chronic pancreatitis - m. elsayed

8/8/2019 Chronic Pancreatitis - M. Elsayed

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Chronic PancreatitisChronic Pancreatitis

By assistant lecturerBy assistant lecturer

MOHAMMAD ELMOHAMMAD EL--SAYEDSAYED


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Chronic pancreatitis is defined as a

continuing chronic inflammatory process ofthe pancreas, characterized by irreversible

morphological changes.

This chronic inflammation can lead tochronic abdominal pain and/or impairment of

endocrine and exocrine function of the

pancreas.


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By definition, chronic pancreatitis is a

completely different process from acute

pancreatitis. In acute pancreatitis, the patient

presents with acute and severe abdominal

pain, nausea, and vomiting.

The pancreas is acutely inflamed

(neutrophils and edema), and the serum

levels of pancreatic enzymes (amylase andlipase) are elevated.


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Full recovery is observed in most patients

with acute pancreatitis, whereas in chronic

pancreatitis, the primary process is a chronic

irreversible inflammation (monocyte and

lymphocyte) that leads to fibrosis with

calcification.


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Epidemiology:Epidemiology:

1-Frequency

In the US: approximately 87,000 cases of

pancreatitis occur annually.

Internationally: Comparing the hospital

admissions data from several cities around

the globe, the overall frequency is similar.


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II-Sex:

Males are affected more commonly thanfemales (6.7 vs 3.2 per100,000 population).

Alcohol-induced illness is more prevalent in

males, idiopathic and hyperlipidemic-

induced pancreatitis is more prevalent in

females, and equal sex ratios are observed in

chronic pancreatitis associated with

hereditary pancreatitis.


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III-Age:

The mean age at diagnosis is 46 years, plusor minus 13 years.

In idiopathic chronic pancreatitis, a bimodal

age distribution has been reported,designated as early-onset form (median age

19.2 y) and late-onset form (median age 56.2

y).


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IV-Race:

Hospitalization rates for blacks are 3 timeshigher than for whites in the United States.


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Pathophysiology:Pathophysiology:

Intraductal plugging and obstruction (eg,alcohol abuse, stones, tumors).

Direct toxins and toxic metabolites ( These

act on the pancreatic acinar cell to stimulatethe release of cytokines, which stimulate the

stellate cells to produce collagen and to

establish fibrosis) (eg. Alcohol, drugs).


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Oxidative stress (eg, alcohol, smoking).

Necrosis-fibrosis (recurrent acute

pancreatitis that heals with fibrosis).

Ischemia (from obstruction and fibrosis)

which is important in exacerbating disease

rather than in initiating disease.


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Autoimmune disorders: Chronic pancreatitis

has been found in association with other

autoimmune diseases, such as Sjgren

syndrome, primary biliary cirrhosis, and

renal tubular acidosis.


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Aetiology:Aetiology:

II--Metabolic:Metabolic:1-Excessive alcohol consumption is the most

common cause, accounting for about 60% of

all cases.

In the affected gland, alcohol appears to

increase protein secretion from acinar cells

while decreasing fluid and bicarbonate

production from ductal epithelial cells.


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The resulting viscous fluid results in

proteinaceous debris becoming inspissated

within the lumen, causing ductular

obstruction.


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A competing theory suggests that the

persistent demands of metabolizing alcohol

causes oxidative stress within the pancreas

and may lead to cellular injury and organ

damage, especially in the setting ofmalnutrition.


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Although 60-70% of chronic pancreatitis

cases are due to alcohol consumption, only

10-15 % of alcoholics develop chronic

pancreatitis.

Other factors may be involved including high

fat and protein diet, deficiency in

antioxidants and trace elements, smoking

and genetic predisposition.


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2-Hyperlipidemia (usually type I and type V)

also may cause chronic pancreatitis;

however, it usually presents with repeated

attacks of acute pancreatitis.

3-Hypercalcemia due to hyperparathyroidism

now is a rare cause of chronic pancreatitis,

probably because automation of serum

chemistries reveals hypercalcemia before itresults in pancreatitis.


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4-Nutritional, or tropical, chronic pancreatitis is

rare in the United States, but it is an

important cause of disease in other parts of

the world.


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IIII--Genetic:Genetic:

1-Hereditaty pancreatitis Autosomal dominantdisorder accounting for about 1% of cases.

2-Cystic fibrosis is one of the most common

genetic abnormalities, is an autosomalrecessive disorder accounting for a small

percent of patients with chronic pancreatitis.


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IIIIII--Idiopathic chronicIdiopathic chronic

pancreatitis:pancreatitis:Accounts for approximately 30% of cases,

has been subdivided into early-onset and

late-onset forms. The cause is not yet known.


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IVIV--ObstructionObstruction of the flow of

pancreatic juice can cause chronicpancreatitis:

Congenital abnormalities such as pancreas

divisum.

Acquired obstructive forms result from blunt

abdominal trauma, stones or tumours.


