Acute pancreatitis is an inflammation of the organ is (and sometimes the adjacent tissue), which is caused by the release of activated pancreatic enzymes. The most common triggers are diseases of the biliary system, and pronounced alcohol consumption. The severity of pancreatitis moves between the light (abdominal pain and vomiting) to the severe form (pancreatic necrosis with a severe inflammatory generally image with shock and multiple organ failure). The diagnosis is based on the clinical picture, serum amylase and lipase. Treatment is supportive with i.v. Hydration, pain medications and fasting.
Acute pancreatitis is an inflammation of the organ is (and sometimes the adjacent tissue), which is caused by the release of activated pancreatic enzymes. The most common triggers are diseases of the biliary system, and pronounced alcohol consumption. The severity of pancreatitis moves between the light (abdominal pain and vomiting) to the severe form (pancreatic necrosis with a severe inflammatory generally image with shock and multiple organ failure). The diagnosis is based on the clinical picture, serum amylase and lipase. Treatment is supportive with i.v. Hydration, pain medications and fasting. Etiology diseases of the biliary tract and alcoholism are responsible for ? 80% of acute pancreatitis. The remaining 20% ??may have (see Fig. Causes of acute pancreatitis) multiple causes. Causes of acute pancreatitis causes medicines as ACE inhibitors, asparaginase, azathioprine, 2 ‘, 3’-dideoxyinosine, furosemide, 6-mercaptopurine, pentamidine, sulfonamides, valproate Infectious Coxsackie B virus, cytomegalovirus, mumps Hereditary Multiple known gene mutations incl. a small percentage of patients with cystic fibrosis Mechanical / str ukturell gallstones, ERCP, trauma, pancreatic or Periampullary carcinoma, Choledochal, sphincter of Oddi stenosis, pancreas divisum Metabolically hypertriglyceridemia, hypercalcemia (incl. Hyperparathyroidism), estrogen intake associated with high blood lipid values ??toxins alcohol, methanol Other pregnancy state after kidney transplantation, ischemia in hypotension or embolism, tropical pancreatitis pathophysiology The precise mechanism involved in transfer of the Sphincter of Oddi by a gallstone or microlithiasis (sludge) to a pancreatitis leads, is not precisely known, although probably the increased intraductal pressure plays a pathogenetic role. Continued alcohol intake (> 100 g / day for 3-5 years) can lead to precipitation of the protein of pancreatic enzymes in the small bile ducts. The gear shifting by these clumps of protein can cause premature activation of pancreatic enzymes. A binge-drinking can cause acute pancreatitis in these patients, but the exact mechanism is unknown. It has identified numerous genetic mutations that predispose to pancreatitis. A form, an autosomal dominant mutation of the cationic Trypsinogengens, causes pancreatitis in 80% of the carrier, while there is obviously a familial pattern. Other mutations show lower penetrance, they are not clinically obvious and therefore not diagnosed unless it carries genetic investigations. The genetic changes that are responsible for cystic fibrosis, increase the risk of both a recurrent acute and chronic pancreatitis. Regardless of the etiology of the pancreatic enzymes (incl. Trypsin, phospholipase A2 and elastase) are activated in the gland. These enzymes can damage tissue and activate the complement system and inflammation cascade with the production of cytokines. This process in turn leads to inflammation, edema, and sometimes necrosis. At low pronounced pancreatitis, inflammation of the pancreas is limited; the mortality rate is <5%. In severe pancreatitis made a significant inflammation, necrosis and hemorrhage of the gland and a systemic inflammatory response; the mortality rate is 10-50%. After 5-7 days, the necrotic pancreatic tissue is infected by intestinal bacteria. Activated enzymes, toxins, and cytokines can enter the systemic circulation and cause severe general inflammatory response with acute respiratory distress syndrome and renal failure. The systemic response is mainly due to a general increase in capillary permeability and a decrease of vascular resistance, which is due to the release of cytokines and chemokines. It is believed that phospholipase A2 damages the alveolar membranes of the lungs. In approximately 40% of patients in and around the pancreas collections of enzyme-rich pancreatic juice and tissue debris occur. Approximately half these accumulations regress spontaneously. For others, it may become infected or form pseudocysts. Pseudocysts have a fibrous capsule without epithelium. You can bleed, rupture or become infected. A fatal course during