Pancreatitis

1. Classification

Acute Pancreatitis (AP)

• Interstitial oedematous pancreatitis - proteolytic enzymes injure the acinar cell, causing oedema and swelling but not necrosis. This constitutes 70-80% of cases and is generally self-limiting.
• Necrotising pancreatitis - the inflammatory response is strong enough to induce cell apoptosis and fat necrosis, which spreads to the pancreatic parenchyma. Necrosis is the major determinant of morbidity and mortality.

• Mild - no organ failure, no local/systemic complications
• Moderately severe - transient organ failure (<48 hours) and/or local complications
• Severe - persistent organ failure (>48 hours), mortality ~29.5%

Chronic Pancreatitis (CP)

2. Etiology

Acute Pancreatitis

• Gallstone pancreatitis is caused by transient or sustained impaction of sludge or a stone within the common channel of the ampulla of Vater
• Hypertriglyceridemia should be considered the etiology when serum TG >1000 mg/dL with no cholelithiasis or significant alcohol use
• Pancreatic neoplasm must be considered on the differential in anyone >40 years
• Post-ERCP pancreatitis occurs in 5-10%, rising to >20% with risk factors (young age, suspected sphincter of Oddi dysfunction, failed/difficult cannulation, pancreatic guidewire placement, history of prior post-ERCP pancreatitis)
• Drugs known to cause AP include valproate, L-asparaginase, prednisone, 6-mercaptopurine, azathioprine
• Viral infections (enteroviruses, EBV, mumps, CMV, HIV-related)
• Genetic causes: SPINK1, CFTR, PRSS1 mutations - particularly relevant in recurrent and pediatric cases

Chronic Pancreatitis

3. Clinical Presentation

Acute Pancreatitis

• Epigastric pain - severe, constant, boring through to the back; partially relieved by leaning forward
• Nausea and vomiting
• Fever and tachycardia in more severe cases
• Abdominal tenderness - epigastric, may be diffuse in severe disease
• Classic signs in hemorrhagic/necrotizing pancreatitis:
  • Grey-Turner sign - flank ecchymosis
  • Cullen's sign - periumbilical ecchymosis
• Severe disease: hypotension, tachycardia, respiratory distress, altered mental status (signs of multi-organ failure)

Chronic Pancreatitis

• Recurrent attacks of epigastric pain, often relentless
• Steatorrhoea and malabsorption (exocrine insufficiency)
• Diabetes mellitus (endocrine insufficiency)
• Weight loss and nutritional deficiencies
• Complications: pseudocysts, biliary stricture, fistulae, mesenteric venous thrombosis, arterial pseudoaneurysm, pancreatic ascites

4. Diagnosis

Diagnostic Criteria

1. Abdominal pain strongly suggestive of acute pancreatitis
2. Serum amylase and/or lipase ≥3 times the upper limit of normal
3. Characteristic findings on abdominal imaging

• Clinically, ~40% of acute cases are recognized only at autopsy, underlining the importance of early diagnosis within 48 hours - Textbook of Family Medicine 9e, p. 1136

Laboratory Tests

• Serum lipase - preferred; sensitivity >90%, remains elevated up to 14 days
• Serum amylase - cleared within 48-72 hours; sensitivity falls to <30% by day 2-4
• Neither marker predicts disease severity
• CRP - useful marker for pancreatic necrosis (though limited specificity)
• LFTs, bilirubin, ALP - elevated with biliary obstruction/CBD stone
• BUN, creatinine - rising levels suggest hemoconcentration and third-spacing; fall in BUN with aggressive hydration is a treatment target
• Hematocrit - may be elevated due to fluid shifts (third-spacing)
• Serum triglycerides when metabolic cause is suspected

Imaging

• Recommended in all patients with AP to evaluate for gallstones/biliary cause
• May show diffuse gland swelling, reduced reflectivity, peripancreatic fluid
• Cannot reliably detect pancreatic necrosis

• Indicated when diagnosis is unclear, or when patient fails to improve in first 48-72 hours
• Best modality to assess presence and extent of pancreatic necrosis, peripancreatic collections
• CT Severity Index (CTSI) / Modified CTSI:

CT of acute pancreatitis - Grainger & Allison's Diagnostic Radiology

Severity Scoring Systems

5. Management

Acute Pancreatitis - General Principles

Fluid Resuscitation (most critical intervention)

• Aggressive IV hydration with isotonic crystalloid at 250-500 mL/hr in all patients unless cardiovascular or renal comorbidities exist
• Higher rates required in hypotension/tachycardia
• Most beneficial in the first 12-24 hours - may minimize or prevent pancreatic necrosis
• Target: decrease in BUN; correction of hemoconcentration
• Lactated Ringer's preferred over normal saline (anti-inflammatory properties)

Pain Management

• Adequate analgesia is essential (IV opioids commonly used)

Nutrition

• If severe (ICU-level SIRS, mechanical ventilation): nasogastric (NG) or nasojejunal (NJ) tube placed + EN initiated within 24-36 hours
• If mild/moderate (ward-level): oral diet offered as tolerated; EN only if oral diet fails to advance after 4 days
• Gastric vs. jejunal feeding: 3 RCTs showed no significant difference in tolerance or clinical outcomes in severe AP
• EN vs. parenteral nutrition (PN): EN significantly reduces:
  • Risk of infected peripancreatic necrosis (OR 0.28, 95% CI 0.15-0.51)
  • Single organ failure (OR 0.25, 95% CI 0.10-0.62)
  • Multi-organ failure (OR 0.41, 95% CI 0.27-0.63)
  • Risk of death (~2.5-fold reduction)
• Source: AGA technical review of 12 RCTs - Sleisenger & Fordtran's GI and Liver Disease, p. (nutrition chapter)

Antibiotics

• Not indicated routinely
• Indicated only for documented infection (e.g., infected pancreatic necrosis, cholangitis)
• Prophylactic antibiotics do not reduce mortality or infection rates in AP

Gallstone Pancreatitis

• ERCP within 24 hours if concurrent acute cholangitis
• ERCP not needed in most patients without evidence of ongoing biliary obstruction
• Without cholangitis/jaundice: use MRCP or EUS to screen for choledocholithiasis first
• Early laparoscopic cholecystectomy (within 3 days) in mild biliary pancreatitis improves outcomes and reduces need for subsequent ERCP
• Standard of care: early cholecystectomy after resolution

Local Complications

• Endoscopic drainage preferred for collections in close apposition to the gastric or duodenal wall (endoscopic cyst-gastrostomy or cyst-duodenostomy)

6. Chronic Pancreatitis Management

• Abstinence from alcohol (patients who continue drinking have more recurrent attacks)
• Pain management - often requires multimodal approach; selected patients may benefit from therapeutic ERCP or pancreatic surgery
• Pancreatic enzyme supplementation with each meal for exocrine insufficiency (malabsorption, steatorrhoea)
• Diabetes management - pancreatic (type 3c) diabetes requiring insulin
• Nutritional support - jejunal feeding used to improve weight and reduce pain; antioxidant supplementation (selenium, ascorbic acid, β-carotene, α-tocopherol, methionine) has shown benefit in some RCTs for pain relief
• ERCP for ductal strictures and stones; endoscopic pancreatic sphincterotomy
• Surgery: lateral pancreaticojejunostomy (Partington-Rochelle) or Whipple procedure for selected cases

• Pseudocyst, abscess
• Bile duct stricture
• Fistula (pancreatic-enteric, pancreaticoplural)
• Pancreatic ascites
• Mesenteric venous thrombosis
• Arterial pseudoaneurysm
• Increased risk of pancreatic adenocarcinoma

7. Prognosis

• Mild AP: >80% recover uneventfully; most cases resolve within 1 week
• Severe AP: mortality ~29.5% (mainly from respiratory or hemodynamic failure, or infected necrosis)
• ~40% of severe acute cases only recognized at autopsy, underscoring need for early clinical vigilance
• CP is progressive; eventual exocrine failure (malabsorption) and endocrine failure (diabetes) are common end points