Acute Pancreatitis Medscape

8/18/2019 Acute Pancreatitis Medscape

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Practice Essentials

Recognizing patients with severe acute pancreatitis as soon as possible is critical for

achieving optimal outcomes. Management depends largely on severity. Medical treatmentof 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.

Essential update! "#" releases new guidelines for diagnosis$management ofasymptomatic neoplastic pancreatic cysts

The "merican #astroenterological "ssociation recommends the following in the

diagnosis and management of asymptomatic neoplastic pancreatic cysts%&' !

or asymptomatic mucinous cysts) a *+year interval is recommended for a cyst of any

size undergoing surveillance) with surveillance being stopped after , years if there is nochange.

Perform surgery only if there is more than one concerning feature on MR- confirmed onendoscopic ultrasonography (ES and only in centers with high volumes of pancreatic

surgery) and there should be no surveillance after surgery if there is no invasive cancer ordysplasia.

The ris/ of malignant transformation of pancreatic cysts is appro0imately 1.*23 per year)

and the ris/ of cancer in cysts without a significant change over a ,+year period is li/ely

to be lower.

The small ris/ of malignant progression in stable cysts is li/ely outweighed by the costs

of surveillance and the ris/s of surgery.

Positive cytology on ES+guided fine+needle aspiration (4" has the highest specificity

for diagnosing malignancy5 if there is a combination of high+ris/ features on imaging)then this is li/ely to increase the ris/ of malignancy even further. Similarly) if a cyst has

both a solid component and a dilated pancreatic duct (confirmed on both ES and MR-)

the specificity for malignancy is li/ely to be high even in the absence of positivecytology.

There is lower immediate postoperative mortality) as well as long+term mortality) for

patients who undergo surgery in high+volume pancreatic centers.

-t seems sensible to offer screening even after the cyst has been resected) provided the patients have not undergone total pancreatectomy. Surveillance should continue as longas the patient remains a good candidate for surgery. MR- every * years may be a

reasonable approach for these patients. The clinician may elect to offer more fre6uent

surveillance in the case of invasive cancer resection) particularly if there is concern thatthe lesion has not been fully resected.

Signs and symptoms



Symptoms of acute pancreatitis include the following!

"bdominal pain (cardinal symptom! 7haracteristically dull) boring) and steady5 usually

sudden in onset and gradually becoming more severe until reaching a constant ache5 mostoften located in the upper abdomen and may radiate directly through to the bac/

4ausea and vomiting) sometimes with anore0ia

8iarrhea

Patients may have a history of the following!

Recent operative or other invasive procedures

amily history of hypertriglyceridemia

Previous biliary colic and binge alcohol consumption (ma9or causes of acute pancreatitis

The following physical findings may be noted) varying with the severity of the disease!

ever (:;3 and tachycardia (;,35 hypotension

"bdominal tenderness) muscular guarding (;<3) and distention (;,35 diminished or

absent bowel sounds

=aundice (*<3

8yspnea (&135 tachypnea5 basilar rales) especially in the left lung

-n severe cases) hemodynamic instability (&13 and hematemesis or melena (,35 pale)diaphoretic) and listless appearance

>ccasionally) e0tremity muscular spasm secondary to hypocalcemia

The following uncommon physical findings are associated with severe necrotizing

pancreatitis!

7ullen sign (bluish discoloration around the umbilicus resulting from hemoperitoneum

#rey+Turner sign (reddish+brown discoloration along the flan/s resulting from

retroperitoneal blood dissecting along tissue planes5 more commonly) patients may have

a ruddy erythema in the flan/s secondary to e0travasated pancreatic e0udate

Erythematous s/in nodules) usually no larger than & cm and typically located on e0tensors/in surfaces5 polyarthritis



See 7linical Presentation for more detail.

8iagnosis

>nce a wor/ing diagnosis of acute pancreatitis is reached) laboratory tests are obtained to

support the clinical impression) such as the following!

