Written by Chin Ming Huay
Last Reviewed: April 2019
Review Due: April 2020
' a new-onset inflammatory disorder of the pancreas with the severity of the disease ranging from mild oedema to pancreatic necrosis and multiple organ failure'
I GET SMASHED
Drugs (e.g. diuretics, NSAIDs and azathioprine)
N.B. Gallstones, excessive alcohol intake and post-ERCP are the most common causes of acute pancreatitis
SIGNS AND SYMPTOMS
Onset: Rapid onset, gradually worsening over several hours
Character: Tight, ‘band-like’
Radiation: Radiates to the back
Associated symptoms: As below
Exacerbating Factors: Worse on moving
Relieving Factors: Lying down, not moving
Severity: Moderate to very severe
Nausea & Vomiting
Loss of appetite (mostly due to pain)
Steatorrhoea (pale stools) and darker urine may be present
In severe pancreatitis:
Grey Turner’s Sign (bruising of the flanks)
Cullen’s Sign (periumbilical bruising)
Signs of hypovolaemia or hypovolaemic shock (including tachycardia, dry mucous membranes, cool peripheries and sweaty/clammy skin)
The pancreas becomes inflamed in response to autodigestion of the pancreatic cells which occurs when the digestive enzymes in pancreatic secretions become activated. This triggers a systemic inflammatory response and significant movement of fluid into the peritoneal cavity (third space losses) due to leaky capillaries therefore leading to hypovolaemia and hypovolaemic shock.
Gallstone pancreatitis is caused by obstruction of the flow of pancreatic enzymes into the duodenum by a gallstone. Trypsinogen is cleaved into trypsin, leading to damage of the pancreatic acinar cells. Increased intracellular calcium may also potentiate activation of trypsinogen.
There are a few different mechanisms involved in alcohol-induced pancreatitis. Alcohol may directly affect the pancreatic acinar cells, causing inflammation and damage to the cell membranes. It may also interfere with calcium homeostasis which may potentiate activation of trypsinogen.
Diagnostic if raised more than 3 times the upper limit of normal, within 24 hours of onset of pain. Levels start to fall back to normal after 3-5 days, so delayed serum amylase testing may show a false negative.
Evidence of gallstone disease
To exclude duodenal perforation which may be another cause of epigastric pain and raised serum amylase, also to exclude ARDS which may be a complication of pancreatitis
To investigate for gallstone disease
To assess pancreatic damage
Treatment for acute pancreatitis is largely supportive. If there is a clear reversible underlying cause, such as gallstones, this should be treated appropriately.
Fluid losses in pancreatitis can be significant. Ensure haemodynamic stability and measure urine output.
Subcutaneous LMWH for prevention of DVT and PE
Early enteral nutrition is preferred however this may be through an NG tube if patient cannot tolerate normal diet
Alcohol - Counselling, referral to addiction services if required and vitamin replacement
Gallstones - ERCP or Cholecystectomy may be indicated
Incidence in the UK ranges from 150 to 420 cases per 1,000,000 people.
Systemic Inflammatory Response
Acute Kidney Injury
Portal Vein Thrombosis
The Glasgow PANCREAS scoring system for pancreatitis indicates severity and predicts mortality.
PaO2 <8.0 kPa
Age >55 years
Neutrophils (Total white cell count) >15 x109/L
Renal (Increase in urea) >1.8mmol/L
Enzymes – Serum LDH >600U/L and serum AST >250U/L
Sugar (Blood glucose) >10 mmol/L
A score >3 suggests severe pancreatitis
0-2 of the above: Mortality <1%
>6 of the above: Mortality can go up to 100%
NICE Guideline 104 Pancreatitis 2018
Zyromski NJ. Acute Pancreatitis. BMJ Best Pract. 2019
Kumar & Clark. Kumar and Clark’s Clinical Medicine, 8th Edition | Parveen Kumar, Michael Clark. Saunders Ltd. 2012.