DISEASES OF PANCREAS

SURGERY UNIT –III

 Pancreas

• Pancreas means all flesh

• A soft yellowish lobulated
gland
• Lies behind the peritoneum on
the posterior abdominal wall,
roughly at the level of of L1~L2
 Pancreas
Four parts
• Head
– Lies within the cancavity of the C-
shaped curvatune of duodenum
– Uncinate process－ a projection to
the left from the lower part of the
head behind the superior
mesenteric vessels.
• Neck－narrow part, overlies the
superior mesenteric vessels and
beginning of the portal vein
• Body－triangular in cross section,
passes upward ang to the left across the
midline
• Tail－extends to the hilum of spleen in
the splenorenal ligament
 Pancreas
• Pancreatic duct
– Main Pancreatic duct
• Begins at tail and throughout
gland
• Joins common bile duct
before entering descending
part of duodenum at major
duodenal papilla
– Accessory pancreatic duct
• Opens 2cm above main duct
at lesser duodenal papilla
EMBRYOLOGICAL DEVELOPMENT
Arterial supply and venous drainage of the pancreas
Function
The pancreas is both an exocrine and an endocrine gland.

The exocrine portion of the gland produces a secretion that

contains enzymes that are capable of hydrolyzing proteins,
fats, and carbohydrates.

The endocrine portion of the gland, the pancreatic islet,

produces the hormones insulin and glucagons that play a key
role in carbohydrate metabolism.
 PANCREAS DISEASES
• Congenital
• Inflammatory
–Acute
–Chronic
• Cysts
• Neoplasms
 Congenital
• Agenesis (very rare)
• Pancreas Divisum (failure of 2 ducts to fuse)
(common)
• Annular Pancreas (pancreas encircles
duodenum) (rare)
• Ectopic Pancreas (very common)
Pancreas divisum
ANNULAR PANCREAS
Acute pancreatitis

acute pancreatitis
 Introduction
• Acute pancreatitis is a condition in which
activated pancreatic enzymes leak into
the substance of the pancreas and initiate
the auto-digestion of the gland.

introduction
 Etiology
Common (90%)
•Gall stones
•Alcohol
•Idopathic
Rare
•Metabolic: hypercalcemia, hypertrigyceridemia
•Drugs: thiazide, azathioprine, sodium valporate,
pentamidine
•Infection: mumps, coxsackie virus
•Post ERCP (due to back pressure of contrast into ductal
system)
•Trauma
•Organ transplantation
•Post surgical
etiology
etiology
 Pathophysiology
• The pancreas secretes the digestive enzymes as
proenzymes which are activated in the intestinal lumen.

• Acute pancreatitis may result when activation occurs in

pancreatic duct system or acinar cells. May include edema
or obstruction of the ampulla of Vater resulting in reflux of
bile into pancreatic ducts or direct injury to the acinar cells.

• The pancreas show edema and necrosis. The release of

enzymes lead to fat necrosis both in the pancreas and in
the peritoneal cavity.

• Premature activation of trypsinogen into trypsin while it is

still in pancreas. Resulting in auto digestion of the
pancreas.
 Defective intracellular Pancreatic duct
transport and secretion obstruction (common
of pancreatic zymogens bile duct stones,
tumors)

+ +

Proenzymes
+ +

Hyperstimulation of Reflux of infected bile

pancreas (alcohol, or duodenal contents
triglycerides) into pancreatic duct
(sphincter of Oddi
dysfunction)

Activated
proteolytic
enzymes Pancreatic
secretory
- trypsin
Acute pancreatitis inhibitors

pathophysiology
pathophysiology
 ABDOMINAL PAIN-Cardinal Symptom
 SITE: usually experienced first in the epigastrium but may be localized to either
upper quadrant or felt diffusely throughout the abdomen or lower chest

 ONSET: characteristically develops quickly, generally following substantial meal.

