Chronic Pancreatitis

From a chronic pancreatitis is a persistent inflammation of the pancreas with permanent organ damage with fibrosis and Gangstrikturen, associated with worsening of exocrine and endocrine function. It can occur as a result of chronic alcohol abuse or be idiopathic. The initial symptoms are recurrent attacks of pain. In later stages of the disease, some patients develop malabsorption and glucose intolerance. The diagnosis is usually by imaging techniques such as ERCP, EUS or secretin Pankreozymin test. Treatment is supportive with pancreatic diet, painkillers gift and enzyme substitution. In some cases, surgical treatment is indicated.

From a chronic pancreatitis is a persistent inflammation of the pancreas with permanent organ damage with fibrosis and Gangstrikturen, associated with worsening of exocrine and endocrine function. It can occur as a result of chronic alcohol abuse or be idiopathic. The initial symptoms are recurrent attacks of pain. In later stages of the disease, some patients develop malabsorption and glucose intolerance. The diagnosis is usually by imaging techniques such as ERCP, EUS or secretin Pankreozymin test. Treatment is supportive with pancreatic diet, painkillers gift and enzyme substitution. In some cases, surgical treatment is indicated. Etiology In the US, less than half of the cases, an alcoholic cause, 15-25% are idiopathic. However, recent data suggest that alcohol less and less as the cause comes into question. Less common causes include hereditary pancreatitis, an autoimmune pancreatitis, hyperparathyroidism, and obstruction of the main passage by stenosis, stones or cancer. In India, Indonesia and Nigeria in children and young adults idiopathic calcific pancreatitis ( “tropical pancreatitis”) occurs. Similar to the pathophysiology of acute pancreatitis the pathogenic mechanism in a gear installation may consist of Proteinpfröpfe. The Proteinpfröpfe be prevented by an excessive secretion of glycoprotein-2, or a lack of Lithostatin, a protein in the pancreatic juice, the Kalziumpräzipitation caused. In chronic inflammation laying persists and leads to fibrosis and changes in the Ganges within the meaning of dilatations and strictures, which can also calcify. A Nervenscheidenhypotrophie and perineural inflammation may contribute to the development of chronic pain. After several years of progressive fibrosis leading to a loss of exocrine and endocrine function. This results in 20-30% of patients within 10 to 15 years, a diabetes mellitus. Symptoms and signs Most patients suffering from episodic abdominal pain. 10-15% have no pain, but a malabsorption. The pain is epigastric, persistent and difficult for several hours or several days. The pain episodes can spontaneously after 6-10 years because the acinar cells that secrete the pancreatic digestive enzymes are increasingly being destroyed. If lipase and protease secretion up to <10% of normal reduced, the patient develops steatorrhea and issues greasy stool or even oil drops and there is a Kreatorrhö (the presence of undigested muscle fibers in the stool). At this time, symptoms of glucose intolerance may occur. Diagnosis Clinical suspicion abdominal CT occasionally magnetic resonance cholangiopancreatography (MRCP), endoscopic ultrasound or ERCP Diagnosis can be difficult because amylase and lipase in serum due to the severe loss of Pankeasfunktion are often normal. In a patient with history of a typical alcohol abuse and recurrent episodes of acute pancreatitis the detection of lime in the pancreas on the abdominal plain may be sufficient. However, such calcifications typically occur in later stages of the disease and the patient also is only at about 30%. In patients without typical history, the presence of a pancreatic tumor must be ruled out as the cause of the pain symptoms: it is an abdominal CT is recommended. The CT can show calcifications and other pathological conditions of the pancreas (eg. As pseudocyst or advanced courses), but may be normal in the early stages of the disease. The MRCP is now often used to diagnose, they can reveal lesions in the pancreas and provides better visualization of ductal changes in chronic pancreatitis. Further investigation procedures in patients with normal CT are an ERCP, an endoscopic ultrasound and the secretin Pankreozymin test. These test methods are very sensitive, but about 5% of patients ERCP can cause acute pancreatitis. In the late stages of the disease, the test method for detecting a pancreatic exocrine dysfunction are pathological. A 72-hour test for the detection of fat in the stool is diagnostic for the presence of steatorrhea, but can not detect the cause. When secretin pancreatic juice is collected via a duodenal tube for analysis, however, this test is only available in some centers. Trypsinogen in serum and chymotrypsin and elastase in the stool can be reduced. When Bentiromid- and when pancreolauryl substances are administered orally, and then analyzed the urine formed by