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Introduction & Definition

What is acute pancreatitis?

  • A common presentation and a surgical emergency
  • Results from an inflammatory process in the pancreas leading to a multisystem disease characterized by a systemic inflammatory response and multi-organ dysfunction syndrome


Pancreatitis is typically established by the presence of two of the following criteria:


1. Abdominal pain consistent with the disease

2. Serum amylase and/or lipase greater than three times the upper limit of normal

3. Characteristic findings from abdominal imaging

How can acute pancreatitis be classified?

Pancreatitis can be classified by severity according to the Revised ATLANTA criteria 2012

  • No organ failure
  • No local complications
  • Transient organ failure (<}48 hours)
  • Local complications +/-
  • Persistent organ failure

*Local complications include:
Acute peripancreatic fluid collection
Pancreatic pseudocyst
Acute necrotic collection
Pleural effusion

Epidemiology, Clinical Course & Prognosis

How common is severe acute pancreatitis?

  • Acute pancreatitis is a common condition
    • Affects between 40 and 70 people per 100,000 population per year
    • Annual incidence is increasing
  • Severe acute pancreatitis (SAP) accounts for 15-20% of cases of pancreatitis

What is the mortality rate of severe acute pancreatitis?

  • Still carries high mortality though overall deaths remain stable despite increased incidence:
    • Reflects recent advances in management
  • Mortality rate of up to 30% reported


What are the causes of acute pancreatitis?

Obstructive / Mechanical
  • Gall stones (50%)
  • Malignancy:
    • Pancreatic ductal carcinoma
    • Ampullary carcinoma
    • Islet cell tumour
    • Sarcoma
    • Lymphoma
  • ERCP (5% of procedures)
  • Trauma
  • Penetrating duodenal ulcer
  • Congenital abnormalities
  • Cystic fibrosis
  • Alcohol (20%)
  • Autoimmune / vasculitic disease
  • Scorpion stings
  • Hypoxemia / ischaemia
  • Drugs
  • Hypothermia
  • Hypercalcemia
  • Hypertriglyceridemia (>20mmol/L)
  • Viruses (Mumps, HIV, CMV, EBV)
  • Other infections
  • Venovenous - requires an external pump


A commonly used mnemonic is: I GET SMASHED

  • Idiopathic
  • Gall stones (50%)
  • Ethanol (20%)
  • Trauma
  • Steroids
  • Mumps and other viruses (EBV, CMV, HIV)
  • Autoimmune diseases (SLE, polyarteritis nodosa, pregnancy)
  • Scorpion stings
  • Hypercalcemia, hyperlipidemia, hypothermia, hypotension (ischemia)
  • ERCP, emboli
  • Drugs

Which drugs are associated with pancreatitis?

  • Steroids
  • Anticonvulsants – sodium valproate
  • Antibiotics – tetracycline, sulfonamides, metronidazole, nitrofurantoin, isoniazid
  • Chemotherapy agents – cisplatin, asparaginase
  • Diuretics – furosemide, thiazide
  • Antihypertensives – ACEi, methyldopa
  • Immunosuppressants – azathioprine, mercaptopurine
  • NSAIDs
  • Statins

Which infections are associated with pancreatitis?

  • Viruses – Mumps, HIV, EBV, CMV, hepatitides, cocksackie, measles, rubella
  • Bacteria – Legionella, Mycoplasma pneumoniae, Salmonella, Campylobacter, Mycobacterium tuberculosis, Legionella
  • Fungi – Aspergillus, cryptosporidium
  • Parasites – Ascaris, Toxoplasma

What are the likely reasons for idiopathic pancreatitis?

  • Often a significant duration between exposure to precipitant and symptoms making diagnosis difficult
  • True idiopathic pancreatitis becoming rarer:
    • Increased diagnostic work-up
    • Recognition of genetic causes of disease


What are the underlying pathophysiological mechanisms in pancreatitis?


What are the symptoms & signs of pancreatitis?

