Acute pancreatitis

Notes

Definition & classification

Acute pancreatitis refers to an acute inflammatory process involving the pancreas. 

Pancreatitis occurs due the uncontrolled release of pancreatic enzymes resulting in autodigestion. Patients may suffer a spectrum of disease from mild abdominal discomfort to multi-organ failure.

Pancreatitis has an annual incidence of 13-45 cases per 100,000, with trends showing that it is becoming more common. It tends to occur more in men and is commonly secondary to alcohol misuse or gallstones. 

Aetiology

Alcohol misuse and gallstones are the most common causes of acute pancreatitis.

Alcohol misuse and gallstones are responsible for upwards of 75% of cases of acute pancreatitis. Other important causes include ERCP and hyperlipidaemia (e.g. hypertriglyceridaemia).

The causes of acute pancreatitis may be remembered with the mnemonic I GET SMASHED.

Pancreatitis pathology

Gallstones

Gallstones are the most common cause of acute pancreatitis, they are responsible for around 40% of cases. Gallstones migrate from the gallbladder to the biliary tree where they may cause obstruction of the ampulla. It is thought that biliary reflux and raised pressures are responsible for the resultant pancreatitis. 

Alcohol

Alcohol has toxic effects on the pancreas and is implicated in around 35% of cases. Though it is known to increase the production of digestive enzymes, the exact mechanism by which it causes pancreatitis remains unclear. 

Alcohol commonly causes chronic pancreatitis with alcoholics suffering acute-on-chronic attacks. It may also induce acute pancreatitis without pre-existing disease following a significant binge.

Other

Acute pancreatitis is a significant complication in those undergoing an endoscopic retrograde cholangiopancreatography (ERCP). It is estimated 1-3% develop the condition following the procedure.

Operations in which the pancreas is handled or mobilised may result in pancreatitis. Infections, trauma, drugs, hyperlipidaemia, hypercalcaemia and hypothermia may all result in acute pancreatitis.

A proportion of cases are idiopathic. It is thought the majority of these occur secondary to unidentified biliary disease.

Pathophysiology

Pancreatitis is caused by the release of enzymes, which undergo autodigestion of pancreatic tissue.

The pancreas has both endocrine and exocrine function. Endocrine function is governed by the islets of Langerhans and the hormones produced include insulin and glucagon. 

The pancreatic ductal cells are responsible for its exocrine function. They produce the ‘pancreatic juice’ composed of bicarbonate and digestive enzymes. One of these enzymes, trypsin, is key to the development of pancreatitis. 

Under normal circumstances the pancreas releases zymogens - inactive enzyme precursors (trypsinogen in the case of trypsin). In pancreatitis, normal zymogen transport fails and trypsinogen is converted to trypsin leading to a cascade of zymogen activation. This triggers the recruitment of inflammatory cells and the release of inflammatory mediators. 

This inflammation causes changes in the vascular bed, which leads to increased permeability and resultant oedema. The condition may be worsened by the release of inflammatory mediators and enzymes into the systemic circulation. This can result in a systemic inflammatory response (SIRS), sepsis and adult respiratory distress syndrome (ARDS).

Clinical features

The presentation of pancreatitis may range from mild abdominal pain to life-threatening shock.

Abdominal pain is the most common presenting symptom. It tends to be epigastric with a sudden and severe onset. It continues as an ache of variable severity, may be worsened on movement and commonly radiates to the back. 

Pancreatitis signs and symptoms

Symptoms

  • Abdominal pain
  • Nausea
  • Vomiting
  • Anorexia
  • Diarrhoea

Signs

  • Abdominal tenderness
  • Abdominal distention
  • Tachycardia
  • Tachypnea
  • Pyrexia

Eponymous signs

Cullen’s sign: peri-umbilical bruising

Grey-Turner’s sign: flank bruising

Severe pancreatitis

Investigations & diagnosis

A serum amylase elevated 3 times above the reference range is considered diagnostic.

Amylase & lipase

Amylase is a digestive enzyme produced by the pancreas and salivary glands. It plays a role in the breakdown of carbohydrates. A patient with clinical features consistent with acute pancreatitis and an elevated amylase can be considered as very likely to have the condition. 

In acute pancreatitis the levels are normally elevated 3 times above the reference range. Levels rise acutely before falling after 3 days (urinary amylase may remain elevated for a longer period). Patients who present late may therefore have a ‘missed peak’. It should be noted that even in severe pancreatitis the amylase may be normal, particularly in those with acute-on-chronic disease. 

