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Drugs & Diseases > Gastroenterology
ACUTE PANCREATITIS
Updated: Jul 14, 2021
* Author: Jeffrey C F Tang, MD; Chief Editor: BS Anand, MD more...
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Sections
Acute Pancreatitis
* Sections Acute Pancreatitis
* Overview
* Practice Essentials
* Background
* Pathophysiology
* Etiology
* Epidemiology
* Prognosis
* Patient Education
* Show All
* Presentation
* History
* Physical Examination
* Show All
* DDx
* Workup
* Approach Considerations
* Laboratory Studies
* Abdominal Radiography
* Ultrasonography
* Computed Tomography Scanning
* Magnetic Resonance Cholangiopancreatography
* Endoscopic Retrograde Cholangiopancreatography
* Image-Guided Aspiration and Drainage
* Genetic Testing
* Histologic Findings
* Staging
* Show All
* Treatment
* Approach Considerations
* Initial Supportive Care
* Antibiotic Therapy
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Overview
PRACTICE ESSENTIALS
Recognizing patients with severe acute pancreatitis as soon as possible is
critical for achieving optimal outcomes. Management depends largely on severity.
Medical treatment of mild acute pancreatitis is relatively straightforward.
Treatment of severe acute pancreatitis involves intensive care. Surgical
intervention (open or minimally invasive) is indicated in selected cases.
SIGNS AND SYMPTOMS
Symptoms of acute pancreatitis include the following:
* Abdominal pain (cardinal symptom): Characteristically dull, boring, and
steady; usually sudden in onset and gradually becoming more severe until
reaching a constant ache; most often located in the upper abdomen and may
radiate directly through to the back
* Nausea and vomiting, sometimes with anorexia
* Diarrhea
Patients may have a history of the following:
* Recent operative or other invasive procedures
* Family history of hypertriglyceridemia
* Previous biliary colic and binge alcohol consumption (major causes of acute
pancreatitis)
The following physical findings may be noted, varying with the severity of the
disease:
* Fever (76%) and tachycardia (65%); hypotension
* Abdominal tenderness, muscular guarding (68%), and distention (65%);
diminished or absent bowel sounds
* Jaundice (28%)
* Dyspnea (10%); tachypnea; basilar rales, especially in the left lung
* In severe cases, hemodynamic instability (10%) and hematemesis or melena
(5%); pale, diaphoretic, and listless appearance
* Occasionally, extremity muscular spasms secondary to hypocalcemia
The following uncommon physical findings are associated with severe necrotizing
pancreatitis:
* Cullen sign (bluish discoloration around the umbilicus resulting from
hemoperitoneum)
* Grey-Turner sign (reddish-brown discoloration along the flanks resulting from
retroperitoneal blood dissecting along tissue planes); more commonly,
patients may have a ruddy erythema in the flanks secondary to extravasated
pancreatic exudate
* Erythematous skin nodules, usually no larger than 1 cm and typically located
on extensor skin surfaces; polyarthritis
See Presentation for more detail.
DIAGNOSIS
Once a working diagnosis of acute pancreatitis is reached, laboratory tests are
obtained to support the clinical impression, such as the following:
* Serum amylase and lipase
* Liver-associated enzymes
* Blood urea nitrogen (BUN), creatinine, and electrolytes
* Blood glucose
* Serum cholesterol and triglyceride
* Complete blood count (CBC) and hematocrit; NLR
* C-reactive protein (CRP)
* Arterial blood gas values
* Serum lactic dehydrogenase (LDH) and bicarbonate
* Immunoglobulin G4 (IgG4): elevated in autoimmune pancreatitis
Diagnostic imaging is unnecessary in most cases but may be obtained when the
diagnosis is in doubt, when pancreatitis is severe, or when a given study might
provide specific information required. Modalities employed include the
following:
* Abdominal radiography (limited role): Kidneys-ureters-bladder (KUB)
radiography with the patient upright is primarily performed to detect free
air in the abdomen
* Abdominal ultrasonography (most useful initial test in determining the
etiology, and is the technique of choice for detecting gallstones)
* Endoscopic ultrasonography (EUS) (used mainly for detection of microlithiasis
and periampullary lesions not easily revealed by other methods)
* Abdominal computed tomography (CT) scanning (generally not indicated for
patients with mild pancreatitis but always indicated for those with severe
acute pancreatitis)
* Endoscopic retrograde cholangiopancreatography (ERCP); to be used with
extreme caution in this disease and never as a first-line diagnostic tool [1]
* Magnetic resonance cholangiopancreatography (MRCP) (not as sensitive as ERCP
but safer and noninvasive)
Other diagnostic modalities include the following:
* CT-guided or EUS-guided aspiration and drainage
* Genetic testing
Acute pancreatitis is broadly classified as either mild or severe. According to
the Atlanta classification, severe acute pancreatitis is signaled by the
following [2] :
* Evidence of organ failure (eg, systolic blood pressure below 90 mm Hg,
arterial partial pressure of oxygen [Pa O2] 60 mm Hg or lower, serum
creatinine level 2 mg/dL or higher, GI bleeding amounting to 500 mL or more
in 24 hours)
* Local complications (eg, necrosis, abscess, pseudocyst)
* Ranson score of 3 or higher or APACHE score of 8 or higher
See Workup for more detail.
