Acute pancreatitis

Last updated
Acute pancreatitis
Other namesAcute pancreatic necrosis [1]
3D Medical Animation Acute Pancreatitis.jpg
Still from 3D medical animation of acute pancreatitis
Specialty Gastroenterology, general surgery

Acute pancreatitis (AP) is a sudden inflammation of the pancreas. Causes include a gallstone impacted in the common bile duct or the pancreatic duct, heavy alcohol use, systemic disease, trauma, elevated calcium levels, hypertriglyceridemia (with triglycerides usually being very elevated, over 1000 mg/dL), certain medications, hereditary causes and, in children, mumps. Acute pancreatitis may be a single event, it may be recurrent, or it may progress to chronic pancreatitis and/or pancreatic failure (the term pancreatic dysfunction includes cases of acute or chronic pancreatitis where the pancreas is measurably damaged, even if it has not failed).

Contents

In all cases of acute pancreatitis, early intravenous fluid hydration and early enteral (nutrition delivered to the gut, either by mouth or via a feeding tube) feeding are associated with lower mortality and complications. [2] Mild cases are usually successfully treated with conservative measures such as hospitalization with intravenous fluid infusion, pain control, and early enteral feeding. If a person is not able to tolerate feeding by mouth, feeding via nasogastric or nasojejunal tubes are frequently used which provide nutrition directly to the stomach or intestines respectively. [2] Severe cases often require admission to an intensive care unit. Severe pancreatitis, which by definition includes organ damage other than the pancreas, is associated with a mortality rate of 20%. [2] The condition is characterized by the pancreas secreting active enzymes such as trypsin, chymotrypsin and carboxypeptidase, instead of their inactive forms, leading to auto-digestion of the pancreas. Calcium helps to convert trypsinogen to the active trypsin, thus elevated calcium (of any cause) is a potential cause of pancreatitis. [2] Damage to the pancreatic ducts can occur as a result of this. Long term complications include type 3c diabetes (pancreatogenic diabetes), in which the pancreas is unable to secrete enough insulin due to structural damage. [2] 35% develop exocrine pancreatic insufficiency in which the pancreas is unable to secrete digestive enzymes due to structural damage, leading to malabsorption. [2]

Signs and symptoms

Common

Common symptoms of acute pancreatitis include abdominal pain, nausea, vomiting, and low to moderate grade fever. [2] [3] The abdominal pain is the most common symptom and it is usually described as being in the left upper quadrant, epigastric area or around the umbilicus, with radiation throughout the abdomen, or to the chest or back. [4] The abdominal pain initially may worsen with eating or drinking but may become constant as the disease progresses. [2] [4] Less common symptoms include hiccups, abdominal bloating and indigestion. [4] Although these are common symptoms, frequently they are not all present; and epigastric pain may be the only symptom. [5]

Grey-Turner's sign (hemorrhagic discoloration of the flanks) or Cullen's sign (hemorrhagic discoloration of the umbilicus) are associated with severe disease. However both signs are rare (occurring in less than 1% of cases of acute pancreatitis) and are not specific nor sensitive for diagnosis of acute pancreatitis. [6] Pleural effusions (fluid in the lung cavity) may occur in up to 34% of people with acute pancreatitis and are associated with a poor prognosis. [7] The 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)) is also associated with acute pancreatitis. [8]

Complications

Complications of acute pancreatitis may occur. Necrotic pancreatitis occurs when inflammation of the pancreas progresses to cell death. Acute fluid collections may form adjacent to the pancreas or necrotic collections (discrete areas of dead tissue) may also form adjacent to or within the pancreas. These may progress to pancreatic pseudocysts and walled off areas of dead tissue which may persist for longer than 4 weeks. Both can become secondarily infected. [2] Other complications include gastric outlet obstruction splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, blood clot of the splenic vein, superior mesenteric vein and portal veins, duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, or pleural effusion. [9] [2]

Systemic complications include acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome, disseminated intravascular coagulation (DIC), hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), and malabsorption due to exocrine failure.[ citation needed ]

Tobacco use, recurrent episodes of acute pancreatitis, pancreatic tissue death, alcoholic pancreatitis are all risk factors for developing chronic pancreatitis. [2]

Causes

Most common

Less common

Pathology

Anatomy of the pancreas Illu pancrease.svg
Anatomy of the pancreas

Pathogenesis

Acute pancreatitis occurs when there is abnormal activation of digestive enzymes within the pancreas. This occurs through inappropriate activation of inactive enzyme precursors called zymogens (or proenzymes) inside the pancreas, most notably trypsinogen. Normally, trypsinogen is converted to its active form (trypsin) in the first part of the small intestine (duodenum), where the enzyme assists in the digestion of proteins. During an episode of acute pancreatitis, trypsinogen comes into contact with lysosomal enzymes (specifically cathepsin), which activate trypsinogen to trypsin. The active form trypsin then leads to further activation of other molecules of trypsinogen. The activation of these digestive enzymes lead to inflammation, edema, vascular injury, and even cellular death. The death of pancreatic cells occurs via two main mechanisms: apoptosis, which is physiologically controlled, and necrosis, which is less organized and more damaging. The balance between these two mechanisms of cellular death 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.

