Acute Pancreatitis

• Acute relapsing pancreatitis
• Acute cholecystitis
• Ascending cholangitis
• Pancreatic pseudocyst
• Perforated viscus

Apart from amylase and lipase, lactate dehydrogenase should be checked. LDH helps assess the extent of tissue injury and it forms part of the Glasgow scoring criteria for severity assessment in acute pancreatitis.

Both amylase and lipase have diagnostic value, but lipase is more specific to the pancreas and remains elevated for longer, making it more reliable.

Amylase is less specific. Elevations can occur in patients with small intestinal obstruction, mesenteric ischaemia, tubo-ovarian disease, renal insufficiency, or macroamylasaemia. It can originate from other tissues such as salivary glands so rarely elevations may reflect parotitis. It has a short half-life so returns to normal within 48 hours, making it falsely reassuring if measured too early or too late. Therefore, lipase is considered the better marker for pancreatitis.

P-amylase (pancreatic amylase) is more specific.
S-amylase comes from salivary glands, so elevations may be due to non-pancreatic causes such as parotitis.

Post-cholecystectomy pancreatitis is usually due to

• Iatrogenic injury that causes obstruction or irritation of the pancreatic duct
• Infection
• Retained or slipped CBD stones, or 
• Post-operative biliary strictures leading to obstruction and pancreatic inflammation.

The most likely cause is retained or recurrent CBD stones causing biliary obstruction. A postoperative stricture is another important possibility, as it can compromise bile drainage and predispose to cholangitis.

The presentation five weeks after the attack is most consistent with a pancreatic pseudocyst, which develops over 4–6 weeks and can produce pressure symptoms from its mass effect.

• A pancreatic pseudocyst is a collection of amylase-rich fluid enclosed within a wall of fibrous or granulation tissue, without an epithelial lining. The contents typically include enzyme-rich fluid, inflammatory exudate and sometimes debris..
• A true cyst has an epithelial lining, whereas a pseudocyst has no epithelial wall and is instead surrounded by fibrous and granulation tissue as a result of inflammation.
• Pancreatic cancer usually has high fluid viscosity, elevated CA19-9, and low amylase levels within the cystic component, while pseudocysts typically have low viscosity, low CA19-9, and high amylase content. CT imaging also helps distinguish them, with pseudocysts showing a simple fluid collection and cancers showing irregular, solid or complex features

• I would assess the patient systematically using the A to E approach following the CRISP protocol
• I would ensure adequate oxygenation, provide analgesia, and begin aggressive intravenous fluid resuscitation
• The patient should be admitted to a high-dependency or intensive care setting for close monitoring of urine output, blood gases, and central venous pressure
• Frequent laboratory assessment is needed, including U&Es, LFTs, coagulation profile, serum calcium and glucose
• Nasogastric drainage may be used initially if vomiting persists
• Antibiotics (Carbapenem and Quinolone) are indicated if there is suspected cholangitis, sepsis, necrosis or if invasive biliary intervention is planned
• Octreotide may be used to reduce pancreatic secretions
• PPI is given to prevent stress ulceration
• CT scanning is required if the patient deteriorates or develops organ failure
• ERCP should be performed within 72 hours for gallstone pancreatitis with evidence of cholangitis
• If the patient cannot maintain enteral intake, nasojejunal feeding is preferred; TPN is reserved for severe or septic cases

Steroids may reduce systemic inflammation by suppressing cytokine release. Some evidence suggests they decrease the length of hospital stay, reduce the need for surgery and improve mortality in severe acute pancreatitis, although they are not universally recommended.

Antibiotics are used in sepsis, infected pancreatic necrosis, and acute cholangitis, and they are routinely administered before ERCP to reduce the risk of infectious complications. Prophylactic antibiotics are not routinely recommended in uncomplicated pancreatitis.