  • Abdominal Pain:
    • Epigastric
    • Radiates to back
    • Severe in nature
    • Alleviated by leaning forward
  • Nausea
  • Systemic features:
    • Tachycardia
    • Pyrexia
  • Vomiting
  • Abdominal distension
  • Peritonism
  • Signs of retroperitoneal haemorrhage (tracks along tissue planes)
    • Grey–Turner’s sign: bruising of the flanks
    • Cullen’s sign: peri-umbilical bruising
    • Fox’s sign: bruising of the inguinal ligament


What are the complications associated with acute severe pancreatitis?

Local (Pancreatic)
  • Interstitial Oedematous pancreatitis:
    • Peripancreatic collection
    • Pseudocyst (pancreatic fluid surrounded by a wall of fibrous or granulation tissue)
    • Abscess (circumscribed collection of pus)
  • Necrotising pancreatitis:
    • Sterile parenchymal necrosis
    • Infected parenchymal necrosis
  • Pancreatic insufficiency (and Type 3c Diabetes)
  • Ascites
  • Portal vein / splenic thrombosis
  • Intraperitoneal bleeding
  • Retroperitoneal bleeding
  • Bowel obstruction
  • Enteric fistulas
  • Intrabdominal hypertension
  • Sepsis
  • Multiorgan failure
  • Respiratory:
    • Respiratory failure
    • ARDS
    • Effusions
  • DIC
  • Renal failure
  • GI Bleeding

What are pancreatic pseudocysts? 

  • A collection of pancreatic secretions resulting from pancreatic duct leakage:
    • Become encased in granulation tissue
  • Occurs in approximately 5% of cases of acute pancreatitis
  • Presentation may be:
    • Asymptomatic
    • Isolated pain
    • Due to complications including bleeding, infection or rupture
  • Rarely, pseudocysts can cause gastric outlet and/or biliary obstruction and thrombosis of splenic or portal veins
  • About 50% will resolve spontaneously:
    • Usually managed conservatively
    • May require interventional management if symptomatic

What is pancreatic necrosis and what are the consequences?

  • Ischaemia and autodigestion lead to necrosis of peri-pancreatic fat and surrounding tissue· Appearance changes over time:
    • Early: appears as a diffuse semi-solid mass with no obvious demarcation
    • Late (>4 weeks): develops a fibrinous wall making it more amenable to intervention·
  • Infected necrosis is associated with significant morbidity and mortality
    • Image-guided needle aspiration of pancreatic tissue is required to confirm the diagnosis
    • Proven infection necessitates drainage/debridement


What are the most common bacteria responsible for infected pancreatic necrosis?

  • Organisms are usually gut-derived:
    • Common pathogens – Escherichia coli, Bacteroides, and Enterococcus
    • Rarer pathogens -Staphylococcus and Pseudomonas
  • Fungal infection rare but more common when prophylactic antibiotics are given

What are the causes of hypoxia in pancreatitis?

Often multifactorial:

  • ARDS due to systemic cytokine release
  • Pleural effusions due to third space fluid mobilization and aggressive fluid resuscitation·
  • Pulmonary oedema (decreased cardiac contractility, capillary leak, fluid resuscitation)·
  • Aspiration pneumonia (decreased level of consciousness, history of vomiting)

Work-Up Summary

How do you work-up the patient with pancreatitis?

To Determine Diagnosis

Diagnosis established by 2 of:

  • Abdominal pain
  • Serum amylase and/or lipase >3x upper limit of normal
  • Characteristic findings from abdominal imaging

Serum Marker

  • Lipase (preferable)
  • Amylase
To Determine Aetiology

History & Examination

  • History of alcohol intake
  • Medication
  • Recent procedures

Laboratory Investigations

  • LFTs
  • Calcium
  • Triglycerides
  • Viral antibodies

Imaging Investigations

  • Abdominal ultrasound
  • To rule out microlithiasis if other investigations negative:
    • Endoscopic ultrasound - first line
    • MRCP
  • CT if persistent organ failure at 6-10 days
To Determine Severity / Prognosis

Scoring Sytstems

  • Atlanta Criteria
  • APACHE II Score
  • Glasgow's Score (at 48 hours)


  • ABG
  • LDH
To Assess for Complications
  • CXR
  • ABG
  • Renal function tests

Laboratory Investigations

Which enzymes can be measured to aid in the diagnosis of pancreatitis and what are their advantages?

