Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 Chronic pancreatitis is an inflammatory disease in which progressive and irreversible structural changes to the pancreas result in a permanent impairment of both the exocrine and endocrine functions. As the pancreas become progressively more scarred, some persons develop diabetes and/or the inability to digest foods, especially fats. Because of the lack of normal pancreatic enzymes, digestion of food and the production of wastes are adversely affected. Abdominal pain is common, especially after eating. Stools become bulky, greasy, foul smelling and tend to float in the water because of their high fat content - a condition known as steatorrhea. The formation of stones in the pancreas is also common. The treatment of chronic pancreatitis depends on 4 factors: the cause of the pancreatitis, the portion of the pancreas involved, the presence or absence os symptoms, and the size of the pancreatic duct. When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is indicated. For persons with disabling symptoms, however, treatment is indicated. Treatment may consist of medications and possibly surgery. The pancreas is a long, slender organ in the upper abdomen. The exocrine area of the pancreas produces digestive juices and the endocrine area makes hormones, such as insulin, that regulate how the body stores and uses food. Both functions are impaired by chronic pancreatitis, an inflammatory disease that causes progressive, irreversible structural changes. Some persons develop diabetes and/or become unable to digest foods, especially fats. The lack of normal pancreatic enzymes adversely affects digestion and waste production. Abdominal pain is common, especially after eating. This illness can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can cause stones to form in the pancreas. In some 70% to 80% of cases, alcoholism is a factor, but other causes can include duct obstruction, nutritional factors and genetic abnormalities. About 30% of cases have no known cause. Symptoms include severe abdominal pain, weight loss and steatorrhea. When symptoms are mild, no treatment is indicated. When needed, treatment focuses on pain control, relieving duct obstruction, correcting digestive problems, and detecting and managing complications. The choice of treatment for you or for the patient you care about, depends on the cause, the portion of the organ involved, symptoms and duct size. This illness requires individual diagnosis and treatment. Not all patients respond to the same therapy. Treatment may consist of medications and, possibly, surgery. The Journal of Gastrointestinal Surgery reports that surgery for chronic pancreatitis " can be performed safely with minimal morbidity and excellent long-term survival. " acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 Chronic pancreatitis is an inflammatory disease in which progressive and irreversible structural changes to the pancreas result in a permanent impairment of both the exocrine and endocrine functions. As the pancreas become progressively more scarred, some persons develop diabetes and/or the inability to digest foods, especially fats. Because of the lack of normal pancreatic enzymes, digestion of food and the production of wastes are adversely affected. Abdominal pain is common, especially after eating. Stools become bulky, greasy, foul smelling and tend to float in the water because of their high fat content - a condition known as steatorrhea. The formation of stones in the pancreas is also common. The treatment of chronic pancreatitis depends on 4 factors: the cause of the pancreatitis, the portion of the pancreas involved, the presence or absence os symptoms, and the size of the pancreatic duct. When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is indicated. For persons with disabling symptoms, however, treatment is indicated. Treatment may consist of medications and possibly surgery. The pancreas is a long, slender organ in the upper abdomen. The exocrine area of the pancreas produces digestive juices and the endocrine area makes hormones, such as insulin, that regulate how the body stores and uses food. Both functions are impaired by chronic pancreatitis, an inflammatory disease that causes progressive, irreversible structural changes. Some persons develop diabetes and/or become unable to digest foods, especially fats. The lack of normal pancreatic enzymes adversely affects digestion and waste production. Abdominal pain is common, especially after eating. This illness can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can cause stones to form in the pancreas. In some 70% to 80% of cases, alcoholism is a factor, but other causes can include duct obstruction, nutritional factors and genetic abnormalities. About 30% of cases have no known cause. Symptoms include severe abdominal pain, weight loss and steatorrhea. When symptoms are mild, no treatment is indicated. When needed, treatment focuses on pain control, relieving duct obstruction, correcting digestive problems, and detecting and managing complications. The choice of treatment for you or for the patient you care about, depends on the cause, the portion of the organ involved, symptoms and duct size. This illness requires individual diagnosis and treatment. Not all patients respond to the same therapy. Treatment may consist of medications and, possibly, surgery. The Journal of Gastrointestinal Surgery reports that surgery for chronic pancreatitis " can be performed safely with minimal morbidity and excellent long-term survival. " acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 Chronic pancreatitis is an inflammatory disease in which progressive and irreversible structural changes to the pancreas result in a permanent impairment of both the exocrine and endocrine functions. As the pancreas become progressively more scarred, some persons develop diabetes and/or the inability to digest foods, especially fats. Because of the lack of normal pancreatic enzymes, digestion of food and the production