 SEVERITY: frequently severe, reaching max. intensity within minutes rather than
hours

 NATURE: “boring through”, “knifing” (illimitable agony)

 DURATION: hours-days

 COURSE: constant (refractory to usual doses of analgesics, not relieved by

vomiting)

 RADIATION: directly to back(50%), chest or flanks

 RELEIVING FACTOR: sitting or leaning/stooping forward (Muslims PRAYER

SIGN)
◦ due to shifting forward of abdominal contents and taking pressure off from inflamed
pancreas

 AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine

 OTHER MANIFESTATIONS
 Nausea, frequent and effortless vomiting, anorexia,diarrhea
◦ Due to reflex pylorospasm
◦ More intense in necrotizing than in edematous pancreatitis

 Persistent retching
◦ despite empty stomach

 Hiccups
◦ Due to gastric distension/diaphragmatic irritation

 Fever
◦ Low grade, seen in infective pancreatitis

 Weakness, Anxiety, Sweating

◦ Indicates severe attack.
 General Physical
Examination
 Appearance: well  gravely ill with profound shock, toxicity
and confusion

 Vitals:
◦ Tachypnea(and dyspnea-10%),
◦ Tachycardia(65%).
◦ Hypotension
◦ temp  high(76%)/normal/low (acute swinging pyrexia in
cholangitis)

 Icterus(28%)
◦ gallstone pancreatitis or due to edema of pancreatic head

 Pallor, cold clammy skin, diaphoresis, dehydration

 ABDOMEN EXAMINATION
 Tenderness + Rebound tenderness:
◦ epigastrium/upper abdomen

 Distension:
◦ Ileus(BS decreased or absent)
◦ ascites with shifting dullness

 Mass in epigastrium(usually absent)

◦ due to inflammation

 Guarding(also called “defense musculaire” )-upper abdomen

◦ tensing of the abdominal wall muscles to guard inflamed organs
within the abdomen from the pain of pressure upon them(i.e.
during palpation)

 Rigidity(involuntary stiffness)-unusual
◦ Tensing of the abdominal wall muscles to guard inflamed organs
even if patient not touched
 Cutaneous Ecchymosis(1 %
cases)*

Acute Hemorrhagic (Necrotizing/fulminant) Pancreatitis

Periperitoneal/retroperitoneal
Hemorrhage

Methemalbumin formed from digested blood

tracks around Fascial planes  hemorrhagic spots and

ecchymosis

FALCIFORM LIGAMENT
in flanks  around umbilicus Below inguinal ligament
(GREY TURNER’S SIGN) (FOX SIGN)
(CULLEN’S SIGN)
 GREY TURNER1 SIGN CULLEN2 SIGN FOX3
SIGN

1.Named after British surgeon George Grey Turner(1877-1951)

2.Named for Thomas Stephen Cullen (1869-1953), Canadian gynecologist who

first described the sign in ruptured ectopic pregnancy in 1916

3.Named after George Henry Fox(1846-1937), American dermatologist

 RESPIRATORY
EXAMINATION
Left sided* Pleural effusion(10-20%) -
exudative

* Due to close approximation of body and tail of pancreas to the left sided
 Other Manifestations
 Subcutaneous fat necrosis
◦ Small(<1 cm), red, tender nodules on
extensor skin of legs

 Purtscher retinopathy(on
fundoscopy)
◦ Activation of complement and agglutination
of blood cells within retinal vessels causing
Ischemic injury of retina
◦ It may cause temporary or permanent
blindness
MANIFESTAIONS OF
COMPLICATIONS
 Hypocalcaemia
◦ circumoral numbness or paresthesia (1st symtpom to
develop).
◦ carpopedal spasm .
◦ Laryngospasm.
◦ generalized seizures
◦ Chvostek sign :
 Depending on calcium level, graded response occur: twitching
first at angle of mouth, then by nose, the eye and the facial
muscles
 Positive in 10 % population in absence of hypocalcaemia
◦ Trousseau sign :
 BP cuff around arm and inflating to 20 mmHg above SBP for 3-5
minutes
 Carpal spasm observed ign(postive even
 More specific and sensitive than chvostek s before
tetany/hyperreflxia)
MANIFESTAIONS OF COMPLICATIONS

