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== Pathogenesis ==
== Pathogenesis ==
The two types of pancreatitis are mild pancreatitis and severe pancreatitis, which are separated based on their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is inflammation and edema of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of [[zymogens]] and inappropriate activation of pancreatic [[zymogens]] inside the pancreas, most notably [[trypsinogen]]. Normally, [[trypsinogen]] is activated to [[trypsin]] in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically [[cathepsin]], with [[trypsinogen]]. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death. The response to this cell death can proceed according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by [[caspases]] which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.
The two types of pancreatitis are mild pancreatitis and severe pancreatitis, which are separated based on whether their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is inflammation and edema of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of [[zymogens]] and inappropriate activation of pancreatic [[zymogens]] inside the pancreas, most notably [[trypsinogen]]. Normally, [[trypsinogen]] is activated to [[trypsin]] in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically [[cathepsin]], with [[trypsinogen]]. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death. The response to this cell death can proceed according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by [[caspases]] which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.


As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage.
As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage.

Revision as of 01:57, 3 October 2011

Acute pancreatitis
SpecialtyGastroenterology Edit this on Wikidata

Acute pancreatitis or acute pancreatic necrosis[1] is a sudden 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 (nil per os or nothing by mouth (NBM)) and aggressive intravenous fluid rehydration, severe cases may require admission to the intensive care unit or even surgery to deal with complications of the disease process.

Symptoms and signs

The most common symptoms and signs include:

Signs which are less common, and indicate severe disease, include:

  • Grey-Turner's sign (hemorrhagic discoloration of the flanks)
  • Cullen's sign (hemorrhagic discoloration of the umbilicus)
  • Pleural effusions (fluid in the bases of the pleural cavity)
  • Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to local toxic lesion of the vessels)
  • Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium, 6–7 cm above the umbilicus)
  • Kamenchik's sign (pain with pressure under the xiphoid process)
  • Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA))[2]
  • Mayo-Robson's point - a point on border of inner 2/3 with the external 1/3 of the line that represents the bisection of the left upper abdominal quadrant, where tenderness on pressure exists in disease of the pancreas. At this point the tail of pancreas is projected on the abdominal wall.[3][4]

Other conditions to consider are:

Although these are common symptoms, they are not always present. Simple abdominal pain may be the sole symptom.

Causes

Most common causes


Less common causes

Causes by demographic

The most common causes of pancreatitis, are as follows:

  • Western countries: In the United States alcohol represents the primary etiology in 65% of acute pancreatitis cases (Sweden (20%), United Kingdom (5%))
  • Eastern countries: gallstones
  • Children: trauma
  • Adolescents and young adults: mumps

Pathogenesis

The two types of pancreatitis are mild pancreatitis and severe pancreatitis, which are separated based on whether their predominant response to cell injury is inflammation or necrosis, respectively. In mild pancreatitis there is inflammation and edema of the pancreas. In severe pancreatitis there are additional features of necrosis and secondary injury to extrapancreatic organs. Both types share a common mechanism of abnormal inhibition of secretion of zymogens and inappropriate activation of pancreatic zymogens inside the pancreas, most notably trypsinogen. Normally, trypsinogen is activated to trypsin in the duodenum where it assists in the digestion of proteins. During an acute pancreatitis episode there is colocalization of lysosomal enzymes, specifically cathepsin, with trypsinogen. Cathepsin activates trypsinogen to trypsin leading to further activation of other molecules of trypsinogen and immediate pancreatic cell death. The response to this cell death can proceed according to either the necrosis or apoptosis mechanism (or a mix between the two). The balance between these two processes is mediated by caspases which regulate apoptosis and have important anti-necrosis functions during pancreatitis: preventing trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If, however, the caspases are depleted due to either chronic ethanol exposure or through a severe insult then necrosis can predominate.

As part of the initial injury there is an extensive inflammatory response due to pancreatic cells synthesizing and secreting inflammatory mediators: primarily TNF-alpha and IL-1. A hallmark of acute pancreatitis is a manifestation of the inflammatory response, namely the recruitment of neutrophils to the pancreas. The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage.