Serum amylase and lipase

?iver+associated enzymes

@lood urea nitrogen (@4) creatinine) and electrolytes

@lood glucose

Serum cholesterol and triglyceride

7omplete blood count (7@7 and hematocrit5 4?R

7+reactive protein (7RP

"rterial blood gas values

Serum lactic dehydrogenase (?8A and bicarbonate

-mmunoglobulin #2 (-g#2

8iagnostic 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 specificinformation re6uired. Modalities employed include the following!

"bdominal radiography (limited role! Bidneys+ureters+bladder (B@ radiography withthe patient upright is primarily performed to detect free air in the abdomen

"bdominal ultrasonography (most useful initial test in determining the etiology) and is

the techni6ue of choice for detecting gallstones

Endoscopic ultrasonography (ES (used mainly for detection of microlithiasis and periampullary lesions not easily revealed by other methods

"bdominal computed tomography (7T scanning (generally not indicated for patients

with mild pancreatitis but always indicated for those with severe acute pancreatitis

Endoscopic retrograde cholangiopancreatography (ER7P5 to be used with e0treme

caution in this disease and never as a first+line diagnostic tool %*'

Magnetic resonance cholangiopancreatography (MR7P5 not as sensitive as ER7P but

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safer and noninvasive

>ther diagnostic modalities include the following!

7T+guided or ES+guided aspiration and drainage

#enetic testing

"cute pancreatitis is broadly classified as either mild or severe. "ccording to the "tlantaclassification) severe acute pancreatitis is signaled by the following%C' !

Evidence of organ failure (eg) systolic blood pressure below D1 mm Ag) arterial partial

pressure of o0ygen %P a > *' ;1 mm Ag or lower) serum creatinine level * mg$d? or

higher) #- bleeding amounting to ,11 m? or more in *2 hours

?ocal complications (eg) necrosis) abscess) pseudocyst

Ranson score of C or higher or "P"7AE score of < or higher

See or/up for more detail.

Management

Medical management of mild acute pancreatitis is relatively straightforward5 however)

patients with severe acute pancreatitis re6uire intensive care.

-nitial supportive care includes the following!

luid resuscitation %2'

4utritional support

"ntibiotic therapy is employed as follows!

"ntibiotics (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

"ntibiotic prophyla0is in severe pancreatitis is controversial5 routine use of antibiotics as prophyla0is 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!

#allstone pancreatitis! 7holecystectomy

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Pancreatic duct disruption! -mage+guided percutaneous placement of a drainage tube into

the fluid collection %,' 5 stent or tube placement via ER7P5 in refractory cases) distal

pancreatectomy or a hipple procedure

Pseudocysts! 4one necessary in most cases5 for large or symptomatic pseudocysts)

percutaneous aspiration) endoscopic transpapillary or transmural techni6ues) or surgicalmanagement

-nfected pancreatic necrosis! -mage+guided aspiration5 necrosectomy

Pancreatic abscess! Percutaneous catheter drainage and antibiotics5 if no response)surgical debridement and drainage

See Treatment and Medication for more detail.

@ac/ground

This article focuses on the recognition and management of acute pancreatitis. Pancreatitisis an inflammatory process in which pancreatic enzymes autodigest the gland. The glandsometimes heals without any impairment of function or any morphologic changes5 this

process is /nown as acute pancreatitis. Pancreatitis can also recur intermittently)

contributing to the functional and morphologic loss of the gland5 recurrent attac/s arereferred to as chronic pancreatitis.

@oth forms of pancreatitis may present in the emergency department (E8 with acute

clinical findings. Recognizing patients with severe acute pancreatitis as soon as possible

is critical for achieving optimal outcomes (see Presentation.

>nce a wor/ing diagnosis of acute pancreatitis is reached) laboratory tests are obtained to

support the clinical impression) to help define the etiology) and to loo/ for complications.8iagnostic imaging is unnecessary in most cases but may be obtained when the diagnosis

is in doubt) when severe pancreatitis is present) or when a given imaging study might

provide specific information needed to answer a clinical 6uestion. -mage+guidedaspiration may be useful. #enetic testing may be considered (see or/up.

Management depends largely on severity. Medical treatment of mild acute pancreatitis is

relatively straightforward. Treatment of severe acute pancreatitis involves intensive care5

the goals of medical management are to provide aggressive supportive care) to decreaseinflammation) 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.