the first few days caused (with refractory shock and renal failure) or respiratory failure (with hypoxemia and adult respiratory distress syndrome) in general by a circulatory collapse. Occasionally, a death occurs as a result of heart failure, caused by an unidentified myocardial inhibitory factor. Cause of death after the first week is usually multi-organ failure. Symptoms and signs Acute episode of pancreatitis caused a constant nagging pain in the upper abdomen, which is typically so hard that large doses of parenteral opioids must be used. The pain radiates in 50% of patients in the back, rare it is initially located in the lower abdomen. The pain occurs abruptly when biliary pancreatitis, in alcoholic pancreatitis he developed against it for several days. The pain usually lasts for several days. Sitting upright and bending forward can reduce the pain, however, it is amplified by coughing, stronger movements and deep breaths. Nausea and vomiting are common. The patient makes an impression acutely ill and sweats. The pulse rate is generally at 100 to 140 beats / min. Breathing is shallow and rapid. Blood pressure can vary in phases. There is a significant orthostatic hypotension. The body temperature is located in or below the normal, but then within hours to increase to 37.7 to 38.3 ° C. Consciousness can be clouded by the semi-coma. Occasionally a sclerenicterus occurs. There is a Zwerchfellhochstand with restricted lung movements and atelectasis. Approximately 20% of patients have a distension in the upper abdomen, which is brought about by expansion or displacement of the stomach as a result of an inflamed pancreas mass. Severe damage to the pancreatic duct leading to ascites (pancreatic ascites). In the upper abdomen usually consists guarding. A lower guarding can also be present in the lower abdomen, however, the rectum is not sensitive to pain, the chair usually occult blood negative. A low to moderate muscle rigidity consists pronounced in the upper, rare in the lower abdomen. Rarely peritoneal irritation results in a board-hard abdomen. Bowel sounds are usually diminished. The Gray Turner's sign (Ekchymoses of the flanks), and Cullen sign (ecchymosis in the Umbilikalregion) are an expression of extravasation of hemorrhagic exudate. An infection of the pancreas or of the surrounding fluid accumulation must be assumed if the patient develops a toxic disease with elevated temperature and an elevated leukocyte count or if deterioration in an initial period of stabilization follows. Diagnostic serum markers (amylase, lipase) Usually, CT at once diagnosed pancreatitis The suspected pancreatitis is always in severe abdominal pain, v. a. in patients with heavy alcohol consumption or known gallstones. Medical conditions which cause similar symptoms, are perforated gastric or duodenal ulcers, Mesenterialinfarkte, strangulation, dissecting aneurysms, biliary colic, appendicitis, diverticulitis, posterior myocardial infarction and hematoma in the abdominal muscles or spleen. The diagnosis is made by the clinical picture, serum markers (amylase and lipase) and exclusion of other causes. Therefore, a number of studies are carried out, typically blood count, electrolytes, calcium, magnesium, glucose, urea, creatinine, amylase and lipase. Further investigations are routine ECG and Abdomenaufnahmen in different positions. A urine-Stix for trypsinogen 2 has a sensitivity and specificity of> 90% in acute pancreatitis. An abdominal ultrasound and CT are usually not required to obtain the specific diagnosis pancreatitis, but used to diagnose an acute abdomen (test method). Laboratory tests Serumamylase- and -lipasekonzentration rise on the first day of acute pancreatitis and go within 3-7 days back to normal. The lipase is specific for pancreatitis, but both enzymes are elevated in renal failure and in various diseases of the abdomen (such as. For example, perforated ulcer, closure of Mesenterialgefäßen, ileus). Other causes of increased serum amylase are functional disorders of the salivary gland, and macroamylasemia amylasesezernierende tumors. Both the amylase as the lipase remain normal if a previous injury to the Azinusgewebes prevents the release of a sufficient amount of enzyme. The serum of patients with hypertriglyceridemia may contain a circulating inhibitor which must be diluted before it can be shown an increase in amylase. The ratio of amylase / creatinine clearance does not have sufficient sensitivity for the diagnosis of pancreatitis and specificity. It is generally used to diagnose a macroamylasemia in the absence of pancreatitis. When macroamylasemia a bound to serum immunoglobulins amylase yields false-high values ??of serum amylase. An analysis of the total