Peripancreatic (duodenal)
necrosis

Gastric
DIC erosions

Hematemesis/
melena
(5%)
 Diagnostic criteria
 Most often established by the presence of two of
the three following criteria:
◦ (i) abdominal pain consistent with the disease,
◦ (ii) serum amylase and/or lipase greater than
three times the upper limit of normal, and/or
◦ (iii) characteristic findings from abdominal
imaging.
 CT and/or MRI of the pancreas should be
reserved for patients
◦ in whom the diagnosis is unclear(typical pain with
normal enzymes)
◦ who fail to improve clinically within the first 48–72
h after hospital admission (e.g., persistent pain,
fever, nausea, unable to begin oral feeding)
◦ to evaluate complications
 WORKUP
 HEMATOLOGICAL investigations
 RADIOLOGICAL investigations
 HEMATOLOGICAL
 BASELINES
◦ CBC:
 Low Hb: prolonged hemetemesis/melena, internal hemorrhage
 Leucocytosis (10,000-30,000/mcL)-infection, non infectious
inflammation
 Low platelets-DIC
 Hct –raised in hemoconcentration
◦ LFT’s:
 raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone
pancreatitis
◦ RFT’s:
 raised BUN/cretainine- ATN ARF
◦ Coagulation profile:
 increased INR-DIC
◦ BSR:
 > 180 mg/dl-diabetes as a sequelae or cause
◦ Serum electrolytes:
 Low sodium/potassium: persistent vomiting
 Hypocalcemia- saponification/fat necrosis
◦ Serum Protein:
 HEMATOLOGICAL
 ABG’s
Acid-Base Disturbance Etiology

Metabolic (Lactic)acidosis with Hypovolemic shock

high anion gap

Hypokalemic Hypochloremic persistent vomiting

metabolic alkalosis

 Etiology specific investigations

Respiratory acidosis ARDS
◦ Serum fasting lipid profile
◦ Serum Calcium (Hypercalcemia  AP
Hypocalcemia)
◦ Autoimmune markers:
 serum autoantibodies such as anti-nuclear antibody
(ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II
antibody, and rheumatoid factor (RF),
 HEMATOLOGICAL
 Pancreatic Enzymes’ Assays
◦ Serum Amylase: Raised Amylase  may not AP
 ONSET: almost immediately Normal Amylase  may be AP
 PEAK: within several hours
 3-4 times upper limit of normal within 24 hrs (90%)
 RETURN to normal in (3-5 days)
 normal at time of admission in 20% cases
 Compared with lipase, returns more quickly to normal values.

SERUM INDICATOR OF HIGHEST

◦ Serum Lipase: PROBABILITY OF DISEASE
 more sensitive/specific than amylase
 Remains elevated longer than amylase(12 days)
 Useful in late presentation and if the cause is High TG
 Pancreatic Enzymes’Assays
◦ Urine Amylase
 More sensitive than serum levels
 Remain elevated for several days after serum levels
returned to normal

◦ Pancreatic-specific amylase (p-amylase)

 Measuring p-amylase instead to total amylase(also
includes salivary amylase) makes diagnosis more
specific(88-93%)
 Plain CXR-PA view
 Left sided Pleural effusion: blunting of costophrenic and
cardiophrenic angles + haziness in lower zones

 Elevated diaphragm on left side

 Linear focal atelactasis of lower lobe of lungs

 ARDS : diffuse alveolar interstitial shadowing

Plain X-ray abdomen erect AP
view
 Sentinel* loop sign
◦ Localized isolated Distended gut loop (Ileus) seen near the site of injured
viscus or inflamed organ

◦ RATIONALE: body's effort to localize the traumatic or inflamed lesions

◦ ETIOLOGY: Localized paralysis followed by accumulation of gas

◦ SITE:
 Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM)
 Acute Appendicitis Right iliac fossa
 Acute Cholecystitis Right Hypochondrium
 Diverticulitis Left iliac fossa
SENTINEL LOOP SIGN
Plain X-ray abdomen erect AP
view
 Colon cut-off sign
◦ Gas filled (Distended) segment of proximal(mainly transverse)
colon associated with narrowing of the splenic flexure
◦ with collapse of descending colon

◦ RANTIONALE: Extension of inflammatory process from the

pancreas into the phrenicocolic ligament via the transverse
mesocolon
 resulting in functional spasm and/or mechanical narrowing of the
splenic flexure at the level where the colon returns to the
retroperitoneum.

