Acute and chronic pancreatitis

Overview

Acute pancreatitis is sudden inflammation of a previously normal pancreas that can return to normal. Most attacks are mild and settle in days, but about a quarter run a complicated course, and severe attacks with persistent organ failure carry a high mortality.

Chronic pancreatitis is continuing inflammation with permanent damage: fibrosis, duct strictures and calcification. It causes chronic pain and, later, failure of exocrine (steatorrhoea) and endocrine (diabetes) function.

Acute pancreatitis

Causes

Pathophysiology (brief)

• A trigger (a small stone at the ampulla, alcohol, high calcium) causes premature activation of trypsinogen to trypsin inside acinar cells.
• Trypsin activates other enzymes → autodigestion, local inflammation and fat necrosis.
• Inflammatory mediators cause SIRS, capillary leak and organ failure (lungs, kidneys, circulation).
• Lipase splits fat into fatty acids that bind calcium (saponification), which is why calcium falls.

Clinical features

• Severe, constant epigastric pain, rising to its peak within minutes, often radiating to the back (about half); relieved by leaning forward.
• Nausea and repeated vomiting.
• Tachycardia, fever, hypotension, tachypnoea; reduced bowel sounds (ileus); upper abdominal tenderness and guarding (rigidity is unusual).
• Jaundice or swinging fever in gallstone pancreatitis (cholangitis).
• Cullen sign (periumbilical bruising) and Grey Turner sign (flank bruising): from retroperitoneal haemorrhage in severe necrotising disease; neither is specific.
• Pleural effusion, ARDS, confusion.
• Tender red skin nodules from subcutaneous fat necrosis.

Diagnosis

Two of three: typical pain, serum amylase or lipase at least 3 times the upper limit of normal, and typical imaging (CT, MRI or ultrasound).

• Serum amylase: rises early and falls back over 3–5 days, so it may be normal in late presenters. The level does not reflect severity.
• Serum lipase: stays raised longer and is slightly more specific; preferred where available.
• Other causes of high amylase: perforated peptic ulcer, mesenteric infarction, bowel obstruction, ruptured ectopic pregnancy, DKA, salivary gland disease, renal failure, macroamylasaemia.

Investigations

• Bloods: FBC, urea and electrolytes, creatinine, glucose, calcium, liver tests, CRP, arterial blood gas, LDH, lipid profile; repeat at 24 and 48 hours for scoring.
• Ultrasound within 24 hours: look for gallstones and a dilated common bile duct.
• Erect chest X-ray: exclude gas under the diaphragm (perforation); shows effusion or ARDS. Abdominal X-ray: may show a sentinel loop (local ileus), colon cut-off sign, gallstones or calcification.
• Contrast-enhanced CT: not for every patient. Use it when the diagnosis is uncertain, in severe attacks (after about 72 hours, as earlier scans under-estimate necrosis), or when the patient deteriorates or a local complication is suspected.
• MRCP or endoscopic ultrasound: look for small stones in the bile duct and microlithiasis in "idiopathic" cases.

Assessing severity

Glasgow (Imrie) criteria (within 48 hours; 3 or more = severe):

Other tools:

• Ranson criteria (5 on admission, 6 at 48 hours; 3 or more = severe).
• APACHE II (can be used at 24 hours; obesity adds risk).
• CRP over 150 mg/L at 48 hours suggests severe disease.
• Revised Atlanta classification (2013):
  • Mild: neither organ failure nor any complication, local or systemic.
  • Moderately severe: organ failure that resolves within 48 hours and/or local complications.
  • Severe: persistent organ failure (over 48 hours), single or multiple. Organ failure is scored by the modified Marshall system (a score of 2 or more in respiratory, renal or cardiovascular systems).

Management

All patients

1. IV fluids: early, generous, goal-directed crystalloid (fluid leaks into tissues and bowel); monitor pulse, BP and urine output; avoid over-filling.
2. Analgesia: opioids are acceptable (patient-controlled if needed).
3. Oxygen with ABG monitoring.
4. Nutrition: eat when able; in severe attacks start early enteral feeding by nasogastric tube (nasojejunal if not tolerated). There is no benefit in "resting" the pancreas; parenteral nutrition carries more infection risk.
5. Antibiotics: not as routine prophylaxis in mild disease. Give them for cholangitis, infected necrosis, or another proven infection (a carbapenem penetrates necrosis well).
6. DVT prophylaxis (LMWH); NG tube only for persistent vomiting.
7. Severe attacks: HDU/ICU, organ support (ventilation, haemofiltration, vasopressors), discuss with a specialist pancreatic unit.

Gallstone pancreatitis

• Urgent ERCP with sphincterotomy and stone clearance if there is cholangitis or ongoing bile duct obstruction (Bailey: within 72 hours in severe gallstone pancreatitis).
• Cholecystectomy during the same admission in mild attacks (or once collections settle in severe ones) to prevent recurrence.

Complications

Kumar: deaths in the first week are from SIRS and organ failure; deaths after the first week are mostly from infected collections or bleeding.