MANAGEMENT
Medical management of mild acute pancreatitis is relatively straightforward;
however, patients with severe acute pancreatitis require intensive care.
Initial supportive care includes the following:
* Fluid resuscitation [3]
* Nutritional support
Antibiotic therapy is employed as follows:
* Antibiotics (usually of the imipenem class) should be used in any case of
pancreatitis complicated by infected pancreatic necrosis but should not be
given routinely for fever, especially early in the presentation
* Antibiotic prophylaxis in severe pancreatitis is controversial; routine use
of antibiotics as prophylaxis against infection in severe acute pancreatitis
is not currently recommended
Surgical intervention (open or minimally invasive) is indicated when an anatomic
complication amenable to a mechanical solution is present. Procedures
appropriate for specific conditions involving pancreatitis include the
following:
* Gallstone pancreatitis: Cholecystectomy
* Pancreatic duct disruption: Image-guided percutaneous placement of a drainage
tube into the fluid collection [4] ; stent or tube placement via ERCP; in
refractory cases, distal pancreatectomy or a Whipple procedure
* Pseudocysts: None necessary in most cases; for large or symptomatic
pseudocysts, percutaneous aspiration, endoscopic transpapillary or transmural
techniques, or surgical management
* Infected pancreatic necrosis: Image-guided aspiration; necrosectomy
* Pancreatic abscess: Percutaneous catheter drainage and antibiotics; if no
response, surgical debridement and drainage
See Treatment and Medication for more detail.
Next: Background
BACKGROUND
This article focuses on the recognition and management of acute pancreatitis.
Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest
the gland. The gland sometimes heals without any impairment of function or any
morphologic changes; this process is known as acute pancreatitis. Pancreatitis
can also recur intermittently, contributing to the functional and morphologic
loss of the gland; recurrent attacks are referred to as chronic pancreatitis.
Both forms of pancreatitis may present in the emergency department (ED) with
acute clinical findings. Recognizing patients with severe acute pancreatitis as
soon as possible is critical for achieving optimal outcomes (see Presentation).
Once a working diagnosis of acute pancreatitis is reached, laboratory tests are
obtained to support the clinical impression, to help define the etiology, and to
look for complications. Diagnostic imaging is unnecessary in most cases but may
be obtained when the diagnosis is in doubt, when severe pancreatitis is present,
or when an imaging study might provide specific information needed to answer a
clinical question. Image-guided aspiration may be useful. Genetic testing may be
considered (see Workup).
Management depends largely on severity. Medical treatment of mild acute
pancreatitis is relatively straightforward. Treatment of severe acute
pancreatitis involves intensive care; the goals of medical management are to
provide aggressive supportive care, to decrease inflammation, to limit infection
or superinfection, and to identify and treat complications as appropriate.
Surgical intervention (open or minimally invasive) is indicated in selected
cases (see Treatment).
Previous
Next: Background
PATHOPHYSIOLOGY
NORMAL PANCREATIC FUNCTION
The pancreas is a gland located in the upper posterior abdomen. It is
responsible for insulin production (endocrine pancreas) and the manufacture and
secretion of digestive enzymes (exocrine pancreas) leading to carbohydrate, fat,
and protein metabolism. Approximately 80% of the gross weight of the pancreas
supports exocrine function, and the remaining 20% is involved with endocrine
function. The focus of this article is on the exocrine function of the pancreas.
The pancreas accounts for only 0.1% of total body weight but has 13 times the
protein-producing capacity of the liver and the reticuloendothelial system
combined, which together make up 4% of total body weight. Digestive enzymes are
produced within the pancreatic acinar cells, packaged into storage vesicles
called zymogens, and then released via the pancreatic ductal cells into the
pancreatic duct, where they are secreted into the small intestine to begin the
metabolic process.
In normal pancreatic function, up to 15 different types of digestive enzymes are
manufactured in the rough endoplasmic reticulum, targeted in the Golgi apparatus
and packaged into zymogens as proenzymes. When a meal is ingested, the vagal
nerves, vasoactive intestinal polypeptide (VIP), gastrin-releasing peptide
(GRP), secretin, cholecystokinin (CCK), and encephalins stimulate the release of
these proenzymes into the pancreatic duct.
The proenzymes travel to the brush border of the duodenum, where trypsinogen,
the proenzyme for trypsin, is activated via hydrolysis of an N-terminal
hexapeptide fragment by the brush border enzyme enterokinase. Trypsin then
facilitates the conversion of the other proenzymes into their active forms.
A feedback mechanism exists to limit pancreatic enzyme activation after
appropriate metabolism has occurred. It is hypothesized that elevated levels of
trypsin, having become unbound from digesting food, lead to decreased CCK and
secretin levels, thus limiting further pancreatic secretion.
