Presented by : Dr.

Siddhant Singh
Moderator : Prof. Dr. Sanjay Kala (MS)
ANATOMY
 J-shaped or retort
shaped.
 Length 15-20 cm
 Breadth 2.5-3.8 cm
 Thickness 1.2-1.8 cm
 Weight 90 gm
 retroperitoneal
Arterial supply
-Splenic A.

-Superior pancreatico-
duodenal artery
(from coeliac trunk)

-Inferior pancreatico-duodenal A.(from superior

mesenteric A)
Venous drainage
-Splenic vein

-Superior
mesenteric
vein

-Portal vein
Nerve supply
 Parasympathetic by
the vagus nerve
controlling secretion .
 Sympathetic from
coeliac & superior
mesenteric plx.
 Secretion is also
controlled by
hormone secretin-
pancreozymine.
Lymphatic drainage
 Head & neck –ventral &
dorsal
pancreaticodudenal
grp LN.

 Body &tail by
pancreatico-splenic
LN.

 Efferents to Coeliac &

sup.mesenteric LN
Pancreatic Secretions
 Exocrine
 Digestive enzymes : secreted by acinar cells
 Bicarbonate : secreted by duct cells

• Endocrine
 Insulin
 Glucagon
 Somatostatin
Acute Pancreatitis
 CLINICAL DEFINITION
 An acute condition presenting with abdominal pain-
usually associated with raised blood/urine pancreatic
enzymes as a result of pancreatic inflammation

 PATHOLOGICAL DEFINITION
 Reversible pancreatic parenchymal injury associated
with inflammation
Acute Pancreatitis
 Acute pancreatitis (AP) is a common acute medical condition
requiring emergent care.
 Yet, no prevalence data are available from India. Only some idea
of incidence can be obtained from patients admitted in tertiary
care centers. At the All India Institute of Medical Sciences
(AIIMS), New Delhi, 276 patients with AP were hospitalized
from January 1997 to June 2002, i.e. about 55 patients per year.
 The incidence of AP has, however, been reported to be much
higher in USA, Finland and Scotland (49.3, 46.6 and 41.9 per
100,000 population, respectively).
 The mortality rate of acute edematous interstitial (mild)
pancreatitis is less than 1%, whereas in patients with
hemorrhagic necrotizing (severe) pancreatitis, it is reported to
be between 10% and 24% (…..Blumgarts)
 Intra-acinar activation of trypsinogen, with
subsequent activation of other pancreatic enzymes, is
thought to play a central role in the pathogenesis.

 Ischemia reperfusion injury is believed to be critical to

disease progression.
ETIOLOGY
 Gall stones (including microlithiasis) (40%)
 Alcohol (30%)
 Hypertriglyceridemia (mainly >1000 mg/dl)
 ERCP (more common with therapeutic)(in upto 5%
patients)
 Blunt trauma abdomen (MCC in children)
 Drugs (sulfonamides, metronidazole, erythromycin,
tetracycline, ART, thiazides, furosemide
 Hypercalcemia
 Miscellaneous causes :
Splenic artery embolization
Scorpion venom sting
Duodenal ulcer perforation
 Although a male/female ratio of 1 : 3 exists for gallstone disease,
acute biliary pancreatitis is observed with a ratio of 1 : 1.4 to 1 :
1.7, suggesting that men with gallstones are at a greater risk of
developing biliary pancreatitis than women with gallstones.

 Further studies have shown that the gender ratio changes with
age. Imrie and colleagues reported a male/female ratio of 1 : 2.7
in younger patients with gallstone pancreatitis, whereas the ratio
changed to 1 : 1.1 in patients older than 50 years.