Pathophysiology

The two types of acute pancreatitis are mild and severe, which are defined based on whether the predominant response to cell injury is inflammation (mild) or necrosis (severe). In mild pancreatitis, there is inflammation and edema of the pancreas. In severe pancreatitis, there is necrosis of the pancreas, and nearby organs may become injured.

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.

Diagnosis

Acute pancreatitis is diagnosed using clinical history and physical examination findings supporting the diagnosis with imaging and pancreatic enzymes (amylase and lipase). The Revised Atlanta Classification requires two out of three of the following findings for the diagnosis: abdominal pain consistent with pancreatitis, elevated amylase or lipase levels greater than 3 times the upper limit of normal, and imaging consistent with acute pancreatitis. [2] [13] Additional labs may be used to identify organ failure for prognostic purposes or to guide fluid resuscitation rate. [2] If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol. [14] Serum lipase is more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis, and is the preferred test in the diagnosis. [15] [16]

Most, but not all individual studies support favor the diagnostic utility of lipase. [17] In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase. [18] 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. [19]

Reduced lipase clearance due to kidney disease, gastrointestinal or hepatobiliary cancers, pancreatic enzyme hypersecretion, critical illness including due to neurosurgical causes have been shown to increase serum lipase and may complicate the diagnosis of acute pancreatitis. [20]

Differential diagnosis

The differential diagnosis includes: [21]

Computed tomography

Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas Akute exsudative Pankreatitis - CT axial.jpg
Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas

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:

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

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

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

The principal value of CT imaging to the treating clinician is the capacity to identify devitalized areas of the pancreas which have become necrotic due to ischaemia. Pancreatic necrosis can be reliably identified by intravenous contrast-enhanced CT imaging, [22] and is of value if infection occurs and surgical or percutaneous debridement is indicated.

Magnetic resonance imaging

While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis, [23] 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. [24] 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. [25]

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. [24] 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. [26] [27]

Ultrasound

Abdominal ultrasonography of acute pancreatitis Ultrasonography of acute pancreatitis.jpg
Abdominal ultrasonography of acute pancreatitis

Ultrasound is less preferred as a diagnostic test for acute pancreatitis, but it may be used in select cases. Abdominal ultrasonography may be obtained if there is concern of a gallstone blocking the pancreatic duct leading to pancreatitis. [2]

Treatment

Early enteral (nutrition given directly to the gut, either by mouth or via feeding tube) nutrition and aggressive intravenous fluid hydration are indicated in all forms and severities of acute pancreatitis and are associated with lower mortality and complications. [2]

Fluid replacement

The specific rate of intravenous fluid replacement in acute pancreatitis is not well established but some experts recommend an initial fluid infusion rate of 5-10 mL of IV fluids per kilogram of body weight per hour and adjusting the rate to meet physiologic parameters such as heart rate, mean arterial pressure, urine output and hematocrit. [2]

Isotonic crystalloid solutions (such as lactated ringers) are preferred over normal saline for fluid resuscitation and are associted with a lower risk of developing systemic inflammatory response syndrome (SIRS). [2]

In the initial stages (within the first 12 to 24 hours) of acute pancreatitis, fluid replacement has been associated with a reduction in morbidity and mortality. [28] [29] [30] [31]

Pain control

Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics.

Opioids are safe and effective at providing pain control in patients with acute pancreatitis. [32] Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given both as a bolus as well as constant infusion. Meperidine has been historically favored over morphine because of the belief that morphine caused an increase in sphincter of Oddi pressure. However, no clinical studies suggest that morphine can aggravate or cause pancreatitis or cholecystitis. [33] In addition, meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite normeperidine, which causes neuromuscular side effects and, rarely, seizures.

Nutritional support

Acute pancreatitis is a catabolic state and with hemodynamic instability or fluid shifts or edema there may be reduced intravascular perfusion to the gut. This reduction in gut perfusion increases the risk of gut necrosis with bacterial translocation with the subsequent risk of sepsis or secondary infections. [2] Enteral nutrition gives one needed caloric intake as well as enhances intestinal motility and blood flow to the gut, reducing these risks. [2] Enteral nutrition (as compared to parenteral nutrition, in which nutrients are given via intravenous infusion) is associated with reduced mortality, reduced risk of multi-organ failure and systemic infection in those with acute pancreatitis. [2] [34] In patients with acute pancreatitis, the American Gastroenterological Association (AGA) recommends early oral nutrition, within 24 hours, rather than keeping the patient fastng (or nothing by mouth). And in those unable to feed orally, the AGA recommends enteral nutrition (via a nasogastric or nasojejunal tube) rather than parenteral nutrition. [35]

Antibiotics

Up to 20 percent of people with acute pancreatitis develop an infection outside the pancreas such as bloodstream infections, pneumonia, or urinary tract infections. [36] These infections are associated with an increase in mortality. [37] Fluid collections around the pancreas or areas within the pancreas that experience tissue death (necrosis) may also become secondarily infected requiring the use of antibiotics. [2] When an infection is suspected, antibiotics should be started while the source of the infection is being determined. However, if cultures are negative and no source of infection is identified, antibiotics should be discontinued.