Because premature activation of pancreatic enzymes within the pancreas leads to
organ injury and pancreatitis, several mechanisms exist to limit this
occurrence. First, proteins are translated into the inactive proenzymes. Later,
posttranslational modification of the Golgi cells allows their segregation into
the unique subcellular zymogen compartments. The proenzymes are packaged in a
paracrystalline arrangement with protease inhibitors.
Zymogen granules have an acidic pH and a low calcium concentration, which are
factors that guard against premature activation until after secretion has
occurred and extracellular factors have triggered the activation cascade. Under
various conditions, disruption of these protective mechanisms may occur,
resulting in intracellular enzyme activation and pancreatic autodigestion
leading to acute pancreatitis.
PATHOGENESIS OF ACUTE PANCREATITIS
Acute pancreatitis may occur when factors involved in maintaining cellular
homeostasis are out of balance. The initiating event may be anything that
injures the acinar cell and impairs the secretion of zymogen granules; examples
include alcohol use, gallstones, and certain drugs.
At present, it is unclear exactly what pathophysiologic event triggers the onset
of acute pancreatitis. It is believed, however, that both extracellular factors
(eg, neural and vascular response) and intracellular factors (eg, intracellular
digestive enzyme activation, increased calcium signaling, and heat shock protein
activation) play a role. In addition, acute pancreatitis can develop when ductal
cell injury leads to delayed or absent enzymatic secretion, as seen in patients
with the CFTR gene mutation.
Once a cellular injury pattern has been initiated, cellular membrane trafficking
becomes chaotic, with the following deleterious effects:
* Lysosomal and zymogen granule compartments fuse, enabling activation of
trypsinogen to trypsin
* Intracellular trypsin triggers the entire zymogen activation cascade
* Secretory vesicles are extruded across the basolateral membrane into the
interstitium, where molecular fragments act as chemoattractants for
inflammatory cells
Activated neutrophils then exacerbate the problem by releasing superoxide (the
respiratory burst) or proteolytic enzymes (cathepsins B, D, and G; collagenase;
and elastase). Finally, macrophages release cytokines that further mediate local
(and, in severe cases, systemic) inflammatory responses. The early mediators
defined to date are tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and
IL-8.
These mediators of inflammation cause an increased pancreatic vascular
permeability, leading to hemorrhage, edema, and eventually pancreatic necrosis.
As the mediators are excreted into the circulation, systemic complications can
arise, such as bacteremia due to gut flora translocation, acute respiratory
distress syndrome (ARDS), pleural effusions, gastrointestinal (GI) hemorrhage,
and renal failure.
The systemic inflammatory response syndrome (SIRS) can also develop, leading to
the development of systemic shock. Eventually, the mediators of inflammation can
become so overwhelming that hemodynamic instability and death ensue.
In acute pancreatitis, parenchymal edema and peripancreatic fat necrosis occur
first; this is known as acute edematous pancreatitis. When necrosis involves the
parenchyma, accompanied by hemorrhage and dysfunction of the gland, the
inflammation evolves into hemorrhagic or necrotizing pancreatitis. Pseudocysts
and pancreatic abscesses can result from necrotizing pancreatitis because
enzymes can be walled off by granulation tissue (pseudocyst formation) or via
bacterial seeding of the pancreatic or peripancreatic tissue (pancreatic abscess
formation).
Li et al compared two sets of patients with severe acute pancreatitis—one with
acute renal failure and the other without it—and determined that a history of
renal disease, hypoxemia, and abdominal compartment syndrome were significant
risk factors for acute renal failure in patients with severe acute pancreatitis.
[5] In addition, patients with acute renal failure were found to have a
significantly greater average length of stay in the hospital and in the
intensive care unit (ICU), as well as higher rates of pancreatic infection and
mortality.
Previous
Next: Background
ETIOLOGY
Long-standing alcohol consumption and biliary stone disease cause most cases of
acute pancreatitis, but numerous other etiologies are known. In 10%-30% of
cases, the cause is unknown, though studies have suggested that as many as 70%
of cases of idiopathic pancreatitis are secondary to biliary microlithiasis.
BILIARY TRACT DISEASE
One of the most common causes of acute pancreatitis in most developed countries
(accounting for approximately 40% of cases) is gallstones passing into the bile
duct and temporarily lodging at the sphincter of Oddi. The risk of a stone
causing pancreatitis is inversely proportional to its size.
It is thought that acinar cell injury occurs secondary to increasing pancreatic
duct pressures caused by obstructive biliary stones at the ampulla of Vater,
although this has not been definitively proven in humans. Occult microlithiasis
is probably responsible for most cases of idiopathic acute pancreatitis.
ALCOHOL
Alcohol use is a major cause of acute pancreatitis (accounting for at least 35%
of cases [6] ). At the cellular level, ethanol leads to intracellular
accumulation of digestive enzymes and their premature activation and release. At
the ductal level, it increases the permeability of ductules, allowing enzymes to
reach the parenchyma and cause pancreatic damage. Ethanol increases the protein
content of pancreatic juice and decreases bicarbonate levels and trypsin
inhibitor concentrations. This leads to the formation of protein plugs that
block pancreatic outflow.
