Acute pancreatitis is an acute inflammatory process of the pancreas, with a cascade of release of inflammatory cytokines and pancreatic enzymes with autodigestion, leading to varying involvement of local tissues or more remote organ systems. Around three-quarters of cases are caused by gallstones or alcohol misuse.
Causes
Causes of acute pancreatitis include:
- I: Idiopathic
- G: Gallstones
- E: Ethanol
- T: Trauma e.g. blunt abdominal trauma, or surgery near the pancreas
- S: Steroids
- M: Mumps (and other infections e.g. Coxsackie B4 virus and Mycoplasma pneumonia)/Malignancy (e.g. pancreatic adenocarcinoma)
- A: Autoimmune e.g. SLE and Sjogren’s syndrome
- S: Scorpion stings/spider bites
- H: Hyperlipidaemia/hypercalcaemia/hyperparathyroidism (and other metabolic disorders)
- E: Endoscopic procedures e.g. endoscopic retrograde cholangiopancreatography (ERCP)
- D: Drugs e.g. thiazide diuretics, azathioprine, tetracyclines, valproate, oestrogens
Clinical features
Suspect acute pancreatitis in any person who presents with acute upper or generalised abdominal pain, particularly if they have a history or clinical features of gallstones or alcohol misuse.
Clinical features of acute pancreatitis include:
- Sudden onset severe upper abdominal pain radiating to the back
- Nausea, anorexia and vomiting
- Epigastric tenderness with associated rebound tenderness, guarding and rigidity in peritonitis
- Abdominal distension
- Cullen’s sign (a bluish discolouration around the umbilicus)
- Grey-Turner’s sign (a bluish discolouration around the flank)
- Fever
- Tachycardia, hypotension and features of shock
Differential diagnosis
Conditions which can present similarly to acute pancreatitis include:
- Perforated peptic ulcer, bowel obstruction, or ischaemic bowel.
- Ruptured abdominal aortic aneurysm.
- Myocardial infarction.
- Biliary colic, acute cholecystitis, or cholangitis.
- Viral hepatitis.
- Gastroenteritis.
Investigations
Initial investigations include:
- Serum lipase or amylase
- Use serum lipase testing (if available) in preference to serum amylase
- Serum lipase and amylase have similar sensitivity and specificity but lipase levels remain elevated for longer (up to 14 days after symptom onset vs. 5 days for amylase)
- A result > 3 times the upper limit of normal confirms the diagnosis of acute pancreatitis in a patient with acute upper abdominal pain
- Beware false positive and false negative results
- FBC
- Leucocytosis
- Elevated haematocrit (>44%) indicates poorer prognosis
- CRP
- CRP > 200 units/L is associated with pancreatic necrosis
- U&Es
- Elevated urea and creatinine may be seen in severe cases
- Pulse oximetry
- Patients may be hypoxaemic requiring supplemental oxygen
- LFTs
- Elevated ALT > 3 times the upper limit of normal predicts gallstone disease as aetiology
- Serum calcium
- May show hypercalcaemia as a rare cause of acute pancreatitis
- CXR
- May show atelectasis and pleural effusion
- Transabdominal ultrasound
- Confirms or excludes gallstones
- May show pancreatic inflammation, peri-pancreatic stranding, calcification or fluid collections
Further investigations to consider include:
- Serum triglycerides
- >11.3 suggests hypertriglyceridaemia as possible cause
- Abdominal CT scan
- Most patients do not need contrast-enhanced computed tomography (CECT) as diagnosis is usually based on clinical presentation and serum lipase/amylase
- CT should be requested where there is diagnostic doubt or in patients who fail to improve within 48 - 72 hours
- Findings may include diffuse or segmental enlargement of the pancreas with irregular contour and obliteration of the peri-pancreatic fat, necrosis, or pseudocysts
- Endoscopic ultrasound/Magnetic resonance cholangiopancreatography
- Use EUS or MRCP in preference to CECT to screen for choledocholithiasis if it is highly suspected in the absence of cholangitis and/or jaundice
- EUS is indicated in patients considered to have idiopathic acute pancreatitis to exclude strictures, occult biliary microlithiasis, neoplasms, and chronic pancreatitis
- Use MRCP if CT is contraindicated (e.g. renal insufficiency, contrast allergy)
Management
Initial treatment of acute pancreatitis may include:
- Resuscitation with intravenous crystalloid fluids.
- Early and adequate fluid replacement is the single most important step in initial treatment. Evidence suggests early fluid resuscitation reduces the risk of organ failure and death.
- Latest evidence suggests a balanced crystalloid (such as Hartmann’s solution, Ringer’s lactate, or PlasmaLyte) may have benefits compared with normal saline, although either choice of fluid is reasonable.
- Start intravenous fluid therapy with 5 to 10 mL/kg/hour and then proceed with goal-directed fluid therapy, titrating intravenous fluids to indicators of end-organ perfusion.
- Supplemental oxygen (to maintain oxygenation of vital organs).
- During initial management, consider the need for blood gas analysis (arterial or venous) to assess both oxygenation and acid-base status if the patient shows signs of deterioration.
- Pain relief and antiemetics.
- Pain is the predominant symptom. Ensure it is treated promptly and effectively.
- Empiric intravenous antibiotics.
- For treatment of associated cholangitis or acute infections, such as chest infection or urinary tract infection.
- Suspect infection based on signs and symptoms such as fever, leukocytosis, and signs of organ dysfunction.
- Early nutritional support.
- Oral feeding can commence in people with mild acute pancreatitis if there is no nausea, vomiting, or abdominal pain. Start a normal oral diet as soon as the patient can tolerate it (ideally within 24 hours).
- Enteral feeding is otherwise preferable and is possible in the majority of people. Start this within 72 hours of presentation.
- Only use parenteral nutrition for patients in whom enteral feeding is not feasible, not tolerated, or failing to meet calorie requirements.
- Severity assessment.
- Use SIRS criteria along with patient risk factors to assess severity in the first 48 hours.
- Never classify a patient as having mild disease until at least 48 hours after onset of symptoms. Many patients who go on to develop severe disease present without signs of organ failure or local complications.
- Calcium and magnesium replacement therapy.
- Emergency endoscopic retrograde cholangiopancreatography (ERCP) within 24 hours for any patient who has concurrent cholangitis.
Complications
Complications develop in 15-20% of people with acute pancreatitis.
Complications of acute pancreatitis include:
- Local complications
- Pancreatic necrosis +/- secondary bacterial infection
- Infected pancreatic necrosis is responsible for 80% of deaths from acute pancreatitis.
- Pseudocyst formation +/- infection, rupture or haemorrhage
- Pancreatic abscess
- Pancreatic fistula
- Prehepatic portal hypertension
- Erosion of a pancreatic, splenic, or peri-pancreatic artery or vein with haemorrhage
- Systemic complications
- Sepsis
- Acute respiratory distress syndrome (ARDS)
- Acute renal failure
- Multiple organ dysfunction
- Disseminated intravascular coagulation (DIC)