 In the group between 60 and 70 years of age, the gender

predominance was reversed; more men than women had biliary
pancreatitis
Gall Stone Pancreatitis
 Most common cause
 F>M
 50-70 years
 Theories :
1. Obstructive : d/t excessive pressure in pancreatic
duct (d/t continuous secretion of pancreatic juice in
the presence of pancreatic duct obstruction).
2. Reflux : stones may impact in the ampulla of Vater
allowing bile salt reflux into pancreas.
Alcohol Pancreatitis
 M>>F (30-45 years)
 Only 5-10% of drinkers develop pancreatitis
 Heavy drinker : >100g/d for atleast 5 years
 Alcohol triggers proinflammatory pathways (NF-kB)
which increases production of TNF-a and IL-1.
 Also decreases pancreatic perfusion, induces sphincter
of oddi spasm, and obstructs pancreatic ducts through
precipitation of proteins inside ducts.
Diagnostic Criteria
Two of the following three features:

 Upper abdo. pain of acute onset often radiating to back

(constant)

 Serum amylase or lipase > 3times normal

 Radiological finding
Clinical Manifestation
 Pain :
 Epigastric/ periumbilical
 Radiates to back
 Constant (if pain disappears or decreases, consider
another diagnosis
 Nausea/ vomiting :
 Upto 90% patients
 Does not relieve the pain
 Severe pancreatitis : abdominal distension, rebound
tenderness, rigidity
 Dehydration, tachycardia, hypotension
Cutaneous manifestations
 Cullen’s sign
 Grey Turner sign
 Fox’s sign (thigh)
 Bryant’s sign (scrotum)

 Rare findings
 Indicate retroperitoneal bleeding a/w severe
pancreatitis
Serum markers
 Serum Amylase
 Elevates within HOURS and can remain elevated for 3-5 days
 High specificity when level >3x normal
 Many false positives

 Urine Amylase
 urinary levels may be more sensitive than serum levels
 Urinary amylase levels usually remain elevated for several days
after serum levels have returned to normal
 Serum Lipase
 The preferred test for diagnosis
 Begins to increase 4-8H after onset of symptoms and peaks at
24H
 Remains elevated for days
 Sensitivity 86-100% and Specificity 60-99%
 >3X normal S&S ~100%
Radiological Findings
 Plain Abdominal Radiograph
 To rule out other causes of pain
 Air fluid levels : d/t ileus
 Colon cut off sign : d/t colonic spasm at splenic flexure
 Widening of duodenal C-loop : d/t pancreatic head edema
 Cut off colon sign
 Ultrasound :
 To visualise gall stones
 Gall stones + raised AST – 97% sensitivity

 CECT : Best Investigation

 Best phase to evaluate : Portal Venous Phase (65-70 seconds
after injection of contrast)
 In case of renal failure : NCCT/MRI
 Various criteria used to diagnose necrosis include non-
enhancement of more than 30% of the pancreatic parenchyma
or an area of greater than 3 cm of the pancreas that does not
enhance.
CT scan findings
 Typical findings :
 Focal or diffuse parenchymal enlargement
 Changes in density because of edema
 Indistinct pancreatic margins owing to inflammation
 Surrounding retroperitoneal fat stranding

• Liquefactive necrosis of pancreatic parenchyma

 Lack of parenchymal enhancement

• Abscess formation
• Haemorrhage
 EUS : for gall stone pancreatitis

 MRI : costly and not for acute phase

may be used in patients with renal impairment
or allergy to iv contrasts

 MRCP : helpful in unexplained/ recurrent pancreatitis

Severity
 A large body of evidence now demonstrates that the
two key determinants of severity in acute pancreatitis
are organ failure— absent, transient, or persistent—
and pancreatic complications— absent, noninfectious,
or infectious.
Ranson’s Criteria
 Released in 1974 by John HC Ranson, this score was
the first widely used in the PA. Initially encompassed
43 clinical and laboratory parameters, and of these,
only 11 have shown to be related to mortality and
morbidity. Therefore, Ranson criteria were amended in
1982 and currently consist of 11 parameters, of which
five are assessed on admission and other during the
first 48 h
 The presence of three or more criteria within 48 h of
admission, classifies as severe pancreatitis.
 It has a sensitivity of 75% to 87%, specificity of 68% to
77.5%, PPV of 28.6% to 49% and NPV of 91% to 94.5%
APACHE II scoring
 It has 12 evaluation parameters, and extra score based
on age and the presence of chronic disease
 It has sensitivity of 76% and specificity of 61.5% to
assess the PA severity.
 8 or more – severe AP
 Advantages of being able to be calculated within the
first 24 h after patient's admission to hospital and can
be performed daily in the evaluation of patient
outcomes.
 The addition of BMI in Apache II score - known as
Apache-O - adds one point to BMI of >25-30
kg/m2 and two points to BMI >30 kg/m2
 Maximum score : 71