Preventative antibiotics are not recommended in people with acute pancreatitis, regardless of the type (interstitial or necrotizing) or disease severity (mild, moderately severe, or severe) [13] [38]

Endoscopic retrograde cholangiopancreatography

In 30% of those with acute pancreatitis, no cause is identified. Endoscopic retrograde cholangiopancreatography (ERCP) with empirical biliary sphincterotomy has an equal chance of causing complications and treating the underlying cause, therefore, is not recommended for treating acute pancreatitis. [39] If a gallstone is detected, ERCP, performed within 24 to 72 hours of presentation with successful removal of the stone, is known to reduce morbidity and mortality. [40] The indications for early ERCP are:

The risks of ERCP are that it may worsen pancreatitis, it may introduce an infection to otherwise sterile pancreatitis, and bleeding.

Surgery

In those with mild acute pancreatitis due to gallstones, cholecystectomy (removal of the gallbladder) is recommended in the hospital and is associated with a reduced risk of pancreatitis recurrence. [2] In those with gallstone pancreatitis who have severe disease, including the presence of peripancreatic fluid collections, cholecystectomy should be delayed as the fluid collections around the pancreas make surgery technically difficult. The peri-pancreatic fluids also carry a risk of becoming secondarily infected with surgery. [2]

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

Surgical options for infected necrosis include:[ citation needed ]

Other measures

Classification by severity: prognostic scoring systems

Acute pancreatitis patients recover in majority of cases. Some may develop abscess, pseudocyst or duodenal obstruction. About 20% of the acute pancreatitis are severe with a mortality of about 20%. [2] Acute pancreatitis can be further divided into mild and severe pancreatitis. Several clinical scoring tools have been developed to determine prognostic information and may guide certain areas of clinical management, such as need for ICU admission. [2]

Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most, [43] [44] but not all [45] studies report that the Apache score may be more accurate. In the negative study of the APACHE-II, the APACHE-II 24-hour score was used rather than the 48-hour score. [45] Some experts recommend using the APACHE II score as well as a serum hematocrit level early during the admission as prognostic indicators. [15]

Ranson score

The Ranson score is used to predict the severity of acute pancreatitis. They were introduced in 1974.

At admission

  • age in years > 55 years
  • white blood cell count > 16000 cells/mm3
  • blood glucose > 11.1 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 any time 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]

Alternative Ranson 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 II score

"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18% mortality [15]

Balthazar score

Developed in the early 1990s by Emil J. Balthazar et al., [46] 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 gradeAppearance on CTCT grade points
Grade ANormal CT0 points
Grade BFocal or diffuse enlargement of the pancreas1 point
Grade CPancreatic gland abnormalities and peripancreatic inflammation2 points
Grade DFluid collection in a single location3 points
Grade ETwo or more fluid collections and / or gas bubbles in or adjacent to pancreas4 points

Necrosis score

Necrosis percentagePoints
No necrosis0 points
0 to 30% necrosis2 points
30 to 50% necrosis4 points
Over 50% necrosis6 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. [47] [48] [49] 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. [50] [51]

Glasgow score

The Glasgow score is valid for both gallstone and alcohol induced pancreatitis, whereas the Ranson score is only for alcohol induced pancreatitis[ citation needed ]. If a patient scores 3 or more it indicates severe pancreatitis and the patient should be considered for transfer to ITU. It is scored through the mnemonic, PANCREAS:

BISAP score

Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation.

Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test performance characteristics for predicting mortality as the APACHE II score. [52] As is a problem with many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as length of hospital stay, need for ICU care, or need for intervention.

Epidemiology

The worldwide incidence of acute pancreatitis has increasing from 1961 to 2016 with an average annual percentage increase of 3%, the increased incidence was seen in North America and Europe. [53] The incidence of acute pancreatitis in the United States is 110-140 cases per 100,000 people. [2]

In the United States the most common causes include gallstones, which are responsible for 21-33% of cases, followed by alcohol (16-27%) and elevated triglycerides (2-5%). [2]

See also

Related Research Articles

<span class="mw-page-title-main">Pancreas</span> Organ of the digestive system and endocrine system of vertebrates

The pancreas is an organ of the digestive system and endocrine system of vertebrates. In humans, it is located in the abdomen behind the stomach and functions as a gland. The pancreas is a mixed or heterocrine gland, i.e., it has both an endocrine and a digestive exocrine function. 99% of the pancreas is exocrine and 1% is endocrine. As an endocrine gland, it functions mostly to regulate blood sugar levels, secreting the hormones insulin, glucagon, somatostatin and pancreatic polypeptide. As a part of the digestive system, it functions as an exocrine gland secreting pancreatic juice into the duodenum through the pancreatic duct. This juice contains bicarbonate, which neutralizes acid entering the duodenum from the stomach; and digestive enzymes, which break down carbohydrates, proteins and fats in food entering the duodenum from the stomach.