Pathophysiology

4ormal pancreatic function

The pancreas is a gland located in the upper posterior abdomen. -t is responsible forinsulin production (endocrine pancreas and the manufacture and secretion of digestive

enzymes (e0ocrine pancreas leading to carbohydrate) fat) and protein metabolism.

"ppro0imately <13 of the gross weight of the pancreas supports e0ocrine function) and

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the remaining *13 is involved with endocrine function. The focus of this article is on the

e0ocrine function of the pancreas.

The pancreas accounts for only 1.&3 of total body weight but has &C times the protein+

producing capacity of the liver and the reticuloendothelial system combined) whichtogether ma/e up 23 of total body weight. 8igestive enzymes are produced within the

pancreatic acinar cells) pac/aged into storage vesicles called zymogens) and then released

via the pancreatic ductal cells into the pancreatic duct) where they are secreted into thesmall intestine to begin the metabolic process.

-n normal pancreatic function) up to &, different types of digestive enzymes are

manufactured in the rough endoplasmic reticulum) targeted in the #olgi apparatus and

pac/aged into zymogens as proenzymes. hen a meal is ingested) the vagal nerves)vasoactive intestinal polypeptide (F-P) gastrin+releasing peptide (#RP) secretin)

cholecysto/inin (77B) and encephalins stimulate 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 4+terminal he0apeptide fragment by the brush border enzyme entero/inase. Trypsin then facilitates the conversion of the

other proenzymes to their active forms.

" feedbac/ mechanism e0ists to limit pancreatic enzyme activation after appropriate

metabolism has occurred. -t is hypothesized that elevated levels of trypsin) having become unbound from digesting food) lead to decreased 77B and secretin levels) thus

limiting further pancreatic secretion.

@ecause premature activation of pancreatic enzymes within the pancreas leads to organ

in9ury and pancreatitis) several mechanisms e0ist to limit this occurrence. irst) proteins

are translated into the inactive proenzymes. ?ater) posttranslational modification of the#olgi cells allows their segregation into the uni6ue subcellular zymogen compartments.

The proenzymes are pac/aged in a paracrystalline arrangement with protease inhibitors.

Gymogen granules have an acidic pA and a low calcium concentration) which are factors

that guard against premature activation until after secretion has occurred and e0tracellular factors have triggered the activation cascade. nder 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

"cute pancreatitis may occur when factors involved in maintaining cellular homeostasisare out of balance. The initiating event may be anything that in9ures the acinar cell and

impairs the secretion of zymogen granules5 e0amples include alcohol use) gallstones) and

certain drugs.

"t present) it is unclear e0actly what pathophysiologic event triggers the onset of acute pancreatitis. -t is believed) however) that both e0tracellular factors (eg) neural and

vascular response and intracellular factors (eg) intracellular digestive enzyme activation)

increased calcium signaling) and heat shoc/ protein activation play a role. -n addition)



acute pancreatitis can develop when ductal cell in9ury leads to delayed or absent

enzymatic secretion) as seen in patients with the 7TR gene mutation.

>nce a cellular in9ury pattern has been initiated) cellular membrane traffic/ing becomes

chaotic) with the following deleterious effects!

?ysosomal and zymogen granule compartments fuse) enabling activation of trypsinogen

to trypsin

-ntracellular trypsin triggers the entire zymogen activation cascade

Secretory vesicles are e0truded across the basolateral membrane into the interstitium)

where molecular fragments act as chemoattractants for inflammatory cells

"ctivated neutrophils then e0acerbate the problem by releasing supero0ide (the

respiratory burst or proteolytic enzymes (cathepsins @) 8) and #5 collagenase5 and

elastase. inally) macrophages release cyto/ines that further mediate local (and) in

severe cases) systemic inflammatory responses. The early mediators defined to date aretumor necrosis factor+alpha (T4+H) interleu/in (-?+;) and -?+<.

These mediators of inflammation cause an increased pancreatic vascular permeability)

leading to hemorrhage) edema) and eventually pancreatic necrosis. "s the mediators are

e0creted into the circulation) systemic complications can arise) such as bacteremia due togut flora translocation) acute respiratory distress syndrome ("R8S) pleural effusions)

gastrointestinal (#- hemorrhage) and renal failure.