◦ Differential DIAGNOSIS:
 IBD
 Carcinoma of colon
 Mesenteric Ischemia
COLON CUT-OFF SIGN
Transcutaneous Abdominal
Ultrasonography
 Not diagnostic
 Should be performed within 24 hours in all patients to
◦ detect gall stones* as a potential cause
◦ Rule out acute cholecystits as differential diagnosis
◦ Detect dilated CBD.

* Identification of gallstones as the etiology should prompt referral for

cholecystectomy to prevent recurrent attacks and potential biliary sepsis.

Gallstone pancreatitis is usually an acute event and resolves when the

stone is removed or passes spontaneously.
 IV Contrast enhanced Computed Tomography Scan

 Provides over 90 % sensitivity and specificity for the

diagnosis of AP….. BUT

 Routine use in patients with AP is unwarranted, as the

diagnosis is apparent in many patients and most have a mild,
uncomplicated course.
 IV Contrast enhanced Computed Tomography Scan*
 INDICATIONS-DIAGNOSTIC

◦ Diagnostic uncertainty (differentiating pancreatitis from other

possible intra-abdominal catastrophes)

◦ Severe acute pancreatitis- distinguish interstitial from necrotizing

pancreatitis
 Necrosis( non enhancement area > 30 % or 3 cm) done at 72
hrs

◦ Systemic complications:
 Progressive deterioration, MOF, sepsis

◦ Localized complications:
 Altered fat and fascial planes, Fluid collection, pseudocyst,
psduoaneurysm,
 Bowel distension, mesenteric edema, hemorrhage
 IV Contrast enhanced Computed Tomography
Scan
 INDICATIONS-DIAGNOSTIC
◦ Initial assessment of prognosis (CT severity index).
◦ Perfusion CT at 3rd day  area of ischemia predict
pancreatic necrosis
 BALTHAZAR CT severity index(CTSI)-1994
Mild (0-3)
moderate (4-
6)
severe (7-10)

CT Severity Inflammation score + Necrosis score

Index
Magnetic Resonant
Cholangiopancreatography

 INDICATION:
◦ diagnosis of suspected biliary and pancreatic duct
obstruction in the setting of pancreatitis.
◦ Repeated attacks of idiopathic acute pancreatitis
(Microlithiasis)
 Endoscopic Ultrasonography
 INDICATIONS

◦ Repeated idiopathic acute pancreatitis*

 occult biliary disease- small stones/sludge
 secretin-stimulated EUS study may reveal
resistance to ductal outflow at the level of the
papilla,
 as evidenced by dilatation of the pancreatic duct to a
greater extent and longer duration than in a healthy
population

◦ Age >40 to exclude malignancy

 especially those with prolong or recurrent course
 RATIONALE: 5 % CA pancreas present as AP
Endoscopic Retrograde
Cholangiopancreatography
INDICATION
Severe gallstone AP or AP with concurrent acute cholangitis/biliary
obstruction/ biliary sepsis/jaundice (due to persistent stone)
ERCP within 24(-72) h of admission
Sphincterotomy /stent and bile duct clearance
It reduces infective complications/mortality

NOT INDICATED
Not needed early in most patients with gallstone pancreatitis who
lack laboratory or clinical evidence of ongoing biliary obstruction

◦ As most of gallstones causing AP readily pass to duodenum and are

lost in stool
◦ Ranson score

• Modified Glasgow score

Bedside Index for Severity in Acute Pancreatitis(BISAP) score

◦ Harmless Acute Pancreatitis Score(HAPS)