<span class="mw-page-title-main">Pancreatitis</span> Inflammation of the pancreas

Pancreatitis is a condition characterized by inflammation of the pancreas. The pancreas is a large organ behind the stomach that produces digestive enzymes and a number of hormones. There are two main types: acute pancreatitis, and chronic pancreatitis.

<span class="mw-page-title-main">Cholecystitis</span> Inflammation of the gallbladder

Cholecystitis is inflammation of the gallbladder. Symptoms include right upper abdominal pain, pain in the right shoulder, nausea, vomiting, and occasionally fever. Often gallbladder attacks precede acute cholecystitis. The pain lasts longer in cholecystitis than in a typical gallbladder attack. Without appropriate treatment, recurrent episodes of cholecystitis are common. Complications of acute cholecystitis include gallstone pancreatitis, common bile duct stones, or inflammation of the common bile duct.

<span class="mw-page-title-main">Abdominal pain</span> Stomach aches

Abdominal pain, also known as a stomach ache, is a symptom associated with both non-serious and serious medical issues. Since the abdomen contains most of the body's vital organs, it can be an indicator of a wide variety of diseases. Given that, approaching the examination of a person and planning of a differential diagnosis is extremely important.

<span class="mw-page-title-main">Chronic pancreatitis</span> Medical condition

Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption. It is a disease process characterized by irreversible damage to the pancreas as distinct from reversible changes in acute pancreatitis. Tobacco smoke and alcohol misuse are two of the most frequently implicated causes, and the two risk factors are thought to have a synergistic effect with regards to the development of chronic pancreatitis. Chronic pancreatitis is a risk factor for the development of pancreatic cancer.

<span class="mw-page-title-main">Gastrointestinal disease</span> Illnesses of the digestive system

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum; and the accessory organs of digestion, the liver, gallbladder, and pancreas.

<span class="mw-page-title-main">Common bile duct stone</span> Medical condition

Common bile duct stone, also known as choledocholithiasis, is the presence of gallstones in the common bile duct (CBD). This condition can cause jaundice and liver cell damage. Treatments include choledocholithotomy and endoscopic retrograde cholangiopancreatography (ERCP).

<span class="mw-page-title-main">Pancreatic enzymes (medication)</span> Amylase, lipase, and protease mixture

Pancreatic enzymes, also known as pancreases or pancrelipase and pancreatin, are commercial mixtures of amylase, lipase, protease and lactase. They are used to treat malabsorption syndrome due to certain pancreatic problems. These pancreatic problems may be due to cystic fibrosis, surgical removal of the pancreas, long term pancreatitis, pancreatic cancer, or MODY 5, among others. The preparation is taken by mouth.

<span class="mw-page-title-main">Pancreatic pseudocyst</span> Medical condition

A pancreatic pseudocyst is a circumscribed collection of fluid rich in pancreatic enzymes, blood, and non-necrotic tissue, typically located in the lesser sac of the abdomen. Pancreatic pseudocysts are usually complications of pancreatitis, although in children they frequently occur following abdominal trauma. Pancreatic pseudocysts account for approximately 75% of all pancreatic masses.

<span class="mw-page-title-main">Pancreatic fistula</span> Leakage of pancreatic secretions into other organs or spaces

A pancreatic fistula is an abnormal communication between the pancreas and other organs due to leakage of pancreatic secretions from damaged pancreatic ducts. An external pancreatic fistula is one that communicates with the skin, and is also known as a pancreaticocutaneous fistula, whereas an internal pancreatic fistula communicates with other internal organs or spaces. Pancreatic fistulas can be caused by pancreatic disease, trauma, or surgery.

<span class="mw-page-title-main">Pancreas divisum</span> Congenital disorder of digestive system

Pancreas divisum is a congenital anomaly in the anatomy of the ducts of the pancreas in which a single pancreatic duct is not formed, but rather remains as two distinct dorsal and ventral ducts. Most individuals with pancreas divisum remain without symptoms or complications. A minority of people with pancreatic divisum may develop episodes of abdominal pain, nausea or vomiting due to acute or chronic pancreatitis. The presence of pancreas divisum is usually identified with cross sectional diagnostic imaging, such as endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP). In some cases, it may be detected intraoperatively. If no symptoms or complications are present, then treatment is not necessary. However, if there is recurrent pancreatitis, then a sphincterotomy of the minor papilla may be indicated.

<span class="mw-page-title-main">Exocrine pancreatic insufficiency</span> Inability to properly digest food due to a lack of digestive enzymes from the pancreas

Exocrine pancreatic insufficiency (EPI) is the inability to properly digest food due to a lack or reduction of digestive enzymes made by the pancreas. EPI can occur in humans and is prevalent in many conditions such as cystic fibrosis, Shwachman–Diamond syndrome, different types of pancreatitis, multiple types of diabetes mellitus, advanced renal disease, older adults, celiac disease, IBS-D, IBD, HIV, alcohol-related liver disease, Sjogren syndrome, tobacco use, and use of somatostatin analogues.

