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Acute pancreatitis is an acute inflammation of the pancreas that can quickly take a fulminant course. Early diagnosis and initiation of treatment is therefore essential.

Acute pancreatitis used to be divided into two forms: the more common edematous pancreatitis (85%) and severe necrotizing pancreatitis (15%).edematous pancreatitis is characterized by edema and granulocyte infiltrates in the interstitium. Fatty tissue necrosis may occur. Necrotizing pancreatitis is characterized by intra- and extrapancreatic fatty tissue and parenchymal necrosis with hemorrhage.

In 2012, the Atlanta Classification divided pancreatitis into an early (first) and a late (second) phase of pancreatitis. In addition, pancreatitis was divided into mild (without organ failure, no local or systemic complications), moderate (organ failure within 48 hours that resolves, local or systemic complications without persistent organ failure) and severe (persistent organ failure that occurs > 48 hours, organ failure).

In the early phase, the occurrence of (multi-)organ failure is prognostically relevant, while in the second phase, possible infections of necrosis (in approx. 25% of patients) are the main concern.

Epidemiology

The worldwide age-related incidence of the disease is 16 (men) or 10.2 (women) per 100,000 inhabitants. The disease occurs particularly between the ages of 40 and 60.

Causes

The most common causes of acute pancreatitis are biliary tract diseases (such as choledocholithiasis, gallstone obstruction, stenosis of the duodenal papilla major) in 45% of cases and alcohol abuse (35%). This is followed by idiopathic pancreatitis (15%) and rarer causes such as viral infections (e.g. mumps), hypertriglyceridemia; iatrogenic after ERCP (endoscopic retrograde cholangiopancreatography) and abdominal trauma. Acute pancreatitis can also be caused by hereditary (e.g. mutations in the trypsinogen gene) and autoimmune (e.g. Sjögren's syndrome) processes. Furthermore, tumors or penetrating ulcers (duodeni/ventriculi) can lead to the development of acute pancreatitis. Pancreatitis has also been described after taking medication, for example enalapril, statins and carbimazole.

Pathogenesis of pancreatitis

Acute pancreatitis leads to intrapancreatic activation of digestive enzymes. The pancreas is thus autodigested by proteolytic enzymes. The acinus cells are damaged and this is followed by an inflammatory reaction with proteolysis, bleeding, edema and vasodilation. In severe cases, the process can lead to necrosis with a possible septic course.

The release of lipases, protestases and elastases can lead to acute hemorrhagic pancreatitis. Calcium ions are bound by the released fatty acids and saponify (saponification).

Capillary leakage and vasodilation remove fluid from the circulation. This fluid accumulates in the pancreas, the surrounding tissue and in the abdominal cavity. Ascites and even hypotension with reduced organ perfusion are the consequences. The kidneys are particularly affected.

Symptoms

Acute pancreatitis is characterized by acute upper abdominal and/or thoracic pain. This often extends into the back in the form of a belt. In the case of gallstones, the pain can be colicky. Painless courses of the disease are very rare. Nausea and vomiting may also occur. The occurrence of meteorism or paralytic (sub-)ileus with scanty bowel sounds is also often described. Ascites or pleural effusions may also occur. In the context of acute pancreatitis, bluish-livid or green-brown ecchymoses may also occur in characteristic localizations, for example periumbilical (Cullen's sign), in the flank area (Grey-Turner's sign) or in the groin. These are rare and prognostically unfavorable. Typical of acute pancreatitis is the "rubber belly" with only moderate tension of the abdominal wall.

Diagnosis

Diagnostic criteria: Acute pancreatitis can be diagnosed according to international guidelines if two of the following criteria are met:

  • The lipase and/or amylase in the serum is elevated by more than three times the norm
  • Upper abdominal pain is present
  • There are characteristic findings on imaging

Diagnostic procedure: The diagnosis of acute pancreatitis begins with a medical history, which includes typical symptoms, a history of gallstones and alcohol consumption. This is followed by a clinical examination of the patient. This should at least include the vital parameters of blood pressure and pulse, the lungs should be auscultated and the body temperature measured. The abdomen is examined for tenderness and tenderness. The bowel sounds are auscultated and attention is paid to signs such as the Grey-Tuner or Cullen sign.

Laboratory chemical parameters: Serum lipase has the highest sensitivity and specificity for the diagnosis of acute pancreatitis. It should be noted with this laboratory parameter that the level of serum lipase does not provide any information on the severity of the pancreatitis and therefore does not allow any prognostic statement to be made.

As part of the diagnosis, it is important to clarify the aetiology of the pancreatitis present, as this has both prognostic and therapeutic consequences. Biliary pancreatitis should be recognized early, as this form of pancreatitis can be treated in a targeted manner using endoscopic stone removal. In order to detect biliary pancreatitis, the cholestasis parameters AP, gGT and bilirubin as well as the transaminases are determined in the laboratory. An increase in GPT to more than 300% of the norm is indicative of biliary genesis (positive predictive value of 95%) and the laboratory parameters for suspected acute pancreatitis should include at least lipase, ALT, gGT, blood count, LDH, CRP, calcium, creatinine, urea, triglycerides and blood glucose.