serum amylase in terms of pancreatic type (P-type) of the isoamylase and salivary gland type (S-type) of the isoamylase increases the accuracy of Serumamylasenbestimmung. However, the level of pancreatic amylase also increases in renal failure and other serious abdominal diseases in which amylase clearance is altered. The leukocytes are usually clearly 12000-20000 / ul increased. increase fluid losses in the “third space” the hematocrit to values ??of 50-55% and indicate a severe inflammatory response. Hyperglycemia may occur. Serum calcium levels may already fall on the first day, as calcium soaps form as a result of increased formation of free fatty acids by pancreatic lipase. The serum bilirubin is increased in 15-25% of patients, because the common bile duct, pancreatic edema komprimiert.Bildgebende method Abdomenübersichtsaufnahmen can calcified stones in the pancreatic ducts (evidence of infection had taken place and thus a chronic pancreatitis), calcified gallstones or a localized ileus in the upper left quadrant or in the middle of the abdomen ( “sentinel loop” of the small intestine, dilation of the transverse colon or Duodenalileus) Show. A chest radiograph can atelectasis or pleural effusion show (in most cases the left-sided or bilateral but rarely confined to the right pleural cavity). A sonography should be performed if the suspected gallstone pancreatitis is (and another etiology is not clear) to gallstones or dilation of the common duct (which stands for a bile duct obstruction) determine. Edema of the pancreas can be represented, which is above the air organ often leads to inaccurate representation of the pancreas. A CT with iv Contrast agent is performed generally to detect necrosis, fluid collections or pseudocysts in principle already diagnosed pancreatitis. It is recommended or particularly in severe pancreatitis occurring complications (such. As hypotension or increasing leukocytosis and fever increase). Intravenous contrast agent facilitates the detection of pancreatic necrosis, on the other hand, it can trigger a pancreatic necrosis in areas of low perfusion (z. B. ischemia). Therefore, should not be performed until a contrast-enhanced CT, when the patient’s fluid balance is balanced. In cases of suspected infection of the pancreas can be diagnosed using a Gram stain or culture pathogens in the liquid, which was won by percutaneous CT-guided needle aspiration of cysts or fluid retention or necrosis. The diagnosis is supported by positive blood cultures and v. a. by the appearance of air bubbles in the retroperitoneum, diagnosed in abdominal CT. The introduction of the magnetic resonance cholangiopancreatography (MRCP) simplifies the selection of imaging techniques in the diagnosis of pancreas. Forecast In edematous pancreatitis is the mortality <5%. In necrotic and hemorrhagic pancreatitis, the mortality rate is 10-50%. Upon infection of the pancreas, the mortality rate is 100%, if not an extensive surgical clearance work of the destroyed necrotic tissue or drainage of the inflammation area are performed. The CT findings correlate with prognosis. It is excellent if the CT is normal or the image of a poor levels Pankreasödems shows (Balthazar Class A or B). In patients with peripankreatischer inflammation or an area of ??fluid accumulation (class C and D) in 10-15% of cases occur abscesses; the incidence of abscesses is> 60% in patients with two or more fluid retention (Class E). The Ranson signs are helpful in predicting the prognosis of acute pancreatitis. Five of the characters can be recorded during recording: age> 55 years plasma glucose> 200 mg / dl (> 11.1 mmol / l) serum LDH> 350 IU / L AST> 250 UL leukocyte count> 16,000 / ul, the other characters Ranson within 48 h after ingestion determined: HCT-reduction> 10% increase in BUN> 5 mg / dl (> 1.78 mmol / l) serum Ca <8 mg / dl (<2 mmol / l) PaO2 <60 mmHg (<7.98 kPa) base deficit> 4 mEq / l (> 4 mmol / l) Estimated sequestration of liquid> 6 l mortality increases with the number of positive signs: If <3 signs are positive, the mortality is <5 % when 3 ? signs are positive, the mortality is 15-20%. Clinical Calculator: APACHE II score system and mortality estimates ( "Acute Physiology and Chronic Health Disease Classification System II") The APACHE II index (see table: The APACHE II scoring system *), carried out on the second day of hospitalization, also correlates with prognosis. Clinical computer. Prognostic criteria for pancreatitis therapy fluid replacement fasting drugs including adequate analgesia and antacid antibiotics in pancreatic drainage of infected pseudo cysts or necrosis An adequate recovery of a balanced fluid balance is essential: up to 6-8 l electrolyte-containing liquid / day may be required. An inadequate fluid replacement increases the risk of pancreatic necrosis. Fasting is indicated until the acute inflammation regresses (z. B. easing of abdominal tension feeling and pain, normalization of serum amylase, return of appetite and improve general well-being). The duration of the fasting period can vary from one day at low pronounced pancreatitis to several weeks. In severe cases, total parenteral nutrition within the first day should be taken to prevent malnutrition. For pain treatment parenteral opioids must be given in sufficient dosage. Although morphine can in principle lead to a contraction of the sphincter of Oddi, this does not reflect the clinical experience. Antiemetic substances (eg. B. prochlorperazine 5-10 mg i.v. every 6 h) can be given for the suppression of vomiting. A nasogastric tube is only necessary if the vomiting occurs or if an ileus is. Parenteral H2 blockers or proton pump inhibitors are administered. to reduce efforts pancreatic secretion with drugs (eg. as anticholinergics, glucagon, somatostatin, octreotide) have no proven beneficial effect. Patients with severe acute pancreatitis should be treated in an intensive care unit, v. a. those with hypotension oliguria, a Ranson score ? 3, APACHE-II-index ? 8 or a diagnosed by CT pancreatic necrosis of> 30%. In the intensive care unit, the vital parameters and urinary excretion are monitored hourly, metabolic parameters (hematocrit, glucose and electrolytes) are determined every 8 h, the arterial blood gases are measured continuously, the central venous pressure or pulmonary artery catheter-determinations are made every 6 h if the patient is hemodynamically unstable or fluid requirement is unclear. Daily provisions should be made for: complete blood count, platelet count, coagulation parameters, total protein with albumin, urea, creatinine, calcium and magnesium. The hypoxemia is treated by administering O2 via a mask. If hypoxemia persists in this way or respiratory distress syndrome occurs, artificial respiration may be necessary. A glucose increase> 170-200 mg / dL (9.4 to 11.1 mmol / l) should be careful with s.c. or iv given insulin to be treated. Hypocalcemia is first treated in the rule if neuromuscular disorders occur: 10-20 ml of 10% strength Ca-gluconate in 1 l i.v. administered over 4-6 h. Chronic alcoholics or patients with documented hypomagnesemia should to obtain Mg-sulfate 1 g / l of liquid to a total replacement of 2-4 g, or until the normalization of the serum magnesium. In case of kidney failure the serum magnesium is controlled and magnesium i.v. administered cautiously. With the restoration of normal levels of magnesium and serum calcium levels return usually the norm. Heart failure should be treated (heart failure: Treatment). A pre-renal azotemia is treated by fluid replacement. Renal failure can mean dialysis (usually peritoneal dialysis). Antibiotic prophylaxis with imipenem can prevent infection of sterile pancreatic necrosis, although a beneficial effect has not been proven to reduce mortality. Infected areas of pancreatic necrosis require surgical clearance work, infected fluid collections around the pancreas can be percutaneously drained. A pseudo-cyst with a rapid increase in size, infection, bleeding or the threat of rupture requires the drainage. Whether the drainage is done percutaneously, surgically or endoscopically, depends on the location of the pseudocyst and medical experience. A peritoneal lavage to remove activated pancreatic enzymes and inflammatory mediators has not ultimately found to be favorable. Surgical intervention is justified in severe blunt or penetrative trauma or uncontrollable sepsis during the first days. Although> 80% of patients with biliary pancreatitis have a spontaneous stone passage, ERCP with sphincterotomy and stone removal is indicated for patients who do not improve within 24 hours. Patients who recover spontaneously are cholecystectomy elective laparoscopic generally. Elective cholangiography is controversial. Summary There are many causes of acute pancreatitis, the most common are biliary diseases and chronic, heavy alcohol consumption. In mild cases, the inflammation of the pancreas is limited, but with increasing severity to pancreatic necrosis, pseudocysts and / or a severe systemic inflammatory response evolve. Once the pancreatitis is diagnosed, then a CT to detect pancreatic necrosis or pseudocyst formation. CT findings and Ranson characters are useful for creating the forecast. Treatment consists of i.v. Fluid replacement, fasting, parenteral analgesics and antacids. Determined complications are treated as required (eg. B. drainage of pseudocyst, antibiotics in infected pancreatic necrosis).