◦ Hong Kong Criteria

• ACUTE PANCREATITIS NON-SPECIFIC SCORING

SYSTEMS
• (ICU SCORING SYSTEMS)

◦ Acute Physiology And Chronic Health Evaluation(APACHE) II

score(12 clinical parameters)
• Sequential Organ Failure Assessment(SOFA) score
Although amylase/lipase are used in
diagnosing pancreatitis, they are NOT
use for predicting severity of disease

◦i.e. patient with normal amylase(raised in

90 % cases) levels may still have severe
acute pancreatitis
 RANSON SCORE-1974
(for alcohol pancreatitis)
ON ADMISSION AFTER 48 HOURS

 Age > 55 yrs  BUN rise >5 mg/dL

 WBC > 16,000/mm3  Pa02 < 60 mmHg ( 8 KPa)

 BSR > 200 mg/dL  Serum Calcium < 8 mg/dL

 AST > 250 IU/L  Base deficit > 4 meq/L

 Fluid Sequestration > 6000 mL

 LDH > 350 IU/L

 Hct fall > 10 %

NOTE: Disease classified as SEVERE when 3 or more factors are
present
 Revised RANSON SCORE-1979
(for Gallstone pancreatitis)
ON ADMISSION AFTER 48 HOURS

 Age > 70 years  BUN rise >5 mg/dL

 WBC > 18,000/mm3  Pa02 < 60 mmHg ( 8 KPa)

 BSR > 220 mg/dL  Serum Calcium < 8 mg/dL

 AST> 250 IU/L  Base deficit > 5 meq/L

 Fluid Sequestration > 4000 ml

 LDH >400 IU/L

 Hct fall > 10 %

NOTE: Disease classified as SEVERE when 3 or more factors are present
 RANSON SCORE

Ranson Mortality rate SEVERITY Interpretation

score

0-2 0-2 % Mild Admit in regular ward

3-5 10-20 % Moderate Admit in ICU/HDU

6-7 40 % Severe Associated with more

systemic complications

>7 >50 % Same as above

 APACHE Scoring System
 Immediate assessment of the severity
of pancreatitis possible

 Unlike ALL pancreatic specific scoring systems,

APACHE includes clinical features of patient
besides laboratory values

 (Clinical findings are more important than lab

findings in predicting SIRS,sepsis and other
complications)
DEMERITS OF AP-specific scoring
systems
 No single laboratory test is accurate to predict
severity in patients with AP.
◦ Even the acute-phase reactant CRP, the most
widely studied inflammatory marker in AP, is not
practical as it takes 72h to become accurate.
 CT and/or MRI imaging also cannot
determine severity early in the course of AP,
as necrosis usually is not present on
admission and may develop after 24 – 48 h.

Thus, in the absence of any available test to

determine severity, CLOSE EXAMINATION
to assess early fluid losses, hypovolemic
shock, and symptoms suggestive of organ
dysfunction is crucial.
 Differential diagnosis
• Perforated peptic ulcer
• Acute cholecystitis and biliary colic
• Acute intestinal obstruction
• Renal colic
• Myocardial infarction
• Vasculitis
• Pneumonia
• Diabetic ketoacidosis

differential diagnosis
 Management
• In most patients it is a mild disease that subsides
spontaneously within several days. Withhold food and
liquids by mouth, bed rest and in patients with severe
pain and ileus nasogastric suction.

