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Acute pancreatitis

Introduction

Acute pancreatitis is a reversible inflammatory condition of the pancreas that varies in intensity from just oedema and adiponecrosis to widespread parenchymal necrosis. It occurs when something causes the digestive enzymes to be activated in the pancreas itself, which self-digest the organ. The disease has a significant mortality, around 5%.

In most patients the disease is mild and patients recover after a few days. However, 20% develop severe (necrotising) pancreatitis with complications or organ failure, which has a high mortality.

Etiology

Acronym GET SMASHED

• Gallstones
• Ethanol (Alcoholism)
• Trauma
• Steroids
• Mumps (and Coxsackie) Virus
• Autoimmune
• Scorpion venom
• Hypercalcaemia, Hyperlipidemia
• ERCP
• Drugs

Other causes are Vascular (shock, arteroembolism, polyarteritis nodosa), mutations (PRSS1, SPINK1), idiopathic, etc.

The most common causes are alcoholism and gallstones in the biliary tract distal to the pancreatic duct. These two factors are responsible for 80% of all cases of acute pancreatitis.

Pathology

We distinguish two forms of acute pancreatitis, oedematous type and necrotising/haemorrhagic type.

Oedematous acute pancreatitis accounts for 80% of cases and is the mildest of the two. Histologically we can see interstitial oedema, inflammatory cell infiltrate, and adiponecrosis but no haemorrhage or interstitial necrosis. It has an almost zero percent mortality rate.

Necrotising or haemorrhagic acute pancreatitis is more severe and accounts for 20% of cases. Histologically we can see patchy necrosis, interstitial oedema, adiponecrosis, inflammatory cell infiltrate, and interstitial haemorrhage. The necrosis may become infected, which worsens the prognosis.

Clinical features

Most patients with acute pancreatitis have acute, persistent, severe epigastric pain which often radiates to the back. This is often described as a “belt-like” pain with the pain being in a belt-like distribution around the abdomen and back.

Nausea/vomiting also occurs in most patients. Other symptoms are rare, unless they’re also associated with the underlying cause (like jaundice due to choledocholithiasis). Patients with severe acute pancreatitis may have fever, tachypnoea, and haemodynamic instability.

In mild acute pancreatitis, the epigastrium may be minimally tender to palpation. In severe acute pancreatitis however, the epigastrium is significantly tender.

Clinical deterioration, failure to improve after a week, or development of sepsis may occur during the disease course if local complications develop (especially if they become infected), or if the oedematous pancreatitis has progressed to a necrotising one.

Diagnosis and evaluation

The diagnosis of acute pancreatitis is made when two of the following are present:

• Acute, persistent, severe epigastric pain (often radiates to the back)
• Elevation in serum lipase or amylase (to > 3 the upper normal limit)
• Characteristic findings of acute pancreatitis on imaging

Imaging may be performed with ultrasound, contrast CT, or MRI. It is not necessary to obtain imaging in uncomplicated cases where the first two criteria are fulfilled.

On abdominal ultrasound, the pancreas appears enlarged and hypoechoic. Local complications (peripancreatic fluid collection/acute necrotic collection) are visible as anechoic masses, with internal echoes if they contain necrosis.

On contrast CT, the pancreas is focally or diffusely enlarged. In oedematous pancreatitis there is heterogenous contrast enhancement. In necrotic pancreatitis there is a lack of contrast enhancement. CT may also show a gallstone.

After the diagnosis is made, the underlying cause must be sought. This includes a thorough history to look for risk factors, serum triglyceride level, calcium level, and abdominal ultrasound for gallstone. Endoscopic ultrasound may be used if initial investigations does not reveal the etiology.

The severity of the pancreatitis must be assessed, both based on clinical assessment and the SIRS score. Severe acute pancreatitis (as determined by the presence of haemodynamic instability, hypoxaemia, acid-based disorder, altered mental status, etc.) should be managed in an intensive care unit. High CRP (> 100 mg/L) suggests necrotising pancreatitis.

Treatment

Management of acute pancreatitis is conservative and supportive. This involves pain control, IV fluids, correction of electrolyte and metabolic abnormalities, and initial nil per os. Mild (oedematous) pancreatitis is self-limited, and so these measures are usually sufficient, and the patient recovers within a week. Feeding should be initialised early but slowly with a soft diet when the pain is decreasing and the inflammatory markers are improving.