Histopathology

The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessel necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces as well as vessel damage. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Due to the pancreas lacking a capsule, the inflammation and necrosis can extend to include fascial layers in the immediate vicinity of the pancreas.

Investigations and diagnosis

  • Acute pancreatitis is diagnosed clinically but requires CT evaluation to differentiate mild acute pancreatitis from severe necrotic pancreatitis. Experienced clinicians were able to detect severe pancreatitis in approximately 34-39% of patients who later had imaging confirmed severe necrotic pancreatitis. Blood studies are used to identify organ failure, offer prognostic information, determine if fluid resuscitation is adequate, and if antibiotics are indicated.
  • Blood Investigations - Full blood count, Renal function tests, Liver Function, serum calcium, serum amylase and lipase, Arterial blood gas, Trypsin-Selective Test
  • Imaging - A triple phase abdominal CT and abdominal ultrasound are together considered the gold standard for the evaluation of acute pancreatitis. Other modalities including the abdominal xray lack sensitivity and are not recommended. An important caveat is that imaging during the first 12 hours may be falsely reassuring as the inflammatory and necrotic process usually requires 48 hours to fully manifest.

Amylase and lipase, serum calcium, glycosuria

    • Elevated serum AMYLASE and LIPASE levels, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis. However, they have no role in assessing disease severity.
  • Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment.
  • Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.
  • Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.
  • If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol.[7]
    • decreased serum Calcium
    • Glycosuria

Regarding selection on these tests, two practice guidelines state:

"It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis"[8]
"Although amylase is widely available and provides acceptable accuracy of diagnosis, where lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade A)"[9]

Most (PMID 15943725, PMID 11552931, PMID 2580467, PMID 2466075, PMID 9436862), but not all (PMID 11156345, PMID 8945483) individual studies support the superiority of the lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase.[10] Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.[11]

Computed tomography

Regarding the need for computed tomography, practice guidelines state:

CT is an important common initial assessment tool for acute pancreatitis. Imaging is indicated during the initial presentation if:

  • the diagnosis of acute pancreatitis is uncertain
  • there is abdominal distension and tenderness, fever>102, or leukocytosis
  • there is a A Ranson score > 3 or APACHE score > 8
  • there is no improvement after 72 hours of conservative medical therapy
  • there has been an acute change in status: fever, pain, or shock

CT is recommended as a delayed assessment tool in the following situations:

  • acute change in status
  • to determine therapeutic response after surgery or interventional radiologic procedure
  • before discharge in patients with severe acute pancreatitis

CT abdomen should not be performed before the 1st 12 hours of onset of symptoms as early CT (<12 h) may result in equivocal or normal findings.

CT Findings can be classified into the following categories for easy recall :

  • Intrapancreatic - diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
  • Peripancreatic / extrapancreatic - irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
  • Locoregional - Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus, etc.

Magnetic resonance imaging

While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis,[12] magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris.[13] Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, and venous thrombosis.[14]

Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP) sequences. MRCP provides useful information regarding the etiology of acute pancreatitis, i.e., the presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies.[13] Clinical trials indicate that MRCP can be as effective a diagnostic tool for acute pancreatitis with biliary etiology as endoscopic retrograde cholangiopancreatography, but with the benefits of being less invasive and causing fewer complications.[15][16]

Endoscopic ultrasound

Main article: Endoscopic ultrasound

Classification by severity

Progression of pathophysiology

Acute pancreatitis patients recover in maximum cases. Some may develop abscess, pseudocyst or duodenal obstruction. In 5 percent cases, it may result in ARDS(acute respiratory distress syndrome), DIC(disseminated intravascular coagulation), etc. Acute pancreatitis can be further divided into mild and severe pancreatitis. Mostly the Atlanta classification (1992) is used. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. About 20% of the acute pancreatitis are severe with a mortality of about 20%. This is an important classification as severe pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common ward.

Necrosis will be followed by a systemic inflammatory response syndrome (SIRS) and will determine the immediate clinical course. The further clinical course is then determined by bacterial infection. SIRS is the cause of bacterial (Gram negative) translocation from the patients colon.

There are several ways to help distinguish between these two forms. One is the above mentioned Ranson Score.