  • Amylase & lipase are enzymes derived from pancreatic acinar cells
  • Both have their own advantages
  • Where possible lipase is recommended as the assay of choice

  • Serum amylase remains most commonly used in clinical practice
  • Diagnosis suggested when level is greater than 3x upper range of normal (>300 IU/L)
  • Less accurate than lipase for diagnosis:
    • May remain within normal levels in as many as one fifth of patients
    • Levels rise quickly and have a serum half life of 2 hours - a single peak in amylase may be missed
  • Non-specific and may be elevated due to other causes
  • Level of elevation does not necessarily correlate with disease severity or prognosis
  • Diagnosis suggested when level is greater than 600 IU/L
  • Greater overall accuracy than amylase
    • Recommended as assay of choice by BSG
    • More sensitive and specific for diagnosis
    • Concentrations are increased for up to 14 days after onset of pancreatitis

Which conditions other than pancreatitis can cause a raised amylase?

  • Intrabdominal pathology
    • Bowel perforation, obstruction, ischaemia
    • Fallopian tube pathology
  • Diabetic ketoacidosis
  • Pneumonia
  • Neoplasm

Imaging Investigations

What is the role of Imaging in pancreatitis?

  • An ultrasound of the RUQ should be performed in all cases to assess for biliary stones and obstruction
  • After negative routine work-up for biliary aetiology, endoscopic ultrasonography (EUS) is recommended as the first step to assess for occult microlithiasis, neoplasms and chronic pancreatitis
  • If EUS is negative MRCP is advised as a second step to identify rare morphologic abnormalities

Which imaging modalities are useful in acute pancreatitis and what might they show?

Abdominal X-ray
Ileus, loss of psoas shadow, sentinel loop, pancreatic calcification, and calcified gallstones
Chest X-ray
Pleural effusions (usually on left) and pulmonary infiltrates
Chest US
Visualization of pleural effusion; guided drainage for diagnosis or treatment of respiratory failure
Abdominal US
Superior to CT at detecting stones in the gallbladder or biliary duct; may be difficult to visualize pancreas, especially in the presence of ileus; free peritoneal fluid
Endoscopic Ultrasound
Combination of endoscopy and high-frequency US; useful if abdominal US/CT fail to detect CBD stones; useful when CT/MRI are not available/feasible
Renal Tract US
If oliguric, to rule out obstruction/pyelonephrosis
Contrast-Enhanced CT
Contrast deficit indicating necrosis, local pathology, e.g. abscess, acute fluid collections (pseudocysts/abscesses usually form after approximately 4 weeks), haemorrhage, thrombosis, pseudoaneurysm; can guide interventional procedures (FNAB and drain placement)
May be of use in the stable patient in whom CT contrast is contraindicated; can delineate necrotic areas; excellent at assessing biliary tree
Haemorrhage localization and guided endovascular management

What is the role of CT in pancreatitis?

  • CT is indicated if the diagnosis is equivocal, to rule out alternative intra-abdominal catastrophes
  • In acute severe pancreatitis, CT is used to detect and stage regional complications such as pancreatic necrosis:
    • Should be performed in those with new or persisting organ failure
    • If the diagnosis is clear, it may be appropriate to delay CT imaging for at least 48–72 h after onset of symptoms because the full extent of pancreatic necrosis cannot be determined until this time
  • Patients with SAP often require multiple contrast-enhanced CT scans to assess progress and screen for complications
  • The risk of contrast nephropathy should be considered in patients who have already had septic, hypoxaemic, and ischaemic insults to the kidneys.

