Acute Pancreatitis

Dr Dilmo Yeldo
DNB Resident
General Medicine
 DEFINITION

• An acute inflammatory process of the pancreas with

variable involvement of other regional tissues or
remote organ System

•Presenti ng with 2 of the following 3 criteria:

1. Symptoms (e.g, Epigastric pain) consistent with
pancreatitis
2. Serum amylase or lipase level greater than 3
times the laboratory’s upper limit of normal
3. Radiologic imaging consistent with
pancreatitis
Causes of Acute Pancreatitis
 PATHOGENESIS

• The initial phase is characterized by intrapancreatic

digestive enzyme activation and acinar cell injury.

• The second phase of pancreatitis involves the

activation, chemoattraction, and sequestration of
leukocytes and macrophages in the pancreas, resulting
in an enhanced intrapancreatic inflammatory reaction.

• The third phase of pancreatitis is due to the effects of

activated proteolytic enzymes and cytokines, released
by the inflamed pancreas, on distant organs
• Activated proteolytic enzymes, especially trypsin, not only
digest pancreatic and peripancreatic tissues but also activate
other enzymes such aselastase and phospholipase A2.

• The active enzymes and cytokines then digest cellular

membranes and cause proteolysis, edema, interstitial
hemorrhage, vascular damage, coagulation necrosis, fat
necrosis, and parenchymal cell necrosis.

• Cellular injury and death result in the liberation of bradykinin

peptides, vasoactive substances, and histamine that can
produce vasodilation, increased vascular permeability, and
edema with profound effects on many organs.

• The systemic inflammatory response syndrome (SIRS) and

acute respiratory distress syndrome (ARDS), as well as
multiorgan failure, may occur as a result of this cascade of local
and distant effect
 Clinical Features
• Acute onset of persistent, severe epigastric abdominal
pain .
• In some patients, the pain may be in the right upper
quadrant or, rarely, confined to the left side.
• In approximately 50 percent of patients, the pain radiates to
the back. The pain persists for several hours to days and may
be partially relieved by sitting up or bending forward.
• Approximately 90 percent of patients have associated nausea
and vomiting which may persist for several hours.
• Patients with severe acute pancreatitis may have dyspnea due to
diaphragmatic inflammation secondary to pancreatitis, pleural
effusions, or adult respiratory distress syndrome.
• There may be significant tenderness to palpation in the
epigastrium or more diffusely over the abdomen.
• Guarding and tenderness may be there.
• Severe pancreatitis may have fever, tachypnea,
hypoxemia, and hypotension.
• Bowel sounds are usually diminished or absent.
• In 10–20% of patients, there are pulmonary findings,
including basilar rales, atelectasis, and pleural effusion.
• In 1 percent of patients with acute pancreatitis,
ecchymotic discoloration may be observed in the
periumbilical region (Cullen's sign) or along the flank
(Grey Turner sign).
• An enlarged pancreas from acute fluid collection, walled
off necrosis, or a pseudocyst may be palpable in the
upper abdomen later in the course of the disease (i.e., 4–
6 weeks).
 INVESTIGATIONS
• CBC -
Low Hb: Hemetemesis/melena, internal hemorrhage
Leucocytosis: infection, non infectious inflammation
Low platelets: DIC
Hct: 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
• Bood Glucose: > 180 mg/dl-diabetes as a sequelae or cause
• Serum Electrolytes: Hyponatremia/Hypokalemia,
Hypocalcemia
• Etiology specific investigations
– Serum fasting lipid profile
– Viral titers
– Serum Calcium (HypercalcemiaAPHypocalcemia)
– Autoimmune markers
• increased serum levels of IgG4
• serum autoantibodies such as anti-nuclear antibody
(ANA), anti-lactoferrin antibody, anti-carbonic
anhydrase II antibody, and rheumatoid factor (RF).