 Score of 25 represents a predicted mortality of ~50%

 Score of >35 represents a predicted mortality of ~80%

SAPS II
 It is an alternative version of the Apache scale, used
most often in the intensive care unit compared with
the Apache.
 It has sensitivity and specificity respectively 87.5% and
77.8% for predicting mortality.
 The Saps II should be applied in the first 24 h of
admission in intensive care unit and consists of 12
immediate variables, while also taking into
consideration the age and comorbidities acquired
before admission.
 The cut-off used is ≥34
SAPS II score Mortality
 29  10%

 40  25%

 52  50%

 64  75%

 77  90%
CT Severity Index
 In 1985 Balthazar et al introduced severity score based on
the presence of pancreatic and peri-pancreatic
inflammation and fluid collections evidenced by computed
tomography.
 This score was achieved without the need to use contrast,
making it impossible to detect pancreatic necrosis,
reducing its prognostic value.
 introduction of intravenous contrast in the CT scan
enabling the detection of pancreatic necrosis.
 It should be noted however, that CTSI in isolation fails to
predict the outcome and needs to be combined with one or
the other clinical criteria to get a reliable assessment of the
severity and expected outcome.
BISAP
 1. Blood urea nitrogen (BUN) > 25 mg/dL
 2. Impaired mental status (Glasgow coma scale score < 15)
 3. Systemic inflammatory response syndrome (SIRS) score
≥2
 4. Age > 60 years and
 5. Pleural effusion.
 It has been developed from the data of about 18,000
patients with AP and has been tested prospectively and
found to be as accurate as APACHE II in predicting severity
and mortality of AP. The great advantage of this scoring
system is ease of its application in day to day practice.
Harmless acute pancreatitis score
(HAPS)

 Absence of rebound tenderness and guarding of the

abdomen, normal hematocrit and normal creatinine
assure the clinician with 98% certainty that the disease
is mild
 Among the single prognostic markers,
hemoconcentration stands out to be a simple, readily
available and yet reliable indicator of bad outcome.
Thus, a hematocrit of 44% or hemoglobin of 14.6
gm/dL or more or a BUN of 33 mg/dL or more are
associated with increased pancreatic necrosis and
complications. It is because of this that early
aggressive fluid replacement is recommended.
CRP
 Peaks after 48-72 hours.

 As a stand-alone prognostic marker, an elevated C-reactive

protein (CRP) concentration of greater than 130 mg/L
predicts a complicated course with a sensitivity of 85% in
the first 72 hours after the onset of symptoms.

 Although detection of elevated CRP levels is sensitive for

the severity of acute pancreatitis, it is not specific for the
disease; other causes of inflammation, such as cholangitis
and pneumonia, need to be ruled out before severity
assessment by measurement of CRP is undertaken
Management
 Diagnostic Assessment of Acute
Pancreatitis
 If the patient presents within 24 hours after the onset
of pain, the elevated serum pancreatic enzymes
predict pancreatitis with a sensitivity of 98%.

 Sensitivity will then steadily decline over the next 5 to

7 days; serum levels will eventually be normal or below
reference levels, even in the presence of acute
necrotizing pancreatitis
 Clinical Assessment of Acute
Pancreatitis
 Although in 75% to 80% of cases, acute pancreatitis is
a mild disease without associated mortality, it is
important to identify the 20% to 25% of patients who
are likely to develop severe disease associated with
major complications and who would benefit from early
intensive care monitoring and treatment.
Treatment
 Three most important issues initially are