Supportive treatment
• Bed rest NPO
• IV fluids; saline or whole blood
• Nasogastric suctioning; if severe nausea, vomiting or
development of paralytic ileus
• Pethidine 3-4 hourly to control pain, avoid morphine
• Oxygen for hypoxia, ventilator may be required for ARDS
• Dopamine may be required for shock nonresponsive to
fluid
management
• Calcium gluconate IV only if hypocalcemia is
associated with tetany
• Fresh frozen plasma for coagulopathy
• Serum albumin for hypoalbuminemia
• Insulin for hyperglycemia
• Total parenteral nutrition for severe cases
• Antibiotics; prophylactic broad spectrum antibiotic is
given even in sterile pancreatitis to prevent infection
• Imipenem 500mg IV 8 hourly or cefuroxime 1.5g IV 8
hourly
• ERCP; when severe pancreatitis results from stone in
biliary tract; particularly if there is jaundice or
cholangitis ERCP with endoscopic sphincterotomy and
stone extraction is indicated
management
 Management
• Fluid Therapy

• Antibiotics

• Analgesics
 Local Complications
• Necrosis
• Pseudocyst
• Ductal Disruption
• Peripancreatic Vascular Complications

• Extra-pancreatic complications
 Fluid Collections
• APFC (acute peripancreatic fluid collection)
• Acute necrotic collection (ANC)

• After 4 Weeks !
• Pancreatic pseudocysts and
• Walled-off pancreatic necrosis (WOPN)
Necrosis
 Necrosis

• Focal or diffuse nonviable pancreatic parenchyma

• Accompanied by peripancreatic fat necrosis.

 Necrosis - Issues
• 30 % - Avascularity

• Sterile Vs Infected

• Avoid Necrosectomy between 4-8 days

 Pancreatic debridement
(necrosectomy)
Principle:
1. Wide removal of devitalized and necrotic tissue
with through exploration and unroofing of all
collections.
2. Assurance of post operative removal of products of
ongoing local inflammation and infection.
 Types
Open:
1. Debridement with closure over drains.
2. Debridement with closure over packing.
3. Debridement with closure over irrigation drains
and postoperative lavage.
Minimally invasive:
1. Laparoscopic/gastroscopic/nephroscopic
necrosectomy
2. Radiology guided necrosectomy
 Approaches
• Gastrocolic:
1. Tissue planes obscured by inflammation.
2. Drain cannot be placed in depth.

• Transmesocolic :
1. Middle colic obscures the path
2. Way to whole of abdomen is opened for
inflammation to spread.
 Pancreatic Pseudocyst
• Pseudocysts are best defined as a localized fluid
collection that is rich in amylase and other pancreatic
enzymes, that has a nonepithelialized wall consisting of
fibrous and granulation tissue, and that usually appears
several weeks after the onset of pancreatitis*.

