Pancreatitis is the inflammation of the pancreas and is most commonly caused by gallstones and excessive alcohol use. These patients typically present with mid-epigastric or left upper quadrant pain which radiates to the back.
Pancreatitis can be either acute or chronic, with acute being reversible pancreatic injury and chronic being progressive pancreatic injury that causes a loss of function. As pancreatitis can become life-threatening, especially in acute pancreatitis, suspected cases should be assessed and treated urgently.
Incidence of acute pancreatitis varies between 5 and 80 per 100,000 around the globe and is on the increase. Mortality rate of acute pancreatitis in the UK ranges between 5-25% depending on severity.
In the UK, 50% of acute pancreatitis is due to gallstones, 25% due to alcohol excess and 25% are considered idiopathic. Idiopathic acute pancreatitis are generally considered to be caused by microlithiasis or biliary sludge in the pancreas.
A useful mnemonic for general causes of pancreatitis is ‘I GET SMASHED’:
- Gallstones/Genetic: gallstones and cystic fibrosis
- Autoimmune pancreatitis
- Scorpion/Spider: venomous stings and bites
- ERCP (as a complication of ERCP procedures)
- Thiazide diuretics
- Valproic acid
The exact mechanism of injury is still uncertain, but evidence suggests abnormality with intracellular calcium accumulation. This interferes with the normal activity of zymogens and lysosome granules and activates enzymes prematurely. The intraluminal activation of proteolytic enzymes causes autodestruction of the pancreatic tissues and subsequently triggers inflammation which exacerbates the degradation. This leads to proteolysis, fat necrosis, haemorrhage and liquefying necrosis.
Acute pancreatitis can present in a variety of ways but the main clinical feature is abdominal pain.
Typical features of abdominal pain from pancreatitis include:
- Site of pain: Pain may be epigastric or right upper quadrant in location.
- Onset of pain Acute or sub-acute onset.
- Characteristic: Sharp, constant pain.
- Radiation: Pain may radiate to the back
- Timing: May last for hours before pain plateaus
- Exacerbating factors: worsen with movement
- Severity: typically severe pain, although does not correlate with severity of disease
Vomiting and nausea is seen in the majority of acute pancreatitis cases. Jaundice and steatorrhoea may occur if obstruction is the cause. Abdominal bruising, such as Cullen’s (periumbilical) or Grey-Turner’s (flank bruising) signs, may also be present.
First-line investigations for any pancreatitis include baseline blood tests and abdominal ultrasound or CT scan. Further imaging investigations can be done using Computer Tomography (CT) and Magnetic Resonance Imaging (MRI) to look for other intra-abdominal complications.
|Serum Amylase or Lipase||If elevated above 3x normal amounts, confirms acute pancreatitis. Both biomarkers offer similar diagnostic accuracy but lipase is more preferable to amylase as it remains elevated for longer.|
|Full Blood Count||Leucocytosis indicates active inflammation. High haematocrit predicts poor prognosis.|
|C Reactive Protein (CRP)||Elevated CRP indicates inflammation and infection and used as early indicator of severity. >200 units/L is suggestive of pancreatic necrosis.|
|Liver Function Test||Mostly normal or slightly elevated alkaline phosphatase (ALP)/ bilirubin/alanine aminotransferase (ALT). Bilirubin can be raised in biliary obstruction.|
|Urea and creatinine||Elevation suggestive of hypovolaemia and increased risk of severe pancreatitis.|
|Liver function tests||Elevated ALT > 3x upper limit suggests a gallstone disease aetiology.|
|Electrolytes||Severe acute pancreatitis produces hypocalcaemia. Hypercalcaemia is an uncommon cause of pancreatitis.|
|Serum triglycerides||>11.3 mmol/L suggests hypertriglyceridaemia as a cause.|
|Arterial blood gas and oximetry||Can identify hypoxia and pH imbalances in context of organ dysfunction|
|Abdominal Ultrasound||Not necessary for diagnosis as pancreatitis is a clinical diagnosis Able to detect presence of gallstones and pancreatic inflammation, calcification or fluid collection|
|Abdominal Computed Tomography,|
|Not necessary for diagnosis but can help if there is diagnostic doubt if there are findings of pancreatic inflammation or peri-pancreatic stranding. It can also identify potential underlying causes, such as gallstones.|
|Chest X ray||Not for diagnostic use but to rule out other diagnosis that may present with epigastric pain|
Initially, assess the patient using the ABCDE approach and manage haemodynamic instability and systemic inflammatory response syndrome (SIRS) if required. The management of haemodynamics and intensive care support is critical in reducing the risk of organ failure and death. Patients should also be given supplemental oxygen if oxygen saturations are low. Prophylactic antibiotics are not needed unless infection is suspected.
