Acute Pancreatitis — Exam Revision

Acute pancreatitis is acute inflammation caused by premature activation of digestive enzymes within the pancreas. Acinar injury and autodigestion trigger local oedema, inflammation and sometimes necrosis. A systemic inflammatory response can produce circulatory, respiratory or renal failure. This explains why a patient with an abdominal complaint may need intensive organ support even when no operation is immediately indicated.

The Revised Atlanta diagnostic rule requires at least two of three findings: characteristic acute epigastric pain, serum lipase or amylase at least three times the upper limit of normal, and imaging consistent with pancreatitis. Typical pain radiates to the back and is accompanied by nausea or vomiting. Two convincing clinical and biochemical criteria can establish the diagnosis without a routine admission CT.

Read the question in layers. First establish pancreatitis; then identify its cause; finally determine the clinical severity. These are different tasks. A raised enzyme concentration alone does not prove pancreatitis, and the numerical height of the enzyme rise does not replace assessment for organ failure. A patient with a clear diagnosis still needs an aetiological work-up to prevent another attack.

Gallstones and alcohol are leading causes, but their relative importance varies across populations. NICE specifically cautions against assuming that pancreatitis is alcohol-related simply because the patient drinks. An unexplained attack should prompt consideration of metabolic causes, drugs, microlithiasis, hereditary disease, autoimmune pancreatitis, tumours and pancreatic duct abnormalities. The aetiological label should follow evidence rather than a mnemonic alone.

The biliary and pancreatic ducts lie close to each other near the duodenum. This anatomy helps explain how a migrating gallstone can trigger pancreatic inflammation. Ultrasound examines gallstones, sludge and duct dilatation. When suspicion remains despite an unrevealing ultrasound, endoscopic ultrasound or MRCP can provide further duct assessment. ERCP is primarily a therapeutic procedure rather than a screening investigation.

Initial testing includes pancreatic enzymes, a full blood count, renal function, electrolytes, liver tests, calcium and triglycerides. BUN and haematocrit trends help assess intravascular volume status and clinical progression. Assess oxygenation and urine output alongside laboratory results. A worsening biochemical trend matters because fluid loss into inflamed tissues may leave the circulating volume depleted despite apparent abdominal fluid accumulation.

Ultrasound answers the biliary question; contrast CT answers the complication question. CT is useful when the diagnosis is uncertain, the clinical course is severe or worsening, or improvement does not occur as expected. It can show pancreatic inflammation, necrosis and peripancreatic collections. Ordering CT routinely for every mild attack adds little when the clinical and enzyme criteria already establish the diagnosis.

A CT image showing surrounding fluid does not by itself name that collection. Look for the time from onset, whether there is a mature wall, and whether solid necrotic debris is present. Those observations distinguish a simple fluid collection from a necrotic collection. The distinction affects the words used in the report and the approach to any later intervention.

Distinguish a severity definition from a prediction score. Atlanta describes the course and complications; BISAP and Ranson estimate the risk of an adverse course. A high prediction score should prompt closer monitoring, but it does not make persistent organ failure appear before it has occurred. Likewise, necrosis is a local complication and does not automatically establish severe disease without persistent organ failure.

Transient organ failure can resolve with treatment. Persistent failure can affect the lungs, circulation or kidneys, singly or together. Serial examination therefore remains central. Read a vignette for the duration of dysfunction rather than reacting only to a CT adjective such as necrotising. This avoids the older teaching error that every local pancreatic complication is sufficient to classify an attack as severe.

BISAP stands for Bedside Index for Severity in Acute Pancreatitis. The total ranges from zero to five, with a higher score indicating greater concern. A score of three or more flags a higher-risk group. Its appeal is the small number of readily available variables. It avoids waiting for the complete delayed Ranson assessment and helps decide how closely the patient should be monitored. It supplements clinical judgement rather than authorising discharge by itself.

Pay particular attention to the BUN threshold and the age threshold. They are different from the change in BUN used in delayed Ranson scoring and from the age cut-offs in the original and modified Ranson systems. The impaired-mental-status item also links to the Glasgow Coma Scale. A pleural effusion contributes to BISAP; it does not need to be a primary lung disease.

The original system uses eleven variables, five at admission and six at forty-eight hours. The modified gallstone system uses ten, with five in each group. Each positive finding scores one point. Keep the two systems separate. Mixing the original admission thresholds with modified delayed thresholds creates a score that belongs to neither system.

A Ranson score of three or more traditionally predicts increased risk of a severe course; it does not replace the current organ-failure definition. The main practical limitation is the wait for the delayed measurements. Ranson cannot provide its complete result at the first assessment. Its fluid-sequestration variable is also less convenient than routine bedside observations. Use the table for examination calculations, while remembering that modern care relies on continuing assessment, early risk tools and the clinical severity definition rather than a single historical score.

Pseudocyst is not a synonym for every post-pancreatitis collection. A pseudocyst has a defined wall and predominantly fluid content. Walled-off necrosis contains necrotic material, so its management can require more than drainage of simple fluid. The four-week boundary describes typical maturation; the actual imaging appearance and clinical context still matter when assigning a name.

Collections may remain sterile, become infected, or produce pain, vomiting and obstruction through mass effect. Infection may cause renewed fever, sepsis or clinical deterioration. A symptomatic collection and an infected collection raise different intervention questions. Size alone is not a universal instruction to operate. Current NICE guidance supports endoscopic approaches when suitable and a percutaneous approach when endoscopic access is not anatomically possible.

• Assess and support circulation, breathing and renal function; reassess the response to treatment.
• Give intravenous crystalloid guided by hydration and perfusion, with attention to fluid overload; provide analgesia and antiemetics.
• Resume oral intake as tolerated and use enteral nutrition when necessary; prolonged routine fasting is inappropriate.
• Do not give prophylactic antimicrobials for uncomplicated pancreatitis or sterile necrosis. Treat suspected or proven infection appropriately.
• Address the cause: biliary obstruction or cholangitis may require ERCP; mild gallstone pancreatitis usually needs definitive gallbladder treatment during the admission.
• Manage infected necrosis with specialist input, considering drainage and a step-up approach rather than automatic immediate open surgery.

Systemic complications include shock, acute respiratory distress syndrome, acute kidney injury and multiorgan dysfunction. Local or vascular problems include necrosis, collections, bleeding, pseudoaneurysm and venous thrombosis. The complications connect pancreatic inflammation to several specialties, which is why severe attacks require coordinated gastroenterology, surgery, radiology, nutrition and critical care input.

Nutritional support is part of treatment, not an optional late step. NICE recommends not withholding food without a clear reason such as vomiting, and favours enteral feeding over parenteral feeding where feasible. Likewise, sterile inflammation is not the same as bacterial infection. Fever or leukocytosis must be interpreted with the overall course rather than triggering routine prophylactic antibiotics.