Pancreatitis

Inflammation of the pancreas from premature activation of digestive enzymes within the gland, causing autodigestion.

Acute pancreatitis is most commonly caused by gallstones or alcohol (together accounting for the large majority of cases), with other causes including hypertriglyceridemia (typically above 11.3 mmol/L), post-ERCP, drugs (azathioprine, thiazides, valproate, GLP-1 agonists, among others), trauma, and, rarely, autoimmune or hereditary pancreatitis.

Chronic pancreatitis represents irreversible fibrosis and progressive exocrine and endocrine dysfunction, most commonly from long-term alcohol use, with recurrent acute pancreatitis, autoimmune pancreatitis, and cystic fibrosis among other causes.

Acute: severe, constant epigastric pain radiating to the back, often relieved by sitting forward, associated with nausea and vomiting.

Examination may show epigastric tenderness, guarding, reduced bowel sounds, and, in severe hemorrhagic pancreatitis, Cullen's sign (periumbilical bruising) or Grey Turner's sign (flank bruising), both uncommon but indicative of severe disease. Systemic features in severe disease include fever, tachycardia, hypotension, and hypoxia reflecting SIRS or evolving organ dysfunction.

Chronic: recurrent or persistent epigastric pain (though a subset of patients become pain free as the gland burns out), steatorrhea and weight loss from exocrine insufficiency, and diabetes mellitus from endocrine insufficiency as islet cell mass is progressively lost.

Acute pancreatitis diagnosis requires two of three: characteristic abdominal pain, serum lipase or amylase greater than three times the upper limit of normal (lipase preferred, more sensitive and specific and remains elevated longer than amylase), and characteristic findings on cross sectional imaging.

Severity assessment uses scoring systems such as the Glasgow Imrie or APACHE II criteria, alongside CRP (a level above 150 mg/L at 48 hours predicts severe disease) and hematocrit trend.

Abdominal ultrasound identifies gallstones as the underlying cause. Contrast enhanced CT is reserved for diagnostic uncertainty or to assess complications (necrosis, pseudocyst, abscess), ideally performed after 72 hours if necrosis is being assessed, since early imaging can underestimate necrotic extent.

Triglycerides, calcium, and a thorough medication history complete the etiological workup when gallstones and alcohol are absent.

Chronic pancreatitis diagnosis uses CT or MRI showing pancreatic calcification, duct dilatation, and atrophy; endoscopic ultrasound for early or equivocal changes; fecal elastase to confirm exocrine insufficiency; and formal assessment for diabetes.

Differentials include perforated peptic ulcer, mesenteric ischemia, biliary colic, cholecystitis, and myocardial infarction (particularly inferior MI, which can mimic epigastric pain).

Acute pancreatitis:

Aggressive IV fluid resuscitation with crystalloid, guided by urine output and hemodynamic response, is the cornerstone of early management. Analgesia should be given generously, typically with opioids.
Early enteral nutrition (oral or nasogastric feeding as tolerated, started within 24 to 72 hours) is preferred over prolonged fasting, since it reduces infectious complications and mortality compared with nil by mouth strategies.
Antibiotics are not given prophylactically and are reserved for confirmed infected necrosis or another proven source of infection.
Gallstone pancreatitis requires cholecystectomy during the same admission for mild disease, or once inflammation has settled for severe disease, to prevent recurrence; ERCP with sphincterotomy is indicated urgently if there is concurrent cholangitis or persistent biliary obstruction.
Severe pancreatitis with organ dysfunction requires ICU or HDU level care. Local complications such as infected pancreatic necrosis are managed with a step up approach, starting with percutaneous or endoscopic drainage before progressing to necrosectomy if needed, since early surgical intervention carries higher mortality than a delayed, minimally invasive strategy.

Chronic pancreatitis:

Alcohol cessation and smoking cessation are essential to slow progression. Analgesia follows a stepwise approach, escalating from simple analgesics to neuropathic agents and, in refractory cases, to endoscopic or surgical intervention (duct decompression, celiac plexus block, or resection).
Pancreatic enzyme replacement therapy is given with meals for exocrine insufficiency, titrated to control steatorrhea and support weight.
Diabetes arising from endocrine insufficiency is managed per standard diabetes principles, though patients are often more prone to hypoglycemia given concurrent glucagon deficiency.
Fat soluble vitamin deficiency (A, D, E, K) should be screened for and replaced.