of wastes are adversely affected. Abdominal pain is common, especially after eating. Stools become bulky, greasy, foul smelling and tend to float in the water because of their high fat content - a condition known as steatorrhea. The formation of stones in the pancreas is also common. The treatment of chronic pancreatitis depends on 4 factors: the cause of the pancreatitis, the portion of the pancreas involved, the presence or absence os symptoms, and the size of the pancreatic duct. When symptoms are mild or absent ( " silent pancreatitis " ) no treatment is indicated. For persons with disabling symptoms, however, treatment is indicated. Treatment may consist of medications and possibly surgery. The pancreas is a long, slender organ in the upper abdomen. The exocrine area of the pancreas produces digestive juices and the endocrine area makes hormones, such as insulin, that regulate how the body stores and uses food. Both functions are impaired by chronic pancreatitis, an inflammatory disease that causes progressive, irreversible structural changes. Some persons develop diabetes and/or become unable to digest foods, especially fats. The lack of normal pancreatic enzymes adversely affects digestion and waste production. Abdominal pain is common, especially after eating. This illness can make stool bulky, fatty and odiferous (that's " steatorrhea " ), and can cause stones to form in the pancreas. In some 70% to 80% of cases, alcoholism is a factor, but other causes can include duct obstruction, nutritional factors and genetic abnormalities. About 30% of cases have no known cause. Symptoms include severe abdominal pain, weight loss and steatorrhea. When symptoms are mild, no treatment is indicated. When needed, treatment focuses on pain control, relieving duct obstruction, correcting digestive problems, and detecting and managing complications. The choice of treatment for you or for the patient you care about, depends on the cause, the portion of the organ involved, symptoms and duct size. This illness requires individual diagnosis and treatment. Not all patients respond to the same therapy. Treatment may consist of medications and, possibly, surgery. The Journal of Gastrointestinal Surgery reports that surgery for chronic pancreatitis " can be performed safely with minimal morbidity and excellent long-term survival. " acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 This is a medical emergency marked by acute abdominal stress. Symptoms are caused by spillage of pancreatic fluids into the abdominal cavity. These fluids contain enzymes which begin to digest and destroy the lining of the intestine and the intestinal wall itself as well as any internal organs it encounters. Pain typically radiates from the pit of the abdomen through to the back with nausea, vomiting, low-grade fever, and shock. Some patients exhibit none of these save shock. There may be evidence of intra-abdominal bleeding. Causes include direct trauma, overindulgence in alcoholic beverages, viral and bacterial infections, duodenal ulcer perforation into the pancreas, certain metabolic insults, and toxicity from some pharmacological drugs. The diagnosis is made by ultrasound with supporting evidence from elevated pancreatic enzyme levels (amylase and lipase). These people usually have elevated white cell counts. Acute pancreatitis is a medical emergency and must be treated in a hospital setting. In addition to the usual management doctors in nutritional medicine have noted that intramuscular selenium followed by repeat doses 24 hours later, then daily doses are useful in the management of this disorder. Only doctors who practice nutritional medicine have a clue about the use of selenium for this indication. In the acute stage of acute pancreatitis the patient should have nothing by mouth, intravenous feeding should be instituted, calcium and magnesium levels maintained, pain managed, and the cause of the disorder treated. This may involve surgery. Chronic pancreatitis may result from one or more bouts of acute pancreatitis and this condition is marked by radiologic evidence of calcification of the pancreas, passage of undigested fat in the stool, diabetes, vitamin B12 deficiency, and poor digestion due to loss of pancreatic enzymes. Also a cyst-like condition may develop requiring surgery. The most important aspect in the treatment of acute pancreatitis is supportive care. This includes replacement of fluid and electrolytes, correction of metabolic abnormalities such as symptomatic hypercalcemiaand nutritional support. Other measures such as the use of nasogastric suction and antibiotics should be decided on a case-by-case basis. Agents that have been used to inhibit pancreatic secretion have not been found to be useful in altering the course in acute pancreatitis. These include somatostatin and glucagon. Protease inhibitors, which are effective in laboratory studies, have not been shown to be useful in clinical pancreatitis. Emergency surgery is not indicated in mild acute pancreatitis. Some surgical procedures such as resection of necrotictissue and peritoneal lavagemay have a role in select patients with severe, progressive necrotizing pancreatitis or pancreatic abscess. Cholecystectomy has been demonstrated to be effective in patients with recurrent acute pancreatitis and microlithiasis (Figure 17). Surgical sphincteroplasty of the pancreatic sphincter is an alternative approach to endoscopic pancreatic sphincterotomy in patients with pancreatic sphincter dysfunction. Although the patient outcome is the same as for the endoscopic approach, it is more invasive, requiring laparotomy and . duodenotomy Sphincteroplasty of the minor papilla is indicated for unsuccessful or failed endoscopic minor papilla sphincterotomy in patients with . pancreas divisum Endoscopic therapy has a therapeutic role in three specific areas in the management of acute pancreatitis: 1) acute gallstone pancreatitis, 2) recurrent pancreatitis due to pancreatic sphincter dysfunction, and 3) recurrent pancreatitis due