ERCP is indicated when there is evidence of common bile duct stones, when the patient presents with acute cholangitis, when there is failure to improve within 48 hours despite optimal medical therapy, and in cases of severe gallstone pancreatitis. In these situations, relieving biliary obstruction is essential in preventing further pancreatic injury.

Use CoFE PAN:

• Co → collections
• Fat stranding
• Edema
• Pseudocyst
• Abscess
• Necrosis

The main scoring systems include:

Glasgow criteria: Uses ((eight clinical and biochemical markers::Use the mnemonic PANCREAS)) to identify severe attacks and a score > 2 indicates ITU admission warranted:

• ((PaO₂::PaO2 < 8 kPa))
• ((Age::Age > 55 years))
• ((Neutrophils::Neutrophils > 15,000))
• ((Calcium::Calcium < 2 mol after 48 hours ))
• Renal function using ((urea::Urea > 16 mmol/L))
• Enzymes ((LDH::LDH > 600 after 48 hours))
• ((Albumin::Albumin < 32 gL after 48 hours))
• Sugar, ((glucose:: Glucose > 10 mmol/L)) .

Ranson’s criteria: uses admission and 48-hour values to estimate mortality for example with 5 points estimated mortality is 40%...

• Criteria at admission: Age > 55, WBC > 16,000, Glucose > 11, AST > 250, LDH > 350
• Criteria after 48 hours of admission: Hct falls ≥ 10%, Fluid sequestration > 6 L, Calcium < 2.0, PO2 < 8 kPa, BUN rises > 1.98 mmol/L after IV fluid hydration, Base deficit > 4 mmol/L

Balthazar CT scoring: Evaluates CT features at 5 days after admission such as oedema, fat stranding, collections and necrosis to assess severity

• Normal pancreas
• Enlargement (oedema) of pancreas
• Inflammatory changes in pancreas and peripancreatic fat
• Ill-defined single peripancreatic fluid collection
• ≥ 2 poorly defined peripancreatic fluid collections

APACHE II: ((APACHE II::Acute Physiologic Assessment and Chronic Health Evaluation)) provides a dynamic, ICU-based assessment of physiological derangement

Use mnemonic I GET SMASHED:

• Idiopathic
• Gallstones
• Ethanol
• Trauma
• Snake bite
• Mumps
• Autoimmune
• Steroids
• Hypercalcemia / hypertriglyceridemia
• ERCP
• ((Drugs::Azathioprine, OCPs, thiazides, corticosteroids))

Acute pancreatitis leads to both local and systemic early and late complications. 

Local complications include pseudocyst formation, abscess, necrotising pancreatitis, fat necrosis, ascites, phlegmon and splenic vein thrombosis.

The gastrointestinal tract may develop ileus or bleeding, and acute renal failure can occur from hypovolaemia.

Systemic complications reflect the intensity of the inflammatory response and include hypovolaemic shock, haemorrhagic pancreatitis, SIRS and multi-organ failure. Haematological problems such as DIC may develop, and hepatobiliary involvement can lead to jaundice, portal vein thrombosis or strictures.

Important metabolic complications include hypocalcaemia, hypomagnesaemia, hypoalbuminaemia and hyperglycaemia.

Respiratory complications are frequent and include ARDS and pleural effusion.

Severe cases can progress to death.

Investigations

• Ultrasound / CT scan / MRCP
• Cyst fluid analysis: Confirm low CA-19-9, CEA, CA-125; low fluid viscosity; high amylase content
• Presence of high amylase 4 weeks after the acute pancreatitis episode is suspicious for pancreatic pseudocyst

It is most frequently located in the lesser peritoneal sac in proximity to the pancreas

Management

• Supportive treatment
• 40% resolve spontaneously
• Intervention ((cystogastrostomy::Cystogastrostomy entails entering the anterior wall of the stomach, fashioning a large hole through the posterior wall into the pseudocyst, and securing stomach and pseudocyst with a circumferential stitch. The pseudocyst then drains into the stomach)) or cystojejunostomy) if persist > 2 months, diameter ≥ 6 cm, symptomatic or infected

