Acute Pancreatitis
Last updated 20th June 2019 - Tom Heaton
, Pancreatitis is inflammation of the pancreas.
It involves activation of proteolytic enzymes that can lead to haemorrhagic necrosis of the pancreatic parenchyma.
This is a good introduction video from Armand Hasudungan: https://www.youtube.com/watch?v=UVof2fZdfjY
Atlanta criteria 2012 revision:
Mild - Acute inflammation of the pancreas with oedema and resolves without complications
Moderate - when the is transient organ failure (<48h) that resolves.
Severe - Acute inflammation of the pancreas with necrosis and develops complications, including persistent organ failure (>48h).
Diagnosis requires 2 out of 3 of:
It involves activation of proteolytic enzymes that can lead to haemorrhagic necrosis of the pancreatic parenchyma.
This is a good introduction video from Armand Hasudungan: https://www.youtube.com/watch?v=UVof2fZdfjY
Atlanta criteria 2012 revision:
Mild - Acute inflammation of the pancreas with oedema and resolves without complications
Moderate - when the is transient organ failure (<48h) that resolves.
Severe - Acute inflammation of the pancreas with necrosis and develops complications, including persistent organ failure (>48h).
Diagnosis requires 2 out of 3 of:
- Appropriate history
- Elevated enzymes (amylase or lipase
- Radiological findings of pancreatitis
Pathophysiology
The pancreas is an endocrine and exocrine gland.
In regards to its exocrine function, it usually produces and secretes proteases, amylases and lipases into the ducts which are then released into the duodenum.
An initial inflammatory trigger can lead to disruption of the normal excretory process, with such enzymes resulting in ‘autodigestion’.
This further pancreatic injury can propagate an inflammatory process and injury.
As well as local consequences, there may be a notable systematic response to the inflammation.
This can then result in the multisystem effects of pancreatitis, including the multi-organ failure seen in severe disease.
In regards to its exocrine function, it usually produces and secretes proteases, amylases and lipases into the ducts which are then released into the duodenum.
An initial inflammatory trigger can lead to disruption of the normal excretory process, with such enzymes resulting in ‘autodigestion’.
This further pancreatic injury can propagate an inflammatory process and injury.
As well as local consequences, there may be a notable systematic response to the inflammation.
This can then result in the multisystem effects of pancreatitis, including the multi-organ failure seen in severe disease.
Aetiology
GET SMASHED is the mnemonic often used
Gallstones
Ethanol
Trauma
Steroids
Mumps (and other viruses)
Autoimmune (SLE, pregnancy)
Scorpion venom
Hypers - hypercalcaemia, hyperlipidaemia, hypothermia, hypotension
ERCP
Drugs - sulfasalazine, azathioprine, NSAIDs, diuretics, metronidazole, ranitidine, valproate, erythromycin, tetracyclines
Gallstone disease is the most common cause.
Alcohol is often the cause associated with the worst outcome.
Idiopathic is also a possible outcome - remember Dublin study though (high rate of gallstone disease on close examination)
Gallstones
Ethanol
Trauma
Steroids
Mumps (and other viruses)
Autoimmune (SLE, pregnancy)
Scorpion venom
Hypers - hypercalcaemia, hyperlipidaemia, hypothermia, hypotension
ERCP
Drugs - sulfasalazine, azathioprine, NSAIDs, diuretics, metronidazole, ranitidine, valproate, erythromycin, tetracyclines
Gallstone disease is the most common cause.
Alcohol is often the cause associated with the worst outcome.
Idiopathic is also a possible outcome - remember Dublin study though (high rate of gallstone disease on close examination)
Presentation
May present in a few ways:
Symptoms
Examination
Very variable - very well to severely ill
- Appropriate history and >3x normal lipase (amylase)
- Unexpected finding on CT
- Post ERCP
- Trauma - cyclist vs handlebars
Symptoms
- Severe upper abdo pain
- Epigastric. Can be RUQ or LUQ
- Usually fairly rapid onset, steadily increasing to peak
- Continuous
- Band like radiation into back
- Nausea and vomiting
- Steatorrhoea
- Anorexia
- Fevers and chills
Examination
Very variable - very well to severely ill
- Abdominal tenderness
- Abdominal distension
- SIRS response
- CVS compromise
- Jaundice
- Features of retroperitoneal haemorrhage
- Grey-Turner sign - flank ecchymosis
- Cullen sign - periumbilical ecchymosis
Assessment
Investigations
Bloods
Imaging
Bloods
- Amylase (x3 time normal)
- Lipase - more specific, longer half life
- FBC - raised WBC
- U&E - renal dysfunction
- LFTS - raised
- LDH - part of Ranson’s criteria
- Hyperglycaemia
- Hypocalcaemia
Imaging
- CT - contrast enhance
- May diagnose in cases of uncertainty
- Can detect structural complications
- CT severity index - extent of necrosis and peripancreatic inflammation
- Abdo US
- Assess for gallstones
- MRI
- CXR
- Assessment of complications
- AXR
- More in assessment of bowel obstruction
Severity Scoring
This can be done in several ways:
Glasgow-Imrie Score
Uses physiological and laboratory values from 48h after admission.