to . pancreas divisum The rationale for endoscopic therapy in each area is the relief of obstruction to flow of pancreatic juice. [top] Although it would seem logical that removal of the gallstones from the common bile duct early in acute gallstone pancreatitis would improve the clinical course, there is a lack of a " predictable " good outcome as suggested by propective clinical trials. It appears, however, that the patients with suspected stones who benefit from early ERCP are those with evidence of biliary obstruction such as jaundice or dilation of the bile duct and severe pancreatitis. Further clinical trials are needed before more definitive recommendations can be made. In a subgroup of patients with acute recurrent pancreatitis and ,microlithiasis endoscopic sphincterotomy has been shown to significantly reduce the frequency of attacks (Figure 18). [top] With the advent of manometric studies of the pancreatic sphincter, many cases of so-called idiopathic recurrent pancreatitis are now known to be a result of pancreatic sphincter dysfunction. Endoscopic pancreatic sphincterotomy may be expected to have a good outcome in up to 90% of these patients. There are two techniques for endoscopic pancreatic sphincterotomy; one is with a pull-type sphincterotome followed by stenting of the pancreatic duct and the second is with a needle-knife sphincterotome performed over a pancreatic stent. Following pancreatic sphincterotomy there may be tissue swelling that could result in obstruction to pancreatic outflow. Therefore, short-term pancreatic stenting is indicated when pancreatic sphincterotomy is performed to maintain patency of pancreatic outflow (Figure 19). [top] Endoscopic minor papilla sphincterotomy is effective treatment for patients with recurrent pancreatitis and pancreas divisum (Figure 20). Good long-term results are found in about 70% of patients but may be significantly less if there are changes of chronic pancreatitis. There are two techniques for endoscopic minor papilla sphincterotomy; one is with a pull-type sphincterotome followed by stenting of the pancreatic duct and the second is with a needle-knife sphincterotome performed over a pancreatic stent (Figure 21). Following pancreatic sphincterotomy there may be tissue swelling that could result in obstruction to pancreatic outflow. Therefore short-term pancreatic stenting is indicated when pancreatic sphincterotomy is performed to maintain patency of pancreatic outflow. [top] acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 INTRODUCTION Background: Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland. The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatitis. It can recur intermittently, contributing to the functional and morphologic loss of the gland. Recurrent attacks are referred to as chronic pancreatitis. Both forms of pancreatitis are present in the ED with acute clinical findings. Pathophysiology: Because the pancreas is located in the retroperitoneal space with no capsule, inflammation can spread easily. In acute pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first. This process is known as acute edematous pancreatitis. When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland, the inflammation evolves into hemorrhagic or necrotizing pancreatitis. Pseudocysts and pancreatic abscesses can result from necrotizing pancreatitis because of enzymes being walled off by granulation tissue (ie, pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic tissue (ie, pancreatic abscess formation). An ultrasound or, preferably, a CT scan can be used detect both. The inflammatory process can cause systemic effects because of the presence of cytokines, such as bradykinins and phospholipase A. These cytokines may cause vasodilation, increase in vascular permeability, pain, and leukocyte accumulation in the vessel walls. Fat necrosis may cause hypocalcemia. Pancreatic B cell injury may lead to hyperglycemia. Frequency: In the US: Annual incidence of acute pancreatitis is 19.5 per 100,000 population and chronic pancreatitis is 8.3 per 100,000 population per year. Mortality/Morbidity: Although acute pancreatitis should be noted, chronic pancreatitis has a more severe presentation as episodes recur. Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock all may be systemic manifestations of acute pancreatitis in its most severe form. Race: Annual incidence of acute pancreatitis in Native American persons is 4 per 100,000 population, in white persons is 5.7 per 100,000 population, and in black persons is 20.7 per 100,000 population. Sex: No predilection exists. Age: The risk for African American persons aged 35-64 years is 10 times higher than for any other group. African American persons are at higher risk than white persons in that same age group. Clinical History: The main presentation of acute pancreatitis is epigastric pain or right upper quadrant pain radiating to the back Nausea and/or vomiting Fever Query the patient about recent surgeries and invasive procedures (ie, endoscopic retrograde cholangiopancreatography) or family history of hypertriglyceridemia. Patients frequently have a history of previous biliary colic and binge alcohol consumption, the major causes of acute pancreatitis. Physical: Tachycardia Tachypnea Hypotension Fever Abdominal tenderness, distension, guarding, and rigidity Mild jaundice Diminished or absent bowel sounds Because of contiguous spread of inflammation (effusion) from the pancreas, lung auscultation may reveal basilar rales, especially in the left lung. Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcemia. Severe cases may have a Grey sign (ie, bluish discoloration of the flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis. Causes: The major causes are long-standing alcohol consumption and biliary stone disease. In developed countries, the most common cause of acute pancreatitis is alcohol abuse. On the cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release. On the ductal level, ethanol increases the permeability of ductules, which allow enzymes to reach the parenchyma, resulting in pancreatic damage. Ethanol increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the formation of protein plugs that block the pancreatic outflow and obstruction. Another major cause of acute pancreatitis is biliary stone disease (eg, cholelithiasis, choledocholithiasis). A biliary stone may lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma. Minor causes of acute pancreatitis Medications, including azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, NSAIDs, mercaptopurine, methyldopa, and tetracyclines Endoscopic retrograde cholangiopancreatography (ERCP) Hypertriglyceridemia (When the triglyceride (TG) level exceeds 1000 mg/U, an episode of pancreatitis is more likely.) Peptic ulcer disease Abdominal or cardiopulmonary bypass surgery, which may insult the gland by ischemia Trauma to the abdomen or back, resulting in sudden compression of the gland against the spine posteriorly Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction Viral infections, including mumps, sackievirus, cytomegalovirus (CMV), hepatitis virus, Epstein-Barr virus (EBV), and rubella Bacterial infections, such as mycoplasma Intestinal parasites, such as ascaris, which can block the pancreatic outflow Pancreas divisum Scorpion and snake bites Vascular factors, such as ischemia or vasculitis DIFFERENTIALS Other Problems to be Considered: Perforated viscus Acute peritonitis Choledocholithiasis Macroamylasemia Macrolipasemia Intestinal obstruction Pancreatic cancer Malabsorption syndromes/processes Workup Lab Studies: A complete blood count (CBC) demonstrates leukocytosis (WBC >12000) with the differential being shifted towards the segmented polymorphs. If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and crossmatch. Measure blood glucose level because it may be elevated from B cell injury in the pancreas. Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl, CO2, P, Mg); a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids. Measure amylase levels, preferably the Amylase P, which is more specific to pancreatic pathology. Levels more than 3 times higher than normal strongly suggest the diagnosis of acute pancreatitis Lipase levels also are elevated and remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase may be elevated in the presence of a normal serum amylase level Perform liver function tests (eg, alkaline phosphatase, serum glutamic-pyruvic transaminase [sGPT], serum glutamic-oxaloacetic transaminase [sGOT], G-GT) and bilirubin, particularly with biliary origin pancreatitis. Imaging Studies: Perform a plain KUB (Kidneys, ureters, bladder) with the patient in the upright position to exclude viscus perforation (ie, air under the diaphragm). In cases with a recurrent episode of chronic pancreatitis, peripancreatic calcifications may be noted Ultrasound can be used as a screening test. If overlying gas shadows secondary to bowel distention are present, it may not be specific CT scan is the most reliable imaging modality in the diagnosis of acute pancreatitis. The criteria for diagnosis are divided by Balthazar and colleagues into 5 grades, as follows: Grade A - Normal pancreas Grade B - Focal or diffuse gland enlargement Grade C - Intrinsic gland abnormality recognized by haziness on the scan Grade D - Single ill-defined collection or phlegmon Grade E - Two or more ill-defined collections or the presence of gas in or nearby the pancreas Other Tests: Para-aminobenzoic acid test (ie, bentiromide [Chymex] test) for chronic pancreatitis Treatment Emergency Department Care: Most of the cases presenting to the ED are treated conservatively, and approximately 80% respond to such treatment. Fluid resuscitation Monitor accurate intake/output and electrolyte balance of the patient. Crystalloids are used, but other infusions, such as packed red blood cells (PRBCs), are occasionally administered, particularly in the case of hemorrhagic pancreatitis. Central lines and Swan-Ganz catheters are used in patients with severe fluid loss and very low blood pressure. Patients should have nothing by mouth, and a nasogastric tube should be inserted to assure an empty stomach and to keep the GI system at rest. Begin parenteral nutrition if the prognosis is poor and if the patient is going to be kept in the hospital for more than 4 days. Analgesics are used to relieve pain. Meperidine is preferred over morphine because of the greater spastic effect of the latter on the sphincter of Oddi. Antibiotics are used in severe cases associated with septic shock or when the CT scan indicates that a phlegmon of the pancreas has evolved. Other conditions, such as biliary pancreatitis associated with cholangitis, also need antibiotic coverage. The preferred antibiotics are the ones secreted by the biliary system, such as ampicillin and third generation cephalosporins. Continuous oxygen saturation should be monitored by pulse oxymetry and acidosis should be corrected. When tachypnea and pending respiratory failure develops, intubation should be performed. Perform CT-guided aspiration of necrotic areas, if necessary. An ERCP may be indicated for common duct stone removal. Consultations: Consult a general surgeon in the following cases: For phlegmon of the pancreas, surgery can achieve drainage of any abscess or scooping of necrotic pancreatic tissue. It should be followed by postoperative lavage of the pancreatic bed. In patients with hemorrhagic pancreatitis, surgery is indicated to achieve hemostasis, particularly because major vessels may be eroded in acute pancreatitis. Patients who fail to improve despite optimal medical treatment or patients who push the Ranson score even further are taken to the operating room. Surgery in these cases may lead to a better outcome or confirm a different diagnosis. In biliary pancreatitis, a sphincterotomy (ie, surgical emptying of the common bile duct) can relieve the obstruction. A cholecystectomy may be performed to clear the system from any source of biliary stones. Medications The goal of pharmacotherapy