Most commonly, the disease develops in patients whose alcohol ingestion is
habitual over 5-15 years. Alcoholics are usually admitted with an acute
exacerbation of chronic pancreatitis. Occasionally, however, pancreatitis can
develop in a patient with a weekend binging habit, and several case reports have
described a sole large alcohol load precipitating a first attack. Nevertheless,
the alcoholic who imbibes routinely remains the rule rather than the exception
for the development of pancreatitis.
Currently, there is no universally accepted explanation for why certain
alcoholics are more predisposed to developing acute pancreatitis than other
alcoholics who ingest similar quantities.
ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY
Pancreatitis occurring after endoscopic retrograde cholangiopancreatography
(ERCP) is probably the third most common type (accounting for approximately 4%
of cases). Whereas retrospective surveys indicate that the risk is only 1%,
prospective studies have shown the risk to be at least 5%.
The risk of post-ERCP acute pancreatitis is increased if the endoscopist is
inexperienced, if the patient is thought to have sphincter of Oddi dysfunction,
or if manometry is performed on the sphincter of Oddi. Aggressive
preintervention intravenous (IV) hydration has been durably shown to prevent
post-ERCP pancreatitis in randomized studies. More recently, rectal indomethacin
has been employed; it has been shown to reduce the incidence of post-ERCP
pancreatitis and is now widely accepted at most institutions. The literature
continues to debate the role of rectal indomethacin. [7]
TRAUMA
Abdominal trauma (approximately 1.5%) causes an elevation of amylase and lipase
levels in 17% of cases and clinical pancreatitis in 5% of cases. Pancreatic
injury occurs more often in penetrating injuries (eg, from knives, bullets) than
in blunt abdominal trauma (eg, from steering wheels, horses, bicycles). Blunt
injury to the abdomen or back may crush the gland across the spine, leading to a
ductal injury.
DRUGS
Considering the small number of patients who develop pancreatitis compared to
the relatively large number who receive potentially toxic drugs, drug-induced
pancreatitis is a relatively rare occurrence (accounting for approximately 2% of
cases) that is probably related to an unknown predisposition. Fortunately,
drug-induced pancreatitis is usually mild.
Drugs definitely associated with acute pancreatitis include the following:
* Azathioprine
* Sulfonamides
* Sulindac
* Tetracycline
* Valproic acid,
* Didanosine
* Methyldopa
* Estrogens
* Furosemide
* 6-Mercaptopurine
* Pentamidine
* 5-aminosalicylic acid compounds
* Corticosteroids
* Octreotide
Drugs probably associated with acute pancreatitis include the following:
* Chlorothiazide and hydrochlorothiazide
* Methandrostenolone (methandienone)
* Metronidazole
* Nitrofurantoin
* Phenformin
* Piroxicam
* Procainamide
* Colaspase
* Chlorthalidone
* Combination cancer chemotherapy drugs (especially asparaginase)
* Cimetidine
* Cisplatin
* Cytosine arabinoside
* Diphenoxylate
* Ethacrynic acid
In addition, there are many drugs that have been reported to cause acute
pancreatitis in isolated or sporadic cases.
LESS COMMON CAUSES
The following causes each account for less than 1% of cases of pancreatitis.
Infection
Several infectious diseases may cause pancreatitis, especially in children.
These cases of acute pancreatitis tend to be milder than cases of acute biliary
or alcohol-induced pancreatitis.
Viral causes include mumps virus, coxsackievirus, cytomegalovirus (CMV),
hepatitis virus, Epstein-Barr virus (EBV), echovirus, varicella-zoster virus
(VZV), measles virus, and rubella virus. Bacterial causes include Mycoplasma
pneumoniae, Salmonella, Campylobacter, and Mycobacterium tuberculosis.
Worldwide, Ascaris is a recognized cause of pancreatitis resulting from the
migration of worms in and out of the duodenal papillae.
Pancreatitis has been associated with AIDS; however, this may be the result of
opportunistic infections, neoplasms, lipodystrophy, or drug therapies.
Hereditary pancreatitis
Hereditary pancreatitis is an autosomal dominant gain-of-function disorder
related to mutations of the cationic trypsinogen gene (PRSS1), which has an 80%
penetrance. Mutations in this gene cause premature activation of trypsinogen to
trypsin.
In addition, the CFTR mutation plays a role in predisposing patients to acute
pancreatitis by causing abnormalities of ductal secretion. At present, however,
the phenotypic variability of patients with the CFTR mutation is not well
understood. Certainly, patients homozygous for the CFTR mutation are at risk for
pancreatic disease, but it is not yet clear which of the more than 800 mutations
carries the most significant risk. In addition, the role of CFTR heterozygotes
in pancreatic disease is unknown.
Mutations in the SPINK1 protein, which blocks the active binding site of
trypsin, rendering it inactive, also probably play a role in causing a
predisposition to acute pancreatitis.