A score of < 3 suggests a low probability of severe pancreatitis.
Ranson’s Criteria
Similar scoring based on physiological and laboratory values.
Has an admission and 48 component.
Admission value of <3 suggests low risk.
48h score can suggest mortality rate.
- Glasgow-Imrie criteria - https://www.mdcalc.com/glasgow-imrie-criteria-severity-acute-pancreatitis
- Ranson's criteria - https://www.mdcalc.com/ransons-criteria-pancreatitis-mortality
- Physiology scores
- SOFA
- APACHE II
- CRP
- CT severity index
Glasgow-Imrie Score
Uses physiological and laboratory values from 48h after admission.
A score of < 3 suggests a low probability of severe pancreatitis.
Ranson’s Criteria
Similar scoring based on physiological and laboratory values.
Has an admission and 48 component.
Admission value of <3 suggests low risk.
48h score can suggest mortality rate.
Critical Care
May be referred to critical care for a few reasons:
Organ dysfunction
Organ dysfunction
- Renal
- CVS
- Resp
- ERCP
Management
No definitive treatment.
Supportive care:
If a triggering cause can be managed then this should be done e.g. gallstones.
Supportive care:
- CVS
- Fluid balance
- Oxygenation
- Nutrition
- Analgesia
- Nausea
If a triggering cause can be managed then this should be done e.g. gallstones.
Nutrition
No evidence for the concept of ‘pancreatic rest’.
The idea behind this is to avoid the stimulation of enzyme secretion and reduce their autodigestive effects too.
Patients with mild pancreatitis may be safely fasted for 3-4 days but patients with severe disease benefit from early nutrition.
Enteral nutrition prevents intestinal atrophy, improving gut mucosal function and thus reducing bacterial translocation and SIRS response.
In severe pancreatitis it has demonstrated fewer complications and reduced cost.
Severe pancreatitis
Mild/mod
The idea behind this is to avoid the stimulation of enzyme secretion and reduce their autodigestive effects too.
Patients with mild pancreatitis may be safely fasted for 3-4 days but patients with severe disease benefit from early nutrition.
Enteral nutrition prevents intestinal atrophy, improving gut mucosal function and thus reducing bacterial translocation and SIRS response.
In severe pancreatitis it has demonstrated fewer complications and reduced cost.
Severe pancreatitis
- Early EN
- Protocolised
- Consider more distal feeding if challenging e.g. post pyloric tube
- Consider PN support of EN if needing extra calorie input
- Control glucose
Mild/mod
- Patients can be fasted for 3-4 days, and maybe up to a week
- EN should be considered after this if there is a failure to resume normal diet
Surgical Intervention
This is uncommon and associated with significant complications.
Indications include:
Indications include:
- Debridement of infected necrosis
- Walled of necrosis (abscess)
- Intra-abdominal hypertension
Complications
Surgical/Anatomical
Systemic
Can also progress to chronic pancreatitis.
Specialist centre referral - failure of conservative treatment of infected necrosis and require debridement
- Pancreatic necrosis
- Threshold of 30% of the pancreas necrotic (non enhancing on scan)
- Threshold of 30% of the pancreas necrotic (non enhancing on scan)
- Infected necrosis
- Gas on CT
- Targeted antibiotics
- Best to get a culture first
- This may require IR intervention
- Gas on CT
- Acute pancreatic fluid collection
- Occurring within 4 weeks and without a well-defined wall
- Occurring within 4 weeks and without a well-defined wall
- Pseudocyst formation
- Fluid collection for >4 weeks and with a well defined wall
- Fluid collection for >4 weeks and with a well defined wall
- Compartment syndrome
- Ileus
- Retroperitoneal haemorrhage
Systemic
- Pain
- SIRS
- MOF
- AKI
- CVS dysfunction
- Third space losses
- Cardiac dysfunction (acidaemia, SIRS cardiomyopathy)
- GI losses
- SVR decrease
- Third space losses
- Respiratory compromise
- Atelectasis
- Oedema
- Effusions
- ARDS
- Atelectasis
- Liver failure
- AKI
- Electrolyte disturbance
- Hypocalcaemia
- Metabolic acidosis
- Hypocalcaemia
Can also progress to chronic pancreatitis.
Specialist centre referral - failure of conservative treatment of infected necrosis and require debridement
Epidemiology
Incidence about 30/100,000/year
Approx 15% are severe.
Mortality rate 1-2% (10% if severe)
Approx 15% are severe.
Mortality rate 1-2% (10% if severe)
Links & References
- Nickson, C. Pancreatitis. LITFL. 2019. https://litfl.com/pancreatitis-ccc/
- Clarke, E. Acute pancreatitis. NW FICM teaching. 2019.
- MDCALC. Glasgow-Imrie score. https://www.mdcalc.com/glasgow-imrie-criteria-severity-acute-pancreatitis
- MDCALC. Ranson’s criteria. https://www.mdcalc.com/ransons-criteria-pancreatitis-mortality
- Hasudungan, A. Acute pancreatitis - overview. Youtube. 2016. https://www.youtube.com/watch?v=UVof2fZdfjY
- Knott, L. Acute pancreatitis. Patient.info. 2016. https://patient.info/doctor/acute-pancreatitis-pro
