Pancreatitis

Pancreatitis management at Shree Hospitals is structured around five clinical steps that address the immediate emergency management of acute pancreatitis, aetiology identification, escalation of care for severe disease, intervention for complications, and long-term chronic pancreatitis management.

 

Acute pancreatitis is a disease where the decisions made in the first 24–48 hours - particularly the volume and rate of intravenous fluid resuscitation and the timing of enteral nutrition - determine whether a mild episode remains mild or deteriorates into severe disease with necrosis and multi-organ failure.

 

Step 1 - Initial Assessment and Severity Stratification

 

All patients presenting with acute-onset severe epigastric pain radiating to the back, with serum lipase or amylase above 3 times the upper limit of normal and supporting imaging, are assessed for acute pancreatitis.

 

Severity stratification at presentation predicts which patients need ICU-level care and which can be managed on a general ward. The BISAP score (Blood urea nitrogen, Impaired mental status, SIRS, Age above 60, Pleural effusion) provides rapid bedside severity assessment.

 

CT severity index (Balthazar score on contrast-enhanced CT) quantifies pancreatic necrosis and peripancreatic inflammation at 48–72 hours from onset - the optimal timing for CT because early CT underestimates necrosis.

 

Organ failure - respiratory (PaO₂/FiO₂ below 300), renal (creatinine above 177 µmol/L), or cardiovascular (systolic BP below 90 despite fluid resuscitation) - defines severe acute pancreatitis by the Revised Atlanta Classification.

 

Step 2 - Aetiology Identification and Causative Management

 

The most common causes of acute pancreatitis in India are gallstones (40–50%), alcohol (30–35%), and hypertriglyceridaemia (increasingly common with rising metabolic syndrome prevalence).

 

Identifying the cause guides specific management. Gallstone pancreatitis - diagnosed by common bile duct stone on ultrasound, elevated bilirubin and ALP, and the clinical picture - requires ERCP with sphincterotomy and stone extraction when associated with cholangitis or persistent biliary obstruction, followed by cholecystectomy during the same admission or within 6 weeks to prevent recurrence.

 

Hypertriglyceridaemia-induced pancreatitis (triglycerides above 1,000 mg/dL) requires triglyceride-lowering therapy - insulin infusion in the acute phase for rapid triglyceride reduction, and long-term fibrate therapy.

 

Alcohol-related pancreatitis mandates addiction counselling and abstinence support.

 

Step 3 - Aggressive Supportive Management and Early Enteral Nutrition

 

The cornerstone of acute pancreatitis management - the intervention that most directly influences outcome - is aggressive intravenous fluid resuscitation in the first 24–48 hours.

 

Pancreatic microvascular insufficiency and capillary leak drive the inflammatory cascade that causes pancreatic necrosis; adequate hydration restores microvascular perfusion and limits necrosis development.

 

We target 250–500ml/hour Ringer's lactate in the first 24 hours, adjusted to clinical response markers - urine output above 0.5ml/kg/hour, improvement in haematocrit and BUN. Analgesia with IV morphine or fentanyl is provided without restriction.

 

Early enteral nutrition via nasojejunal tube - commencing within 48 hours of admission - is superior to parenteral (intravenous) nutrition in severe pancreatitis and significantly reduces infectious complications and mortality. Prophylactic antibiotics are not routinely administered in acute pancreatitis - their use is restricted to confirmed infected pancreatic necrosis.

 

Step 4 - Intervention for Pancreatic Complications

 

Pancreatic fluid collections develop in 30–50% of severe acute pancreatitis - acute peripancreatic fluid collections, acute necrotic collections, pseudocysts (fluid without necrotic debris, arising 4 or more weeks post-acute episode), and walled-off necrosis (WON - organised necrotic debris within a fibrous capsule, 4+ weeks).

 

Asymptomatic pseudocysts and WON are managed conservatively. Symptomatic or infected collections require drainage. EUS-guided transmural drainage - positioning a lumen-apposing metal stent (LAMS) through the gastric or duodenal wall directly into the collection cavity - is the preferred minimally invasive approach for pseudocysts and WON with adequate wall maturation.

 

For infected WON requiring solid debris removal, direct endoscopic necrosectomy through the LAMS or video-assisted retroperitoneal debridement (VARD) are performed by our interventional team.

 

Step 5 - Chronic Pancreatitis Management

 

Chronic pancreatitis - progressive, irreversible fibrotic replacement of pancreatic parenchyma - results in exocrine insufficiency (steatorrhoea, malabsorption, weight loss) and endocrine failure (post-pancreatitis diabetes, Type 3c). Exocrine pancreatic insufficiency (EPI) is treated with pancreatic enzyme replacement therapy (PERT) - pancreatin capsules (Creon or equivalent) containing lipase, amylase, and protease, taken with every meal and snack, titrated to resolution of steatorrhoea and weight stabilisation.

 

Type 3c diabetes (diabetes following pancreatic disease) requires careful insulin management - often characterised by brittle glucose control with hypoglycaemia risk due to concurrent glucagon deficiency.

 

Pain management in chronic pancreatitis follows a stepwise approach: analgesics, abstinence, EUS-guided coeliac plexus block, and in selected patients, ERCP with pancreatic duct stenting or surgical decompression (Partington-Rochelle or Frey procedure) for dilated duct disease.