Pancreatic diseases are diseases that affect the pancreas, an organ in most vertebrates and in humans and other mammals located in the abdomen. The pancreas plays a role in the digestive and endocrine system, producing enzymes which aid the digestion process and the hormone insulin, which regulates blood sugar levels. The most common pancreatic disease is pancreatitis, an inflammation of the pancreas which could come in acute or chronic form. Other pancreatic diseases include diabetes mellitus, exocrine pancreatic insufficiency, cystic fibrosis, pseudocysts, cysts, congenital malformations, tumors including pancreatic cancer, and hemosuccus pancreaticus.

<span class="mw-page-title-main">Biliary colic</span> Medical condition in which gallstones cause acute pain

Biliary colic, also known as symptomatic cholelithiasis, a gallbladder attack or gallstone attack, is when a colic occurs due to a gallstone temporarily blocking the cystic duct. Typically, the pain is in the right upper part of the abdomen, and can be severe. Pain usually lasts from 15 minutes to a few hours. Often, it occurs after eating a heavy meal, or during the night. Repeated attacks are common. Cholecystokinin - a gastrointestinal hormone - plays a role in the colic, as following the consumption of fatty meals, the hormone triggers the gallbladder to contract, which may expel stones into the duct and temporarily block it until being successfully passed.

The Ranson criteria form a clinical prediction rule for predicting the prognosis and mortality risk of acute pancreatitis. They were introduced in 1974 by the English-American pancreatic expert and surgeon Dr. John Ranson (1938–1995).

<span class="mw-page-title-main">Sphincter of Oddi dysfunction</span> Medical condition

Sphincter of Oddi dysfunction refers to a group of functional disorders leading to abdominal pain due to dysfunction of the Sphincter of Oddi: functional biliary sphincter of Oddi and functional pancreatic sphincter of Oddi disorder. The sphincter of Oddi is a sphincter muscle, a circular band of muscle at the bottom of the biliary tree which controls the flow of pancreatic juices and bile into the second part of the duodenum. The pathogenesis of this condition is recognized to encompass stenosis or dyskinesia of the sphincter of Oddi ; consequently the terms biliary dyskinesia, papillary stenosis, and postcholecystectomy syndrome have all been used to describe this condition. Both stenosis and dyskinesia can obstruct flow through the sphincter of Oddi and can therefore cause retention of bile in the biliary tree and pancreatic juice in the pancreatic duct.

<span class="mw-page-title-main">Pancreatitis (veterinary)</span> Medical condition

Pancreatitis is a common condition in cats and dogs. Pancreatitis is inflammation of the pancreas that can occur in two very different forms. Acute pancreatitis is sudden, while chronic pancreatitis is characterized by recurring or persistent form of pancreatic inflammation. Cases of both can be considered mild or severe. It is currently undecided whether chronic pancreatitis is a distinct disease or a form of acute pancreatitis. Other forms such as auto-immune and hereditary pancreatitis are presumed to occur but there existence has not been proven.

Pancreatic abscess is a late complication of acute necrotizing pancreatitis, occurring more than 4 weeks after the initial attack. A pancreatic abscess is a collection of pus resulting from tissue necrosis, liquefaction, and infection. It is estimated that approximately 3% of the patients with acute pancreatitis will develop an abscess.

A pancreatic injury is some form of trauma sustained by the pancreas. The injury can be sustained through either blunt forces, such as a motor vehicle accident, or penetrative forces, such as that of a gunshot wound. The pancreas is one of the least commonly injured organs in abdominal trauma.

<span class="mw-page-title-main">Pancreatic cyst</span> Medical condition

A pancreatic cyst is a fluid filled sac within the pancreas. The prevalence of pancreatic cysts is 2-15% based on imaging studies, but the prevalence may be as high as 50% based on autopsy series. Most pancreatic cysts are benign and the risk of malignancy is 0.5-1.5%. Pancreatic pseudocysts and serous cystadenomas are considered benign pancreatic cysts with a risk of malignancy of 0%.

