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Acute pancreatitis

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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 relatively high 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. Having many episodes of acute pancreatitis may lead to chronic pancreatitis.

Etiology

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.

There are multiple possible causes, memorised by the acronym "I GET SMASHED"

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

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 three 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

In case of jaundice, elevated bilirubin, elevated liver tests or cholestatic enzymes, gallstone or another obstruction of the biliary tree is the likely cause.

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. Ultrasound is usually the first choice modality. If complications are suspected, CT is usually the better first choice.

On abdominal ultrasound, the pancreas appears enlarged, oedematous, and hypoechoic. There may be peripancreatic fluid and the margins of the pancreas are indistinct. 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 if present, as well as any complication. Like on ultrasonography, there may be peripancreatic fluid and the pancreatic margins may be indistinct.

Etiology

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.

Severity assessment

The severity of the pancreatitis must be assessed, both based on clinical assessment and the SIRS score. High CRP (> 100 mg/L) suggests necrotising pancreatitis. Important to note that serum lipase/amylase are not predictors of severity, and so the degree of enzyme elevation does not correlate with the severity of the disease.

Treatment

Management of acute pancreatitis is conservative and supportive, as it's usually self-limiting. This involves pain control, IV fluids (large amounts), and correction of electrolyte and metabolic abnormalities. 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. In more severe cases, the patient should be nil per os (no oral feeding). Severe acute pancreatitis (as determined by the presence of haemodynamic instability, hypoxaemia, acid-base disorder, altered mental status, etc.) should be managed in an intensive care unit.

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 has recently been established that feeding through nasogastric tube does not stimulate the pancreas either.

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.

Indications for surgical treatment in acute pancreatitis

Surgery is playing a smaller and smaller role in the management of acute pancreatitis, as supportive and non-invasive therapy have improved and research has shown that these are superior to surgery in many cases. As such, acute pancreatitis is no longer a surgical disease but rather a disease of internal medicine, and surgery is only very rarely performed for this disease. Nevertheless, there remain a few indications for surgery in acute pancreatitis.

  • Infected necrotising pancreatitis (acute necrotic collection or walled-off necrosis)
  • Biliary pancreatitis
  • Abdominal compartment syndrome

Acute necrotic collection is an early complication of acute pancreatitis characterised by non-encapsulated necrotic material. Walled-off necrosis is a late (> 4 weeks) complication which is similar but encapsulated. Both may be sterile or infected.

Abdominal compartment syndrome is defined as intraabdominal hypertension (> 20 mmHg) and new-onset organ dysfunction. Severe pancreatitis may cause abdominal compartment syndrome due to tissue oedema.

Treatment of infected pancreatic necrosis

Infected pancreatic necrosis (infected acute necrotic collection or infected walled-off necrosis) is the main indication for surgery in acute pancreatitis, and requires treatment for drainage or removal, as well as antibiotics. Treatment usually follows a step-up approach, where percutaneous drainage with radiological guidance is the first line, with endoscopic transgastric necrosectomy being second line and surgical necrosectomy being third line.

Necrosectomy refers to removal of infected pancreatic necrosis. Surgical necrosectomy is usually performed in a minimal invasive (laparoscopic) manner with retroperitoneal access, necrosectomy, and drainage. Necrosectomy is never performed for sterile necrosis; for that, only conservative therapy is used.

Treatment of biliary pancreatitis

If the patient has concomitant cholangitis, they should be treated with urgent ERCP and sphincterotomy. In all cases of biliary pancreatitis, ERCP should be performed. Cholecystectomy should be performed after recovery of the acute illness.

In mild biliary pancreatitis, cholecystectomy is performed during the same admission, after the patient has stabilised. In severe biliary pancreatitis, early biliary surgery worsens the prognosis and so cholecystectomy is performed later as an elective procedure instead. Endoscopic sphincterotomy is an alternative for those unfit for surgery.

Treatment of abdominal compartment syndrome

Surgical decompression of the abdominal cavity is indicated for abdominal compartment syndrome. Decompression can be achieved with a midline incision (laparotomy) or percutaneously. The incision is then temporarily closed with a patch, negative pressure systems, or with a silo. This technique is called temporary abdominal closure and prevents fluid loss and prevents evisceration.

Abdominal compartment syndrome is rare and was not described in the lecture and is therefore probably not important.

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.