International Guidelines

  • The indication for initial CT assessment in acute pancreatitis can be:
    • Diagnostic uncertainty
    • Confirmation of severity based on clinical predictors of severe acute pancreatitis
    • Failure to respond to conservative treatment or in the setting of clinical deterioration
  • Optimal timing for initial CT assessment is at least 72-96 hours after onset of symptoms
  • Follow up CT or MR in acute pancreatitis is indicated when there is a lack of clinical improvement, clinical deterioration, or especially when invasive intervention is considered

Severity & Prognostic Scoring

How can acute pancreatitis severity be classified and scored?

  • A number of systems exist to identify severity and prognosticate pancreatitis
    • Considered advantageous over clinical judgement alone
    • Useful in determining optimum location of care
  • Limitations exist with many of the scoring systems:
    • Cumbersome to complete
    • Require 48 hours to gather variables for some scores
    • Lack accuracy in early stages
    • Limited clinical value
Classification Systems

Atlanta Criteria

  • Divides pancreatitis in to two pathophysiological types:
    • Interstitial oedematous pancreatitis
    • Necrotising pancreatitis
    • Classifies severity as mild, moderate and severe
  • Determined by presence of local features and organ failure
Prognostic Scoring Systems
Disease Specific


  • Ransoms:
    • Originally designed for gallstone-induced pancreatitis
    • Uses age, nine laboratory parameters plus fluid requirements to calculate a score over 48 hours
    • A score of >3 at 48 hours indicates the presence of severe pancreatitis
  • Glasgow-Imrie:
    • Requires 48 hours to complete
    • Uses age and seven laboratory parameters to predict severe pancreatitis


  • Balthazar CT grade
    • A score of >8 at 24 hours defines severe acute pancreatitis

What is the Atlanta Classification for pancreatitis?


Classified according to the Revised ATLANTA criteria 2012

  • No organ failure
  • No local complications
  • Transient organ failure (<48 hours)
  • Local complications +/-
  • Persistent organ failure

*Local complications include:
Acute peripancreatic fluid collection
Pancreatic pseudocyst
Acute necrotic collection
Pleural effusion

What is Ranson’s score for pancreatitis?

  • Ranson’s score is used to determine the severity and predict the mortality of acute pancreatitis
  • Five parameters are assessed on admission and the other six are assessed 48 hours post-admission
  • One point is given for each parameter met:
On Admission
  • Age >55 years
  • WCC >16,000
  • LDH >350 U/I
  • AST >250 U/I
  • Glucose >11 mmol/L
At 48 hours
  • Haematocrit fall >10%
  • Urea rise >1.8 mmol/L despite fluid resuscitation
  • Calcium <2 mmol/L
  • pO2 <8.0 kPa
  • Base deficit >5 mEq/L
  • Fluid needs of >6 L
  • The estimated mortality from pancreatitis by these criteria, according to the score generated, are as follows:
    • 0-2 = 1%
    • 3-4 = 15%
    • 5-6 = 40%
    • >6 = 100%

Management Summary

How do you manage the patient with severe acute pancreatitis?