Aside from pancreatitis there are a number of causes of elevated amylase. These include parotitis, bowel obstruction, intestinal inflammation and ruptured ectopic pregnancy. 

Some centres prefer to use serum lipase. Again, levels elevated 3 times above the reference range are indicative of pancreatitis. Lipase has a longer half-life and as such levels may remain elevated longer than amylase. Raised levels are more specific for pancreatic disease than amylase.  

Bedside

  • Observations
  • ECG (if tachycardic or deranged electrolytes) 
  • Beta-HCG

Bloods

  • Amylase/lipase
  • FBC
  • UE
  • CRP
  • LFT (including AST)
  • Bone profile
  • LDH
  • Serum glucose
  • Lipids
  • Arterial blood gas (used for scoring acute pancreatitis)

Imaging

Ultrasound: used to demonstrate gallstones or a dilated common bile duct. The pancreas may be visualised.

Computed tomography: used to confirm diagnosis when uncertainty remains and to exclude complications of disease.

Glasgow score

The Glasgow score, completed in the first 48hrs, helps to assess the severity of acute pancreatitis.

Glasgow score

A score of > 3 indicates severe pancreatitis, these patients have a high mortality and should be managed on a high-dependency unit.

Management

Management consists of supportive care, nutrional support and in rare cases surgical intervention.

Supportive

Pain is the most common complaint and patients should receive adequate analgesia. Morphine can be used, but it can lead to spasm of the sphincter of Oddi. Pethidine and buprenorphine are alternatives. 

Patients require fluid resuscitation to compensate for third-space losses. They may need aggressive intravenous fluids, particularly in the first 24 hours. A careful fluid balance should be recorded and monitored. 

Nutrition

Our understanding of how to best manage nutrition in patients with acute pancreatitis continues to evolve. In mild cases, a low fat diet may be reintroduced once tolerated by the patient (i.e. the pain has settled and they have an appetite). 

In patients with severe disease other options must be explored. Enteral feeding is preferred to total parenteral nutrition. It is thought enteral feeding helps maintain the mucosa and prevent translocation of bacteria. Nasojejunal feeding is commonly used.

TPN should be used in patients with ileus or where nutritional requirements are not being met. 

Antibiotics

Antibiotics are not routinely indicated in acute pancreatitis and they should not be used prophylactically. 

Infection remains a significant cause of mortality in pancreatitis. Antibiotics should be commenced in patients with suspected infected pancreatic necrosis.

Surgery

Patients with gallstone pancreatitis should have a cholecystectomy during the same admission to avoid recurrence and readmission.

An endoscopic retrograde cholangiopancreatography and sphincterotomy is indicated in those with obstructive LFTs, a dilated common bile duct or severe gallstone pancreatitis. 

Complications

The recovery from an acute pancreatitis may be complicated by necrosis, pseudocyst or abscess formation.

Acute pancreatitis may be a severe and systemic condition. Complications are those of a severe and dysregulated inflammatory response including adult respiratory distress syndrome, multiorgan dysfunction syndrome as well as electrolyte abnormalities, hyperglycaemia and sepsis. Here we focus on three pancreatitis specific complications.

Pancreatic necrosis

In certain cases continued inflammation leads to localised thrombosis and haemorrhage within the pancreas. A necrotic area forms that may be diagnosed on dynamic spiral CT.

Though initially sterile there is a 40-70% chance of infection. Infected pancreatic necrosis is responsible for 80% of deaths related to acute pancreatitis. Patients with evidence of an inflammatory response should have a CT guided fine needle aspiration and culture. Culture positive patients are generally managed with surgical debridement, drainage and antibiotics.

Pancreatic pseudocyst

These are peripancreatic collections of pancreatic fluid that persist for four weeks (prior to this they are termed acute peripancreatic fluid collections).

If asymptomatic these can be monitored but they frequently cause pain and fullness. In addition they may be complicated by rupture or haemorrhage. Pseudocysts that are symptomatic or large require endoscopic, radiological or surgical management. 

Abscess

These are localised collections of infection that may present weeks following the acute attack 

A pancreatic abscess should be suspected in those with continued pyrexia or elevated white cells. Treatment is with antibiotics and drainage.

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