This probably explains the predisposition, rather than the cause, of acute
pancreatitis in these patients. If enough mutant enzymes become activated
intracellularly, they can overwhelm the first line of defense (ie, pancreatic
secretory trypsin inhibitor) and resist backup defenses (ie, proteolytic
degradation by mesotrypsin, enzyme Y, and trypsin itself). Activated mutant
cationic trypsin can then trigger the entire zymogen activation cascade.
Hypercalcemia
Hypercalcemia from any cause can lead to acute pancreatitis. Causes include
hyperparathyroidism, excessive doses of vitamin D, familial hypocalciuric
hypercalcemia, and total parenteral nutrition (TPN). Routine use of automated
serum chemistries has allowed earlier detection and reduced the frequency of
hypercalcemia manifesting as pancreatitis.
Developmental abnormalities of pancreas
The pancreas develops from two buds stemming from the alimentary tract of the
developing embryo. There are two developmental abnormalities commonly associated
with pancreatitis: pancreas divisum and annular pancreas.
Pancreas divisum is a failure of the dorsal and ventral pancreatic ducts to fuse
during embryogenesis. Probably a variant of normal anatomy, it occurs in
approximately 5% of the population (see the images below); in most cases, it may
actually protect against gallstone pancreatitis. It appears that the presence of
a stenotic minor papillae and an atretic duct of Santorini are additional risk
factors that together contribute to the development of acute pancreatitis
through an obstructive mechanism (although this is controversial).
Acute pancreatitis. This image was obtained from a patient with pancreas divisum
associated with minor papilla stenosis causing recurrent pancreatitis. Because
pancreas divisum is relatively common in the general population, it is best
regarded as a variant of normal anatomy and not necessarily as a cause of
pancreatitis. In this case, note the bulbous contour of the duct adjacent to the
cannula. This appearance has been termed Santorinicele. Dorsal duct outflow
obstruction is a probable cause of pancreatitis when Santorinicele is present,
and it is associated with a minor papilla that accommodates only a guide wire.
View Media Gallery
Acute pancreatitis. Recurrent pancreatitis was associated with pancreas divisum
in an elderly man. The pancreatogram of the dorsal duct shows distal stenosis
with upstream chronic pancreatitis. After the stenosis was dilated and stented,
his pain resolved and the patient improved clinically during 1 year of quarterly
stent exchanges. Follow-up computed tomography (CT) scans showed resolution of
the inflammatory mass. Although ductal biopsies and cytology were repeatedly
negative, the patient's pain and pancreatitis returned when the stents were
removed. He developed duodenal outflow obstruction and was sent to surgery;
during the Whipple procedure, periampullary adenocarcinoma (of minor papilla)
was revealed.
View Media Gallery
Annular pancreas is an uncommon congenital anomaly in which a band of pancreatic
tissue surrounds the second part of the duodenum. Usually, it does not cause
symptoms until later in life. This condition is a rare cause of acute
pancreatitis, probably through an obstructive mechanism.
Sphincter of Oddi dysfunction can lead to acute pancreatitis by causing
increased pancreatic ductal pressures. However, the mechanism of pancreatitis
induced by such dysfunction in patients without elevated sphincter pressures on
manometry remains controversial.
Hypertriglyceridemia
Clinically significant pancreatitis usually does not occur until a person’s
serum triglyceride level reaches 1000 mg/dL. It is associated with type I and
type V hyperlipidemia. Although this view is somewhat controversial, most
authorities believe that the association is caused by the underlying derangement
in lipid metabolism rather than by pancreatitis causing hyperlipidemia. This
type of pancreatitis tends to be more severe than alcohol- or gallstone-induced
disease.
Tumors
Obstruction of the pancreatic ductal system by a pancreatic ductal carcinoma,
ampullary carcinoma, islet cell tumor, solid pseudotumor of the pancreas,
sarcoma, lymphoma, cholangiocarcinoma, or metastatic tumor can cause acute
pancreatitis. The chances of pancreatitis occurring when a tumor is present are
approximately 14%. Pancreatic cystic neoplasms, such as intraductal
papillary-mucinous neoplasm (IPMN), mucinous cystadenoma, or serous cystadenoma,
can also cause pancreatitis.
Toxins
Exposure to organophosphate insecticide can cause acute pancreatitis. Scorpion
and snake bites may also be causative; in Trinidad, the sting of the scorpion
Tityus trinitatis is the most common cause of acute pancreatitis.
Hyperstimulation of pancreas exocrine secretion appears to be the mechanism of
action in both instances.
Surgical procedures
Acute pancreatitis may occur in the postoperative period of various surgical
procedures (eg, abdominal or cardiopulmonary bypass surgery, which may damage
the gland by causing ischemia). Postoperative acute pancreatitis is often a
difficult diagnosis to confirm, and it has a higher complication rate than
pancreatitis associated with other etiologies. The mechanism is unclear.
Vascular abnormalities
Vascular factors, such as ischemia or vasculitis, can play a role in causing
acute pancreatitis. Vasculitis can predispose patients to pancreatic ischemia,
especially in those with polyarteritis nodosa and systemic lupus erythematosus.