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VV--Autoimmune pancreatitis:Autoimmune pancreatitis:

Is uncommon and accounts probably for lessthan 1% of cases of chronic pancreatitis.

Clinical characteristics include diffuse

enlargement of the pancreas, diffuse andirregular narrowing of the main pancreatic

duct, increased circulating levels of gamma

globulin (IgG4), the presence ofautoantibodies, and a possible association

with other autoimmune diseases.


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Clinical picture:Clinical picture:

Abdominal pain:

The most common symptom.

The patient experiences intermittent attacks

of severe pain, often in the mid or left upper

abdomen and occasionally radiating to the

back and lasting for several hours.


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A small percentage of patients (20%) have

painless chronic pancreatitis and present

with signs or symptoms of pancreatic

exocrine or endocrine insufficiency.


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Other symptoms associated with chronic

pancreatitis include diarrhea and weightloss. This may be due either to fear of eating

(eg, postprandial exacerbation of pain) or

due to pancreatic exocrine insufficiency and

steatorrhea).


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Examination:Examination:

During an attack, patients may assume aDuring an attack, patients may assume acharacteristic position in an attempt toin an attempt to

relieve their abdominal pain (leaningrelieve their abdominal pain (leaning

forward).forward).


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Occasionally, a tender fullness or mass may

be palpated in the epigastrium, suggesting

the presence of a pseudocyst or an

inflammatory mass in the abdomen.

Patients with advanced disease (ie, patients

with steatorrhea) exhibit decreased

subcutaneous fat, temporal wasting, sunken

supraclavicular fossa, and other physical

signs of malnutrition.


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Complications:Complications: PseudocystPseudocyst..

Secondary infection.Secondary infection.

Mechanical obstruction of the duodenum and

common bile duct.

Pancreatic ascites.

Pleural effusion.

Splenic vein thrombosis with portal

hypertension.


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Pseudoaneurysm of splenic artery.

Diabetes mellitus is a late manifestation inabout one third of patients. The tendency to

develop ketoacidosis is low.


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Investigations:Investigations:

1-Blood tests Serum amylase and lipase levels may be

slightly elevated in chronic pancreatitis; high

levels are found only during acute attacks ofpancreatitis.


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While low concentrations of serum trypsinare relatively specific for advanced chronic

pancreatitis, they are not sensitive enough to

be helpful in most patients with mild-to-

moderate disease.

Laboratory studies to identify causative

factors include serum calcium andtriglyceride levels.


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2-Fecal tests:

Neither qualitative nor quantitative fecal fatanalysis can detect early disease because

maldigestion and malabsorption do not

occur until more than90% of the pancreas

has been destroyed, steatorrhea is a

manifestation of advanced chronic

pancreatitis.


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Assays of fecal chymotrypsin and human

pancreatic elastase 1 have the samelimitations but are useful in confirming

advanced chronic pancreatitis with exocrine

insufficiency.


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3-Pancreatic function tests:

A-Direct tests: These tests are the most

sensitive and can be used to detect chronic

pancreatitis at its earliest stage; however,

they are somewhat invasive, and expensive.


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Determination in duodenal aspirates:

Intubation of the duodenum usually isperformed. The output of pancreatic

bicarbonate, protease, amylase, and lipase

then is measured in the duodenal aspirates.


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Determination in pancreatic juice: This test

generally is performed in conjunction with

(ERCP). The pancreatic duct is freely

cannulated, and the pancreatic juice then is

aspirated out of the duct as it is produced.The output of pancreatic bicarbonate,

protease, amylase, and lipase are measured.


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B-Indirect tests:

Noninvasive tests of pancreatic functionhave been developed for detecting chronic

pancreatitis.

In principle, these tests work via oraladministration of a complex substance

(bentiromide) that is hydrolyzed by a specific

pancreatic enzyme to release a marker

substance (PABA).


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The intestine absorbs the marker, which then

is measured in the serum or urine. Thesetests are capable of detecting moderate-to-

severe chronic pancreatitis.

The presence of renal, intestinal, and liverdisease may interfere with the accuracy of

these tests.


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4-Imaging studies:

A-Abdominal x-ray:

Pancreatic calcifications, often considered

pathognomonic of chronic pancreatitis, are

observed in approximately 30% of cases.


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B-Abdominal US:

Can reveal pancreatic duct dilatation,calcifications, pseudocysts, pancreatic

ductal stones.


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C-EUS:

To diagnose chronic pancreatitis requires thepresence of at least 3 criteria of the

followings:

Ductal findings: dilated main duct, ductirregularities, hyperechoic duct margins,

stones and calcifications.


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Parenchymal findings:

hyperechoic foci, hyperechoic strands, glandlobularity and cystic cavities.


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D-Computed tomography scan:

Pseudocysts, calcifications and pncreaticduct dilatation can be observed in chronic

pancreatitis.


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E-MRCP:

Noninvasive

It can assess both pancreatic parenchyma

and ducts at the same time.

It can detect pancreatic duct dilatation,ductal narrowing and filling defects.