is to relieve pain and minimize complications. Drug Category: Antibiotics - Used to cover the microorganisms that may grow in biliary pancreatitis and acute necrotizing pancreatitis. The empiric antibiotic regimen usually is based on the premise that enteric anaerobic and aerobic gram-bacilli microorganisms are often the cause of pancreatic infections. Once culture sensitivities are made, adjustments in the antibiotic regimen can be done. Drug Name Ceftriaxone (Rocephin)- Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Adult Dose 1-2 g IM/IV once or divided bid Pediatric Dose 50-75 mg/kg/d IM/IV divided q12h Contraindications Documented hypersensitivity Interactions Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin Drug Name Ampicillin (Marcillin, Omnipen)- Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally. Adult Dose 250-500 IM/IV mg q6h Pediatric Dose 25-50 mg/kg/d IM/IV divided q6-8h Contraindications Documented hypersensitivity; viral mononucleosis Interactions Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction Drug Category: Analgesics - Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and has sedating properties, which are beneficial for patients who have sustained trauma or have painful lesions. Drug Name Meperidine (Demerol)- Analgesic with multiple actions similar to those of morphine. May produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine. Adult Dose 15-35 mg/h IV; 50-150 mg IM q3-4h Pediatric Dose 1.1-1.8 mg/kg IM q3-4h Contraindications Documented hypersensitivity; MAOIs; upper airway obstruction or significant respiratory depression; during labor when delivery of premature infant is anticipated Interactions Monitor for increased respiratory and CNS depression with coadministration of cimetidine; hydantoins may decrease effects; avoid with protease inhibitors Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in head injuries because may increase respiratory depression and CSF pressure (use only if absolutely necessary); caution when using postoperatively and with history of pulmonary disease (suppresses cough reflex; substantially increased dose levels may aggravate or cause seizures because of tolerance, even if no prior history of convulsive disorders; monitor closely for morphine-induced seizure activity if seizure history exists Drug Category: Antibiotics - Used to cover the microorganisms that may grow in biliary pancreatitis and acute necrotizing pancreatitis. The empiric antibiotic regimen usually is based on the premise that enteric anaerobic and aerobic gram-bacilli microorganisms are often the cause of pancreatic infections. Once culture sensitivities are made, adjustments in the antibiotic regimen can be done. Drug Category: Analgesics - Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and has sedating properties, which are beneficial for patients who have sustained trauma or have painful lesions. Followup Further Inpatient Care: Transfer patients with Ranson scores of 0-2 to a hospital floor. Transfer patients with Ranson scores 3-5 to an intensive care unit. Transfer patients with Ranson scores higher than 5 to an intensive care unit with emergency surgery as a possibility. Further Outpatient Care: The patient should be followed routinely with physical examination and amylase and lipase assays. Complications: Infected pancreatic necrosis may result from seeding of bacteria into the inflammation. An acute pseudocyst is an effusion of pancreatic juice that is walled off by granulation tissue after an episode of acute pancreatitis. Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is possible because of erosion of large vessels. Intestinal obstruction or necrosis may occur. Common bile duct obstruction may be caused by a pancreatic abscess, pseudocyst, or biliary stone that caused the pancreatitis. An internal pancreatic fistula from pancreatic duct disruption or a leaking pancreatic pseudocyst may occur. Prognosis: Ranson developed a series of different criteria for the severity of acute pancreatitis. Present on admission Older than 55 years WBC higher than 16,000 per mcL Blood glucose higher than 200 mg/dL Serum lactate dehydrogenase (LDH) more than 350 IU/L SGOT (ie, aspartate aminotransferase [AST]) greater than 250 IU/L Developing during the first 48 hours Hematocrit fall more than 10% BUN increase more than 8 mg/dL Serum calcium less than 8 mg/dL Arterial oxygen saturation less than 60 mm Hg Base deficit higher than 4 mEq/L Estimated fluid sequestration higher than 600 mL A Ranson score of 0-2 has a minimal mortality rate. A Ranson score of 3-5 has a 10%-20% mortality rate. A Ranson score higher than 5 has a mortality rate of more than 50% and is associated with more systemic complications. Patient Education: Educate patients about the disease and advise then to avoid alcohol in binge amounts and to discontinue any risk factor, such as fatty meals and abdominal trauma. acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 23, 2002 Report Share Posted December 23, 2002 INTRODUCTION Background: Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland. The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatitis. It can recur intermittently, contributing to the functional and morphologic loss of the gland. Recurrent attacks are referred to as chronic pancreatitis. Both forms of pancreatitis are present in the ED with acute clinical findings. Pathophysiology: Because the pancreas is located in the retroperitoneal space with no capsule, inflammation can spread easily. In acute pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first. This process is known as acute edematous pancreatitis. When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland, the inflammation evolves into hemorrhagic or necrotizing pancreatitis. Pseudocysts and pancreatic abscesses can result from necrotizing pancreatitis because of enzymes being walled off by granulation tissue (ie, pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic tissue (ie, pancreatic abscess formation). An ultrasound or, preferably, a CT scan can be used detect both. The inflammatory process can cause systemic effects because of the presence of cytokines, such as bradykinins and phospholipase A. These cytokines may cause vasodilation, increase in vascular permeability, pain, and leukocyte accumulation in the vessel walls. Fat necrosis may cause hypocalcemia. Pancreatic B cell injury may lead to hyperglycemia. Frequency: In the US: Annual incidence of acute pancreatitis is 19.5 per 100,000 population and chronic pancreatitis is 8.3 per 100,000 population per year. Mortality/Morbidity: Although acute pancreatitis should be noted, chronic pancreatitis has a more severe presentation as episodes recur. Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock all may be systemic manifestations of acute pancreatitis in its most severe form. Race: Annual incidence of acute pancreatitis in Native American persons is 4 per 100,000 population, in white persons is 5.7 per 100,000 population, and in black persons is 20.7 per 100,000 population. Sex: No predilection exists. Age: The risk for African American persons aged 35-64 years is 10 times higher than for any other group. African American persons are at higher risk than white persons in that same age group. Clinical History: The main presentation of acute pancreatitis is epigastric pain or right upper quadrant pain radiating to the back Nausea and/or vomiting Fever Query the patient about recent surgeries and invasive procedures (ie, endoscopic retrograde cholangiopancreatography) or family history of hypertriglyceridemia. Patients frequently have a history of previous biliary colic and binge alcohol consumption, the major causes of acute pancreatitis. Physical: Tachycardia Tachypnea Hypotension Fever Abdominal tenderness, distension, guarding, and rigidity Mild jaundice Diminished or absent bowel sounds Because of contiguous spread of inflammation (effusion) from the pancreas, lung auscultation may reveal basilar rales, especially in the left lung. Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcemia. Severe cases may have a Grey sign (ie, bluish discoloration of the flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis. Causes: The major causes are long-standing alcohol consumption and biliary stone disease. In developed countries, the most common cause of acute pancreatitis is alcohol abuse. On the cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release. On the ductal level, ethanol increases the permeability of ductules, which allow enzymes to reach the parenchyma, resulting in pancreatic damage. Ethanol increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the formation of protein plugs that block the pancreatic outflow and obstruction. Another major cause of acute pancreatitis is biliary stone disease (eg, cholelithiasis, choledocholithiasis). A biliary stone may lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma. Minor causes of acute pancreatitis Medications, including azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, NSAIDs, mercaptopurine, methyldopa, and tetracyclines Endoscopic retrograde cholangiopancreatography (ERCP) Hypertriglyceridemia (When the triglyceride (TG) level exceeds 1000 mg/U, an episode of pancreatitis is more likely.) Peptic ulcer disease Abdominal or cardiopulmonary bypass surgery, which may insult the gland by ischemia Trauma to the abdomen or back, resulting in sudden compression of the gland against the spine posteriorly Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction Viral infections, including mumps, sackievirus, cytomegalovirus (CMV), hepatitis virus, Epstein-Barr virus (EBV), and rubella Bacterial infections, such as mycoplasma Intestinal parasites, such as ascaris, which can block the pancreatic outflow Pancreas divisum Scorpion and snake bites Vascular factors, such as ischemia or vasculitis DIFFERENTIALS Other Problems to be Considered: Perforated viscus Acute peritonitis Choledocholithiasis Macroamylasemia Macrolipasemia Intestinal obstruction Pancreatic cancer Malabsorption syndromes/processes Workup Lab Studies: A complete blood count (CBC) demonstrates leukocytosis (WBC >12000) with the differential being shifted towards the segmented polymorphs. If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and crossmatch. Measure blood glucose level because it may be elevated from B cell injury in the pancreas. Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl, CO2, P, Mg); a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids. Measure amylase levels, preferably the Amylase P, which is more specific to pancreatic pathology. Levels more than 3 times higher than normal strongly suggest the diagnosis of acute pancreatitis Lipase levels also are elevated and remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase may be elevated in the presence of a normal serum amylase level Perform liver function tests (eg, alkaline phosphatase, serum glutamic-pyruvic transaminase [sGPT], serum glutamic-oxaloacetic transaminase [sGOT], G-GT) and bilirubin, particularly with biliary origin pancreatitis. Imaging Studies: Perform a plain KUB (Kidneys, ureters, bladder) with the patient in the upright position to exclude viscus perforation (ie, air under the diaphragm). In cases with a recurrent episode of chronic pancreatitis, peripancreatic calcifications may be noted Ultrasound can be used as a screening test. If overlying gas shadows secondary to bowel distention are present, it may not be specific CT scan is the most reliable imaging modality in the diagnosis of acute pancreatitis. The criteria for diagnosis are divided by Balthazar and colleagues into 5 grades, as follows: Grade A - Normal pancreas Grade B - Focal or diffuse gland enlargement Grade C - Intrinsic gland abnormality recognized by haziness on the scan Grade D - Single ill-defined collection or phlegmon Grade E - Two or more ill-defined collections or the presence of gas in or nearby the pancreas Other Tests: Para-aminobenzoic acid test (ie, bentiromide [Chymex] test) for chronic pancreatitis Treatment Emergency