Autoimmune pancreatitis
Autoimmune pancreatitis, a relatively newly described entity, is an extremely
rare cause of acute pancreatitis (prevalence, 0.82 per 100,000 individuals).
When it does cause acute pancreatitis, it is usually in young people
(approximately age 40 years) who may also suffer from other autoimmune diseases.
The pathogenesis is unclear, but it is potentially related to immunoglobulin
(Ig) G4 autoimmune disease. [8]
Previous
Next: Background
EPIDEMIOLOGY
UNITED STATES STATISTICS
Acute pancreatitis has an approximate incidence of 40-50 cases per year per
100,000 adults. [9] In 2009, approximately 275,000 hospitalizations were
attributed to acute pancreatitis. [10] In 2007, approximately 220,000 patients
with acute pancreatitis were admitted to non–federally funded hospitals. In
1998, 183,000 patients with acute pancreatitis were admitted. This trend in
rising incidence has been recognized over the past several decades. [9, 11, 12,
13]
INTERNATIONAL STATISTICS
Worldwide, the incidence of acute pancreatitis ranges between 5 and 80 per
100,000 population, with the highest incidence recorded in the United States and
Finland. [14] In Luneburg, Germany, the incidence is 17.5 cases per 100,000
people. In Finland, the incidence is 73.4 cases per 100,000 people. Similar
incidence rates have been reported in Australia. The incidence of disease
outside North America, Europe, and Australia is less well known.
In Europe and other developed nations, such as Hong Kong, more patients tend to
have gallstone pancreatitis, whereas in the United States, alcoholic
pancreatitis is most common.
AGE-RELATED DEMOGRAPHICS
The median age at onset depends on the etiology. [15] The following are median
ages of onset for various etiologies:
* Alcohol-related - 39 years
* Biliary tract–related - 69 years
* Trauma-related - 66 years
* Drug-induced etiology - 42 years
* ERCP-related - 58 years
* AIDS-related - 31 years
* Vasculitis-related - 36 years
Hospitalization rates increase with age. For people aged 35-75 years, the rate
doubles for males and quadruples for females.
SEX-RELATED DEMOGRAPHICS
Generally, acute pancreatitis affects males more often than females. In males,
the etiology is more often related to alcohol; in females, it is more often
related to biliary tract disease. Idiopathic pancreatitis has no clear
predilection for either sex.
RACE-RELATED DEMOGRAPHICS
The hospitalization rates of patients with acute pancreatitis per 100,000
population are 3 times higher for blacks than whites. These racial differences
are more pronounced for males than females. The risk for African Americans aged
35-64 years is 10 times higher than for any other group. African Americans are
at a higher risk than whites in that same age group.
The annual incidence of acute pancreatitis in Native Americans is 4 per 100,000
population; in whites, 5.7 per 100,000 population; and in blacks, 20.7 per
100,000 population. [16]
Previous
Next: Background
PROGNOSIS
The overall mortality in patients with acute pancreatitis is 10%-15%. Patients
with biliary pancreatitis tend to have a higher mortality than patients with
alcoholic pancreatitis. This rate has been falling over the last 2 decades as
improvements in supportive care have been initiated. Type 2 diabetes mellitus
has also been associated with higher severity and mortality in the setting of
acute pancreatitis. [17] In patients with severe disease (organ failure), who
account for about 20% of presentations, mortality is approximately 30%. [18]
This figure has not decreased in the past 10 years. In patients with pancreatic
necrosis without organ failure, the mortality approaches zero.
In the first week of illness, most deaths result from multiorgan system failure.
In subsequent weeks, infection plays a more significant role, but organ failure
still constitutes a major cause of mortality. Acute respiratory distress
syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and
hypotensive shock all may be systemic manifestations of acute pancreatitis in
its most severe form.
Identifying patients in the greatest need of aggressive medical treatment by
differentiating their disease severity as mild or severe is recommended. In mild
disease, the pancreas exhibits interstitial edema, an inflammatory infiltrate
without hemorrhage or necrosis, and, usually, minimal or no organ dysfunction.
In severe disease, the inflammatory infiltrate is severe, associated with
necrosis of the parenchyma, often accompanied by evidence of severe gland
dysfunction, and it may be associated with multiorgan system failure.
Different strategies have been used to assess the severity of acute pancreatitis
and predict outcome (see Workup and Staging). Several clinical scoring systems
(eg, Ranson criteria, Glasgow, Imrie) are available. The APACHE II scoring
system, though cumbersome, appears to be the best validated (see the APACHE II
Scoring System calculator). Biological markers have also been used for this
purpose. Genetic markers are being studied and have not yet come into clinical
use.
Peritoneal lavage has a high specificity (93%); however, it has a low
sensitivity (54%). Dynamic CT scanning of the abdomen is widely available and
useful in predicting the outcome of acute pancreatitis. When the Balthazar
criteria (see Workup and Computed Tomography Scanning) are used, sensitivity is
87% and specificity is 88%.