Fluid replacement
Pain relief
Nutrition
Fluid Therapy
 No high-level evidence describes the optimal resuscitation
fluid, required fluid rate, or best marker to guide
resuscitation and indicate its adequacy.
 It is not even known whether colloids or crystalloids are
more effective in improving pancreatic microcirculation
and outcome.
 The initial goal of fluid resuscitation is to restore
circulating blood volume (euvolemia), with the aim of
normalizing heart rate, blood pressure, central venous
pressure, and urine output, even though these do not
reflect the adequacy of pancreatic and splanchnic
perfusion.
Fluid Therapy
 Experts and various guidelines started recommending fluid
replacement with crystalloids at a rate of 300–350 ml per
hour, especially in those with raised hematocrit and BUN.
 According to the Mayo group, 33% of the first 72 hours of
fluid volume requirement should be administered within
24 hours of presentation.
 In a recent study, it was seen that administration of more
than 4 liters of fluid during the initial 24 hours was
associated with increased risk of respiratory insufficiency
and a longer stay in the ICU.
 In general, urine output should be restored at greater
than 0.5 mL/h/kg body weight, and the central venous
pressure should be restored to between 8 and 12 cm
H2O.

 Adequate fluid resuscitation is likely when the

hematocrit is restored to between 30% and 35%.
Pain Management
 the NSAID of choice is metamizole (2 g/8 h IV), and
the opioid of choice is buprenorphine (0.3 g/4 h IV).
Nutrition
 Since AP is a hypercatabolic condition, prompt and adequate
provision of nutrition is essential.
 Enteral nutrition (EN) is far superior to parenteral nutrition
(PN)
 Used high protein, low fat, semi-elemental feeding because
reduced pancreatic digestive enzymes.
 To ensure tolerance of EN, it is usually commenced at a low rate
of 25 to 30 mL/h and increased incrementally over a day or more,
until the desired caloric intake is reached. (30 kcal/kg and 1.5
g/kg of protein daily based on ideal body weight)
 Signs that the formula is not tolerated include
- gastric residual volumes >400 cc
- vomiting (with nasogastric feeding)
- bloating
- diarrhea (>5 watery stools or >500 mL/d)
 Metabolic Complications
- Correction of electrolyte imbalance - Ca,Mg
- Cautiously for hyperglycemia

 Cardiovascular Care
 Respiratory Care
 Deep vein thrombosis prophylaxis
 Nasogastric (NG) tube insertion may be more practical
than nasojejunal (NJ), as the latter often requires
endoscopy or radiology expertise, the transfer of
patients within the hospital, and a delay in starting
feeding.
 However, NJ EN has been preferred to NG EN because
of a fear about pancreatic stimulation. (all forms of
EN, with the exception of NJ feeding, stimulate
pancreatic secretion)
Prophylactic antibiotics
 Although this is still an area of debate
 Not indicated for mild attack
 suggest imipenem or meropenem
for 14 days for patients with proven necrosis

 The ACG guidelines do not recommend. if used,

should be restricted to patients with pancreatic
necrosis (>30 %) and continue no more than 14 d.
 Guidelines from the Italian Association recommend
antibiotics for patients with CT-proven necrosis
 MANAGEMENT OF SYSTEMIC
COMPLICATIONS
 Most patients with acute pancreatitis have an initial
sudden inflammatory respiratory syndrome response,
others develop multiple organ dysfunction syndrome
(MODS) in the first few days, and some develop MODS
later in response to infectious complications .
 Patients with severe and critical acute pancreatitis are
best managed in an intensive care environment to allow
for optimal monitoring of fluid resuscitation and organ
function and the early identification of life-threatening
local or systemic complications.
MANAGEMENT OF LOCAL
COMPLICATIONS
 Type of Intervention
STEP DOWN APPROACH STEP UP APPROACH

Many consider open surgical drainage with
necrosectomy to be the gold standard in
the management of infected pancreatic
necrosis, and they reserve less invasive
interventions for subsequent
complications, such as percutaneous tube
drainage of residual fluid complications
Advocates starting with less invasive
interventions, such as percutaneous or
endoscopic drainage, and only employing
open surgical techniques later in the
disease course in those who fail to respond

