Acute pancreatitis

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Acute pancreatitis

  1. 1. ACUTEACUTE PANCREATITISPANCREATITIS
  2. 2.  The pancreas is a gland located in theThe pancreas is a gland located in the upper, posterior abdomen and isupper, posterior abdomen and is responsible for insulin production andresponsible for insulin production and the manufacture and secretion ofthe manufacture and secretion of digestive enzymes leading todigestive enzymes leading to carbohydrate, fat, and proteincarbohydrate, fat, and protein metabolism. Approximately 80% ofmetabolism. Approximately 80% of the gross weight of the pancreasthe gross weight of the pancreas supports exocrine function, while thesupports exocrine function, while the remaining 20% is involved withremaining 20% is involved with endocrine functionendocrine function
  3. 3. The principal function of the exocrineThe principal function of the exocrine pancreas is to make food-digestingpancreas is to make food-digesting enzymes. In normal pancreatic function,enzymes. In normal pancreatic function, up to 15 different types of digestiveup to 15 different types of digestive enzymes are manufactured in the roughenzymes are manufactured in the rough endoplasmic reticulum.endoplasmic reticulum.
  4. 4.  In acute pancreatitis there are not onlyIn acute pancreatitis there are not only symptoms of acute inflammation in thesymptoms of acute inflammation in the pancreas are present. There are thepancreas are present. There are the sings of hemorrhages and necroticsings of hemorrhages and necrotic processes, which are caused byprocesses, which are caused by autodigestion of tissues by pancreaticautodigestion of tissues by pancreatic enzymes.enzymes.  Secondary infection and multiorganSecondary infection and multiorgan system failure may be associated withsystem failure may be associated with autodigestion process.autodigestion process.
  5. 5. FrequencyFrequency  In the US: In 2002, 230,000 patients withIn the US: In 2002, 230,000 patients with acute pancreatitis were admitted toacute pancreatitis were admitted to nonfederally funded hospitals. In 1998,nonfederally funded hospitals. In 1998, 183,000 patients with acute pancreatitis183,000 patients with acute pancreatitis were admitted. This rend in rising incidencewere admitted. This rend in rising incidence has been recognized over the past severalhas been recognized over the past several decades.decades.  Internationally: In Germany the frequency isInternationally: In Germany the frequency is 17.5 cases per 100,000 people. In Finland,17.5 cases per 100,000 people. In Finland, the frequency is 73.4 cases per 100,000the frequency is 73.4 cases per 100,000 people.people.
  6. 6.  The overall mortality rate of patients with acuteThe overall mortality rate of patients with acute pancreatitis is 10-15%. Patients with biliarypancreatitis is 10-15%. Patients with biliary pancreatitis tend to have a higher mortalitypancreatitis tend to have a higher mortality rate than patients with alcoholic pancreatitis.rate than patients with alcoholic pancreatitis.  In patients with severe disease (necrosisIn patients with severe disease (necrosis and/or organ failure), the mortality rate isand/or organ failure), the mortality rate is approximately 30%. This rate in mortality hasapproximately 30%. This rate in mortality has not dropped in the last 10 years.not dropped in the last 10 years.  In the first week of illness, most deaths resultIn the first week of illness, most deaths result from multiorgan system failure. In subsequentfrom multiorgan system failure. In subsequent weeks, infection plays a more significant role,weeks, infection plays a more significant role, but organ failure still constitutes a major causebut organ failure still constitutes a major cause of mortality.of mortality.
  7. 7. PathophysiologyPathophysiology Acute pancreatitis may occur when factorsAcute pancreatitis may occur when factors involved in maintaining cellular homeostasis areinvolved in maintaining cellular homeostasis are out of balance. The initiating event may beout of balance. The initiating event may be anything that injures the acinar cell and impairs theanything that injures the acinar cell and impairs the secretion of zymogen granules, such as alcoholsecretion of zymogen granules, such as alcohol use, gallstones, and certain drugs.use, gallstones, and certain drugs. In addition, acute pancreatitis can develop whenIn addition, acute pancreatitis can develop when ductal cell injury leads to delayed or absentductal cell injury leads to delayed or absent enzymatic secretion, such as with the CFTR geneenzymatic secretion, such as with the CFTR gene mutation.mutation. The mechanisms by which alcohol or gallstonesThe mechanisms by which alcohol or gallstones cause destruction to pancreatic acinar cells are notcause destruction to pancreatic acinar cells are not currently known.currently known.
