ACUTE PANCREATITIS

DR.RAHUL GARG
M.D.MEDICINE(Std.)
S.N.M.C.,AGRA
DR. RAHUL GARG

DEFINITIONS
Atlanta Symposium definition of acute pancreatitis
: An acute inflammatory process of the pancreas
with variable involvement of other regional tissues
or remote organ systems.
Acute pancreatitis is best defined clinically by a
patient presenting with two of the following
criteria:
(1)Symptoms, such as epigastric pain, consistent
with the disease.
(2)A serum amylase or lipase greater than three
times the upper limit of normal.

CAUSES OF ACUTE
PANCREATITS
COMMON CAUSE

Gall Stones ( including microlithiasis ) ( 40%)

Alcohol ( acute and chronic alcoholism (30%)
Hypertriglyceridmia ( mainly over >1000 mg/ dl )
ERCP ( Specially after billary manometry)
Trauma (specially after blunt trauma )
Post operative ( abdominal and non abdominal)
Drugs (azathioprin, 6 mp , sulfonamides,
estrogen, anti HIV protease inhibitor , Vaproic
acid ,thiazide,erythromycin,acetaminophen)
Annular pancreas,Choledochocele

CLINICAL FEATURE
HISTORY
Abdominal pain :
Severity

mild tolerable discomfort

Severe constant incapacitating distress

Character
steady and boring in character
Site
located in epigastrium and
Periumblical region
Radiation radiation to back and chest,
lower abdomen flanks.
Agg /releaving factor pain increases when pt in supine
and relieved by sitting with trunk
flexed and knee drawn up

Nausea/ vomiting / abdominal distention

PHYSICAL EXAMINATION
Hypo or hyperthermia(<98.6or>100.4f)
Tachycardia (>90beats/min)
Hypotension and shock (BP<90mmhg)
Jaundice infrequentely occure due to edema of the head of
pancrease and compression of intrahepatic portion of cbd.
Erythematous skin nodules due to subcutaneous fact necrosis
In 10 20% patients pulmonary findings
Basilar rales
atelcectesis
left sided pleural effusion

Abdominal tenderness and rigidity

Bowel sound diminished and absent
Palpable pancreatic pseudocyst in upper abdomen
In severe necrotizing pancreatitis
Cullens sing : faint blue discoloration around umlicus
Turner,s sing: blue red purpel or grey brown discoloration of the flanks
Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition

LABORATORY DIAGNOSIS
PANCREATIC ENZYMES
Diagnosis of acute pancreatitis relies on at least a three-fold elevation of amylase
or lipase in the blood.
Serum Amylase(30-180 IU/L)
It rises within 6 to 12 hours of onset (half-life, 10 hours).
The serum amylase is usually increased on the first day of symptoms, and it
remains elevated for three to five days in uncomplicated attacks.
Sensitivity is greater than 85%, the serum amylase may be normal or minimally
elevated in fatal pancreatitis, during a mild attack or an attack superimposed on
chronic pancreatitis , or during recovery from acute pancreatitis also in
hypertriglyceridemia-associated pancreatitis.
Hyperamylasemia is not specific for pancreatitis because it occurs in many
conditions other than acute pancreatitis.
. Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition

 Serum Lipase(0-160 IU/L)

The sensitivity of serum lipase is similar to that
of serum amylase and is between 85% and 100%.
Lipase may have greater specificity for
pancreatitis than amylase.
Serum lipase always is elevated on the first day
of illness and remains elevated longer than does
the serum amylase.
Some believe that serum lipase is preferable to
that of serum amylase , whereas others find no
clear advantage .

 Secretin-pancreozymin (CCK) test

Secretin leads to increased output of pancreatic
juice and HCO3; CCK leads to increased output of
pancreatic enzymes.
Sensitive enough to detect occult disease;
involves duodenal intubation and fluoroscopy
,only role in acute on chronic pancreatitis.

Other Pancreatic Enzymes

They include PLA2, trypsin/typsinogen,

carboxylester lipase, carboxypeptidase A,
colipase, elastase, and ribonuclease.
None, alone or in combination, are better than
serum amylase or lipase

Other blood test White blood cell count -Increased

Haematocrit->44 show poor prognosis, moniter daily.
Serum Creatinine and serum electrolytes

AST,ALT,alkaline phosphatase, and bilirubin also may

increase .
MCV- Alcoholic patients tend to have a higher MCV .
Serum triglyceride levels- increase in acute
pancreatitis, but also with alcohol use, uncontrolled
diabetes mellitus, or defective triglyceride
metabolism

RADIAOLIGICAL
Chest X- ray / X ray abdomen errect
See for pulmonary complication pleural effusion
Rule out other diagnosis,specially a perforation
USG- Specially for diagnosis of gall stone
Helical CT Scan (Contrast Enhanced ,After 48 -72hrs
of onset)
Helpful to know severity and prognosis
Allows estimation of presence and extend of pancreatic
necrosis.
Conferm the cinical impression of acute pancreatitis in
face of normal s. Amylase.
Severe allergy and renal impairment(s.crt>2mg/dl) are
contraindication for contrast use.
EUS and/or MRCP are better than CT for choledocolithiasis.