*Brun A, Agarwal N, Pitchumoni CS. Fluid collections in

and around the pancreas in acute pancreatitis. J Clin
Gastroenterol. Aug 2011;45(7):614-25.
 Pancreatic Pseudocyst
• Most common cystic lesions of the pancreas,
accounting for 75-80% of such masses
• Location
– One third of cysts are in the head region and two
third in the region of body of pancreas
– Lesser peritoneal sac in proximity to the pancreas
– Large pseudocysts can extend into the paracolic
gutters, pelvis, mediastinum
• May be loculated
• May be single or multiple
 Composition
• Thick fibrous capsule – not a true epithelial
lining
• Pseudocyst fluid
– Similar electrolyte concentrations to plasma
– High concentration of amylase, lipase, and
enterokinases such as trypsin
 Pathophysiology
• Pancreatic ductal disruption 2 to
1. Acute pancreatitis – Necrosis
2. Chronic pancreatitis – Elevated pancreatic duct
pressures from strictures or ductal calculi
3. Trauma
4. Ductal obstruction and pancreatic neoplasms
 Pathophysiology
• Acute Pancreatitis
– Pancreatic necrosis causes ductular disruption,
resulting in leakage of pancreatic juice from
inflamed area of gland, accumulates in space
adjacent to pancreas
– Inflammatory response induces formation of
distinct cyst wall composed of granulation tissue,
organizes with connective tissue and fibrosis
 Pathophysiology
• Chronic Pancreatitis
– Pancreatic duct chronically obstructed  ongoing
proximal pancreatic secretion leads to secular
dilation of duct – true retention cyst
– Formed micro cysts can eventually coalesce and
lose epithelial lining as enlarge
 Presentation
• Symptoms
– Abdominal pain > 3 weeks (80 – 90%)
– Nausea / vomiting
– Early satiety
– Bloating, indigestion
• Signs
– Tenderness
– Abdominal fullness/mass
– Icterus / pleural effusion
– Peritoneal signs indicate ruptured or infected cyst
Cohen et al: Pancreatic pseudocyst. In: Cameron JL, ed. Current Surgical Therapy. 7th ed.;
2001: 543-7
 Diagnosis
• Clinically suspect a pseudocyst
– Episode of pancreatitis fails to resolve
– Amylase levels persistantly high
– Persistant abdominal pain
– Epigastric mass palpated after pancreatitis
 Work up
• Amylase and lipase levels are often elevated but
may be within reference ranges.
• Bilirubin and liver function test (LFTs) findings
may be elevated if the biliary tree is involved.
• Analysis of the cyst fluid may help differentiate
pseudocysts from tumors. Attempt to exclude
tumors in any patient who does not have a clear
history of pancreatitis. Carcinoembryonic antigen
(CEA) and CA-125 tumor marker levels are low in
pseudocysts and elevated in tumors.
 Sonographic evaluation
• cystic fluid collections in
and around the
pancreas may be
visualized by ultrasound
– 75 -90% sensitive
the technique is limited
by the operator’s skill
the patient's habitus
any overlying bowel
gas.
 Abdominal CT scan
• It has a sensitivity of 90-
100% and is not operator
dependent.
• The pancreas may appear
irregular or have
calcifications.
• The CT scan provides a very
good appreciation of the
wall thickness of the
pseudocyst and billiary or
enteric obstruction which is
useful in planning therapy. Pseudocyst compressing the stomach wall
posteriorly
 Endoscopic ultrasound (EUS)
• EUS is not necessary to
establish a diagnosis but
is very important in
planning therapy,
particularly if endoscopic
drainage is contemplated.
• Transmural drainage may
be performed only when
the symptomatic
pseudocyst is positioned
next to the gut wall
 ERCP Vs. MRCP
• ERCP is not necessary in
diagnosing pseudocysts;
however, it is useful in
planning drainage
strategy.

• MRCP to establish the

relationship of the
pseudocyst to the
pancreatic ducts
 Natural History of Pseudocyst
• ~50% resolve spontaneously
• Size
– Nearly all <4cm resolve spontaneously
– >6cm 60-80% persist, necessitate intervention
• Cause
– Traumatic, chronic pancreatitis <10% resolve
• Multiple cysts – few spontaneously resolve
• Duration - Less likely to resolve if persist > 6-8
weeks
 Differential Diagnosis
• Acute fluid collections
• Pancreatic cancer
• Pancreatic necrosis and pancreatic abscess
• Von Hippel-Lindau Disease
• Pancreatic pseudoaneurysm
 Treatment
• Initial
– NPO
– TPN
– Octreotide
• Antibiotics if infected
• 1/3 – 1/2 resolve spontaneously
 Medication
No medications are specific to the treatment
of pancreatic pseudocysts.
 Antibiotics are an adjunct to drainage of
infected pseudocysts.
Octreotide can be useful as an adjunct to
catheter drainage. Used to reduce pancreatic
exocrine secretion.
 Intervention
• Indications for drainage
– Presence of symptoms (> 6 wks)
– Enlargement of pseudocyst ( > 6 cm)
– Complications
– Suspicion of malignancy
 Intervention
– External Drainage
Percutaneous drainage
Open Drainage
– Internal Drainage
Endoscopic
Transpapillary Drainage
Transmural drainage ( Transgastric or Transduodenal)
Laparoscopic Drainage
Cysto-gastrostomy
Cysto-jejunostomy
Open Surgical drainage
Cysto-gastrostomy
Cysto-jejunostom (Roux-en-Y)
– Pancreatic Rescection
 Excision of the pseudocyst
Pancreaticoduodenectomy
 Percutaneous Drainage
 Continuous drainage until output < 50 ml/day + amylase
activity ↓
 Failure rate 16%
 Recurrence rates 7%
 Complications
 Conversion into an infected
pseudocyst (10%)
 Catheter-site cellulitis
 Damage to adjacent organs
 Pancreatico-cutaneous fistula
 GI hemorrhage