IV fluids resuscitation is always a priority. IV crystalloids, such as Hartmann’s solution or normal saline, should be given at 5-10 ml/kg/hour initially. Afterwards, fluid therapy can be adjusted based on indicators of end-organ perfusion such as heart rate, mean arterial output and urinary output.
The timing of nutrition (or the ‘pancreatic rest’ theory) has been debated. However, current evidence suggests earlier oral feeding provides better outcomes. Hence, it is important to establish feeding as soon as the patient can tolerate it. Oral feeding is preferred over enteral tube feeding, which is preferred over total parenteral nutrition. Patients should only be kept nil by mouth only if necessary (e.g. vomiting, ileus or anticipating surgery).
Offer analgesics (paracetamol, NSAIDs and opioids) to control pain and follow the standard pain ladder approach.
Antiemetics should also be given if a patient has nausea or is vomiting; IV ondansetron is commonly given.
For pancreatitis secondary to gallstones, consider ERCP if there is concurrent cholangitis or pancreatitis is due to gallstone. Cholecystectomy should also be performed after the acute episode resolves.
For pancreatitis secondary to alcohol, patients should be provided alcohol abstinence support after they are stabilised. Treatment for alcohol withdrawal should also be considered if the patient has a history of chronic alcohol abuse.
Complications may be detected using contrast-enhanced abdominal CT after the first 4 days of presentation as complications, such as pancreatic necrosis, take time to develop.
As acute pancreatitis can be life-threatening, it is important to identify its severity and act accordingly (for example, involve critical care early if needed). Pancreatitis can be classified and assessed based on clinical features or radiological findings, however, current evidence suggests that scoring tools may be of limited value.
A mortality estimation scoring system with 11 criteria. A point is scored for each of the following during admission:
- WBC > 16,000
- Age > 55
- Glucose >10 mmol/L
- AST >250
- LDH > 350
A point is scored for each of the following at 48 hours after admission:
- Hct drop of > 10% from admission
- Blood Urea Nitrogen increase by > 1.79 mmol/L from admission,
- Ca2+ < 2 mmol/L
- PaO₂ < 7.9 kPa
- Base deficit >4 mg/dL
- Fluid needs >6 L within 48 hours
A severity scoring system with 8 criteria at 48 hours after admission. A point is scored for each of the following:
- PaO₂ < 7.9 kPa
- Age > 55
- WBC > 15×10⁹/L
- Ca < 2mmol/L
- Urea > 16mmol/L
- LDH > 600 IU/L
- Albumin <32g/L
- Glucose > 10 mmol/L
Atlanta and Balthazar Classifications
The Atlanta classification includes mild, moderate and severe pancreatitis based on the amount of organ failure or local/systemic complications present.
Balthazar classification is a radiological approach based on the amount of pancreatic inflammation visible on CT (with contrast), with A, B, C, D and E representing increasing amounts of inflammatory changes, fluid collection and necrosis seen on CT.
Acute pancreatitis is associated with both short-term and long-term outcomes.
- Sepsis, ARDS, SIRS
- Acute renal failure
- Pancreatic abscess
- This occurs when peripancreatic fluid collections becomes infected and can become fatal
- This generally presents with fever and haemodynamic instability 2-4 weeks after pancreatitis
- Pancreatic pseudocysts
- Pseudocysts are encapsulated fluid collections with high enzyme concentrations
- The walls limits the spread of the pancreatic fluid and can rupture or become infected
- Pseudocysts typically present with pain and a palpable mass and often resolve spontaneously
- Enteric fistula
- Chronic pancreatitis