The systemic inflammatory response syndrome (S-RS can also develop) leading to the

development of systemic shoc/. Eventually) the mediators of inflammation can become

so overwhelming to the body that hemodynamic instability and death ensue.-n acute pancreatitis) parenchymal edema and peripancreatic fat necrosis occur first5 this

is /nown as acute edematous pancreatitis. hen 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 resultfrom necrotizing pancreatitis because enzymes can be walled off by granulation tissue

(pseudocyst formation or via bacterial seeding of pancreatic or peripancreatic tissue

(pancreatic abscess formation.

?i et al compared * set of patients with severe acute pancreatitisIone with acute renalfailure and the other without itIand determined that a history of renal disease)

hypo0emia) and abdominal compartment syndrome are significant ris/ factors for acuterenal failure in patients with severe acute pancreatitis.%;' -n addition) patients with acuterenal failure were found to have a significantly greater average length of stay in the

hospital and in the intensive care unit (-7) as well as higher rates of pancreatic

infection and mortality.

Etiology

?ong+standing alcohol consumption and biliary stone disease cause most cases of acute






pancreatitis) but numerous other etiologies are /nown. -n &1+C13 of cases) the cause is

un/nown) though studies have suggested that as many as :13 of cases of idiopathic

pancreatitis are secondary to biliary microlithiasis.

@iliary tract disease

>ne of the most common causes of acute pancreatitis in most developed countries(accounting for appro0imately 213 of cases is gallstones passing into the bile duct and

temporarily lodging at the sphincter of >ddi. The ris/ of a stone causing pancreatitis is

inversely proportional to its size.

-t is thought that acinar cell in9ury occurs secondary to increasing pancreatic duct pressures caused by obstructive biliary stones at the ampulla of Fater) although this has

not been definitively proven in humans. >ccult microlithiasis is probably responsible for

most cases of idiopathic acute pancreatitis.

"lcohol

"lcohol use is a ma9or cause of acute pancreatitis (accounting for at least C,3 of cases%:'. "t the cellular level) ethanol leads to intracellular accumulation of digestive enzymes

and their premature activation and release. "t 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 9uice anddecreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the

formation of protein plugs that bloc/ pancreatic outflow.

Most commonly) the disease develops in patients whose alcohol ingestion is habitual over

,+&, years. "lcoholics are usually admitted with an acute e0acerbation of chronic pancreatitis. >ccasionally) however) pancreatitis can develop in a patient with a wee/end

binging habit) and several case reports have described a sole large alcohol load

precipitating a first attac/. 4evertheless) the alcoholic who imbibes routinely remains therule rather than the e0ception.

7urrently) there is no universally accepted e0planation for why certain alcoholics are

more predisposed to developing acute pancreatitis than other alcoholics who ingest

similar 6uantities.

Endoscopic retrograde cholangiopancreatography

Pancreatitis occurring after endoscopic retrograde cholangiopancreatography (ER7P is

probably the third most common type (accounting for appro0imately 23 of cases.hereas retrospective surveys indicate that the ris/ is only &3) prospective studies have

shown the ris/ to be at least ,3.

The ris/ of post+ER7P acute pancreatitis is increased if the endoscopist is ine0perienced)

if the patient is thought to have sphincter of >ddi dysfunction) or if manometry is performed on the sphincter of >ddi. 4o medical measures) with the e0ception of

aggressive preintervention intravenous (-F hydration) have been durably shown to

prevent post+ER7P pancreatitis in randomized studies.



Trauma

"bdominal trauma (appro0imately &.,3 causes an elevation of amylase and lipase levels

in &:3 of cases and clinical pancreatitis in ,3 of cases. Pancreatic in9ury occurs more

often in penetrating in9uries (eg) from /nives) bullets than in blunt abdominal trauma (eg)from steering wheels) horses) bicycles. @lunt in9ury to the abdomen or bac/ may crush

the gland across the spine) leading to a ductal in9ury.

8rugs

7onsidering the small number of patients who develop pancreatitis compared to the

relatively large number who receive potentially to0ic drugs) drug+induced pancreatitis is arelatively rare occurrence (accounting for appro0imately *3 of cases that is probably

related to an un/nown predisposition. ortunately) drug+induced pancreatitis is usually

mild.

