystitis (ultrasound), myocardial infarction (ECG), and intestinal obstruction (CT).
5.2 Chronic Pancreatitis¶
Distinguish from IBS, peptic ulcer, and biliary disease using imaging and pancreatic function tests.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis requires two of: abdominal pain, elevated lipase/amylase, or imaging. Labs: elevated lipase (>3× ULN), hypocalcemia, and hyperglycemia.
Table 359-3: Severity Assessment¶
| Parameter | Criteria |
|---|---|
| SIRS | ‡2 of: temp, HR, RR, WBC |
| Hemoconcentration | Hematocrit >44% |
| BISAP Score | ‡3 (BUN, mental status, SIRS, age, pleural effusion) |
| APACHE II | ‡8 at 24h |
6.1 Laboratory Tests¶
Serum lipase/amylase, CBC, electrolytes, calcium, and CRP. Fecal elastase-1 for exocrine insufficiency.
6.2 Imaging¶
Abdominal ultrasound (initial), CT (for necrosis), MRCP (duct imaging), and EUS (for early detection).
7. MANAGEMENT & TREATMENT¶
Fluid resuscitation (lactated Ringer’s), NPO, analgesia, and monitoring. Complications require drainage, surgery, or endoscopic intervention.
Table 359-7: Complications of Chronic Pancreatitis¶
| Complication | Description |
|---|---|
| Exocrine Insufficiency | Steatorrhea, fat-soluble deficiencies |
| Diabetes Mellitus | Insulin deficiency, 80% prevalence |
| Complication | Description |
|---|---|
| Pseudocysts | Encapsulated fluid collections |
| Pancreatic Cancer | 4% risk in 20 years |
| Splanchnic Thrombosis | Varices, portal vein occlusion |
7.1 Acute Pancreatitis¶
Aggressive IV fluids, avoid ERCP unless needed. Nutritional support with enteral feeding. Antibiotics for infected necrosis.
7.2 Chronic Pancreatitis¶
Pancreatic enzyme replacement, pain management (opioids, gabapentin), and surgery for pseudocysts or strictures.
8. PROGNOSIS & COMPLICATIONS¶
Mortality 1–5% for acute; chronic leads to diabetes (80%), malnutrition, and pancreatic cancer (4% risk). Complications include SIRS, ARDS, and multiorgan failure.
8.1 Acute Complications¶
Necrosis, pseudocysts, sepsis, and systemic inflammation. Mortality increases with multiorgan failure.
8.2 Chronic Complications¶
Diabetes, exocrine insufficiency, calcifications, and increased cancer risk. Long-term morbidity and reduced quality of life.
9. SPECIAL CONSIDERATIONS¶
Autoimmune pancreatitis (AIP) with IgG4 elevation, hereditary pancreatitis (PRSS1), and pancreas divisum. Management varies by etiology.
9.1 Autoimmune Pancreatitis¶
Type 1 (IgG4-related) vs. Type 2 (duct-centric). Treated with steroids and immunosuppressants.
9.2 Hereditary Pancreatitis¶
PRSS1 mutations cause early-onset disease with high cancer risk. Genetic counseling recommended.
10. KEY POINTS & CLINICAL PEARLS¶
- Acute pancreatitis: fluid resuscitation is critical; avoid ERCP unless indicated. 2. Chronic pancreatitis: manage pain and exocrine insufficiency. 3. AIP responds to steroids; differentiate from other causes. 4. Genetic testing for PRSS1/CFTR in recurrent cases. 5. Monitor for complications like pseudocysts and cancer.