A previously well 48 year old male, presents to ED with a 48 hour history of severe epigastric pain radiating to his back. On surgical examination he is extremely tender with guarding.
HR 140, BP 100/60, CRT 5 Secs, RR 25, Sp02 97% on 60% oxygen.
Notable blood results:
- Hb 185 g/dl
- WCC 12
- Urea 18.9
- Cr 134
- Bili 32, ALT 75, GGT 20, ALP 23
- Amylase 2150
- Lactate 7.5
A CT Chest/Abdomen/Pelvis is requested that shows an inflamed pancreas consistent with acute pancreatitis.
After several litres of fluid resuscitation but with minimal change to his physiological parameters, he is referred to critical care for ongoing management and monitoring.
What are the causes of Pancreatitis?
The causes of pancreatitis are many, but can be condensed into the acronym ‘I GET SMASHED’ (Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpions and snakes, Hyperlipidaemia and hypercalcaemia, ERCP, Drugs)
The most common causes in the UK are Gallstones and Alcohol.
Idiopathic Pancreatitis is diagnosis of exclusion.
How is the diagnosis made?
The diagnosis of Pancreatitis requires two or more of the following
- Pain consistent with Acute Pancreatitis
- A rise in Biochemical Markers – Amylase or Lipase (more specific) >3 times upper limit of normal
- Imaging confirming Acute Pancreatitis
How do we classify severity of pancreatitis?
The revised Atlanta classification quantifies severity as:1
- Mild – absence of organ failure or complications
- Moderate – transient organ failure or local/systemic complications without persistent organ failure
- Severe – persistent >48 hours organ failure.
There are many other scoring systems available designed to predict complications or disease course. They have a low specificity and low positive predictive value and are therefore not sufficiently reliable to deviate from generic risk predictors such as EWS/APACHE II.2
Investigation of Acute Pancreatitis
- FBC, U&E’s, LFT’s, Coagulation, Bone profile
- Ultrasound +/- MRCP
- CT (initially if diagnostic uncertainty, more specific after 3-5 days)
Management of Acute Pancreatitis
Management is largely supportive but there are specific aspects that all should be aware of when considering ongoing management.
- Fluids (large sequestration in severe inflammation)
- Analgesia (ensure able to deep breathe/cough effectively)
- Endocrine/Exocrine support (e.g. insulin)
- Organ support
1. Nutrition (ESPEN Guidelines 2020)3
Early v Late
- Early feeding (<48 hours) has shown a reduction in infected necrosis, organ failure and need for invasive intervention
- Those with mild pancreatitis can eat and drink as soon as able. The majority can tolerate diet and do not require gut rest
- Enteral Support should be considered within 24-72 hours if oral diet is not possible
Route of Delivery
- Parenteral Nutrition was once thought to be beneficial as it could potentially limit activation of the pancreatic exocrine system, but parenteral nutrition is not without its own risks and complications
- Enteral feeding has beneficial effects on maintenance of both function and structure of the gut mucosa, particularly with respect to prevention of bacterial translocation
- There is consistent evidence that enteral feeding reduces mortality and infective complications.
- When enteral feeding is indicated NG feed should be the first line. NJ feeding is reserved for those who fail to establish feed via the NG route.
- Elemental feeds have been suggested as a way of reducing pancreatic stimulation. There is inadequate evidence to support the use of these at present. This also applies to probiotics and immune-nutrition
- Mild Pancreatitis – Consider cholecystectomy before discharge
- The role of prophylactic antibiotics to prevent infection in pancreatitis has been long debated
- The most recent literature appears to suggest no benefit in mortality or morbidity with prophylactic antibiotic therapy
- Antibiotics should be used where evidence of infected pancreatic necrosis exists (or signs of extra-pancreatic infection)4
- Detecting evidence of infected necrosis can often be clinically challenging
- Procalcitonin (PCT) may be a useful tool when suspecting infected necrosis
4.Involvement of Local HPB Team
- The following patients should be referred:
- Severe acute pancreatitis or inpatient for >2 Weeks 5
- Presence of any local complication
Intervention for local complications of acute pancreatitis is associated with a high morbidity and mortality, particularly early in the disease process. If possible, delaying intervention leads to improved surgical outcome.
Intervention for infected pancreatic necrosis is often required, as this rarely improves with antibiotics alone.
- Pancreatic Necrosis
- Venous Thrombosis
- Pseudoaneurysm (risk of bleed)
- Abdominal Compartment Syndrome
Indications for Intervention
a) Percutaneous/Endoscopic Drainage
>4 weeks post onset of pancreatitis:
- Ongoing organ failure with a collection not thought to be infected necrosis
- Gastric outlet, biliary, or intestinal obstruction due to a ‘walled off’ necrotic collection
- Symptomatic or growing pseudocyst
>8 weeks post onset of pancreatitis:
- Ongoing pain and/or discomfort with an associated collection
b) Surgical Intervention
- Escalation following failure to resolve via a percutaneous/endoscopic intervention
- Abdominal compartment syndrome with failed conservative measures
- Failed endovascular control of bleeding peri-pancreatic vessels
- Ischaemic bowel or gallbladder due to acute pancreatitis
- Fistulation between bowel and peripancreatic collection
- Multi-Organ Failure
3.Potential Long Term Requirements
- Dietary enzyme supplements
Key take home messages
- Pancreatitis is a multi-system pro-inflammatory disease associated with many complications
- The majority of presentations with pancreatitis are self-limiting
- Severe Acute Pancreatitis mortality is approximately 40%
- Early enteral feeding is preferred
- Routine antibiotics are not required unless there is evidence of an infective complication
- Early MDT and specialist involvement is recommended
- Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1): 102-111.
- Robert JH, Frossard JL, Mermillod B, et al. Early prediction of acute pancreatitis: prospective study comparing computed tomography scans, Ranson, Glasgow, Acute Physiology and Chronic Health Evaluation II scores, and various serum markers. World J Surg 2002;26(5): 612-619.
- Arvanitakis M, Ockenga J, Bezmarevic M, et al. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr 2020;39(3): 612-631.
- Leppäniemi A, Tolonen M, Tarasconi A, et al. WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg 2019;14: 27.