Suppiah et al examined the prognostic value of the neutrophil-lymphocyte ratio
(NLR) in 146 consecutive patients with acute pancreatitis. [19] They found that
elevation of the NLR during the first 48 hours of hospital admission was
significantly associated with severe acute pancreatitis and was an independent
negative prognostic indicator. The NLR is calculated from the white cell
differential and provides an indication of inflammation.
Khan et al examined the prognostic value of Modified Early Warning Score (MEWS)
in identifying severe acute pancreatitis in 200 patients admitted to a single
institution. [20] The investigators tracked the highest and mean daily scores.
They found that patients with a high MEWS value > 2 on day one or mean value >
1.2 on day two was most accurate in predicting severe acute pancreatitis. The
investigators concluded that MEWS is a reliable, safe, and inexpensive score
that can be used easily at all levels of health care for prognosticating
patients with acute pancreatitis.
In a retrospective study of data from 822 patients hospitalized with acute
pancreatitis, Mikolasevic et al found that patients who had nonalcoholic fatty
liver at admission (n = 198; 24.1%) had a statistically higher incidence of
moderately severe (35.4% vs 14.6%) and severe acute pancreatitis (20.7% vs 9.6%)
than those without nonalcoholic fatty liver. [21] Moreover, these patients had
higher (1) C-reactive protein levels not only on the day of admission but also
at day 3, (2) APACHE II scores at admission, (3) CT scan severity index, and (4)
occurrence of organ failure and local complications. Although mortality was also
higher in the nonalcoholic fatty liver group compared to the group without this
disease, the difference was not statistically significant. [21]
COMPLICATIONS
Acute fluid collections may occur, typically early in the course of acute
pancreatitis. These are primarily detected by imaging studies rather than by
physical examination. Because they lack a defined wall and usually regress
spontaneously, most acute fluid collections require no specific therapy.
An acute pseudocyst is a collection of pancreatic fluid that is walled off by
granulation tissue after an episode of acute pancreatitis; it requires 4 or more
weeks to develop. Although pseudocysts are sometimes palpable on physical
examination, they are usually detected with abdominal ultrasonography or
computed tomography (CT).
Intra-abdominal infection is common. Within the first 1-3 weeks, fluid
collections or pancreatic necrosis can become infected and jeopardize clinical
outcome. From 3 to 6 weeks, pseudocysts may become infected or a pancreatic
abscess may develop. A pancreatic abscess is a circumscribed intra-abdominal
collection of pus, within or in proximity to the pancreas. It is believed to
arise from localized necrosis, with subsequent liquefaction that becomes
infected.
The intestinal flora is the predominant source of bacteria causing the
infection. The usual suspects are Escherichia coli (26%), Pseudomonas species
(16%), Staphylococcus species (15%), Klebsiella species (10%), Proteus species
(10%), Streptococcus species (4%), Enterobacter species (3%), and anaerobic
organisms (16%). Fungal superinfections may occur weeks or months into the
course of severe necrotizing pancreatitis.
Pancreatic necrosis is a nonviable area of pancreatic parenchyma that is often
associated with peripancreatic fat necrosis and is principally diagnosed with
the aid of dynamic spiral CT scans. Distinguishing between infected and sterile
pancreatic necrosis is an ongoing clinical challenge. Sterile pancreatic
necrosis is usually treated with aggressive medical management, whereas almost
all patients with infected pancreatic necrosis require surgical debridement or
percutaneous drainage if they are to survive.
Hemorrhage into the gastrointestinal (GI) tract, retroperitoneum, or the
peritoneal cavity is possible because of erosion of large vessels. Intestinal
obstruction or necrosis may occur. Common bile duct obstruction may be caused by
a pancreatic abscess, pseudocyst, or biliary stone that caused the pancreatitis.
An internal pancreatic fistula from pancreatic duct disruption or a leaking
pancreatic pseudocyst may occur.
In the weeks (to months) following presentation, the physician’s attention
shifts to developing signs of intra-abdominal infection, pancreatic pseudocyst,
intra-abdominal hemorrhage, colon perforation, obstruction or fistulization, and
multiorgan system failure.
Previous
Next: Background
PATIENT EDUCATION
Educate patients about the disease, and advise them to avoid alcohol in binge
amounts and to discontinue any risk factor, such as fatty meals and abdominal
trauma.
For patient education resources, see the Cholesterol Center, as well as
Pancreatitis and Gallstones.
Previous
Clinical Presentation
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51. Duzenci D, Yalnız M, Ispiroglu M. Comparison between prognostic indicators
in organ insufficiency with acute pancreatitis. Ulus Travma Acil Cerrahi
Derg. 2021 Jul. 27(4):410-20. [QxMD MEDLINE Link].
Media Gallery
* Acute pancreatitis. Suspected acute pancreatitis. Etiologic factors and forms
of acute pancreatitis. Ranson criteria.
* Acute pancreatitis. Mild pancreatitis. Favorable prognostic signs for acute
pancreatitis. Medical management and studies used for acute pancreatitis.
* Acute pancreatitis. Prognostic indicators for severe pancreatitis and
intensive care unit management.
* Acute pancreatitis. Diagnosis and treatment of necrotizing pancreatitis.