Key Principles

  • Aggressive fluid resuscitation and pain management
  • Early ERCP if indicated
  • Early enteral feeding (preferably via NG route)
  • Avoid early surgical intervention for necrotic pancreatitis
  • Vigilant supportive care to avoid complications
Initial Resuscitation & Supportive Care
  • ABCDE approach treating abnormalities as found
  • Manage airway and breathing:
    • If intubation may be required, aspiration a major risk
    • Multifactorial causes for respiratory failure (ARDS, diaphragmatic splinting (pain, intra-abdominal oedema or fluid collections) or pleural effusions)
  • Optimise haemodynamics:
    • Early and aggressive fluid resuscitation
    • May require vasopressor support if severe systemic inflammatory response
    • Maintain UO >0.5 ml/Kg
  • Manage electrolyte abnormalities:
    • Vigilance over hypocalcaemia and arrhythmias
  • Ensure optimal analgesia:
    • PCA usually required
    • Some support use of thoracic epidural
    • Aim to prevent further atelectasis
  • Correct coagulopathy in the setting of VTE
  • Optimise nutrition:
    • Early enteral feeding (within 72 hours):
      • Nasogastric - effective in 80%
      • Nasojejunal second line
    • No advantages for early TPN - only after 7 days if enteral fails
  • Vigilance to good supportive care - often long stays and prone to complications
    • Strict glycaemic control
    • DVT prophylaxis (balance against risk of intrabdominal haemorrhage)
    • Stress ulcer prophylaxis
    • VAP bundles
    • Aseptic precautions
Specific Management
  • Management of biliary obstruction
    • Early ERCP indicated to remove gallstone (within 72 hours)
    • Coagulation should be corrected
    • Surgical management of gallstones during same hospital admission or within 2 weeks
  • Management of infected collection / necrosis
    • Prophylactic antibiotics not routinely recommended
    • If clinical sepsis ensure blood cultures taken and treat as per surviving sepsis
    • If >30% pancreatic necrosis, should undergo FNA to obtain material for culture 7–14 days after the onset of the pancreatitis
    • If infected abscess confirmed post-needle aspiration prescribed according to local guidelines
    • If infected will require definitive intervention (Ideally delay until 4 weeks):
      • Radiological drainage first line - successful in 50%
      • Endoscopic drainage
      • Surgical drainage (delay until clear demarcation)
  • If evidence of retroperitoneal gas on CT:
    • Broad spectrum antibiotics
    • Surgical drainage or debridement
    • Delayed surgery (>2 weeks):
      • Associated with increased survival
      • Allows demarcation of necrotic and preserved tissue
Referral & Deposition
  • All patients with sever acute pancreatitis should be manages on HDU
  • Refer all with persisting organ failure or requiring intervention to regional centre

Critical Care Admission & Referral

Which patients with pancreatitis should be admitted to critical care?

  • UK guidelines state that all patients with acute severe pancreatitis should be managed on the high dependency unit (HDU):
    • Can be difficult in practice – ensure all referred to the critical care outreach team for regular review and escalation of care if deterioration occurs
  • Particular features which suggest critical care admission may be beneficial include:
    • Age 70 years or older
    • Body mass index over 30 kg/m2
    • Hypotension not responsive to fluid resuscitation
    • >30% necrosis of the pancreas
    • Pleural effusions
    • Three or more of Ranson’s criteria
    • CRP > 150 mg/L at 48 hours

 (Adapted from World Association Guidelines)

Which patients with pancreatitis should be referred to the regional centre?

  • All patients with necrotizing pancreatitis with the following features should be referred to a regional HPB centre for discussion:
    • Greater than 30% necrosis of the pancreas or ANCs on early CT (within seven days of admission)
    • Persisting organ dysfunction for greater than 48 h requiring organ support (e.g. ventilation, renal replacement therapy)
    • Infected WON requiring drainage or necrosectomy, gastric or duodenal outflow obstruction secondary to acute peripancreatic collections, pseudocyst or WON
    • Evidence of haemorrhage on CT

Supportive Management

Which patients should receive antibiotics in severe acute pancreatitis?

  • Antibiotics should be used in any case of pancreatitis complicated by infected pancreatic necrosis but should not be given routinely for fever, especially early in the presentation:
    • Carbapenem usually the best class due to penetration in to pancreatic tissue
    • Fungal infection should be considered in severe infected pancreatic necrosis
  • Image-guided FNA should be used to gain material for culture when:
    • Necrosis and features of sepsis
    • 30% necrosis and persistent symptoms at 7-14 days
  • Antibiotic prophylaxis in severe pancreatitis is controversial:
    • Trials performed in this area show great heterogeneity with a variety of antibiotics used for different durations
    • Routine use of against infection is not currently recommended
    • If used may increase the risk of fungal superinfection


What nutrition therapy should patients with severe acute pancreatitis receive?