Markers of Severity within 24 Hours

BMI>30
SIRS [temperature >38 or <36C (>100.4 or
96.8F), Pulse >90, Tachypnea >24, WBC >12,000]
Hemoconcentration (Hct >44%)
BISAP
(B) Blood urea nitrogen (BUN) >22 mg%
(I) Impaired mental status
(S) SIRS: 2/4 present
(A) Age >60 years
(P) Pleural effusion
Organ Failure

Atlanta Criteria for Severe Acute

Pancreatitis
Organ Failure
a.

Shock: systolic blood pressure <90 mm Hg

b.

Pulmonary insufficiency: Pao2 60 mm Hg

c.

Renal failure: serum creatinine >2 mg/dL

d.

Gastrointestinal bleeding: >500 mL/24 hr

Local Complications
a.
b.

Necrosis
Abscess

--

Ranson'sPrognosticCriteria

NON-GALLSTONE
GALLSTONE PANCREATITIS
PANCREATITIS
At Admission

Age >55yr
Age >70yr
White blood cells
>18,000/mm3
3
>16,000/mm
Blood glucose >200mg/dL
>220mg/dL
Serum lactate dehydrogenase
>400IU/L
>350IU/L
Serum aspartate
>250IU/L
aminotransferase >250IU/L
During Initial 48hr

Hematocrit decrease of >10

>10%
%
Blood urea nitrogen increase
>2mg/dL
of >5mg/dL
Serum calcium <8mg/dL
<8mg/dL
Arterial po2 <60mmHg
NA

SEVERITY INDEX IN ACUTE

PANCREATITIS
Grade of Acute pancreatitis

Points

NORMAL PANCREAS

PANCREATIC ENLARGMENT ALONE FOCAL OR DIFFUSE

WITH CONTOUR IRREGULARITIES AND
INHOMOGENOUS ATTENUATION

B+PERIPANCREATIC INFLAMMATION

C+ONE PERIPANCREATIC FLUID COLLECTION

D+TWO OR MORE PERIPANCREATIC OR

RETROPERITONEAL FLUID COLLECTION OR GAS
COLLECTION

DEGREE OF PANCREATIC NECROSIS

1

NO NECROSIS

NECROSIS OF <33% PANCREASE

NECROSIS OF 33%-50% OF PANCREASE

NECROSIS OF > 50% OF PANCREASE

CT SEVERITY INDEX ( CT SI )BALTHAZAR

SCORE+NECROSIS SCORE
CT GRADE + NECROSIS GRADE

Contrast-enhanced computed tomography shows

diffuse swelling of the pancreas (P) with peripancreatic
inflammatory changes (arrows). The pancreas was well
perfused without evidence of necrosis. G, gallbladder.

Acute pancreatic necrosis. Contrast-enhanced c t demonstrates

focal areas of decreased perfusion in the pancreatic parenchyma
(arrows) with surrounding peripancreatic inflammation. The
necrosis was estimated to involve less than 30% of the pancreas.
G, gallbladder

MANAGEMENT;
Patients with acute pancreatitis require adequate
intravenous hydration and adequate analgesia to
eliminate or markedly reduce pain.
The patient is usually on npo until any nausea
and vomiting have subsided.
Opiate dosing is monitored carefully and adjusted
on a daily basis according to ongoing needs.
Nasogastric intubation is not used routinely
because it is not beneficial in mild pancreatitis.
It is used only to treat gastric or intestinal ileus
or intractable nausea and vomiting.
Similarly, proton pump inhibitors or H2-receptor
blocking agents are not beneficial and not used.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth

 The patient should be carefully monitored for any

signs of early organ failure such as hypotension,
vital signs and urinary output.
Tachypnea should not be assumed to be due to
abdominal pain; monitoring oxygen saturation
and, if needed, blood gases is advised and
oxygen supplementation is mandatory if there is
hypoxemia.
Any patient who exhibits signs of early organ
dysfunction should be immediately transferred to
intensive care monitoring.

FLUID RESUSCITATION;
The goal is to decrease the hematocrit.
Laboratory and clinical studies with intravenous
dextran to promote hemodilution have suggested
efficacy in preventing severe disease.
One of the markers of severity of pancreatitis defined
by Ranson and colleagues is intravascular losses
(fluid sequestration).
Requirements of a 70-kg person during the first 48
hours, is should be at least 250 to 300 mL/hour for
48 hours.
The rate of volume replacement is more important

 Maintaining adequate intravascular volume in

patients with severe disease may require 5 to 10 L
of fluid such as isotonic saline daily for the first
several days (200 to 400 mL/hour).
In a patient with unclear cardiac output, a SwanGanz catheter can be useful .

Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth

edition

RESPIRATORY CARE;
Hypoxemia (oxygen saturation <90%) requires
supplemental oxygen.
Current guidelines recommend the initial
routine use of nasal cannula oxygen to all
ARDS
is the
serious
respiratory complication
patients
withmost
acute
pancreatitis.
of acute pancreatitis.
It generally occurs between the second and
seventh day of illness (but can be present on
admission) .
Chest radiography may show multilobar alveolar
infiltrates.
Treatment is endotracheal intubation with positive
end-expiratory pressure ventilation, often with
low tidal volumes to protect the lungs from
volutrauma.

 Cardiac complications of severe acute

pancreatitis include congestive heart failure,
myocardial infarction, cardiac dysrhythmia, and
cardiogenic shock.

If hypotension persists even with appropriate

fluid resuscitation, intravenous dopamine may
help maintain the systemic blood pressure.

Dopamine does not impair the microcirculation of

the pancreas as do other vasoconstrictors.

METABOLIC COMPLICATION;
Hyperglycemia may present but usually
normalizes as the inflammatory process subsides.
Blood sugars fluctuate, and insulin should be
administered cautiously.
Reduced serum ionized calcium may occur and
cause neuromuscular irritability.
If hypomagnesemia coexists, magnesium
replacement should restore serum calcium to
normal.
Once the serum magnesium is normal, signs or
symptoms of neuromuscular irritability may
require administering intravenous calcium
gluconate as long as the serum potassium is
normal and digitalis is not being given.

Prophylactic Antibiotics;
The majority of organisms detected were gramnegative aerobic or anaerobic species (Escherichia
coli, Enterobacter aerogenes, Pseudomonas
aeruginosa, Proteus species, Klebsiella
pneumoniae, Citrobacter freundii, and Bacteroides
species), with occasional gram positives and rare
fungi .
Imipenem, fluoroquinolones (ciprofloxacin,
ofloxacin, pefloxacin), and metronidazole are the
drugs that achieved the highest inhibitory
concentrations in pancreatic tissue, whereas
aminoglycosides did not.
Recently there is no current recommendation of

ENDOSCOPY AND NUTRITION

Endoscopic early removal of a possibly impacted
gallstone in improving the outcome of gallstone
pancreatitis remains a controversial issue.

Severe acute gallstone pancreatitis with

ascending cholangitis (jaundice and fever) is an
indication for urgent ERCP .
Studies demonstrate that enteral nutrition is
cheaper and safer and is preferable in patients
with severe acute pancreatitis.
It is still unclear, however, when nutrition should
be initiated and for how long it needs to be
continued.

Clear fluid diet should be given on 3 rd - 6th day

and regular diet from 5th - 7th day.
The decision to reintroduce oral intake is done
by the following criteria
Resolution of abdominal pain
The patient is hungry
Organ dysfunction if recent has improved
In sever pancreatitis in which much longer
restriction of oral feed needed parenteral
neutriton must be maintained by lipid infusion .

OTHER DRUGS;
Gabexate mesylate is pancreatic protease
inhibitor in acute pancreatitis found no effect on
the 90-day mortality rate, but a reduced incidence
of complication.

The antisecretory hormone somatostatin or its

synthetic analog octreotide(1microgm/kg slow iv 68 hrly) have failed to show evidence of efficacy .

The use of anti-inflammatory cytokines has

lexipafant have not shown clear efficacy.

ROLE OF SURGERY;

Cholecystectomy should be performed as soon

as the patient has recovered and the acute
inflammatory process has subsided.

A second potential role for surgery in

pancreatitis is to debride pancreatic necrosis
(necrosectomy) .

COMPLICATION;LOCAL
Necrosis
Sterile / infected

Pancreatic fluid collection

Pancreatic abscess
Pancreatic pseudocyst
Pancreatic ascitis

Involvement of contiguous organ by

necrotising pancreatitis
Massive intraperitioneal haemorrhage
Thrombosis of blood vessels

Obstructive jaundice

SYSTEMIC
Pulmonary
Pleural effusion
Atelectasis
Pneumonitis
ARDS

Cardiovascular
Hypotension / hypervolemia
Sudden death
Pericardial effusion

Hematological
DIC

GI haemorrhage
Peptic ulcer disease
Erosive gastritis
Hemorrhagic pancreatitis erosion in blood vessel
Portal vein thrombosis

SYSTEMIC
Renal
Oliguria
Azotemia
Renal artery / vein thrombosis

Metabolic
Hyperglycemia
Hypertriglyceridemia
Hypocalcemia
Purtschers retinopathy ( due to occulsion of post
retinal artery by aggregated granulocyte)

CNS
Psychosis
Fat emboli

Fat necrosis
Subcutaneous tissue - erythematous nodule

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