Acute Pancreatitis

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Acute Pancreatitis

​​​​​​Increasing incidence

Mortality = 5 - 30% (Depending on severity)

How does this differ from Chronic Pancreatitis?

Limited damage to the secretory function of the gland & no gross structural damage

Aetiology = GET SMASHED

Gallstones

Ethanol (Alcohol)

Trauma

Steroids

Mumps

Autoimmune disease (e.g. SLE)

Scorpion venom

Hypercalcaemia

ERCP (Endoscopic Retrograde Cholangio-pancreatography

Drugs (e.g. Azathioprine, NSAIDs or Diuretics)

Majority of cases will be due to gallstones and alcohol.

No evident cause will be found in 10-20% of patients

Pathogenesis

Premature & exaggerated activation of digestive enzymes within the pancreas

Leading to increased vascular permeability & fluid loss into the transcellular

Enzymes released from pancreas into circulation

Causes autodigestion of fats & blood vessels

Resulting in fat necrosis & sometimes haemorrhage into the retroperitoneal space

Free fatty acids formed in fat necrosis can cause the release of free fatty acids that react with serum Ca to form chalky deposits in fatty tissue resulting in hypocalcaemia

Severe end-stage pancreatitis will result in partial /complete necrosis of the pancreas

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Clinical Features

Symptoms

Severe epigastric pain radiating through to back

N+V

Signs

Common signs include:

Epigastric tenderness

Soft abdo w normal sounds USUALLY

Signs of severe acute pancreatitis:

Guarding / Rigid abdo

Circulatory instability

Rarer signs:

Signs of retroperitoneal haemorrhage

Grey Turner's Sign = Bruising in the flanks

Cullen's Sign = Bruising around umbilicus

Tetany = Involuntary movements due to hypocalcaemia (secondary to fat necrosis)

Jaundice / Cholangitis due to gallstone pathology

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Differential Diagnoses

AAA - Symptomatic / Ruptured

Chronic pancreatitis

Aortic dissection

Duodenal ulcer

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Investigations

Bloods

Routine (FBC, U&E's)

Serum amylase

Diagnostic if 3x the upper limit of normal BUT no correlation to disease severity

Also raised in

Bowel perforation

Ectopic pregnancy

Mesenteric ischaemia

DKA

LFT's

To assess for concurrent cholestatic element

ALT > 150 has +ve predictive value of 85% for gallstones as underlying cause

Serum lipase

Raised serum lipase indicates acute pancreatitis (more accurate)

Imaging

USS abdo

To investigate underlying cause

Gallstones demonstrated by dilation of the bile ducts

Abdo XR

Sentinal loop sign = Dilated proximal bowel loop adjacent to the pancreas

Happens due to localised inflammation

CXR

Look for pleural effusion or ARDS (Acute resp distress syndrome)

Contrast-enhanced CT scan

If assessment and tests inconclusive

Or suspicion of complications

After 48 hrs, shows pancreatic oedema & swelling as well as other complications

Pancreas won't enhance when necrotic / necrosing

Any CT scan used to assess the severity of the disease should only be done 6 - 10 days after admission in patients with features of persistent inflammatory response or organ failure because they increase hospital stay without improvement in clinical outcome.

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Management

No curative management so supportive measures are the mainstay of treatment

1. Supportive measures

Admit to ICU / High-dependency unit if severe acute pancreatitis

High-flow O2

IV fluid resuscitation

NG tube

If patient vomitting profusely

If the patient is able to eat, oral intake can be encouraged.

Catheterisation

Monitor urine output & start fluid chart

Aim for UO > 0.5 ml/kg/hr

Check U&E's regularly.

Opioid analgesia

2. Broad-spectrum antibiotic (e.g. Imipenem)

Use only as prophylaxis against infection in confirmed pancreatic necrosis

3. Treat the underlying cause

Early laparoscopic cholecystectomy when gallstones are the cause

Referral to appropriate services when alcohol excess is the cause

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Complications

Systemic complications include:

Disseminated Intravascular Coagulation (DIC)

Acute Resp. Distress Syndrome (ARDS)

Hypocalcaemia

Hyperglycaemia

Due to destruction of Islets of Langerhans causing disturbed insulin metabolism

Hypovolaemic shock & Multiorgan failure

Local complications:

Pancreatic Necrosis = Ischaemic infarction of pancreatic tissue

Due to ongoing inflammation

Therefore suspect when evidence of persistent systemic inflammation for more than 7-10 days

Confirmed by CT imaging.

Treated with pancreatic necrosectomy (Open / endoscopic) typically 3-5 weeks after onset of symptoms

Infection prone

Suspect infection if patient deteriorates alongside raised infection markers, +ve blood cultures or low density within pancreas on CT

Definitive diagnosis confirmed by fine needle aspiration of necrosis

Pancreatic Pseudocyst = Collection of fluid containing pancreatic enzymes, blood & necrotic tissue occuring within or adjacent to the pancreas

Most commonly found in the lesser sac, obstructing the gastro-epiploic foramen by inflammatory adhesions

Formed week after initial acute pancreatitis episode

Lack epithelial lining (hence pseudocyst)

Surrounded by vascular & fibrotic wall

Found either incidentally on imaging or due to symptoms of mass effect (e.g. biliary obstruction, gastric outlet obstruction)

Prone to haemorrhage, rupture and infection.

Likely to spontaneously resolve (50%), unless present longer than 6 weeks.

Treatment = Surgical debridement or endoscopic drainage