  • Early EN is now standard of care in patients with acute pancreatitis
    • Recent research suggests improved outcomes compared with previous strategies of pancreatic rest with TPN
    • Guidance recommends commencing within 72 hours if intolerant of oral intake
  • Enteral nutrition in acute pancreatitis can be administered via either the nasojejunal or nasogastric route:
    • Many recommend early NJ feeding and supported by ESPEN guidance
    • Two trials have also found no difference in outcomes in patients fed gastrically versus jejunally
    • Nasogastric usually successful in 80% of patients
    • Nasojejunal feeding should be used if intra-abdominal pressures are >15mmHg
  • Parenteral nutrition can be administered in acute pancreatitis as second-line therapy if nasojejunal tube feeding is not tolerated (pain, ileus,  nausea)


(NICE & ESPEN Guidelines)

What are the advantages of enteral nutrition in pancreatitis?

  • Cheaper
  • Avoids need for central line
  • Safer – associated with fewer complications
  • Better outcome overall
  • Maintains intestinal mucosal barrier
  • Prevents bacterial translocation

Specific Management

What are the indications for surgical and radiological interventions in severe acute pancreatitis?

  • Relieving biliary obstruction (e.g. ERCP)
  • Removing infected intra- and extra-pancreatic necrosis (Necrosectomy)
  • Pancreatic duct disruption
  • Management of symptomatic masses due to pseudocysts or sterile necrosis:
    • Gastric outlet or intestinal obstruction
    • Persistent pain

What is the role of ERCP in severe acute pancreatitis?

  • ERCP is indicated in all patients with biliary pancreatitis and cholangitis:
    • Ideally within 72 hours of onset of pain with proven or suspected gallstone aetiology
    • Urgent ERCP (<24 hrs) is required in patients with acute cholangitis
  • Allows sphincterotomy or stenting
  • Usually requires elective intubation and ventilation – high risk of respiratory complications

What should be done to prevent recurrence in gallstone pancreatitis?

  • All patients with severe acute pancreatitis due to gallstones should have a cholecystectomy to prevent recurrence:
    • Should ideally be performed during the same admission once symptoms have resolved
    • If unable should be booked on an elective list within two weeks of discharge

How should pancreatic necrosis be managed?

  • Management depends upon whether necrosis is sterile or infected:

    • Patients with >30% necrosis or clinical suspicion of sepsis should undergo guided fine needle aspiration for cultures

    • Sterile necrosis- debridement and/or drainage is not recommended 

    • Infected necrosis – Optimal interventional strategy usually percutaneous catheter or endoscopic drainage first line. Can be followed by surgical necrosectomy if required.

What interventions are available to manage pancreatic necrosis?

  • Aim of drainage is to remove infected material without breaching the peritoneum
  • Optimum method remains controversial – usually dependent upon local resources and expertise:
Percutaneous Drainage
  • Associated with fewer complications than surgical necrosectomy though no mortality benefit
  • Avoids surgical necrosectomy in30-50% of cases
  • Can be considered as a bridge to surgery in patients to unstable placement of a drainage tube into the fluid collection
Endoscopic Transluminal Drainage
  • Like percutaneous drainage associated with less morbidity and cost than surgical necrosectomy
  • Involves insertion of a stent to drain necrotic cavity into gastric or duodenal lumen
  • Used only in carefully selected patients and is dependent on local expertise.
Surgical Necrosectomy
  • Once the gold standard now less frequently used as first line
  • Debridement is done bluntly with hydrosonic irrigation frequently used to avoid vascular injury
  • May require multiple operations to achieve adequate debridement

What are the suggested timings for intervention in necrotising pancreatitis?

  • Intervention for removal of necrosis should be delayed where possible until at least 4 weeks after initial presentation:

    • Allows collection to become walled off

    • Associated with decreased mortality compared to earlier intervention


The Guidewire
Trainee in ICM & Anaesthesia


The Guidewire
Trainee in ICM & Anaesthesia