8rugs definitely associated with acute pancreatitis include the following!

"zathioprine

Sulfonamides

Sulindac

Tetracycline

Falproic acid)

8idanosine

Methyldopa

Estrogens

urosemide

;+Mercaptopurine

Pentamidine

,+aminosalicylic acid compounds

7orticosteroids

>ctreotide

8rugs probably associated with acute pancreatitis include the following!



7hlorothiazide and hydrochlorothiazide

Methandrostenolone (methandienone

Metronidazole

4itrofurantoin

Phenformin

Piro0icam

Procainamide

7olaspase

7hlorthalidone

7ombination cancer chemotherapy drugs (especially asparaginase

7imetidine

7isplatin

7ytosine arabinoside

8ipheno0ylate

Ethacrynic acid

-n addition) there are many drugs that have been reported to cause acute pancreatitis in

isolated or sporadic cases.

?ess common causes

The following causes each account for less than &3 of cases of pancreatitis.

-nfection

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.

Firal causes include mumps virus) co0sac/ievirus) cytomegalovirus (7MF) hepatitis

virus) Epstein+@arr virus (E@F) echovirus) varicella+zoster virus (FGF) measles virus)

and rubella virus. @acterial causes include Mycoplasma pneumoniae) Salmonella)7ampylobacter) and Mycobacterium tuberculosis. orldwide) "scaris is a recognized

cause of pancreatitis resulting from the migration of worms in and out of the duodenal



papillae.

Pancreatitis has been associated with "-8S5 however) this may be the result of

opportunistic infections) neoplasms) lipodystrophy) or drug therapies.

Aereditary pancreatitis

Aereditary pancreatitis is an autosomal dominant gain+of+function disorder related to

mutations of the cationic trypsinogen gene (PRSS&) which has an <13 penetrance.Mutations in this gene cause premature activation of trypsinogen to trypsin.

-n addition) the 7TR mutation plays a role in predisposing patients to acute pancreatitis

by causing abnormalities of ductal secretion. "t present) however) the phenotypic

variability of patients with the 7TR mutation is not well understood. 7ertainly) patientshomozygous for the 7TR mutation are at ris/ for pancreatic disease) but it is not yet

clear which of the more than <11 mutations carries the most significant ris/. -n addition)

the role of 7TR heterozygotes in pancreatic disease is un/nown.

Mutations in the SP-4B& protein) which bloc/s the active binding site of trypsin)rendering it inactive) also probably play a role in causing a predisposition to acute pancreatitis.

This probably e0plains the predisposition) rather than the cause) of acute pancreatitis in

these patients. -f enough mutant enzymes become activated intracellularly) they can

overwhelm the first line of defense (ie) pancreatic secretory trypsin inhibitor and resist bac/up defenses (ie) proteolytic degradation by mesotrypsin) enzyme J) and trypsin

itself. "ctivated mutant cationic trypsin can then trigger the entire zymogen activation

cascade.

Aypercalcemia

Aypercalcemia from any cause can lead to acute pancreatitis. 7auses includehyperparathyroidism) e0cessive doses of vitamin 8) familial hypocalciuric

hypercalcemia) and total parenteral nutrition (TP4. Routine use of automated serum

chemistries has allowed earlier detection and reduced the fre6uency of hypercalcemia

manifesting as pancreatitis.

8evelopmental abnormalities of pancreas

The pancreas develops from * buds stemming from the alimentary tract of the developingembryo. There are * 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 appro0imately ,3 ofthe population (see the images below5 in most cases) it may actually protect against

gallstone pancreatitis. -t appears that the presence of stenotic minor papillae and an atretic

duct of Santorini are additional ris/ factors that together contribute to the development ofacute pancreatitis through an obstructive mechanism (although this is controversial.



Pancreas

divisum

associated withminor papilla

stenosis

causingrecurrent

pancreatitis.