Prognostic indices

In predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most,[17][18] but not all[19] studies report that the Apache score may be more accurate. In the negative study of the Apache II,[19] the Apache II 24 hr score was used rather than the 48 hour score. In addition, all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless, only the Apache II can be fully calculated upon admission. As the Apache II is more cumbersome to calculate, presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need prognostication with the Apache II; however, this approach is not studied. The Apache II score can be calculated at www.sfar.org.

Practice guidelines state:

2006: "The two tests that are most helpful at admission in distinguishing mild from severe acute pancreatitis are APACHE-II score and serum hematocrit. It is recommended that APACHE-II scores be generated during the first 3 days of hospitalization and thereafter as needed to help in this distinction. It is also recommended that serum hematocrit be obtained at admission, 12 h after admission, and 24 h after admission to help gauge adequacy of fluid resuscitation."[8]
2005: "Immediate assessment should include clinical evaluation, particularly of any cardiovascular, respiratory, and renal compromise, body mass index, chest x ray, and APACHE II score"[9]

Ranson Score

Main article: Ranson criteria

Ranson criteria is a clinical prediction rule for predicting the severity of acute pancreatitis. It was introduced in 1974.[1]

At admission

  • age in years > 55 years
  • white blood cell count > 16000 cells/mm3
  • blood glucose > 10 mmol/L (> 200 mg/dL)
  • serum AST > 250 IU/L
  • serum LDH > 350 IU/L

At 48 hours

  • Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
  • Hematocrit fall > 10%
  • Oxygen (hypoxemia PO2 < 60 mmHg)
  • BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
  • Base deficit (negative base excess) > 4 mEq/L
  • Sequestration of fluids > 6 L

The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both gallstone and alcoholic pancreatitis.

Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2]

Ranson's score

Ranson's score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT)

Interpretation If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or

Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality

APACHE

Main article: APACHE II

"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18% mortality[8] Online calculator

  • Hemorrhagic peritoneal fluid
  • Obesity
  • Indicators of organ failure
  • Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
  • PO2 <60 mmHg
  • Oliguria (<50 mL/h) or increasing BUN and creatinine
  • Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>

Balthazar scoring

Developed in the early 1990s by Emil J. Balthazar et al.,[20] the Computed Tomography Severity Index (CTSI) is a grading system used to determine the severity of acute pancreatitis. The numerical CTSI has a maximum of ten points, and is the sum of the Balthazar grade points and pancreatic necrosis grade points:

Balthazar Grade

Balthazar Grade Appearance on CT CT Grade Points
Grade A Normal CT 0 points
Grade B Focal or diffuse enlargement of the pancreas 1 point
Grade C Pancreatic gland abnormalities and peripancreatic inflammation 2 points
Grade D Fluid collection in a single location 3 points
Grade E Two or more fluid collections and / or gas bubbles in or adjacent to pancreas 4 points

Necrosis Score

Necrosis Percentage Points
No necrosis 0 points
0 to 30% necrosis 2 points
30 to 50% necrosis 4 points
Over 50% necrosis 6 points

CTSI's staging of acute pancreatitis severity has been shown by a number of studies to provide more accurate assessment than APACHE II, Ranson, and C-reactive protein (CRP) level.[21][22][23][24] However, a few studies indicate that CTSI is not significantly associated with the prognosis of hospitalization in patients with pancreatic necrosis, nor is it an accurate predictor of AP severity.[25][26]

Treatment

Pain control

Originally it was thought that analgesia should not be provided by morphine because it may cause spasm of the sphincter of Oddi and worsen the pain, so the drug of choice was meperidine. However, due to lack of efficacy and risk of toxicity of meperidine, more recent studies have found morphine the analgesic of choice.[citation needed] Meperidine may still be used by some practitioners in more minor cases, or where morphine is contraindicated.

Bowel rest

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest. Approximately 20% of patients have a relapse of pain during acute pancreatitis.[27] Approximately 75% of relapses occur within 48 hours of oral refeeding.

The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than parenteral feeding prior to oral refeeding.[27] IMRIE scoring is also useful.

Nutritional support

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced risk of aspiration.

Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the trachea even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea).

