Pancreatitis — MRCS Part B Applied surgical science and critical care

Acute pancreatitis on a CT, moving through its causes, severity scoring and complications, and ending with the adult respiratory distress syndrome it can produce.

Differential and initial management

Severe epigastric pain radiating to the back with vomiting: pancreatitis, a perforated ulcer, cholecystitis and cholangitis, a leaking aortic aneurysm, mesenteric ischaemia, an inferior myocardial infarction. Resuscitate first: oxygen, large-bore access, intravenous crystalloid titrated to urine output, analgesia, antiemetic, a catheter, and nil by mouth only while vomiting. Bloods: amylase or lipase (three times the upper limit), full count, urea and electrolytes, liver function, calcium, glucose, gases, CRP and lipids. An erect chest radiograph for free air, an ultrasound for gallstones and a dilated duct. CT is for diagnostic doubt or, after three or four days, to look for necrosis; it does not need to be done on admission.

Causes

Gallstones and alcohol account for about four-fifths. The rest: post-ERCP, trauma, drugs (azathioprine, thiazides, valproate, steroids), hypercalcaemia and hypertriglyceridaemia, viral infection (mumps, coxsackie), autoimmune disease, scorpion venom, and idiopathic. In this patient the likely cause is the one the scan or ultrasound shows; it matters because gallstone pancreatitis needs the stones dealt with (ERCP early if there is cholangitis, and cholecystectomy on the same admission or within two weeks) to prevent it happening again.

Severity scoring

The modified Glasgow (Imrie) score at 48 hours: PaO2 under 8 kPa, age over 55, neutrophils over 15, calcium under 2, urea over 16, LDH over 600 or AST over 200, albumin under 32, glucose over 10 (“PANCREAS”); three or more predicts severe disease. Ranson's criteria are the older equivalent. APACHE II on admission, a CRP over 150 at 48 hours, and the Atlanta classification (mild, moderately severe with transient organ failure or local complications, severe with persistent organ failure) are the others to name.

Complications

Local: peripancreatic fluid collections, pseudocyst after four weeks, necrosis and infected necrosis, abscess, splenic vein thrombosis, pseudoaneurysm and haemorrhage. Systemic: hypovolaemia, acute kidney injury, ARDS, DIC, hypocalcaemia, hyperglycaemia, and sepsis. Long term: chronic pancreatitis, exocrine and endocrine failure.

Calcium

Within the acinar cell, a sustained rise in cytosolic calcium activates trypsinogen to trypsin prematurely, which sets off the other enzymes and digests the gland; this is how alcohol, bile acids and hypercalcaemia are all thought to start the process. Later, calcium is lost from the blood into areas of fat necrosis as calcium soaps, which is why hypocalcaemia is a marker of severity.

ARDS

Acute hypoxaemic respiratory failure within a week of an insult, with bilateral infiltrates on the film not explained by cardiac failure or overload, and a PaO2/FiO2 ratio below 300 mmHg on at least 5 cmH2O of PEEP (the Berlin definition, which grades mild, moderate and severe). Inflammatory mediators from the pancreas injure the pulmonary capillary endothelium and alveolar epithelium; protein-rich fluid floods the alveoli, surfactant is lost, alveoli collapse, and the lung becomes stiff with shunting and hypoxaemia. Management is supportive on the intensive care unit: lung-protective ventilation with low tidal volumes (6 ml/kg) and limited plateau pressures, PEEP, prone positioning in severe cases, conservative fluid once resuscitated, and treatment of the pancreatitis and any sepsis driving it.