Instrumental diagnostics

The next step should be sonography. This can be used to visualize necrosis, abscesses, ascites, choledocholithiasis or dilated bile ducts. If a biliary etiology cannot be ruled out with the help of laboratory parameters and sonography, endosonography can help. With its help, prepapillary concretions in particular can be detected better than with conventional ultrasound.

ERCP can visualize the biliary and pancreatic duct system and at the same time offers intervention options (e.g. stone extraction and/or bile duct stenting in the case of cholestasis). Alternatively, an MRI cholangiopancreaticography (MRCP) can be performed if available and if expertise is available.

Assessment of the course of pancreatitis

A distinction must be made between severe pancreatitis and mild pancreatitis, as the severe form requires early intensive medical monitoring.

Various methods are available for differentiation:

  • Ranson criteria (a meaningful result is only possible after 2 days)
  • APACHE II score (a meaningful result is only possible after 2 days)
  • BISAP score (Bedside Index for Severity in Acute Pancreatitis)
  • Computed tomography with intravenous contrast medium (this method is not reliable in assessing the extent of the disease in the early phase of the disease, but only achieves sufficient significance 7 days after admission). The necroses that can be detected by CT usually only develop after 3-5 days. There is also a risk of triggering acute kidney failure during the examination.
  • The laboratory chemical gold standard is the determination of C-reactive protein (CRP): an increase in CRP >15mg/dl indicates necrotizing pancreatitis. This parameter is also only sufficiently predictive after 2-3 days.

The onset of pain and the occurrence of hyperglycemia have been shown to be prognostic parameters. In acute necrotizing pancreatitis, the onset is usually fulminant. An increase in haematocrit also shows a high negative predictive value for the occurrence of necrotizing pancreatitis. Other prognostically unfavorable parameters are leukocytosis (>16 g/l), an age >55 years, a body mass index >30, a serum calcium concentration <2 mmol/l and a lactate dehydrogenase >350 U/l.

Therapy

All acute pancreatitis should be monitored in hospital, as the course and severity are difficult to predict, especially in the initial stage. Intensive medical care is indicated at an early stage, particularly in the case of necrotizing pancreatitis.

Specific therapeutic measures are available for biliary pancreatitis, hypercalcemia and hypertriglyceridemia. No causal therapy is available for the remaining acute pancreatitis.

With regard to the effect of antibiotics in acute pancreatitis, the study situation is contradictory. One meta-analysis showed a reduction in mortality with antibiotics, while other studies were unable to confirm this. Prophylactic antibiotics are not recommended. Antibiotics can be used if necessary.

If the biliary origin of the pancreatitis is proven, ERCP is useful and can help to reduce complications. ERCP should be performed within 72 hours. With regard to the nutrition of patients, parenteral nutrition is now increasingly being replaced by early enteral nutrition, unless there are indications to the contrary (e.g. intestinal paralysis).

A further important aspect of the treatment of acute pancreatitis is the adequate analgesia of patients. An opiod-based stepwise regimen is currently recommended. Acute pancreatitis is usually associated with early intravascular hypovolemia. Early volume administration within the first 12-24 hours is therefore recommended. According to expert opinion, it is difficult to assess the level of volume administration in acute pancreatitis due to the fear of pulmonary overhydration. On the other hand, the fluid requirement is often underestimated, especially in the mild edematous form.

Hemodynamic monitoring must be carried out at an early stage, especially in severe pancreatitis or severe pre-existing conditions such as heart failure. Volume-based preload parameters such as global end-diastolic volume or intrathoracic blood volume can be used for this purpose, as they appear to be more favorable than central venous pressure or a pulmonary artery catheter.

Most guidelines recommend a conservative treatment approach for necrotizing pancreatitis without evidence of germs. If necrosis occurs, a minimally invasive step-up approach starting with primary endoscopic drainage and, if necessary, endoscopic necrosectomy may result in a better prognosis.

Prognosis

Mild edematous pancreatitis usually has a mild course with complete resolution of symptoms without organ failure, while necrotizing pancreatitis is associated with systemic inflammatory and organic complications. In acute pancreatitis, an inflammatory reaction can occur within a very short time. Bacterial infection of pancreatic necoses can lead to pancreatitis-associated organ failure and is therefore an important prognostic marker. The mortality rate for infected necroses (approx. 25%) is higher than for sterile necroses (approx. 5%). In severe cases, necrotizing pancreatitis can progress to life-threatening systemic inflammatory response syndrome (SIRS) with multiple organ failure. The mortality rate for the mild form of pancreatitis is approx. 1%.

Prophylaxis

Acute pancreatitis can be triggered by excessive alcohol abuse. Reducing or avoiding alcohol can contribute to the prevention of acute pancreatitis. Avoiding hypertriglyceridemia can also help to prevent acute pancreatitis.