These two approaches have been subjected to an RCT demonstrating that a minimally
invasive step-up approach results in a reduced rate of the composite endpoint of major
complications or death in patients with necrotizing pancreatitis and suspected or
confirmed infected necrotic tissue.
Treatment of associated condition
 Gallstone pancreatitis
 ERCP should be performed within 72 hours in those
with a high suspicion of persistent bile duct stones
 EUS & MRCP should be considered in case that clinical
is not improving sufficiently
 Cholecystectomy
Therapeutic Endoscopic Retrograde
Cholangiopancreatography
 ERCP with endoscopic sphincterotomy (ES) has been
promoted as a proven intervention in patients with
acute biliary pancreatitis since the early 1990s.
 This was based on the findings of two RCTs, from the
United Kingdom and Hong Kong, of early ERCP
(within 24 to 48 hours of admission) with or without
ES versus conservative treatment.
 Both trials demonstrated that early ERCP was
associated with a reduction in complications, but not
in mortality, and only in patients with predicted severe
acute pancreatitis.
 Some evidence suggests that the duration of biliary
obstruction, rather than the predicted severity of acute
pancreatitis, is the most important determinant of
outcome.
 This is probably due to concomitant cholangitis
secondary to the obstruction and probably best
explains the usefulness of ERCP in the context of acute
biliary pancreatitis.
 Two important meta-analyses were published in 2008.
The first found that compared with conservative
treatment, early ERCP in patients with both predicted
mild and predicted severe acute pancreatitis did not
decrease the incidence of local pancreatic
complications or mortality rate. The second meta-
analysis was designed to negate the confounding effect
of acute cholangitis and demonstrated no benefit of
early ERCP over conservative treatment in terms of
complications and mortality in patients with predicted
mild and predicted severe acute pancreatitis
 The conclusion to be drawn from these studies is
that early ERCP is indicated in patients with acute
pancreatitis if acute cholangitis is evident but not
for those with just cholestasis.
Cholecystectomy
• Should be performed after recovery in all patient with gallstone
pancreatitis

• Failure to perform a cholecystectomy is associated with a 25-30%

risk of recurrent acute pancreatitis, cholecystitis, or cholangitis
within 6-18 weeks

• In mild pancreatitis case, can usually be performed safely within

7 days after recovery

 In severe pancreatitis case ,delaying for at least 3-6 wks

may be reasonable
 If high suspicion of CBD stones, preoperative
ERCP is the best test that therapeutic intervention
will be required
 If low suspicion,intraoperative cholangiogram
during cholecystectomy may be preferable to avoid
the morbidity associated with ERCP
Complications
New Classification Based on
Contrast-Enhanced CT
 Interstitial Edematous Pancreatitis
 Acute Peripancreatic Fluid Collection
 Pancreatic Pseudocyst

 Necrotizing Pancreatitis
 Acute Necrotic Collection
 Walled-Off Necrosis
Peripancreatic Fluid Collection
Occurring within the first 4 weeks in the setting of
interstitial edematous pancreatitis.

 CECT Criteria
 Homogeneous fluid adjacent to pancreas confined by
peripancreatic fascial planes
 No recognizable wall

 Treatment :
 Sterile – conservative
 Infected – percutaneous drainage + i.v Antibiotics
Pancreatic Pseudocyst
 In 5-15 % who have peripancreatic fluid collection after
AP
 Capsule made of collagen and granulation tissue
 Develops in 4-8 weeks
 C/F : in 50% patients
persistent pain, early satiety, nausea, weight loss
 Cyst fluid analysis – Carcinoembryonic antigen (CEA)
and CEA-125 (low in pseudocysts and elevated in
tumors); fluid viscosity (low in pseudocysts and
elevated in tumors); amylase (usually high in
pseudocysts and low in tumors)
Investigations :
Abdominal computed tomography (CT) – The
criterion standard for pancreatic pseudocysts
Endoscopic retrograde cholangiopancreatography
(ERCP) – Not necessary for diagnosis but useful in
planning drainage strategy.
Magnetic resonance imaging (MRI) – Not necessary for
diagnosis but useful in detecting a solid component to the
cyst and in differentiating between organized necrosis and
a pseudocyst
Endoscopic ultrasonography – Not necessary for
diagnosis but very important in planning therapy,
particularly if endoscopic drainage is contemplated
 Percutaneous aspiration :
 <50% have complete resolution. Rest need repeat aspiration /
2nd technique.
 Can be considered in pseudocyst in tail of pancreas, ,100 ml
vol, low intracystic amylase.

