Acute pancreatitis

Pathophysiology

In acute pancreatitis, pancreatic enzymes are hyper-activated and prematurely activated. The inflammatory response of the pancreas also increases vascular permeability and as a result the pancreatic enzymes such as lipase cause breakdown of fatty tissue resulting in fat necrosis.

Fat necrosis can end up releasing free fatty acids (FFAs) which react with serum calcium to form chalk deposits and also result in hypocalcaemia.

Blood vessels may also become digested through protease leading to a retroperitoneal haemorrhage.

⚠️ Causes

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“I GET SMASHED”

• I - Idiopathic
• G - Gallstones
• E - Ethanol (Alcohol)
• T - Trauma
• S - Steroids
• M - Mumps
• A - Autoimmune (SLE or Sjogren’s)
• S - Scorpion sting
• H - Hypercalcaemia, hyperlipidaemia, hypothermia
• E - Endoscopic retrograde cholangiopancreatography
• D - Drugs
• NSAIDs
• Diuretics
• Sodium valproate
• Mesalazine
• Azathioprine/Asparaginase
• Thiazides/Tetracycline
• Statins/Sulfonamides/Sodium Valproate
• Hydrochlorothiazide
• Estrogens
• Ethanol
• Protease inhibitors and NRTIs

10-20% of patients will have no cause evident, however.

😷 Signs and symptoms

Patients may experience severe epigastric pain that may radiate to the back. Pain may be slightly relieved when sitting forward.

Nausea and vomiting is also present often.

On examination there may be epigastric tenderness with/without guarding.

2 signs to look out for (but are not so common) are:

A. Cullen’s sign - bruising around the umbilicus

B. Grey Turner’s sign - bruising in the flank regions.

Both of these indicate retroperitoneal haemorrhage mentioned prior.

Jaundice may also be present if due to gallstones. Tetany (intermittent muscle spasms) may also occur as a result of calcium deficiency.

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We can also use Trousseau and Chvostek signs for hypocalcaemia.

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Purtscher retinopathy is a rare association with pancreatitis. It may result in temporary/permanent blindness.

🔍 Investigations

As with any acute abdomen a series of tests need to be carried out.

These include:

Pancreatitis has a lot of overlapping symptoms to peritonitis. It is very important to assess serum amylase as it can differentiate acute pancreatitis (no surgical treatment required) from peritonitis, which can require a laparotomy.

📷 Imaging

🥇 Ultrasound is our first line investigation for gallstones.

MRCP may be indicated if USS has not detected gallstones.

A CT abdomen may be used to assess any complications such as necrosis, abscesses, fluid collections, but is not required unless any complication is suspected.

Imaging may not be needed if there is the characteristic pain (severe epigastric pain radiating to the back sometimes) + raised amylase/lipase 3x above normal.

🔢 Scoring System

Scoring for pancreatitis is achieved through the Glasgow scoring system. The criteria can be remembered using the PANCREAS mnemonic.

1. P - PaO2: <8kPa
2. A - Age: >55y/o
3. N - Neutrophils: WBC >15x 10^9/L
4. C - Calcium: <2mmol/L
5. R - uRea: >16mmol/L
6. E - Enzymes: LDH > 600u/L & AST >200 u/L
7. A - Albumin: <32g/L
8. S - Sugar: >10mmol/L

0 or 1 - mild pancreatitis

2 - moderate pancreatitis

3+ - severe pancreatitis

🧰 Management

Treatment involves support of symptoms and treating the underlying cause:

1. 🥇 IV fluids - one of the key management protocols in acute pancreatitis is early and aggressive fluid resuscitation which is to correct the third space losses and increase tissue perfusion with the aim of preventing severe inflammatory response syndrome which can lead to pancreatic necrosis.
2. Oxygen
3. NG tube - patients with acute pancreatitis should not routinely be made 'nil-by-mouth’ if the patient is able to eat.
4. Catheterisation - to monitor urine output (at least >0.5ml/kg/hr).
5. Opioid analgesia
6. Broad-spectrum antibiotic prophylaxis - such as imipenem when pancreatic necrosis is confirmed.

The underlying cause should be treated, such as ERCP or cholecystectomy for gallstones.

Alcoholic patients should be advised on alcohol cessation and referred to the necessary services.

❗️Complications

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Local complications

• Necrosis of the pancreas and subsequent infection - the continuous inflammation may lead to an ischaemic infarction. The necrosed tissue is prone to infection.
• Pseudocyst - collection of fluid with enzymes, blood and necrotic tissue. They are surrounded by vascular and fibrotic tissue instead of epithelial tissue (hence pseudo). About 1/2 resolve spontaneously while those that last need drainage or debridement. The indications for active drainage would be signs of infection, mass effect on abdominal organs or a persisting pseudocyst beyond 12 weeks from it developing. Even in cases where patients are symptomatic from a pseudocyst, it is often managed conservatively as the risks of a procedure outweigh the symptoms it causes. The best of the procedural options would be radiological fine-needle aspiration.