References

  1. ↑ Sommermeyer L (December 1935). "Acute Pancreatitis". American Journal of Nursing . 35 (12): 1157–1161. doi:10.2307/3412015. JSTOR   3412015.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 Mederos, Michael A.; Reber, Howard A.; Girgis, Mark D. (26 January 2021). "Acute Pancreatitis: A Review". JAMA. 325 (4): 382–390. doi:10.1001/jama.2020.20317. PMID   33496779.
  3. ↑ "Pancreatitis". Mayo Clinic. Retrieved 14 October 2020.
  4. 1 2 3 Quinlan, JD (1 November 2014). "Acute pancreatitis". American Family Physician. 90 (9): 632–9. PMID   25368923.
  5. ↑ "Symptoms & Causes of Pancreatitis". The National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 4 October 2020.
  6. ↑ Wright, William F. (1 June 2016). "Cullen Sign and Grey Turner Sign Revisited". Journal of Osteopathic Medicine. 116 (6): 398–401. doi:10.7556/jaoa.2016.081.
  7. ↑ Zeng, Tingting; An, Jing; Wu, Yanqiu; Hu, Xueru; An, Naer; Gao, Lijuan; Wan, Chun; Liu, Lian; Shen, Yongchun (12 December 2023). "Incidence and prognostic role of pleural effusion in patients with acute pancreatitis: a meta-analysis". Annals of Medicine. 55 (2). doi:10.1080/07853890.2023.2285909.
  8. ↑ Sriram Bhat M (2018-10-31). SRB's Clinical Methods in Surgery. JP Medical Ltd. pp. 488–. ISBN   978-93-5270-545-0.
  9. ↑ Bassi C, Falconi M, Butturini G, Pederzoli P (2001). "Early complications of severe acute pancreatitis". In Holzheimer RG, Mannick JA (eds.). Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt.
  10. ↑ Rawla P, Sunkara T, Thandra KC, Gaduputi V (December 2018). "Hypertriglyceridemia-induced pancreatitis: updated review of current treatment and preventive strategies". Clinical Journal of Gastroenterology. 11 (6): 441–448. doi:10.1007/s12328-018-0881-1. PMID   29923163. S2CID   49311482.
  11. 1 2 Rawla P, Bandaru SS, Vellipuram AR (June 2017). "Review of Infectious Etiology of Acute Pancreatitis". Gastroenterology Research. 10 (3): 153–158. doi:10.14740/gr858w. PMC   5505279 . PMID   28725301.
  12. ↑ Chung JW, Ryu SH, Jo JH, Park JY, Lee S, Park SW, Song SY, Chung JB (January 2013). "Clinical implications and risk factors of acute pancreatitis after cardiac valve surgery". Yonsei Medical Journal. 54 (1): 154–9. doi:10.3349/ymj.2013.54.1.154. PMC   3521256 . PMID   23225812.
  13. 1 2 Tenner S, Baillie J, DeWitt J, Vege SS (September 2013). "American College of Gastroenterology guideline: management of acute pancreatitis". The American Journal of Gastroenterology. 108 (9): 1400–15, 1416. doi: 10.1038/ajg.2013.218 . PMID   23896955. S2CID   12610145.
  14. ↑ Gumaste VV, Dave PB, Weissman D, Messer J (November 1991). "Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis". Gastroenterology. 101 (5): 1361–6. doi: 10.1016/0016-5085(91)90089-4 . PMID   1718808.
  15. 1 2 3 Banks PA, Freeman ML, et al. (Practice Parameters Committee of the American College of Gastroenterology) (October 2006). "Practice guidelines in acute pancreatitis". The American Journal of Gastroenterology. 101 (10): 2379–400. doi: 10.1111/j.1572-0241.2006.00856.x . PMID   17032204. S2CID   1837007.
  16. ↑ UK Working Party on Acute Pancreatitis (May 2005). "UK guidelines for the management of acute pancreatitis". Gut. 54 (Suppl 3): iii1–9. doi:10.1136/gut.2004.057026. PMC   1867800 . PMID   15831893.
  17. ↑ [ improper synthesis? ]In support of the superiority of the lipase: Without support for the superiority of the lipase:
    • Ignjatović S, Majkić-Singh N, Mitrović M, Gvozdenović M (November 2000). "Biochemical evaluation of patients with acute pancreatitis". Clinical Chemistry and Laboratory Medicine. 38 (11): 1141–4. doi:10.1515/CCLM.2000.173. PMID   11156345. S2CID   34932274.
    • Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP (December 1996). "What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study". Mayo Clinic Proceedings. 71 (12): 1138–44. doi:10.4065/71.12.1138. PMID   8945483.
  18. ↑ Smith RC, Southwell-Keely J, Chesher D (June 2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ Journal of Surgery. 75 (6): 399–404. doi:10.1111/j.1445-2197.2005.03391.x. PMID   15943725. S2CID   35768001.
  19. ↑ Corsetti JP, Cox C, Schulz TJ, Arvan DA (December 1993). "Combined serum amylase and lipase determinations for diagnosis of suspected acute pancreatitis". Clinical Chemistry. 39 (12): 2495–9. doi: 10.1093/clinchem/39.12.2495 . PMID   7504593.