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F-ERCP:

Provides the most accurate visualization of

the pancreatic ductal system and has been

regarded as the criterion standard for

diagnosing chronic pancreatitis.

Findings include characteristic chain of

lakes beading of the main pancreatic duct,

and intraductal filling defects.


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Treatment:Treatment:

1-Behavior modification:

Cessation of alcohol consumption andCessation of alcohol consumption and

tobacco smoking are important. In earlytobacco smoking are important. In early--

stage alcoholstage alcohol--induced chronicinduced chronic

pancreatitis, lasting pain relief can occurpancreatitis, lasting pain relief can occur

after abstinence from alcohol, but, inafter abstinence from alcohol, but, in

advanced stages, abstinence does notadvanced stages, abstinence does not

always lead to symptomatic improvement.always lead to symptomatic improvement.


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Patients continuing to abuse alcoholPatients continuing to abuse alcohol

develop either marked physicaldevelop either marked physical

impairment or have a death rate 3 timesimpairment or have a death rate 3 times

higher than those abstaining.higher than those abstaining.


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2-Medical tratment:

A-Analgesics: to relieve tha abdominal pain.: to relieve tha abdominal pain.

B-Hormones:: Reduction of pancreatic exocrineReduction of pancreatic exocrine

secretion. Subcutaneous injection ofsecretion. Subcutaneous injection of

octreotide (Sandostatin) at 200 mcg tidoctreotide (Sandostatin) at 200 mcg tid

provided relief of pain in 66% of patients.provided relief of pain in 66% of patients.


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C-Antidepressants: (Amitriptyline

hydrochloride)

In addition to alleviating coexistent

depression, tricyclic antidepressants may

ameliorate pain and potentiate the effects ofopiates.


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D-Pancreas enzyme supplements:

Used as a dietary supplement to aiddigestion in patients with pancreatic enzyme

deficiency. Several preparations are

available. Eg. Pancrelipase: assists in

digestion of protein, starch, and fat.


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3-Endoscopic treatment:

I-Papillary stenosis: In appropriately selectedIn appropriately selectedpatients, a pancreatic duct sphincterotomypatients, a pancreatic duct sphincterotomy

will facilitate drainage, reduce ductalwill facilitate drainage, reduce ductal

pressures, and may help alleviate pain.pressures, and may help alleviate pain.II-Pancreatic duct strictures: performing aperforming a

pancreatic sphincterotomy, dilating thepancreatic sphincterotomy, dilating the

stricture, and placing a stent.W

hile technicalstricture, and placing a stent.W

hile technicalsuccess is achieved in more than 90% ofsuccess is achieved in more than 90% of

patients, nearly 20% will have a complication.patients, nearly 20% will have a complication.


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III-Pancreatic duct stones:

Requires a pancreatic duct sphincterotomy

and stricture dilation to enable their

extraction.

In addition to various endoscopic

techniques, extracorporeal shockwave

lithotripsy often is necessary to break up

impacted or large stones into smaller pieces

suitable for removal.


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IV-Pancreatic pseudocysts:

Noncommunicating pseudocysts that bulgeinto the foregut are treatable by endoscopic

transduodenal or transgastric

pseudocystostomy.

The success rate is 85%, with a 17%

complication rate, and the transduodenal

approach has fewer complications and

recurrences than the transgastric approach.


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4-Surgical treatment:

I-Pancreatic duct drainage: In patients with aIn patients with a

dilated pancreatic duct,dilated pancreatic duct,

pancreaticojejunostomy is indicated. Thepancreaticojejunostomy is indicated. The

operative mortality rate is about 3%, and painoperative mortality rate is about 3%, and pain

relief is obtained in approximately 75% ofrelief is obtained in approximately 75% of

patients.patients.


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II-Pancreatic resection: If the disease is limited

to the head of the pancreas, aWhipple

operation (pancreaticoduodenectomy) can

produce good results.

In patients with intractable pain and diffuse

disease with nondilated ducts, a subtotal or

total pancreatectomy can be offered.


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III-Total pancreatectomy and islet

autotransplantation:

In selected patients, the long-term morbidity

caused by diabetes following total

pancreatectomy can be avoided.

This involves harvesting the islets from the

resected pancreas and injecting them into

the portal system, which then lodges them in

the liver.


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IV- Drainage of pseudocyst:

The indications include rapid enlargement,

compression of surrounding structures

(duodenal, biliary obstruction or vascular

occlusion), pain, or signs of infection and

abscess formation, suspected malignancy,

hemorrhage and intraperitoneal rupture.


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Prognosis:Prognosis:

The prognostic factors associated withThe prognostic factors associated withchronic pancreatitis are age at diagnosis,chronic pancreatitis are age at diagnosis,

smoking, continued use of alcohol, and thesmoking, continued use of alcohol, and the

presence of liver cirrhosis.presence of liver cirrhosis.

The overall survival rate is 70% at 10 years

and 45% at 20 years.

The risk of developing pancreatic cancer isapproximately 4% at 20 years.


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chronic pancreatitis - m. elsayed

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