@ecause pancreas

divisum is

relatively

common ingeneral

population) it

is best

regarded as variant of normal anatomy and not necessarily as cause of pancreatitis. -n thiscase) note bulbous contour of duct ad9acent to cannula. This appearance has been termed

Santorinicele. 8orsal duct outflow obstruction is a probable cause of pancreatitis whenSantorinicele is present and associated with a minor papilla that accommodates only

guide wire.

Recurrent

pancreatitisassociated with

pancreas

divisum in an

elderly man.Pancreatogram

of the dorsal

duct showsdistal stenosis

with upstream

chronic pancreatitis.

"fter the

stenosis wasdilated and

stented) pain

resolved and the patient improved clinically during & year of 6uarterly stent e0changes.ollow+up 7T scans showed resolution of the inflammatory mass. "lthough ductal

biopsies and cytology were repeatedly negative) pain and pancreatitis returned when

stents were removed. Patient developed duodenal outflow obstruction and was sent to

surgery5 hipple procedure revealed periampullary adenocarcinoma (of minor papilla.

"nnular pancreas is an uncommon congenital anomaly in which a band of pancreatic



tissue surrounds the second part of the duodenum. sually) 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 >ddi dysfunction can lead to acute pancreatitis by causing increased pancreatic ductal pressures. Aowever) the role of pancreatitis induced by such

dysfunction in patients without elevated sphincter pressures on manometry remains

controversial.

Aypertriglyceridemia

7linically significant pancreatitis usually does not occur until a personKs serumtriglyceride level reaches &111 mg$d?. -t is associated with type - and type F

hyperlipidemia. "lthough 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 moresevere than alcohol+ or gallstone+induced disease.

Tumors

>bstruction 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 chance of pancreatitis occurring when a tumor is present is appro0imately &23. Pancreatic cystic

neoplasm) such as intraductal papillary+mucinous neoplasm (-PM4) mucinous

cystadenoma) or serous cystadenoma) can also cause pancreatitis.

To0ins

E0posure to organophosphate insecticide can cause acute pancreatitis. Scorpion and

sna/e bites may also be causative5 in Trinidad) the sting of the scorpion Tityus trinitatis isthe most common cause of acute pancreatitis. Ayperstimulation of pancreas e0ocrine

secretion appears to be the mechanism of action in both instances.

Surgical procedures

"cute pancreatitis may occur in the postoperative period of various surgical procedures

(eg) abdominal or cardiopulmonary bypass surgery) which may damage the gland bycausing 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.

Fascular abnormalities

Fascular factors) such as ischemia or vasculitis) can play a role in causing acute pancreatitis. Fasculitis can predispose patients to pancreatic ischemia) especially in those

with polyarteritis nodosa and systemic lupus erythematosus.

"utoimmune pancreatitis

"utoimmune pancreatitis) a relatively newly described entity) is an e0tremely rare cause



of acute pancreatitis (prevalence) 1.<* per &11)111 individuals. hen it does cause acute

pancreatitis) it is usually in young people (appro0imately 21 years who also suffer from

inflammatory bowel disease. The pathogenesis is unclear.

Epidemiology

nited States statistics"cute pancreatitis has an incidence of appro0imately 21 cases per year per &11)111

adults.%<' -n *11:) nearly **1)111 patients with acute pancreatitis are e0pected to be

admitted to nonLfederally funded hospitals. -n &DD<) &<C)111 patients with acute pancreatitis were admitted. This trend in rising incidence has been recognized over the

past several decades.%D'

-nternational statistics

orldwide) the incidence of acute pancreatitis ranges between , and <1 per &11)111

population) with the highest incidence recorded in the nited States and inland.%&1' -n?uneburg) #ermany) the incidence is &:., cases per &11)111 people. -n inland) the

incidence is :C.2 cases per &11)111 people. Similar incidence rates have been reported in"ustralia. The incidence of disease outside 4orth "merica) Europe) and "ustralia is less

well /nown.

-n Europe and other developed nations) such as Aong Bong) more patients tend to havegallstone pancreatitis) whereas in the nited States) alcoholic pancreatitis is most

common.

"ge+related demographics

The median age at onset depends on the etiology.%&&' The following are median ages of

onset for various etiologies!

