Chronic Pancreatitis — Written Clinical Reasoning

Part A — Diagnosis, aetiology and staging

Diagnosis

The diagnosis is chronic pancreatitis, established by the combination of characteristic clinical features (chronic recurrent epigastric pain radiating to the back, steatorrhoea, weight loss, and new-onset diabetes), objective exocrine insufficiency (faecal elastase 65 micrograms per gram, indicating severe insufficiency), and characteristic irreversible imaging (a dilated irregular main pancreatic duct with calcifications and parenchymal atrophy on CT). No further diagnostic testing is required to confirm the diagnosis in this advanced case. The 2016 mechanistic consensus defines chronic pancreatitis as a pathological fibroinflammatory syndrome of the pancreas producing irreversible structural damage with permanent loss of exocrine and endocrine function ^[1].

Aetiological framework — the TIGAR-O classification

The aetiology should be classified using the TIGAR-O mechanistic framework ^[2]. This patient's disease is toxic-metabolic, driven by chronic heavy alcohol use, with smoking as the likely cofactor (which must be asked about, as it independently accelerates fibrosis and markedly increases pancreatic cancer risk). The other categories — idiopathic, genetic (PRSS1, SPINK1, CFTR, CTRC), autoimmune (type 1 IgG4-related, type 2), recurrent and severe acute pancreatitis, and obstructive — should be considered if the alcohol history is uncertain or atypical features are present (young age, a positive family history, painless obstructive jaundice suggesting autoimmune pancreatitis). In this patient the alcohol history is sufficient, but I would check a lipid panel, calcium, and serum IgG4 to exclude coexistent hypertriglyceridaemia, hypercalcaemia, and autoimmune pancreatitis.

Staging

The disease is in the burnt-out (insufficiency) phase: the steatorrhoea and type 3c diabetes indicate that the gland has lost more than 90 per cent of its exocrine secretory capacity and a large proportion of its endocrine function. The pain may eventually abate as the parenchyma is destroyed, but at present it remains a major problem. ^[1]