  8. 8. Once a cellular injury pattern has been initiated, cellularOnce a cellular injury pattern has been initiated, cellular membranemembrane trafficking becomes chaotic, with the following deleterioustrafficking becomes chaotic, with the following deleterious effects:effects: 1. Lysosomal and zymogen granule compartments fuse,1. Lysosomal and zymogen granule compartments fuse, enabling activation of trypsinogen to trypsin.enabling activation of trypsinogen to trypsin. 2. Intracellular trypsin triggers the entire zymogen activation2. Intracellular trypsin triggers the entire zymogen activation cascade.cascade. 3. Secretory vesicles are extruded across the basolateral3. Secretory vesicles are extruded across the basolateral membrane into the interstitium, where molecular fragmentsmembrane into the interstitium, where molecular fragments act as chemoattractants for inflammatory cells. Activatedact as chemoattractants for inflammatory cells. Activated neutrophils then exacerbate the problem by releasingneutrophils then exacerbate the problem by releasing superoxide (the respiratory burst) or proteolytic enzymessuperoxide (the respiratory burst) or proteolytic enzymes (cathepsins B, D, and G; collagenase; and elastase).(cathepsins B, D, and G; collagenase; and elastase). Finally, macrophages release cytokines that further mediateFinally, macrophages release cytokines that further mediate local (and, in severe cases, systemic) inflammatorylocal (and, in severe cases, systemic) inflammatory responses.responses.
  9. 9. These mediators of inflammation cause anThese mediators of inflammation cause an increase pancreatic permeability, leading toincrease pancreatic permeability, leading to hemorrhage, edema, and eventually pancreatichemorrhage, edema, and eventually pancreatic necrosis. As the mediators are excretednecrosis. As the mediators are excreted into the circulation, systemic complications caninto the circulation, systemic complications can arise, such as bacteremia due to gut floraarise, such as bacteremia due to gut flora translocation, acute respiratory distresstranslocation, acute respiratory distress syndrome,pleural effusions, gastrointestinalsyndrome,pleural effusions, gastrointestinal hemorrhage, and renal failure. Eventually, thehemorrhage, and renal failure. Eventually, the mediators of inflammation can become somediators of inflammation can become so overwhelming to the body that hemodynamicoverwhelming to the body that hemodynamic instability and death ensue.instability and death ensue.
  10. 10. EtiologyEtiology  Bile and digestive – pancreatic reflux.Bile and digestive – pancreatic reflux.  Obstruction and hypertension ofObstruction and hypertension of biliary and pancreatic ducts.biliary and pancreatic ducts.  Blood supply disturbance ofBlood supply disturbance of pancreas.pancreas.  Allergic and toxic process.Allergic and toxic process.  Peptic ulcer disease.Peptic ulcer disease.  Injuries.Injuries.
  11. 11. RaceRace The hospitalization rates of patients withThe hospitalization rates of patients with acute pancreatitis per 100,000 populationacute pancreatitis per 100,000 population are 3 times higher for blacks than whites.are 3 times higher for blacks than whites. These racial differences are moreThese racial differences are more pronounced for males than females.pronounced for males than females. In Europe and other developed nations suchIn Europe and other developed nations such as Hong Kong, more patients tend to haveas Hong Kong, more patients tend to have gallstone pancreatitis. Whereas in thegallstone pancreatitis. Whereas in the United States, alcoholic pancreatitis is mostUnited States, alcoholic pancreatitis is most common.common.
  12. 12. SexSex In general, acute pancreatitis affectsIn general, acute pancreatitis affects males more often than females.males more often than females. The etiology in males is more oftenThe etiology in males is more often related to alcohol; in females, torelated to alcohol; in females, to biliary tract disease.biliary tract disease. Idiopathic pancreatitis has no clearIdiopathic pancreatitis has no clear predilection for either sex.predilection for either sex.