Patients with severe pancreatitis require NPO for longer time, and so should receive a nasojejunal or nasogastric tube for feeding (rather than parenteral nutrition) for long-term NPO. Up until recently, it was believed that food had to be delivered distally to the sphincter of Oddi to prevent the food from stimulating the pancreas. However, it was recently discovered that feeding through nasogastric tube does not stimulate the pancreas either.

If the pancreatitis is caused by gallstones and the patient has cholangitis, they should be treated with urgent ERCP and sphincterotomy. If the pancreatitis is caused by gallstones but there is no cholangitis, cholecystectomy should be performed after recovery of the acute illness. See also topic B53 of surgery.

Local complications should only be treated if they become infected, never if they’re sterile. This involves antibiotic therapy and percutaneous or endoscopic drainage. Surgery is a last-line option. See topic B53 of surgery – traumatology for details on these treatments.

Complications

• Acute peripancreatic fluid collections
• Pseudocysts
• Acute necrotic collection
• Walled-off necrosis

Acute peripancreatic fluid collections are possible early (< 4 weeks) complications of oedematous acute pancreatitis. These fluid collections do not contain necrosis and are non-encapsulated.

Pseudocysts are possible late (> 4 weeks) complications of oedematous acute pancreatitis. The pseudocyst is formed when liquefied areas of necrotic pancreatic tissue becomes walled off by fibrous tissue. It’s not a true cyst as it’s not lined by epithelium. These cysts may resolve themselves, become infected or compress adjacent structures.

Acute necrotic collection is a non-encapsulated necrotic fluid collection which can occur in the first weeks after necrotising acute pancreatitis. They may become infected.

Walled-off necrosis is similar to acute necrotic collection, but it’s encapsulated and occurs later (> 4 weeks). They may also become infected.

Chronic pancreatitis

Introduction

Chronic pancreatitis is characterised by chronic inflammation of the pancreas with replacement of normal parenchyme by fibrotic scar tissue, which causes chronic abdominal pain and pancreatic insufficiency.

Etiology

The causes of chronic pancreatitis are classified using a system termed TIGAR-O, which is also an acronym.

• Toxic-metabolic factors
  • Alcohol abuse
  • Tobacco smoking
  • Hypertriglyceridaemia
• Idiopathic
• Genetic (hereditary pancreatitis, cystic fibrosis)
• Autoimmune
• Recurring acute pancreatitis
• Obstructive chronic pancreatitis
  • Tumour of papilla of Vater
  • Duct sclerosis
  • Ductal stones

Clinical features

Abdominal pain in the epigastric region which radiates to the back and nausea/vomiting are the most common symptoms.

Complications of loss of pancreatic function can cause pancreoprivic diabetes mellitus, maldigestion and malabsorption, osteoporosis, and steatorrhoea.

Diagnosis and evaluation

Contrast CT or MRI with MRCP will show pancreatic atrophy and parenchymal calcification.

If other investigations are not diagnostic, pancreatic functional diagnostics may be used (see below).

The most likely underlying cause of the chronic pancreatitis must be sought, based on history of exposure to risk factors, lab tests, and possibly genetic testing. Notably, a considerable alcohol intake is necessary to cause chronic pancreatitis, an average of five units daily for five years or more. However, in a significant proportion of cases remain idiopathic.

Treatment

Treatment for chronic pancreatitis unfortunately is not curative. Patients should avoid risk factors like smoking and alcohol, and they should consume low-fat, small meals. Painkillers are often necessary for chronic abdominal pain.

Coeliac ganglion block (topic B47 of surgery-traumatology) is an option for refractory pain.

Patients with diagnosed exocrine pancreatic insufficiency require pancreatic enzyme supplementation, which is to be taken with foods.

For surgical treatment of chronic pancreatitis, see topic B54 of surgery.

Complications

Chronic pancreatitis may lead to chronic malabsorption and steatorrhoea due to the loss of exocrine pancreas function, and diabetes mellitus due to loss of endocrine pancreas function.

Functional diagnostics of pancreatic insufficiency

Direct pancreatic functional testing

IV administration of pancreas-stimulating hormones (secretin or cholecystokinin) stimulates the secretion of pancreatic juice. This fluid can be collected by an oroduodenal tube or an upper endoscope and measured. A bicarbonate concentration of this fluid of < 80 mEq/L is diagnostic of exocrine pancreatic insufficiency.

Direct tests are more sensitive than indirect tests, but also more expensive and difficult to perform.

Indirect pancreatic functional testing

Measuring the amount of elastase in the stool can be used for diagnosis of exocrine pancreatic insufficiency.