pancreatic enzymes cleavage products of these substances. In the early stages of the disease this exocrine test methods are less sensitive than ERCP, or endoscopic ultrasonography. Therapy infusions fasting drugs incl. Adequate analgesia and acid blockers pancreatic enzyme supplements Occasionally drainage of pseudocysts (surgical or endoscopic) Recurrence requires a similar therapeutic approach as in acute pancreatitis with fasting, i.v. Hydration and analgesics. When food is taken again, the patient must avoid alcohol and a low-fat comply (<25 g / day) diet (to reduce pancreatic enzyme secretion). An H2-blockers or proton pump inhibitors knn säurestimulierte reduce the release of secretin and thereby reduce the formation of pancreatic juice. Very often, these measures do not relieve pain, so that increasing amounts of opiates are required, the risk of dependence. The medical treatment of pain in chronic pancreatitis is often unsatisfactory. The replacement of pancreatic enzymes can reduce chronic pain by causing a reduction in Cholezystokininfreisetzung and thus a reduction of pancreatic enzyme secretion. The supplementation is successful in less pronounced idiopathic pancreatitis than in an alcoholic pancreatitis. The enzyme replacement is also used for the treatment of steatorrhea. Numerous preparations are available, there should be a Lipasedosis of at least 30,000 units are used. Release tablets should not be used, the tablets are given with meals. Co-administration of H2 blockers or proton pump inhibitors is recommended in order to prevent denaturation of the enzymes by acid. The response to therapy is shown in weight gain, reduction in stool frequency, disappearance of oil droplets in the stool and improvement of the general condition. Clinical response is documented by the demonstration of reduced fat in the stool by enzyme therapy. In particularly strong expression of the steatorrhea and ineffectiveness of these measures medium chain triglycerides should be administered as a source of fat (they are absorbed without the aid of pancreatic enzymes) with the simultaneous corresponding reduction in the dietary fat content. On replacement of fat-soluble vitamins (A, D, K) must be ensured, incl. Vitamin E, which has antioxidant properties. Surgical therapy can effectively contribute to pain relief. A pseudocyst of the pancreas, which causes chronic pain can effectively in an immediately adjacent abutting structure (eg. As the stomach) or in a disused loop of the jejunum are derived (via Roux-Y-Zystojejunostomie). In an extension of the pancreas main course to> 5-8 mm a pancreaticojejunostomy leads (Puestow operation) at 70-80% of the patients for pain relief. When the main course is not expanded, partial resection shows similar therapeutic results; this is carried out either as a distal pancreatectomy (with pronounced attack of the tail of the pancreas) or as Whipple operation (pronounced at infestation of the pancreatic head). Operational methods should be reserved for patients who are abstinent and able to treat their diabetic metabolic disorder that may be reinforced by pancreatic resection. Some pseudo cysts can be drained endoscopically. Endoscopic ultrasound-guided denervation of the celiac plexus with alcohol and bupivacaine may cause pain relief. In the event of a pronounced Papillenstriktur or stenosis in the distal pancreatic duct ERCP with sphincterotomy, stent or insert a dilation can be effective. Oral antidiabetic drugs are usually not sufficient for treatment of diabetic metabolism in chronic pancreatitis. In the dose of insulin you must be careful because the concurrent reduction in glucagon secretion by the alpha cells means that hypoglycemic states are left unchecked in insulin therapy and thus a prolonged hypoglycemia can occur. Patients with chronic pancreatitis are at increased risk of pancreatic carcinoma. The worsening of symptoms, v. a. the development of a stricture in the pancreatic duct, should cause an immediate investigation because of a possible cancer. To this investigation includes the brush cytology and determination of tumor markers (eg. As CA 19-9 and carcinoembryonic antigen). Summary Recurrent attacks of acute pancreatitis can cause gear damage, persistent chronic inflammation and ultimately fibrosis, leading to pancreatic insufficiency. The patients have episodic abdominal pain, followed by signs of malabsorption in later disease. Serum amylase and lipase may be normal, especially in the later course of the disease; the imaging is effected by CT, MRCP and occasionally ERCP or endoscopic ultrasonography. In patients with symptoms of malabsorption tests of exocrine function to be performed. The treatment is the same as that of acute pancreatitis and consists in i.v. Fluid replacement, fasting, the administration of parenteral analgesics and antacids and additionally oral pancreatic enzyme supplements and / or insulin as needed.

Health Life Media Team

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