• Infection: Abscess, sepsis
• Rupture into gut (→ GI bleed, internal fistula) or into peritoneum (→ peritonitis)
• Enlargement putting pressure on bile duct (→ obstructive jaundice) or on bowel (→ bowel obstruction)
• Vascular erosion leading to hemorrhage into cyst or haemoperitoneum
• Pain
• Diaphragmatic compression (→ tachypnoea)

Management requires a multidisciplinary approach involving gastroenterology or hepatology, haematology and interventional radiology. Because of haemorrhage, LMWH is contraindicated. Radiological intervention—usually coiling or embolisation—is the treatment of choice.

Complications include injury to surrounding structures, haemorrhage, failure of occlusion, and infection.

Pain should be managed following the WHO analgesic ladder, starting with paracetamol, then weak opioids such as codeine, and escalating to strong opioids like Pethidine/Meperidine or PCA. Morphine is traditionally avoided due to theoretical sphincter of Oddi spasm. NSAIDs are avoided as some NSAIDs, such as naproxen, are known to potentially cause acute pancreatitis as a side effect; they can precipitate renal failure in a patient who is already intravascularly depleted, and they can also contribute to gastric mucosal injury and ulceration.

CRP is a nonspecific acute-phase reactant produced by the liver in response to inflammation.

Tachypnoea may be due to ARDS, sympathetic over-activation, or diaphragmatic compression by a pseudocyst.

No

Hypocalcaemia in acute pancreatitis arises through two mechanisms that occur at different stages of the illness.

In the early phase, pancreatic enzymes leak into surrounding tissues and cause autodigestion of mesenteric fat. This releases free fatty acids that bind to circulating calcium, forming insoluble calcium soaps. As calcium becomes trapped in these soaps, serum calcium levels fall. This stage may also involve transient hypoparathyroidism and hypomagnesaemia, which further reduce the availability of calcium.

In the later phase, hypocalcaemia develops mainly due to sepsis and the accompanying surge in circulating catecholamines. These mediators drive calcium into the intracellular compartment, lowering extracellular calcium concentrations. The fall in serum calcium triggers increased parathyroid hormone secretion, but despite this compensatory response, hypocalcaemia persists because the underlying inflammatory state continues to shift calcium intracellularly.

Pancreatic enzymes destroy beta cells in the islets of Langerhans resulting in ↓ insulin. Additionally, stress response increases serum glucose.

Endocrine:

• Alpha cells → Glucagon
• Beta cells → Insulin
• Delta cells → Somatostatin
• PP cells → Pancreatic polypeptide

Exocrine:

• Digestive enzymes: lipase, amylase, proteases, ((enterokinase::Enterokinase activates the pancreatic enzyme trypsinogen into its active form, trypsin. Once activated, trypsin then activates other inactive pancreatic enzymes (zymogens) into their active forms, such as chymotrypsinogen to chymotrypsin. This process is crucial for protein digestion in the small intestine))

Toxic metabolite NAPQI accumulates when glutathione is depleted. It causes hepatocyte necrosis and interferes with vital liver functions.

• Grey Turner sign → flank bruising
• Cullen sign → periumbilical bruising

Contrast-enhanced CT scan of the abdomen. Necrotic areas appear as hypodense, non-enhancing regions compared with the viable pancreatic tissue. CT not only confirms necrosis but also helps assess collections, pseudocysts and complications such as abscess formation.

Pancreaticoduodenectomy, a major surgical operation in which the

• the head of the pancreas,
• the duodenum,
• the gallbladder, and
• the common bile duct

... are removed en bloc.

The remaining pancreas, bile duct and stomach are then reattached to the jejunum to restore gastrointestinal continuity. It is typically performed for cancers of the pancreatic head or periampullary region.