* Acute pancreatitis. Treatment of and studies used for pancreatic pseudocysts.
* Acute pancreatitis. Idiopathic recurrent pancreatitis. Etiologies for acute
pancreatitis.
* Acute pancreatitis. Pancreatic abscess. Definition of an abscess.
* Acute pancreatitis. A patient with acute gallstone pancreatitis underwent
endoscopic retrograde cholangiopancreatography. The cholangiogram showed no
stones in the common bile duct and multiple small stones in the gallbladder.
The pancreatogram shows narrowing of the pancreatic duct in the area of genu,
resulting from extrinsic compression of the ductal system by inflammatory
changes in the pancreas.
* Acute pancreatitis. This image was obtained from a patient with pancreas
divisum associated with minor papilla stenosis causing recurrent
pancreatitis. Because pancreas divisum is relatively common in the general
population, it is best regarded as a variant of normal anatomy and not
necessarily as a cause of pancreatitis. In this case, note the bulbous
contour of the duct adjacent to the cannula. This appearance has been termed
Santorinicele. Dorsal duct outflow obstruction is a probable cause of
pancreatitis when Santorinicele is present, and it is associated with a minor
papilla that accommodates only a guide wire.
* Acute pancreatitis. A normal-appearing ventral pancreas is seen in a patient
with recurrent acute pancreatitis. Dorsal pancreas (not pictured) showed
evidence of chronic pancreatitis.
* Acute pancreatitis. Endoscopic retrograde cholangiopancreatography excluded
suppurative cholangitis and established the presence of anular pancreas
divisum. The dorsal pancreatogram showed extravasation into the
retroperitoneum, and sphincterotomy was performed on the minor papilla. A
pigtail nasopancreatic tube was then inserted into the dorsal duct and out
into the retroperitoneal fluid collection. The other end of the tube was
attached to bulb suction and monitored every shift.
* Acute pancreatitis. Although percutaneous drains remove loculated fluid
collections elsewhere in the abdomen, a nasopancreatic tube drains the
retroperitoneal fluid collection. One week later, the retroperitoneal fluid
collection was much smaller (the image is reversed in a horizontal
direction). By this time, the patient was off pressors and was ready to be
extubated.
* Acute pancreatitis. Recurrent pancreatitis was associated with pancreas
divisum in an elderly man. The pancreatogram of the dorsal duct shows distal
stenosis with upstream chronic pancreatitis. After the stenosis was dilated
and stented, his pain resolved and the patient improved clinically during 1
year of quarterly stent exchanges. Follow-up computed tomography (CT) scans
showed resolution of the inflammatory mass. Although ductal biopsies and
cytology were repeatedly negative, the patient's pain and pancreatitis
returned when the stents were removed. He developed duodenal outflow
obstruction and was sent to surgery; during the Whipple procedure,
periampullary adenocarcinoma (of minor papilla) was revealed.
of 13
TABLES
* Table 1. Risk Factors for Post-ERCP Pancreatitis.
Table 1. Risk Factors for Post-ERCP Pancreatitis.
Acute pancreatitis (any) or a history of post-ERCP pancreatitis Younger age
Female sex Absence of bile duct stones More than 10 attempts to cannulate the
papilla of Vater Pancreatic duct cannulation Contrast medium injection of the
pancreatic system Pancreatic sphincterotomy Sphincter of Oddi dysfunction
Back to List
CONTRIBUTOR INFORMATION AND DISCLOSURES
Author
Jeffrey C F Tang, MD Senior Staff Gastroenterologist, Henry Ford Health System
Jeffrey C F Tang, MD is a member of the following medical societies: American
College of Gastroenterology, American College of Physicians, American Medical
Association, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Coauthor(s)
Johnathon T Markus, MD Fellow, Department of Gastroenterology, Henry Ford
Hospital
Johnathon T Markus, MD is a member of the following medical societies: American
Association for the Study of Liver Diseases, American Gastroenterological
Association, American Medical Association, American Society for Gastrointestinal
Endoscopy
Disclosure: Nothing to disclose.
Chief Editor
BS Anand, MD Professor, Department of Internal Medicine, Division of
Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American
Association for the Study of Liver Diseases, American College of
Gastroenterology, American Gastroenterological Association, American Society for
Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Acknowledgements
Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical
Center
Tushar Patel, MB, ChB is a member of the following medical societies: American
Association for the Study of Liver Diseases and American Gastroenterological
Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of
Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug
Reference
Disclosure: Medscape Salary Employment
Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie
University, Halifax, Nova Scotia, Canada; Professor, Department of Internal
Medicine, Division of Gastroenterology, University of Alberta, Edmonton,
Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College
of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Paul Yakshe, MD Assistant Professor of Medicine, University of Minnesota,
Medical Director of Pancreas and Biliary Clinic, Department of Medicine,
Division of Gastroenterology, Hepatology, and Nutrition, Fairview University
Medical Center
Paul Yakshe, MD is a member of the following medical societies: American College
of Gastroenterology, American Pancreatic Association, and American Society for
Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
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