  13. 13. AgeAge The following are median ages of onset forThe following are median ages of onset for various etiologies:various etiologies:  Alcohol-related - 39 yearsAlcohol-related - 39 years  Biliary tract–related - 69 yearsBiliary tract–related - 69 years  Trauma-related - 66 yearsTrauma-related - 66 years  Drug-induced etiology - 42 yearsDrug-induced etiology - 42 years  Endoscopic retrogradeEndoscopic retrograde cholangiopancreatography (ERCP)–related -cholangiopancreatography (ERCP)–related - 58 years58 years  AIDS-related - 31 yearsAIDS-related - 31 years  Vasculitis-related - 36 yearsVasculitis-related - 36 years
  14. 14. HistoryHistory The cardinal symptom of acute pancreatitis isThe cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically dull,abdominal pain, which is characteristically dull, boring, and steady. Usually, the pain is suddenboring, and steady. Usually, the pain is sudden in onset and gradually intensifies in severityin onset and gradually intensifies in severity until reaching a constant ache. Most often, it isuntil reaching a constant ache. Most often, it is located in the upper abdomen, usually in thelocated in the upper abdomen, usually in the epigastric region, but it may be perceivedepigastric region, but it may be perceived more on the left or right side, depending onmore on the left or right side, depending on which portion of the pancreas is involved. Thewhich portion of the pancreas is involved. The pain radiates directly through the abdomenpain radiates directly through the abdomen to the back in approximately one half of casesto the back in approximately one half of cases
  15. 15. ClassificationClassification Clinico – anatomical formsClinico – anatomical forms Edematous pancreatitisEdematous pancreatitis Fatty pancreatitisFatty pancreatitis Hemorrhagic pancreatitisHemorrhagic pancreatitis Mixed pancreatitisMixed pancreatitis Purulent pancreatitisPurulent pancreatitis
  16. 16. Periods of APPeriods of AP  Period of hemodynamic disturbancesPeriod of hemodynamic disturbances and pancreatogenic shock.and pancreatogenic shock.  Period of functional insufficiency ofPeriod of functional insufficiency of parenchymatous organs.parenchymatous organs.  Period of degenerative and purulentPeriod of degenerative and purulent complications.complications.
  17. 17. ComplicationsComplications  Toxic: pancreatogenic plevritis,Toxic: pancreatogenic plevritis, “pancreatic lung”, hepatic and kidney“pancreatic lung”, hepatic and kidney necrosis, erosive-hemorrhagicnecrosis, erosive-hemorrhagic gastropathy, delirium, coma.gastropathy, delirium, coma.  Necrotic: pancreatical mass, pancreaticalNecrotic: pancreatical mass, pancreatical abscess, abdominal abscess, phlegmonabscess, abdominal abscess, phlegmon of retroperitoneal fatty tissue, pseudocystof retroperitoneal fatty tissue, pseudocyst of pancreas.of pancreas.
  18. 18.  Visceral: external and internal fistulas.Visceral: external and internal fistulas.  Arrosive hamorrhage.Arrosive hamorrhage.  Peritonitis.Peritonitis.  Vessels thrombosis.Vessels thrombosis.
  19. 19. Atlanta's classification,Atlanta's classification, 19921992  Interstitial pancreatitisInterstitial pancreatitis  Pancreonecrosis (aseptical,Pancreonecrosis (aseptical, inflectional)inflectional)  Parapancreatitis (fluid inParapancreatitis (fluid in parapancretical fatty tissue)parapancretical fatty tissue)  Pseudocyst of pancreasPseudocyst of pancreas  Abscess of pancreasAbscess of pancreas
  20. 20. Nausea and vomiting are often presentNausea and vomiting are often present along with accompanying anorexia.along with accompanying anorexia. Diarrhea can also occur.Diarrhea can also occur. Positioning can be important, becausePositioning can be important, because the discomfort frequently improves withthe discomfort frequently improves with the patient in the supine position.the patient in the supine position. The duration of pain varies but typicallyThe duration of pain varies but typically lasts more than a day. It is the intensitylasts more than a day. It is the intensity and persistence of the pain thatand persistence of the pain that usually causes patients to seek medicalusually causes patients to seek medical attention.attention.