Local collections

Pseudocyst

• Causes early satiety, fullness, a mass, persistently raised amylase.
• Complications: infection, rupture (peritonitis, GI bleeding), bleeding into the cyst (pseudoaneurysm), pressure on the stomach, duodenum or bile duct (jaundice).
• Larger (over 6 cm), older (over 12 weeks) and thick-walled cysts are less likely to resolve, but these alone are not reasons to drain.
• Drainage: endoscopic (EUS-guided) cystgastrostomy or surgical internal drainage (cystgastrostomy or cystjejunostomy). Simple percutaneous drainage to the skin tends to recur or form a fistula.
• Distinguish from a cystic neoplasm (cyst fluid CEA high in mucinous tumours).

Infected necrosis

• Suspect when fever, rising CRP and organ failure appear after the first week; gas bubbles in the collection on CT are suggestive; fine-needle aspiration can confirm.
• Mortality may reach about 50% (Bailey).
• Step-up approach: antibiotics, then percutaneous or endoscopic drainage, then minimally invasive or open necrosectomy if needed. Delay debridement until the collection is walled off (about 4 weeks) where possible.
• Sterile necrosis should not be drained.

Chronic pancreatitis

Causes

• Alcohol: the main cause (about 60–80% in developed countries), although only a small minority of heavy drinkers develop it; smoking adds risk.
• Tropical (idiopathic juvenile) pancreatitis: seen in South Asia; young patients, large ductal stones, early diabetes; malnutrition and genetic factors (e.g. SPINK1) implicated.
• Genetic: hereditary pancreatitis (PRSS1 cationic trypsinogen gain-of-function, autosomal dominant), SPINK1, CFTR (cystic fibrosis).
• Autoimmune pancreatitis: type 1 is part of IgG4-related disease (raised IgG4, older men, bile duct and other organs); type 2 is linked to IBD. Both respond to steroids.
• Obstruction: duct stricture after trauma or acute pancreatitis, tumour, pancreas divisum.
• Metabolic: hypercalcaemia, hypertriglyceridaemia. Recurrent acute pancreatitis. Idiopathic.

Clinical features

• Pain: epigastric, boring, radiating to the back, often worse after alcohol or fatty meals; episodic or constant; may lead to opioid dependence.
• Weight loss (fear of eating, malabsorption).
• Exocrine failure: steatorrhoea (pale, bulky, greasy, floating stools), mainly from lack of lipase; deficiency of fat-soluble vitamins.
• Endocrine failure: diabetes (about 30% in Kumar), usually late; often unstable because glucagon is lost as well, so hypoglycaemia is common.
• Jaundice (bile duct stricture in the fibrosed head).

Investigations

• Amylase and lipase are often normal (gland "burnt out").
• Imaging:
  • Plain abdominal X-ray: speckled calcification along the pancreas.
  • CT: best for calcification, atrophy, dilated duct, pseudocysts; also looks for cancer.
  • MRCP (with secretin): irregular, dilated and strictured main duct ("chain of lakes"), dilated side branches.
  • Endoscopic ultrasound: sensitive for early changes.
• Function tests: faecal elastase (low; unaffected by enzyme supplements); faecal fat; glucose and HbA1c.
• IgG4 if autoimmune pancreatitis is suspected.

Management

1. Stop alcohol and smoking: the single most important step for pain and progression.
2. Pain: stepwise analgesia, avoiding long-term strong opioids where possible; treat obstruction; coeliac plexus block for intractable pain; pain team input.
3. Pancreatic enzyme replacement (pancreatin capsules) with every meal and snack. Add a PPI or H2 blocker, because gastric acid inactivates lipase and pancreatic bicarbonate output is low.
4. Diet: a normal fat intake with adequate enzymes (very low-fat diets worsen malnutrition); medium-chain triglycerides in severe steatorrhoea (absorbed without lipase); replace vitamins A, D, E, K and B12.
5. Diabetes: usually needs insulin; beware hypoglycaemia.
6. Endoscopic therapy: stone removal, lithotripsy, duct stents, drainage of pseudocysts.
7. Surgery for intractable pain or complications: drainage of a dilated duct (side-to-side pancreaticojejunostomy) or resection of a diseased head (e.g. duodenum-preserving head resection or pancreaticoduodenectomy).
8. Steroids for autoimmune pancreatitis.

Complications

Pseudocyst, bile duct or duodenal obstruction, splenic vein thrombosis (isolated gastric varices), pancreatic ascites or pleural effusion, pancreatic cancer (higher risk, especially hereditary and in smokers), diabetes, malnutrition and osteoporosis.

Acute vs chronic at a glance

Quick revision

• Acute: gallstones 50–70%, alcohol about 25%; check calcium and triglycerides.
• Diagnosis: pain + amylase/lipase 3 times normal (or CT).
• Lipase lasts longer; erect CXR excludes perforation.
• Glasgow (PANCREAS) or Ranson 3 or more at 48 h = severe; CRP over 150 mg/L.
• Atlanta severe = organ failure over 48 h.
• Fluids, analgesia, oxygen, early NG feeding; no routine antibiotics.
• ERCP for cholangitis/obstruction; cholecystectomy in the same admission.
• Pseudocyst: 4 weeks or more, fibrous wall; drain only if symptomatic.
• Chronic: pain, steatorrhoea, diabetes, calcification; enzymes with meals plus PPI.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Bailey & Love's surgery textbook).

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