Antibiotics

A meta-analysis by the Cochrane Collaboration concluded that antibiotics help with a number needed to treat of 11 patients to reduce mortality.[28] However, the one study in the meta-analysis that used a quinolone, and a subsequent randomized controlled trial that studied ciprofloxacin were both negative.[29]

Carbapenems

An early randomized controlled trial of imipenem 0.5 gram intravenously every eight hours for two weeks showed a reduction in from pancreatic sepsis from 30% to 12%.[30]

Another randomized controlled trial with patients who had at least 50% pancreatic necrosis found a benefit from imipenem compared to pefloxacin with a reduction in infected necrosis from 34% to 20%[31]

A subsequent randomized controlled trial that used meropenem 1 gram intravenously every 8 hours for 7 to 21 days stated no benefit; however, 28% of patients in the group subsequently required open antibiotic treatment vs. 46% in the placebo group. In addition, the control group had only 18% incidence of peripancreatic infections and less biliary pancreatitis that the treatment group (44% versus 24%).[32]

Summary

In summary, the role of antibiotics is controversial. One recent expert opinion (prior to the last negative trial of meropenem[32]) suggested the use of imipenem if CT scan showed more than 30% necrosis of the pancreas.[33]

ERCP

Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 to 72 hours of presentation, is known to reduce morbidity and mortality.[34] The indications for early ERCP are as follows :

  • Clinical deterioration or lack of improvement after 24 hours
  • Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen

The disadvantages of ERCP are as follows :

  • ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis
  • The inherent risks of ERCP i.e. bleeding

It is worth noting that ERCP itself can be a cause of pancreatitis.

Surgery

Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii) complications. The most common cause of death in acute pancreatitis is secondary infection. Infection is diagnosed based on 2 criteria

  • Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)
  • Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the pancreas.

Surgical options for infected necrosis include:

  • Minimally invasive management - necrosectomy through small incision in skin (left flank) or stomach
  • Conventional management - necrosectomy with simple drainage
  • Closed management - necrosectomy with closed continuous postoperative lavage
  • Open management - necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)

Other measures

  • Pancreatic enzyme inhibitors are not proven to work.[35]
  • The use of octreotide has not been shown to improve outcome.[36]

Complications

Complications can be systemic or locoregional.

  • Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage)
  • Locoregional complications include pancreatic pseudocyst and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis

Epidemiology

  • Annual incidence in the U.S. is 18 per 100,000 population. In a European cross-sectional study, incidence of acute pancreatits 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.[37] Another study showed a lower incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963-74) over time.[38]