  21. 21. Atypical acute pancreatitis may beAtypical acute pancreatitis may be misdiagnosed. In a study of patientsmisdiagnosed. In a study of patients with pancreatitis discovered at autopsy,with pancreatitis discovered at autopsy, 13% presented with abdominal pain,13% presented with abdominal pain, 19% had disease that occurred in the19% had disease that occurred in the postoperative setting, and 68%postoperative setting, and 68% presented with various cardiac,presented with various cardiac, pulmonary, hepatic, renal,pulmonary, hepatic, renal, abdominal, and metabolic disturbancesabdominal, and metabolic disturbances
  22. 22. PhysicalPhysical  Fever (76%) and tachycardia (65%) areFever (76%) and tachycardia (65%) are common abnormal vital signs.common abnormal vital signs.  Abdominal tenderness, muscular guardingAbdominal tenderness, muscular guarding (68%), and distension (65%) are observed in(68%), and distension (65%) are observed in most patients.most patients.  Bowel sounds are often hypoactive dueBowel sounds are often hypoactive due to gastric and transverse colonic ileus.to gastric and transverse colonic ileus.  Guarding tends to be more pronounced in theGuarding tends to be more pronounced in the upper abdomen.upper abdomen.  A minority of patients exhibit jaundice (28%).A minority of patients exhibit jaundice (28%).
  23. 23.  Some patients experience dyspneaSome patients experience dyspnea (10%), which may be caused by irritation(10%), which may be caused by irritation of the diaphragm (resulting fromof the diaphragm (resulting from inflammation), pleural effusion, or a moreinflammation), pleural effusion, or a more serious condition, such as acuteserious condition, such as acute respiratory distress syndrome.respiratory distress syndrome.  In severe cases, hemodynamic instabilityIn severe cases, hemodynamic instability is evident (10%) and hematemesis oris evident (10%) and hematemesis or melena sometimes develops (5%).melena sometimes develops (5%).  In addition, patients with severe acuteIn addition, patients with severe acute pancreatitis are often pale, diaphoretic,pancreatitis are often pale, diaphoretic, and listlessand listless
  24. 24. A few uncommon physical findings are associated withA few uncommon physical findings are associated with severe necrotizing pancreatitis.severe necrotizing pancreatitis.  The Cullen sign is a bluish discoloration around theThe Cullen sign is a bluish discoloration around the umbilicus resulting from hemoperitoneum.umbilicus resulting from hemoperitoneum.  The Grey-Turner sign is a reddish-brown discolorationThe Grey-Turner sign is a reddish-brown discoloration along the flanks resulting from retroperitoneal bloodalong the flanks resulting from retroperitoneal blood dissecting along tissue planes.dissecting along tissue planes.  More commonly, patients may have a ruddy erythemaMore commonly, patients may have a ruddy erythema in the flanks secondary to extravasated pancreaticin the flanks secondary to extravasated pancreatic exudate.exudate.  Erythematous skin nodules may result from focalErythematous skin nodules may result from focal subcutaneous fat necrosis. These are usually notsubcutaneous fat necrosis. These are usually not more than 1 cm in size and are typically located onmore than 1 cm in size and are typically located on extensor skin surfaces. In addition, polyarthritis isextensor skin surfaces. In addition, polyarthritis is occasionally seenoccasionally seen
  25. 25.  The Mondor sing – violet sports on theThe Mondor sing – violet sports on the body and fasebody and fase  The Holsted sing – cyanosis of skin ofThe Holsted sing – cyanosis of skin of abdominal wallabdominal wall  The Grunvald sing – petechial skin rashThe Grunvald sing – petechial skin rash in the navel areain the navel area
  26. 26.  The Korte sing – regional tension ofThe Korte sing – regional tension of anterior abdominal wall in epigastriaanterior abdominal wall in epigastria region, along the projection of pancreasregion, along the projection of pancreas  The Mayo – Robson sing – palpationThe Mayo – Robson sing – palpation pain in the left costal-vertebral anglepain in the left costal-vertebral angle  The Gobye sing – abdominal distensionThe Gobye sing – abdominal distension in upper regionin upper region  The Voskresensky sing – absence ofThe Voskresensky sing – absence of pulsation of abdominal aorta in epigastriapulsation of abdominal aorta in epigastria region (sing of parapancreaticalregion (sing of parapancreatical infiltration)infiltration)

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