Department Care: Most of the cases presenting to the ED are treated conservatively, and approximately 80% respond to such treatment. Fluid resuscitation Monitor accurate intake/output and electrolyte balance of the patient. Crystalloids are used, but other infusions, such as packed red blood cells (PRBCs), are occasionally administered, particularly in the case of hemorrhagic pancreatitis. Central lines and Swan-Ganz catheters are used in patients with severe fluid loss and very low blood pressure. Patients should have nothing by mouth, and a nasogastric tube should be inserted to assure an empty stomach and to keep the GI system at rest. Begin parenteral nutrition if the prognosis is poor and if the patient is going to be kept in the hospital for more than 4 days. Analgesics are used to relieve pain. Meperidine is preferred over morphine because of the greater spastic effect of the latter on the sphincter of Oddi. Antibiotics are used in severe cases associated with septic shock or when the CT scan indicates that a phlegmon of the pancreas has evolved. Other conditions, such as biliary pancreatitis associated with cholangitis, also need antibiotic coverage. The preferred antibiotics are the ones secreted by the biliary system, such as ampicillin and third generation cephalosporins. Continuous oxygen saturation should be monitored by pulse oxymetry and acidosis should be corrected. When tachypnea and pending respiratory failure develops, intubation should be performed. Perform CT-guided aspiration of necrotic areas, if necessary. An ERCP may be indicated for common duct stone removal. Consultations: Consult a general surgeon in the following cases: For phlegmon of the pancreas, surgery can achieve drainage of any abscess or scooping of necrotic pancreatic tissue. It should be followed by postoperative lavage of the pancreatic bed. In patients with hemorrhagic pancreatitis, surgery is indicated to achieve hemostasis, particularly because major vessels may be eroded in acute pancreatitis. Patients who fail to improve despite optimal medical treatment or patients who push the Ranson score even further are taken to the operating room. Surgery in these cases may lead to a better outcome or confirm a different diagnosis. In biliary pancreatitis, a sphincterotomy (ie, surgical emptying of the common bile duct) can relieve the obstruction. A cholecystectomy may be performed to clear the system from any source of biliary stones. Medications The goal of pharmacotherapy is to relieve pain and minimize complications. Drug Category: Antibiotics - Used to cover the microorganisms that may grow in biliary pancreatitis and acute necrotizing pancreatitis. The empiric antibiotic regimen usually is based on the premise that enteric anaerobic and aerobic gram-bacilli microorganisms are often the cause of pancreatic infections. Once culture sensitivities are made, adjustments in the antibiotic regimen can be done. Drug Name Ceftriaxone (Rocephin)- Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Adult Dose 1-2 g IM/IV once or divided bid Pediatric Dose 50-75 mg/kg/d IM/IV divided q12h Contraindications Documented hypersensitivity Interactions Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin Drug Name Ampicillin (Marcillin, Omnipen)- Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally. Adult Dose 250-500 IM/IV mg q6h Pediatric Dose 25-50 mg/kg/d IM/IV divided q6-8h Contraindications Documented hypersensitivity; viral mononucleosis Interactions Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction Drug Category: Analgesics - Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and has sedating properties, which are beneficial for patients who have sustained trauma or have painful lesions. Drug Name Meperidine (Demerol)- Analgesic with multiple actions similar to those of morphine. May produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine. Adult Dose 15-35 mg/h IV; 50-150 mg IM q3-4h Pediatric Dose 1.1-1.8 mg/kg IM q3-4h Contraindications Documented hypersensitivity; MAOIs; upper airway obstruction or significant respiratory depression; during labor when delivery of premature infant is anticipated Interactions Monitor for increased respiratory and CNS depression with coadministration of cimetidine; hydantoins may decrease effects; avoid with protease inhibitors Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in head injuries because may increase respiratory depression and CSF pressure (use only if absolutely necessary); caution when using postoperatively and with history of pulmonary disease (suppresses cough reflex; substantially increased dose levels may aggravate or cause seizures because of tolerance, even if no prior history of convulsive disorders; monitor closely for morphine-induced seizure activity if seizure history exists Drug Category: Antibiotics - Used to cover the microorganisms that may grow in biliary pancreatitis and acute necrotizing pancreatitis. The empiric antibiotic regimen usually is based on the premise that enteric anaerobic and aerobic gram-bacilli microorganisms are often the cause of pancreatic infections. Once culture sensitivities are made, adjustments in the antibiotic regimen can be done. Drug Category: Analgesics - Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and has sedating properties, which are beneficial for patients who have sustained trauma or have painful lesions. Followup Further Inpatient Care: Transfer patients with Ranson scores of 0-2 to a hospital floor. Transfer patients with Ranson scores 3-5 to an intensive care unit. Transfer patients with Ranson scores higher than 5 to an intensive care unit with emergency surgery as a possibility. Further Outpatient Care: The patient should be followed routinely with physical examination and amylase and lipase assays. Complications: Infected pancreatic necrosis may result from seeding of bacteria into the inflammation. An acute pseudocyst is an effusion of pancreatic juice that is walled off by granulation tissue after an episode of acute pancreatitis. Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is possible because of erosion of large vessels. Intestinal obstruction or necrosis may occur. Common bile duct obstruction may be caused by a pancreatic abscess, pseudocyst, or biliary stone that caused the pancreatitis. An internal pancreatic fistula from pancreatic duct disruption or a leaking pancreatic pseudocyst may occur. Prognosis: Ranson developed a series of different criteria for the severity of acute pancreatitis. Present on admission Older than 55 years WBC higher than 16,000 per mcL Blood glucose higher than 200 mg/dL Serum lactate dehydrogenase (LDH) more than 350 IU/L SGOT (ie, aspartate aminotransferase [AST]) greater than 250 IU/L Developing during the first 48 hours Hematocrit fall more than 10% BUN increase more than 8 mg/dL Serum calcium less than 8 mg/dL Arterial oxygen saturation less than 60 mm Hg Base deficit higher than 4 mEq/L Estimated fluid sequestration higher than 600 mL A Ranson score of 0-2 has a minimal mortality rate. A Ranson score of 3-5 has a 10%-20% mortality rate. A Ranson score higher than 5 has a mortality rate of more than 50% and is associated with more systemic complications. Patient Education: Educate patients about the disease and advise then to avoid alcohol in binge amounts and to discontinue any risk factor, such as fatty meals and abdominal trauma. acute vs. chronic > Are most of the members of this site chronic sufferers? I was just > diagnosed with pancreatitis, but they are not sure if it is acute or > chronic. I cant get to a specialist until early Jan. > > It is my understanding that acute is bad, but that many acute cases > get better and do not come back. I am more concerned about chronic. > Even then, there are treatments, right? Enzymes, possible > surgeries? I am very depressed right now because I want to live for > a good thirty more years and am concerned. I do not drink, and an > ultrasound did not reveal any stones, just a slightly " inhomogeneous " > pancreas and my lipase and amylase were elevated (lipase 4x normal). > > I am 31. > > Thanks > > > > > PANCREATITIS Association, Intl. > Online e-mail group > > To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 24, 2002 Report Share Posted December 24, 2002 , You are correct that you can have acute panc, recover and never have another problem. The thing I would think is important would be to try and find the cause of the acute panc and then prevent future attacks. I have found that diagnosing chronic panc is anything but simple and straightforward. At this point I have not been diagnosed with chronic panc. I have 'recurring acute panc'. W acute vs. chronic Are most of the members of this site chronic sufferers? I was just diagnosed with pancreatitis, but they are not sure if it is acute or chronic. I cant get to a specialist until early Jan. It is my understanding that acute is bad, but that many acute cases get better and do not come back. I am more concerned about chronic. Even then, there are treatments, right? Enzymes, possible surgeries? I am very depressed right now because I want to live for a good thirty more years and am concerned. I do not drink, and an ultrasound did not reveal any stones, just a slightly " inhomogeneous " pancreas and my lipase and amylase were elevated (lipase 4x normal). I am 31. Thanks PANCREATITIS Association, Intl. Online e-mail group To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 24, 2002 Report Share Posted December 24, 2002 , You are correct that you can have acute panc, recover and never have another problem. The thing I would think is important would be to try and find the cause of the acute panc and then prevent future attacks. I have found that diagnosing chronic panc is anything but simple and straightforward. At this point I have not been diagnosed with chronic panc. I have 'recurring acute panc'. W acute vs. chronic Are most of the members of this site chronic sufferers? I was just diagnosed with pancreatitis, but they are not sure if it is acute or chronic. I cant get to a specialist until early Jan. It is my understanding that acute is bad, but that many acute cases get better and do not come back. I am more concerned about chronic. Even then, there are treatments, right? Enzymes, possible surgeries? I am very depressed right now because I want to live for a good thirty more years and am concerned. I do not drink, and an ultrasound did not reveal any stones, just a slightly " inhomogeneous " pancreas and my lipase and amylase were elevated (lipase 4x normal). I am 31. Thanks PANCREATITIS Association, Intl. Online e-mail group To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 24, 2002 Report Share Posted December 24, 2002 , You are correct that you can have acute panc, recover and never have another problem. The thing I would think is important would be to try and find the cause of the acute panc and then prevent future attacks. I have found that diagnosing chronic panc is anything but simple and straightforward. At this point I have not been diagnosed with chronic panc. I have 'recurring acute panc'. W acute vs. chronic Are most of the members of this site chronic sufferers? I was just diagnosed with pancreatitis, but they are not sure if it is acute or chronic. I cant get to a specialist until early Jan. It is my understanding that acute is bad, but that many acute cases get better and do not come back. I am more concerned about chronic. Even then, there are treatments, right? Enzymes, possible surgeries? I am very depressed right now because I want to live for a good thirty more years and am concerned. I do not drink, and an ultrasound did not reveal any stones, just a slightly " inhomogeneous " pancreas and my lipase and amylase were elevated (lipase 4x normal). I am 31. Thanks PANCREATITIS Association, Intl. Online e-mail group To reply to this message hit & quot;reply & quot; or send an e-mail to: Pancreatitis (AT) Yahoo Quote Link to comment Share on other sites More sharing options...
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