  20. ↑ Hameed AM, Lam VW, Pleass HC (February 2015). "Significant elevations of serum lipase not caused by pancreatitis: a systematic review". HPB. 17 (2): 99–112. doi:10.1111/hpb.12277. PMC   4299384 . PMID   24888393.
  21. ↑ Bailey & Love's/24th/1123
  22. ↑ Larvin M, Chalmers AG, McMahon MJ (June 1990). "Dynamic contrast enhanced computed tomography: a precise technique for identifying and localising pancreatic necrosis". BMJ. 300 (6737): 1425–8. doi:10.1136/bmj.300.6737.1425. PMC   1663140 . PMID   2379000.
  23. ↑ Arvanitakis M, Koustiani G, Gantzarou A, Grollios G, Tsitouridis I, Haritandi-Kouridou A, Dimitriadis A, Arvanitakis C (May 2007). "Staging of severity and prognosis of acute pancreatitis by computed tomography and magnetic resonance imaging-a comparative study". Digestive and Liver Disease. 39 (5): 473–82. doi:10.1016/j.dld.2007.01.015. PMID   17363349.
  24. 1 2 Scaglione M, Casciani E, Pinto A, Andreoli C, De Vargas M, Gualdi GF (October 2008). "Imaging assessment of acute pancreatitis: a review". Seminars in Ultrasound, CT and MRI. 29 (5): 322–40. doi:10.1053/j.sult.2008.06.009. PMID   18853839.
  25. ↑ Miller FH, Keppke AL, Dalal K, Ly JN, Kamler VA, Sica GT (December 2004). "MRI of pancreatitis and its complications: part 1, acute pancreatitis". AJR. American Journal of Roentgenology. 183 (6): 1637–44. doi:10.2214/ajr.183.6.01831637. PMID   15547203.
  26. ↑ Testoni PA, Mariani A, Curioni S, Zanello A, Masci E (June 2008). "MRCP-secretin test-guided management of idiopathic recurrent pancreatitis: long-term outcomes". Gastrointestinal Endoscopy. 67 (7): 1028–34. doi:10.1016/j.gie.2007.09.007. PMID   18179795.
  27. ↑ Khalid A, Peterson M, Slivka A (August 2003). "Secretin-stimulated magnetic resonance pancreaticogram to assess pancreatic duct outflow obstruction in evaluation of idiopathic acute recurrent pancreatitis: a pilot study". Digestive Diseases and Sciences. 48 (8): 1475–81. doi:10.1023/A:1024747319606. PMID   12924639. S2CID   3066587.
  28. ↑ Working Group IAP/APA Acute Pancreatitis Guidelines (2013). "IAP/APA evidence-based guidelines for the management of acute pancreatitis". Pancreatology. 13 (4 Suppl 2): e1–15. doi: 10.1016/j.pan.2013.07.063 . hdl: 1854/LU-8582111 . PMID   24054878.
  29. ↑ Talukdar R, Swaroop Vege S (April 2011). "Early management of severe acute pancreatitis". Current Gastroenterology Reports. 13 (2): 123–30. doi: 10.1007/s11894-010-0174-4 . PMID   21243452. S2CID   38955726.
  30. ↑ Trikudanathan G, Navaneethan U, Vege SS (August 2012). "Current controversies in fluid resuscitation in acute pancreatitis: a systematic review". Pancreas. 41 (6): 827–34. doi:10.1097/MPA.0b013e31824c1598. PMID   22781906. S2CID   1864635.
  31. ↑ Gardner TB, Vege SS, Chari ST, Petersen BT, Topazian MD, Clain JE, Pearson RK, Levy MJ, Sarr MG (2009). "Faster rate of initial fluid resuscitation in severe acute pancreatitis diminishes in-hospital mortality". Pancreatology. 9 (6): 770–6. doi:10.1159/000210022. PMID   20110744. S2CID   5614093.
  32. ↑ Basurto Ona X, Rigau Comas D, Urrútia G (July 2013). "Opioids for acute pancreatitis pain". The Cochrane Database of Systematic Reviews. 7 (7): CD009179. doi:10.1002/14651858.CD009179.pub2. PMID   23888429.
  33. ↑ Helm JF, Venu RP, Geenen JE, Hogan WJ, Dodds WJ, Toouli J, Arndorfer RC (October 1988). "Effects of morphine on the human sphincter of Oddi". Gut. 29 (10): 1402–7. doi:10.1136/gut.29.10.1402. PMC   1434014 . PMID   3197985.
  34. ↑ Al-Omran, Mohammed; AlBalawi, Zaina H; Tashkandi, Mariam F; Al-Ansary, Lubna A (20 January 2010). "Enteral versus parenteral nutrition for acute pancreatitis". Cochrane Database of Systematic Reviews (1): CD002837. doi:10.1002/14651858.CD002837.pub2. PMC   7120370 . PMID   20091534.
  35. ↑ Crockett, Seth D.; Wani, Sachin; Gardner, Timothy B.; Falck-Ytter, Yngve; Barkun, Alan N.; Crockett, Seth; Falck-Ytter, Yngve; Feuerstein, Joseph; Flamm, Steven; Gellad, Ziad; Gerson, Lauren; Gupta, Samir; Hirano, Ikuo; Inadomi, John; Nguyen, Geoffrey C.; Rubenstein, Joel H.; Singh, Siddharth; Smalley, Walter E.; Stollman, Neil; Street, Sarah; Sultan, Shahnaz; Vege, Santhi S.; Wani, Sachin B.; Weinberg, David (March 2018). "American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis". Gastroenterology. 154 (4): 1096–1101. doi:10.1053/j.gastro.2018.01.032. PMID   29409760.