Gumaste et al: Pancreatic pseudocyst. Gastroenterologist 1996 Mar; 4(1): 33-43

External Drainage
 Endoscopic Drainage
• Transenteric drainage
– Cystogastrostomy
– Cystoduodenostomy
• Transpapillary drainage
– 40-70% of pseudocysts communicate
with pancreatic duct
– ERCP with sphincterotomy, balloon
dilatation of pancreatic duct strictures
and stent placement beyond strictures
 Open Surgical Options
Internal drainage
– Cystogastrostomy

– Cystojejunostomy
• Permanent resolution confirmed
in b/w 91%–97% of patients*

– Cystoduodenostomy
• Can be complicated by duodenal fistula
and bleeding at anastomotic site
 Which is the preferred intervention?
• Surgical drainage with laproscopic or
traditional approach – gold standard.
• Percutaneous catheter drainage – high chance
of persistant pancreatic fistula.
• Endoscopic drainage - less invasive, becoming
more popular, technically demanding
• Surgery necessary in complicated pseudocyts,
failed nonsurgical, and multiple pseudocysts.
 Follow up
Dietry Advice: Patients may eat a low-fat diet
as tolerated.
 Patients who have endoscopically placed
stents must be monitored via serial CT scans
to observe resolution of the cyst. Stents may
then be endoscopically removed after
resolution.
Closely monitor patients with percutaneous
drains for pain, infection, or catheter
migration. Remove the drain when drainage
ceases
 Complications
• Infection
– S/S – Fever, worsening abd pain, systemic signs of
sepsis
– CT – Thickening of fibrous wall or air within the
cavity
• GI obstruction
• Perforation
• Hemorrhage
• Thrombosis – SV (most common)
• Pseudoaneurysm formation – Splenic artery (most
common), GDA, PDA
 Prognosis
• Most pseudocysts resolve without
interference, and patients do well without
intervention.
• Outcome is much worse for patients who
develop complications. The presence of
pancreatic necrosis is a poor prognostic sign.
• The failure rate for drainage procedures is
about 10%, the recurrence rate is about 15%,
and the complication rate is 15-20%.
 Pancreatic Ductal Disruption
• Unilateral pleural effusion,

• Pancreatic ascites, or

.Enlarging fluid collection.

 Duct Disruption - Management
• Focal, placement of a bridging stent via
endoscopic retrograde cholangiopancreatography
usually promotes duct healing.

• When ductal disruption occurs in an area of

widespread necrosis, optimum management
needs a multidisciplinary team of therapeutic
endoscopists, interventional radiologists, and
surgeons
 Hemorrhagic Pancreatitis:
• Used with caution, and this term is not a
synonym for necrotizing pancreatitis.

• Hemorrhage is more commonly associated

with pseudoaneurysm formation, an erosion
of peripancreatic blood vessels leading to
hemoperitoneum.
 Peripancreatic vascular complications
• Splenic vein thrombosis 20% of those who undergo
imaging

• The risk of bleeding 5%

• No elective splenectomy

• Pseudo aneurysms in 4–10% of cases.

• Rx - Mesenteric angiography with transcatheter arterial

embolisation
 Vascular Rupture
• Due to irritative effects of liberated activated
enzymes on vascular structures

• Pressure necrosis of inflammatory debris or

fluid collections on surrounding structures.

• Rupture of the splenic artery, splenic vein, or

portal vein possible – Highly Mortality
 Splenic Complications:

• Pseudocysts

• Splenic vein thrombosis

• Infarction and necrosis of the spleen

• Splenic rupture and

• Hematoma.
 Internal Fistulae / Obstruction
• Tail of the pancreas can obstruct or fistulize
into the small or large bowel.

• The most common site is the left colon.

Thank you