"lcohol+related + CD years

@iliary tractLrelated + ;D years

Trauma+related + ;; years

8rug+induced etiology + 2* years

ER7P+related + ,< years

"-8S+related + C& years

Fasculitis+related + C; years

Aospitalization rates increase with age. or people aged C,+:, years) the rate doubles formales and 6uadruples for females.

Se0+related demographics



#enerally) acute pancreatitis affects males more often than females. -n males) the etiology

is more often related to alcohol5 in females) it is more often related to biliary tract disease.

-diopathic pancreatitis has no clear predilection for either se0.

Race+related demographics

The hospitalization rates of patients with acute pancreatitis per &11)111 population are Ctimes higher for blac/s than whites. These racial differences are more pronounced for

males than females. The ris/ for "frican "mericans aged C,+;2 years is &1 times higher

than for any other group. "frican "mericans are at a higher ris/ than whites in that sameage group.

The annual incidence of acute pancreatitis in 4ative "mericans is 2 per &11)111

population5 in whites) ,.: per &11)111 population5 and in blac/s) *1.: per &11)111

population.%&*'

Prognosis

The overall mortality in patients with acute pancreatitis is &1+&,3. Patients with biliary

pancreatitis tend to have a higher mortality than patients with alcoholic pancreatitis. This

rate has been falling over the last * decades as improvements in supportive care have

been initiated. -n patients with severe disease (organ failure) who account for about *13of presentations) mortality is appro0imately C13.%&C'This figure has not decreased in the

past &1 years. -n patients with pancreatic necrosis without organ failure) the mortality

approaches zero.

-n the first wee/ of illness) most deaths result from multiorgan system failure. -nsubse6uent wee/s) infection plays a more significant role) but organ failure still

constitutes a ma9or cause of mortality. "cute respiratory distress syndrome ("R8S) acute

renal failure) cardiac depression) hemorrhage) and hypotensive shoc/ all may be systemic

manifestations of acute pancreatitis in its most severe form.

-dentifying patients in greatest need of aggressive medical treatment by differentiating

their disease severity as mild or severe is recommended. -n mild disease) the pancreas

e0hibits interstitial edema) an inflammatory infiltrate without hemorrhage or necrosis)

and) usually) minimal or no organ dysfunction. -n severe disease) the inflammatoryinfiltrate 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.

8ifferent strategies have been used to assess the severity of acute pancreatitis and predictoutcome (see or/up and Staging. Several clinical scoring systems (eg) Ranson criteria)

#lasgow) -mrie are available. The "P"7AE -- scoring system) though cumbersome)appears to be the best validated (see the "P"7AE -- Scoring System calculator.@iological mar/ers have also been used for this purpose. #enetic mar/ers are being

studied and have not yet come into clinical use.

Peritoneal lavage has a high specificity (DC35 however) it has a low sensitivity (,23.

8ynamic 7T scanning of the abdomen is widely available and useful in predicting the

outcome of acute pancreatitis. hen the @althazar criteria (see or/up and 7omputed


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http://reference.medscape.com/calculator/apache-ii-scoring-system



Tomography are used) sensitivity is <:3 and specificity is <<3.

Suppiah et al e0amined the prognostic value of the neutrophil+lymphocyte ratio (4?R in

&2; consecutive patients with acute pancreatitis.%&2' They found that elevation of the

4?R during the first 2< hours of hospital admission was significantly associated withsevere acute pancreatitis and was an independent negative prognostic indicator. The 4?R

is calculated from the white cell differential and provides an indication of inflammation.

Patient Education

Educate patients about the disease) and advise them to avoid alcohol in binge amountsand to discontinue any ris/ factor) such as fatty meals and abdominal trauma.

or patient education resources) see the 7holesterol 7enter ) as well as Pancreatitisand

#allstones.

http://www.emedicinehealth.com/cholesterol/center.htm

http://www.emedicinehealth.com/pancreatitis/article_em.htm

http://www.emedicinehealth.com/gallstones/article_em.htm

http://www.emedicinehealth.com/cholesterol/center.htm

http://www.emedicinehealth.com/pancreatitis/article_em.htm

http://www.emedicinehealth.com/gallstones/article_em.htm

Documents

Acute Pancreatitis Medscape