See also

References

  1. ^ Sommermeyer, Lucille (December 1935). "Acute Pancreatitis". American Journal of Nursing Io. 35 (12). Philadelphia, PA: Lippincott Williams & Wilkins: 1157–1161. doi:10.2307/3412015. JSTOR 3412015.
  2. ^ http://max.1gb.ru/surg/s16_pract.shtml
  3. ^ http://www.sgmu.ru/edu/learn/student/eman/pediatrics/investigation/digestion.pdf
  4. ^ Пропедевтика детских болезней с уходом за детьми, Капитан Т.В., 2006, page 290
  5. ^ A new source of drug-induced acute pancreatitis: codeine, Patrick Hastier, M.D., Martin J.M. Buckley, M.R.C.P.I., Emmanuel P. Peten, M.D., Nicolas Demuth, M.D., Remy Dumas, M.D., Jean-Francois Demarquay, M.D., Fancois-Xavier Caroli-Bosc, M.D., Jean-Pierre Delmont, M.D. a
  6. ^ Pancreatitis due to codeine, Moreno Escobosa MC, Amat López J, Cruz Granados S, Moya Quesada MC.
  7. ^ Gumaste V, Dave P, Weissman D, Messer J (1991). "Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis". Gastroenterology. 101 (5): 1361–6. PMID 1718808.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ a b c Banks P, Freeman M (2006). "Practice guidelines in acute pancreatitis". Am J Gastroenterol. 101 (10): 2379–400. doi:10.1111/j.1572-0241.2006.00856.x. PMID 17032204.
  9. ^ a b UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut. 54 Suppl 3: iii1. doi:10.1136/gut.2004.057026. PMC 1867800. PMID 15831893. Cite error: The named reference "pmid15831893" was defined multiple times with different content (see the help page).
  10. ^ Smith R, Southwell-Keely J, Chesher D (2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ J Surg. 75 (6): 399–404. doi:10.1111/j.1445-2197.2005.03391.x. PMID 15943725.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Corsetti J, Cox C, Schulz T, Arvan D (1993). "Combined serum amylase and lipase determinations for diagnosis of suspected acute pancreatitis". Clin Chem. 39 (12): 2495–9. PMID 7504593.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Arvanitakis M, Koustiani G, Gantzarou A, Grollios G, Tsitouridis I, Haritandi-Kouridou A, Dimitriadis A, Arvanitakis C (2007). "Staging of severity and prognosis of acute pancreatitis by computed tomography and magnetic resonance imaging-a comparative study". Dig Liver Dis. 39 (5): 473–482. doi:10.1016/j.dld.2007.01.015. PMID 17363349.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ a b Scaglione M, Casciani E, Pinto A, Andreoli C, De Vargas M, Gualdi GF (2008). "Imaging assessment of acute pancreatitis: a review". Semin Ultrasound CT MR. 29 (5): 322–340. doi:10.1053/j.sult.2008.06.009. PMID 18853839.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Miller FH, Keppke AL, Dalal K, Ly JN, Kamler VA, Sica GT (2004). "MRI of pancreatitis and its complications: part 1, acute pancreatitis". AJR Am J Roentgenol. 183 (6): 1637–1644. PMID 15547203.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Testoni PA, Mariani A, Curioni S, Zanello A, Masci E (2008). "MRCP-secretin test-guided management of idiopathic recurrent pancreatitis: long-term outcomes". Gastrointest Endosc. 67 (7): 1028–1034. doi:10.1016/j.gie.2007.09.007. PMID 18179795.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Khalid A, Peterson M, Slivka A (2003). "Secretin-stimulated magnetic resonance pancreaticogram to assess pancreatic duct outflow obstruction in evaluation of idiopathic acute recurrent pancreatitis: a pilot study". Dig Dis Sci. 48 (8): 1475–1481. doi:10.1023/A:1024747319606. PMID 12924639.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Larvin M, McMahon M (1989). "APACHE-II score for assessment and monitoring of acute pancreatitis". Lancet. 2 (8656): 201–5. doi:10.1016/S0140-6736(89)90381-4. PMID 2568529.
  18. ^ Yeung Y, Lam B, Yip A (2006). "APACHE system is better than Ranson system in the prediction of severity of acute pancreatitis". Hepatobiliary Pancreat Dis Int. 5 (2): 294–9. PMID 16698595.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ a b Chatzicostas C, Roussomoustakaki M, Vlachonikolis I, Notas G, Mouzas I, Samonakis D, Kouroumalis E (2002). "Comparison of Ranson, APACHE II and APACHE III scoring systems in acute pancreatitis". Pancreas. 25 (4): 331–5. doi:10.1097/00006676-200211000-00002. PMID 12409825.{{cite journal}}: CS1 maint: multiple names: authors list (link) (comment=this study used a Apache cutoff of >=10)
