Acute pancreatitis overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
Dutch physician and anatomist, Nicholaes Tulp | Dutch physician and anatomist, Nicholaes Tulp, gave the first clear description of [[acute pancreatitis]] in 1652. The first [[systemic]] analysis of acute pancreatitis was presented by Reginald Huber Fitz in 1889. During the 20th century there were many theories about whether surgery should be the initial approach to the treatment of acute pancreatitis. Hans Chiari in 1896 proposed that the basic mechanism of the disease was autodigestion of [[pancreas]]. The father of modern anatomical pathology, Giovanni Battista Morgagni gave the first description of pancreatic [[Pseudocyst|pseudocysts]]. | ||
==Classification== | ==Classification== | ||
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There are many causes for acute pancreatitis. The most common causes include; [[idiopathic]], [[alcohol]], [[gallstones]], [[trauma]], [[steroids]], scorpion bites, [[mumps]], [[autoimmune diseases]], [[ERCP]], and certain [[medications]]. | There are many causes for acute pancreatitis. The most common causes include; [[idiopathic]], [[alcohol]], [[gallstones]], [[trauma]], [[steroids]], scorpion bites, [[mumps]], [[autoimmune diseases]], [[ERCP]], and certain [[medications]]. | ||
==Differentiating Acute | ==Differentiating Acute Pancreatitis from Other Diseases== | ||
Acute pancreatitis should be differentiated from other conditions that may produce symptoms similar to that of acute pancreatitis. These conditions include [[gallstones]], pancreatic cysts, [[Pancreatic pseudocyst|pancreatic pseudocysts]], and [[chronic pancreatitis]]. | Acute pancreatitis should be differentiated from other conditions that may produce symptoms similar to that of acute pancreatitis. These conditions include [[gallstones]], pancreatic cysts, [[Pancreatic pseudocyst|pancreatic pseudocysts]], and [[chronic pancreatitis]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The annual incidence in the U.S. is 18 per 100,000 population. In a European cross-sectional study, the [[incidence]] of acute | The annual incidence in the U.S. is 18 per 100,000 population. In a European cross-sectional study, the [[incidence]] of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes. | ||
==Risk Factors== | ==Risk Factors== | ||
There are several factors that can put someone at risk for acute pancreatitis. The most common cause and the most common risk factor is heavy alcohol use. Other risk factors include [[trauma]], [[family history]], [[Hypertriglyceridemia (patient information)|hypertriglyceridemia]], [[cystic fibrosis]], [[renal failure]], [[SLE]], being on certain [[medications]], and male gender. | There are several factors that can put someone at risk for acute pancreatitis. The most common cause and the most common risk factor is heavy alcohol use. Other risk factors include [[trauma]], [[family history]], [[Hypertriglyceridemia (patient information)|hypertriglyceridemia]], [[cystic fibrosis]], [[renal failure]], [[SLE]], being on certain [[medications]], and the male gender. | ||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
Pancreatitis can be mild or severe, and the natural history depends upon the severity of the condition, and the timeliness of intervention. Acute pancreatitis can result in complications such as [[hemorrhagic]] pancreatitis, multisystem organ failure, [[infection]], [[SIRS]], [[ARDS]], [[hyperglycemia]], [[hypocalcemia]], [[shock]], [[hemorrhage]], [[thrombosis]], [[common bile duct obstruction]], and development of [[chronic pancreatitis]]. Prognosis can be determined with the use of many criteria such as Ranson's criteria, the Glasgow score, the [[APACHE II]] score, and the BISAP score. | Pancreatitis can be mild or severe, and the natural history depends upon the severity of the condition, and the timeliness of intervention. Acute pancreatitis can result in complications such as [[hemorrhagic]] pancreatitis, multisystem organ failure, [[infection]], [[SIRS]], [[ARDS]], [[hyperglycemia]], [[hypocalcemia]], [[shock]], [[hemorrhage]], [[thrombosis]], [[common bile duct obstruction]], and development of [[chronic pancreatitis]]. Prognosis can be determined with the use of many criteria such as Ranson's criteria, the Glasgow score, the [[APACHE II]] score, and the BISAP score. | ||
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[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category: | [[Category:Up-to-date]] | ||
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Latest revision as of 17:00, 29 January 2021
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Acute pancreatitis Microchapters |
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Diagnosis |
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Treatment |
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Acute pancreatitis overview On the Web |
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American Roentgen Ray Society Images of Acute pancreatitis overview |
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Risk calculators and risk factors for Acute pancreatitis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Tarek Nafee, M.D. [3]
Overview
Acute pancreatitis is a rapidly-onset inflammation of the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures, such as NPO (abstaining from any oral intake) and IV fluid rehydration, severe cases may require admission to the ICU or even surgery (often more than one intervention) to deal with complications of the disease process.