  36. ↑ Besselink MG, van Santvoort HC, Boermeester MA, Nieuwenhuijs VB, van Goor H, Dejong CH, Schaapherder AF, Gooszen HG (March 2009). "Timing and impact of infections in acute pancreatitis". The British Journal of Surgery. 96 (3): 267–73. doi: 10.1002/bjs.6447 . PMID   19125434. S2CID   2226746.
  37. ↑ Wu BU, Johannes RS, Kurtz S, Banks PA (September 2008). "The impact of hospital-acquired infection on outcome in acute pancreatitis". Gastroenterology. 135 (3): 816–20. doi:10.1053/j.gastro.2008.05.053. PMC   2570951 . PMID   18616944.
  38. ↑ Jafri NS, Mahid SS, Idstein SR, Hornung CA, Galandiuk S (June 2009). "Antibiotic prophylaxis is not protective in severe acute pancreatitis: a systematic review and meta-analysis". American Journal of Surgery. 197 (6): 806–13. doi:10.1016/j.amjsurg.2008.08.016. PMID   19217608.
  39. ↑ Canlas KR, Branch MS (December 2007). "Role of endoscopic retrograde cholangiopancreatography in acute pancreatitis". World Journal of Gastroenterology. 13 (47): 6314–20. doi: 10.3748/wjg.v13.i47.6314 . PMC   4205448 . PMID   18081218.
  40. ↑ Apostolakos MJ, Papadakos PJ (2001). The Intensive Care Manual. McGraw-Hill Professional. ISBN   978-0-07-006696-0.
  41. ↑ DeCherney AH, Lauren N (2003). Current Obstetric & Gynecologic Diagnosis & Treatment. McGraw-Hill Professional. ISBN   978-0-8385-1401-6.
  42. ↑ Peitzman AB, Schwab CW, Yealy DM, Fabian TC (2007). The Trauma Manual: Trauma and Acute Care Surgery. Lippincott Williams & Wilkins. ISBN   978-0-7817-6275-5.
  43. ↑ Larvin M, McMahon MJ (July 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. S2CID   26047869.
  44. ↑ Yeung YP, Lam BY, Yip AW (May 2006). "APACHE system is better than Ranson system in the prediction of severity of acute pancreatitis". Hepatobiliary & Pancreatic Diseases International. 5 (2): 294–9. PMID   16698595. Archived from the original on 2006-10-26.
  45. 1 2 Chatzicostas C, Roussomoustakaki M, Vlachonikolis IG, Notas G, Mouzas I, Samonakis D, Kouroumalis EA (November 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. S2CID   27166241.
  46. ↑ Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH (February 1990). "Acute pancreatitis: value of CT in establishing prognosis". Radiology. 174 (2): 331–6. doi:10.1148/radiology.174.2.2296641. PMID   2296641.
  47. ↑ 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?" (PDF). Abdominal Imaging. 32 (1): 111–5. doi:10.1007/s00261-006-9034-y. PMID   16944038. S2CID   20809378.
  48. ↑ Leung TK, Lee CM, Lin SY, Chen HC, Wang HJ, Shen LK, Chen YY (October 2005). "Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome". World Journal of Gastroenterology. 11 (38): 6049–52. doi: 10.3748/wjg.v11.i38.6049 . PMC   4436733 . PMID   16273623.
  49. ↑ Vriens PW, van de Linde P, Slotema ET, Warmerdam PE, Breslau PJ (October 2005). "Computed tomography severity index is an early prognostic tool for acute pancreatitis". Journal of the American College of Surgeons. 201 (4): 497–502. doi:10.1016/j.jamcollsurg.2005.06.269. PMID   16183486.
  50. ↑ Triantopoulou C, Lytras D, Maniatis P, Chrysovergis D, Manes K, Siafas I, Papailiou J, Dervenis C (October 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): 238–42. doi:10.1097/MPA.0b013e3180619662. PMID   17895844. S2CID   24245362.
  51. ↑ Mortelé KJ, Mergo PJ, Taylor HM, Wiesner W, Cantisani V, Ernst MD, Kalantari BN, Ros PR (October 2004). "Peripancreatic vascular abnormalities complicating acute pancreatitis: contrast-enhanced helical CT findings". European Journal of Radiology. 52 (1): 67–72. doi:10.1016/j.ejrad.2003.10.006. PMID   15380848.
  52. ↑ Papachristou GI, Muddana V, Yadav D, O'Connell M, Sanders MK, Slivka A, Whitcomb DC (February 2010). "Comparison of BISAP, Ranson's, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis". The American Journal of Gastroenterology. 105 (2): 435–41, quiz 442. doi:10.1038/ajg.2009.622. PMID   19861954. S2CID   41655611.
  53. ↑ Iannuzzi, Jordan P.; King, James A.; Leong, Jessica Hope; Quan, Joshua; Windsor, Joseph W.; Tanyingoh, Divine; Coward, Stephanie; Forbes, Nauzer; Heitman, Steven J.; Shaheen, Abdel-Aziz; Swain, Mark; Buie, Michael; Underwood, Fox E.; Kaplan, Gilaad G. (January 2022). "Global Incidence of Acute Pancreatitis Is Increasing Over Time: A Systematic Review and Meta-Analysis". Gastroenterology. 162 (1): 122–134. doi:10.1053/j.gastro.2021.09.043. PMID   34571026.
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