  20. ^ Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH (1990). "Acute pancreatitis: value of CT in establishing prognosis". Radiology. 174 (2): 331–336. PMID 2296641.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Gürleyik G, Emir S, Kiliçoglu G, Arman A, Saglam A (2005). "Computed tomography severity index, APACHE II score, and serum CRP concentration for predicting the severity of acute pancreatitis". JOP. 6 (6): 562–567. PMID 16286706.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ Knoepfli AS, Kinkel K, Berney T, Morel P, Becker CD, Poletti PA (2007). "Prospective study of 310 patients: can early CT predict the severity of acute pancreatitis?". Abdom Imaging. 32 (1): 111–115. doi:10.1007/s00261-006-9034-y. PMID 16944038.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Leung TK, Lee CM, Lin SY, Chen HC, Wang HJ, Shen LK, Chen YY (2005). "Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome". World J Gastroenterol. 11 (38): 6049–6052. PMID 16273623.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Vriens PW, van de Linde P, Slotema ET, Warmerdam PE, Breslau PJ (2005). "Computed tomography severity index is an early prognostic tool for acute pancreatitis". J Am Coll Surg. 201 (4): 497–502. doi:10.1016/j.jamcollsurg.2005.06.269. PMID 16183486.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Triantopoulou C, Lytras D, Maniatis P, Chrysovergis D, Manes K, Siafas I, Papailiou J, Dervenis C (2007). "Computed tomography versus Acute Physiology and Chronic Health Evaluation II score in predicting severity of acute pancreatitis: a prospective, comparative study with statistical evaluation". Pancreas. 35 (3): 238–242. doi:10.1097/MPA.0b013e3180619662. PMID 17895844.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ Mortelé KJ, Mergo PJ, Taylor HM, Wiesner W, Cantisani V, Ernst MD, Kalantari BN, Ros PR (2004). "Peripancreatic vascular abnormalities complicating acute pancreatitis: contrast-enhanced helical CT findings". Eur J Radiol. 52 (1): 67–72. doi:10.1016/j.ejrad.2003.10.006. PMID 15380848.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ a b Petrov MS, van Santvoort HC, Besselink MG, Cirkel GA, Brink MA, Gooszen HG (2007). "Oral Refeeding After Onset of Acute Pancreatitis: A Review of Literature". The American Journal of Gastroenterology. 102 (9): 2079. doi:10.1111/j.1572-0241.2007.01357.x. PMID 17573797.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Villatoro E, Bassi C, Larvin M (2006). "Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis". Cochrane Database Syst Rev (4): CD002941. doi:10.1002/14651858.CD002941.pub2. PMID 17054156.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ Isenmann R, Rünzi M, Kron M, Kahl S, Kraus D, Jung N, Maier L, Malfertheiner P, Goebell H, Beger H (2004). "Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial". Gastroenterology. 126 (4): 997–1004. doi:10.1053/j.gastro.2003.12.050. PMID 15057739.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ Pederzoli P, Bassi C, Vesentini S, Campedelli A (1993). "A randomized multicenter clinical trial of antibiotic prophylaxis of septic complications in acute necrotizing pancreatitis with imipenem". Surgery, gynecology & obstetrics. 176 (5): 480–3. PMID 8480272.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ Bassi C, Falconi M, Talamini G; et al. (1998). "Controlled clinical trial of pefloxacin versus imipenem in severe acute pancreatitis". Gastroenterology. 115 (6): 1513–7. doi:10.1016/S0016-5085(98)70030-7. PMID 9834279. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  32. ^ a b Dellinger EP, Tellado JM, Soto NE; et al. (2007). "Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double-blind, placebo-controlled study". Ann. Surg. 245 (5): 674–83. doi:10.1097/01.sla.0000250414.09255.84. PMC 1877078. PMID 17457158. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  33. ^ Whitcomb D (2006). "Clinical practice. Acute pancreatitis". N Engl J Med. 354 (20): 2142–50. doi:10.1056/NEJMcp054958. PMID 16707751.
  34. ^ Apostolakos, Michael J. (2001). The Intensive Care Manual. McGraw-Hill Professional. ISBN 0-07-006696-5. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  35. ^ DeCherney, Alan H. (2003). Current Obstetric & Gynecologic Diagnosis & Treatment. McGraw-Hill Professional. ISBN 0-8385-1401-4. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  36. ^ Peitzman, Andrew B. (2007). The Trauma Manual: Trauma and Acute Care Surgery. Lippincott Williams & Wilkins. ISBN 0-7817-6275-8. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); line feed character in |publisher= at position 20 (help)
  37. ^ Eland IA, Sturkenboom MJ, Wilson JH, Stricker BH (2000). "Incidence and mortality of acute pancreatitis between 1985 and 1995". Scand. J. Gastroenterol. 35 (10): 1110–6. doi:10.1080/003655200451261. PMID 11099067.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ Goldacre MJ, Roberts SE (2004). "Hospital admission for acute pancreatitis in an English population, 1963-98: database study of incidence and mortality". BMJ. 328 (7454): 1466–9. doi:10.1136/bmj.328.7454.1466. PMC 428514. PMID 15205290.
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