• Percutaneous drainage :
 Contraindications : significant pancreatic necrosis / solid
debris in pseudocyst
 Lack of safe access route
 Pseudocyst H’ge
 Complete obstruction of main pancreatic duct (controversial)
 Endoscopic approach :
 Favourable factors : pseudocyst in head and body
 <1 cm pseudocyst wall thickness
 Pseudocyst secondary to chronic pancreatitis / trauma

 Complications : sepsis > shock > h’ge > renal failure >
ventilator dependent respiratory failure
 External drainage of pseudocyst :
 When gross infection found at the time of surgery / when
immature thin walled pseudocyst wall is found.
 Pseudocyst cavity opened , contents evacuated, closed
suction drain
 Complication : pancreatico cutaneous fistula
 Treatment :

Asymptomatic, <4cm, located in tail, no obstruction

of pancreatic duct :
OBSERVATION (spontaneous regression in 70%)

Symptomatic : transgastric/ transduodenal endoscopic

drainage
if fails : surgical drainage
Cystogastrostomy / cystoduodenostomy / Roux-
en-Y cystojejunostomy
Complications of Pseudocyst
 Infection :
 Now termed “PANCREATIC ABSCESS” (instead of infected
pseudocyst)
 T/t : percutaneous drainage  if fails (pus too thick/
multiloculated collection)  open operative drainage

• Haemorrhage :
 MCC : splenic art (~50%) > gastroduodenal art >
pancreaticoduodenal art
 Pathogenesis : erosion of vessel  Pseudoaneurysm  rupture
 Mx : stable pt : embolisation of pseudoaneurysm/ source vessel
unstable pt : surgical exploration
 Obstruction :
 D/t mass effect : MC : duodenal obstruction
 May obstruct IVC, ureter, mediastinum, pleura

• Rupture :
 Spontaneous rupture is the least common complication (< 3%)
 Silent rupture : rupture / fistulise into stomach/ small bowel
Pancreatic Necrosis
 CECT – Areas of low attenuation (<40-50 HU)
 Upto 20% patients of AP develop pancreatic necrosis.
 Main complication : infection (risk of infection is
related to amount of necrosis)(E.coli, Klebsiella,
Pseudomonas, Enterococcus)
 Start i.v antibiotics – 1st line carbapenems
 Treatment :
Endoscopic drainage with large bore stent
+Possible endoscopic debridement
+/- percutaneous drainage

If fails:
Open debridement with necrosectomy with closed
continuous irrigation / open packaging
ANC (acute necrotic collection)
 A collection containing variable amounts of both fluid
and necrosis associated with necrotising pancreatitis;
the necrosis can involve the pancreatic parenchyma
and/or the peripancreatic tissues
 CECT criteria
 Occurs only in the setting of acute necrotising pancreatitis
 Heterogeneous and non-liquid density of varying degrees in
different locations (some appear homogeneous early in their
course)
 No definable wall encapsulating the collection
 Location—intrapancreatic and/or extrapancreatic
WON (walled-off necrosis)
 A mature, encapsulated collection of pancreatic
and/or peripancreatic necrosis that has developed a
well defined inflammatory wall. WON usually occurs
>4 weeks after onset of necrotising pancreatitis.

 CECT criteria
 Heterogeneous with liquid and non-liquid density with
varying degrees of loculations (some may appear
homogeneous)
 Well defined wall, that is, completely encapsulated
 Location—intrapancreatic and/or extrapancreatic
 Maturation usually requires 4 weeks after onset of acute
necrotising pancreatitis
Pancreatic Ascites
 Very rare
 d/t complete disruption of pancreatic duct
 Treatment :
Abdomen drainage + endoscopic placement of stent
across disruption
if fails : surgery (distal resection and closure of
proximal stump)
Pancreaticopleural fistula
 Rare
 MC after alcoholic pancreatitis
 Treatment :
-chest drainage
-inj. Octreotide
if fails : endoscopic sphincterotomy and stent
placement
if fails : surgery (distal resection and closure of
proximal stump)
Vascular Complications
 Rare
 MC- splenic artery
 Pancreatic elastase damages vessels : pseudoaneurysm
 C/F : sudden abdominal pain, hypotension,
tachycardia
 T/t : artery embolisation/ ligation
Pancreatico-cutaneous fistula
 Rare
 T/t : conservative