Historical Perspective
Dutch physician and anatomist, Nicholaes Tulp, gave the first clear description of acute pancreatitis in 1652. The first systemic analysis of acute pancreatitis was presented by Reginald Huber Fitz in 1889. During the 20th century there were many theories about whether surgery should be the initial approach to the treatment of acute pancreatitis. Hans Chiari in 1896 proposed that the basic mechanism of the disease was autodigestion of pancreas. The father of modern anatomical pathology, Giovanni Battista Morgagni gave the first description of pancreatic pseudocysts.
Classification
Acute pancreatitis can either be classified according to its phase (early or late), or according to its level of severity.
Pathophysiology
The pathophysiology of acute pancreatitis involves acute inflammation and edema of the pancreas. The process is mediated by the abnormal activation of trypsinogen to trypsin inside the pancreas, and the involvement of other mediators such as cathepsin, lysosomal enzymes, and caspases. Intrapancreatic activation of amylase and lipase is what causes necrosis of pancreatic cells.
Causes
There are many causes for acute pancreatitis. The most common causes include; idiopathic, alcohol, gallstones, trauma, steroids, scorpion bites, mumps, autoimmune diseases, ERCP, and certain medications.
Differentiating Acute Pancreatitis from Other Diseases
Acute pancreatitis should be differentiated from other conditions that may produce symptoms similar to that of acute pancreatitis. These conditions include gallstones, pancreatic cysts, pancreatic pseudocysts, and chronic pancreatitis.
Epidemiology and Demographics
The annual incidence in the U.S. is 18 per 100,000 population. In a European cross-sectional study, the incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes.
Risk Factors
There are several factors that can put someone at risk for acute pancreatitis. The most common cause and the most common risk factor is heavy alcohol use. Other risk factors include trauma, family history, hypertriglyceridemia, cystic fibrosis, renal failure, SLE, being on certain medications, and the male gender.
Natural History, Complications and Prognosis
Pancreatitis can be mild or severe, and the natural history depends upon the severity of the condition, and the timeliness of intervention. Acute pancreatitis can result in complications such as hemorrhagic pancreatitis, multisystem organ failure, infection, SIRS, ARDS, hyperglycemia, hypocalcemia, shock, hemorrhage, thrombosis, common bile duct obstruction, and development of chronic pancreatitis. Prognosis can be determined with the use of many criteria such as Ranson's criteria, the Glasgow score, the APACHE II score, and the BISAP score.
Screening
There is no established screening recommendations for pancreatitis in the general population.
Diagnosis
History and Symptoms
Patient history should include the evaluation of risk factors for pancreatitis, such as heavy alcohol use, certain medications, family history, history of autoimmune diseases, and history of gallstone diseases. Common symptoms of acute pancreatitis include severe epigastric abdominal pain (which worsens on eating) radiating to the back and and the shoulder blades, anorexia, nausea, vomiting, diarrhea, fever and chills. There may also be symptoms of indigestion and abdominal bloating.
Physical Examination
Physical examination findings in acute pancreatitis can include fever, tachycardia, abdominal tenderness, distension, jaundice, pallor, and discoloration of the flanks and umbilicus.
Laboratory Findings
Laboratory tests that should be obtained include a complete blood count, liver function tests, serum amylase and lipase, serum calcium levels, arterial blood gas, and blood glucose levels.
CT
Although ultrasound imaging and CT scanning of the abdomen can be used to confirm the diagnosis of pancreatitis, neither is usually necessary as a primary diagnostic modality. In addition, CT contrast may exacerbate pancreatitis, although this is disputed.
MRI
MRI can also be used and has some advantages over the use of CT. One of the advantages is that there is less chance of contrast induced nephropathy. In addition, the organs and vessels can be visualized better, and it is easier to distinguish between mild and severe pancreatitis.
Ultrasound
Although ultrasound imaging and CT scanning of the abdomen can be used to confirm the diagnosis of pancreatitis, neither is usually necessary as a primary diagnostic modality.
Other Imaging Findings
Other Diagnostic Studies
ERCP in acute pancreatitis is used both to treat pancreatitis, and to determine the cause of idiopathic pancreatitis. There are specific indications for when to use ERCP, and one must keep in mind that ERCP is also a cause of pancreatitis.
Treatment
Medical Therapy
Medical therapy for acute pancreatitis includes pain control, bowel rest, nutritional support, intravenous fluids, and occasionally antibiotics. ERCP is also a possible treatment for acute pancreatitis, but can also cause pancreatitis.
Surgery
Surgery in the treatment of acute pancreatitis is indicated for infected pancreatic necrosis, in cases of diagnostic uncertainty and in the presence of complications.
Primary Prevention
Primary prevention against the development of acute pancreatitis includes avoiding aspirin in children and alcohol abuse, as well as genetic counseling, immunization and proper safety precautions to avoid abdominal trauma.
Secondary Prevention
The secondary prevention of acute pancreatitis primarily focuses on prevention of recurrence. The secondary prevention of acute pancreatitis varies according to the underlying etiology of the primary event. Cholecystectomy, alcohol abstinence, withdrawal of aggravating medications, weight control, and control of hyperlipidemia are among the most common methods of preventing recurrence of acute pancreatitis.