Referral: hepatobiliary or pancreatic surgery for gallstone pancreatitis requiring cholecystectomy, necrotizing pancreatitis requiring drainage, or chronic pancreatitis requiring duct decompression; gastroenterology for ERCP and ongoing chronic pancreatitis management.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Haemochromatosis

Also known as: Hemochromatosis, Iron overload

Disorder of iron overload, most commonly hereditary (autosomal recessive, predominantly caused by HFE gene mutations, particularly C282Y homozygosity, most prevalent in populations of Northern European descent), causing inappropriately increased intestinal iron absorption and progressive deposition in the liver, heart, pancreas, joints, skin, and pituitary gland.

Secondary iron overload occurs from repeated blood transfusion (see Sickle Cell Disease and Leukemia entries) or, less commonly, from excessive iron intake or ineffective erythropoiesis in conditions such as thalassemia.

Early disease is often asymptomatic or presents with nonspecific fatigue and arthralgia (classically affecting the second and third metacarpophalangeal joints, sometimes termed the iron fist sign).

As iron accumulation progresses, organ specific features emerge: hepatomegaly progressing to cirrhosis and a markedly increased risk of hepatocellular carcinoma even in the absence of established cirrhosis, distinguishing this cause from most other cirrhotic etiologies; bronze or slate grey skin pigmentation (from both iron deposition and increased melanin); diabetes mellitus (from pancreatic iron deposition, historically termed bronze diabetes when combined with the skin pigmentation and cirrhosis); cardiomyopathy (restrictive or dilated, with associated arrhythmia) and heart failure; hypogonadism from pituitary iron deposition (reduced libido, erectile dysfunction, amenorrhea); and arthropathy as above.

Transferrin saturation is the most sensitive initial screening test, elevated (generally above 45%) even before ferritin rises significantly, and is the preferred first test in suspected cases or family screening.

Serum ferritin is elevated but, as an acute phase reactant, can be raised by inflammation, infection, alcohol use, or metabolic syndrome independent of true iron overload, so it should always be interpreted alongside transferrin saturation and clinical context rather than in isolation.

Genetic testing for HFE mutations (C282Y and H63D) confirms hereditary hemochromatosis once biochemical iron overload is identified.

Liver biopsy with hepatic iron index, once the primary confirmatory test, is now reserved for cases where genetic testing is negative or equivocal despite biochemical evidence of overload, or to assess the degree of fibrosis in patients with very high ferritin (generally above 1000 micrograms per liter) who are at higher risk of established cirrhosis.

MRI can quantify hepatic and cardiac iron content non-invasively and is increasingly used both for diagnosis and for monitoring treatment response, particularly in transfusion related secondary overload.

Differentials include other causes of chronic liver disease with elevated ferritin (alcohol related liver disease, MASLD, viral hepatitis, all of which can cause a reactive ferritin elevation without true iron overload), and secondary iron overload from transfusion or ineffective erythropoiesis.

Therapeutic phlebotomy is the mainstay of treatment for hereditary hemochromatosis: weekly or twice weekly venesection of approximately 450 to 500 mL initially, continued until ferritin falls to the target range (generally 50 to 100 micrograms per liter), followed by maintenance phlebotomy every few months thereafter to keep iron stores within target range lifelong.

Treatment initiated before the onset of cirrhosis or diabetes can prevent these complications entirely and restores normal life expectancy, which is why early identification through family screening of first degree relatives once an index case is diagnosed is a central part of management.

Dietary advice includes avoiding iron supplements and excessive vitamin C intake (which enhances iron absorption), and moderating alcohol intake given the compounding effect on liver injury, though strict dietary iron restriction is not generally necessary once phlebotomy is established.

Iron chelation therapy (deferasirox, deferoxamine, or deferiprone) is reserved for secondary iron overload where phlebotomy is not feasible due to underlying anemia, such as in transfusion dependent conditions.

Once cirrhosis has developed, hepatocellular carcinoma surveillance (six monthly ultrasound with or without AFP) continues indefinitely even after iron stores are normalized by treatment, since established cirrhosis carries ongoing cancer risk regardless of subsequent iron status.

Referral: hepatology or gastroenterology for diagnosis confirmation and management; hematology for phlebotomy program coordination; genetic counseling and screening for first degree relatives once an index case is confirmed.

That completes the GI/Hepatobiliary group (items 1 to 17). Send the word when you want the next group (Cardiology and Respiratory, items 18 to 28).

Pancreatitis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management