• The electrocardiogram is occasionally abnormal in acute

pancreatitis with ST-segment and T-wave abnormalities
simulating myocardial ischemia.
 PANCREATIC ENZYMES ASSAY
• Serum Amylase:
Peak within several hours.
3-4 times upper limit of normal within 24 hrs (90%)
Compared with lipase, returns more quickly to values
below the upper limit of normal.

• Serum Lipase:
More sensitive/specific than amylase
Remains elevated longer than amylase(12 days)

• Serum amylase and lipase values threefold or more

above normal virtually clinch the diagnosis.
 CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE

ABDOMEN GYNECOLOGY

• Small bowel obstructionsche • Ruptured Ectopic pregnancy

• Acute appendicitis • Torsion of an ovarian cyst
• Cholecystitis
• Perforated Duodenal Ulcer OTHERS
• Gastroenteritis
• Parotitis (Mumps)
• Biliary peritonitis
• Spasm of sphincter of Oddi • Macroamylasaemia

• Opioids administration
• Brain injury(CVA)-
Hyperstimulation of pancreas
 USG
• In patients with acute pancreatitis, the pancreas
appears diffusely enlarged and hypoechoic on
abdominal ultrasound. Gallstones may be
visualized in the gallbladder or the bile duct
• Peripancreatic fluid appears as an anechoic collection
on abdominal ultrasound. These collections may
demonstrate internal echoes in the setting of
pancreatic necrosis
 CT
• CT is the most important imaging test for the diagnosis of
acute pancreatitis and its intra-abdominal complications.
• CT in acute pancreatitis are to
(1)exclude other serious intra-abdominal conditions (e.g.,
mesenteric infarction or a perforated ulcer)
(2) stage the severity of acute pancreatitis, and
(3)determine whether complications of pancreatitis are
present (e.g., involvement of the GI tract or nearby blood
vessels and organs, including liver, spleen, and kidney).
• Pancreatic necrosis manifested as perfusion defects after IV
contrast may not appear until 48 to 72 hours after onset of
acute pancreatitis.
• Any severe acute pain in the abdomen or back
should suggest the possibility of acute
pancreatitis.
• The diagnosis is established by two of the
following three criteria:

(1) typical abdominal pain in the epigastrium that

may radiate to the back,
(2) threefold or greater elevation in serum lipase
and/or amylase, and
(3) confirmatory findings of acute pancreatitis on
cross-sectional abdominal imaging.
Roles of Advanced Imaging Techniques
• MRI is helpful in distinguishing walled-off
necrosis from a pseudocyst.
• Endoscopic ultrasonography highly sensitive test
for detecting cholelithiasis and
choledocholithiasis and could be an alternative to
MRCP, which has limited accuracy for detecting
smaller gallstones or sludge.
 Phases of Acute Pancreatitis
Two phases of acute pancreatitis have been defined, early (<2
weeks) and late (>2 weeks).

In the early phase of acute pancreatitis, which lasts 1–2 weeks,

severity is defined by clinical parameters rather than
morphologic findings.
Most patients exhibit SIRS, and if this persists, patients are
predisposed to organ failure.
Three organ systems should be assessed to define organ failure:
respiratory, cardiovascular, and renal.
Persistent organ failure (>48 h) is the most important clinical
finding in regard to severity of the acute pancreatitis episode.
Organ failure that affects more than one organ is considered
multisystem organ failure.
The late phase is characterized by a protracted course of
illness.
The important clinical parameter of severity, as in the early
phase, is persistent organ failure.
These patients may require supportive measures such as
renal dialysis, ventilator support, or need for supplemental
nutrition via the nasojejunal or parenteral route.
The radiographic feature of greatest importance to
recognize in this phase is the development of necrotizing
pancreatitis on CT imaging.
Necrosis generally prolongs hospitalization and, if infected,
may require operative, endoscopic, or
percutaneous intervention.
 Scoring systems
• Ranson ’s Criteria
• Acute Physiology and Chronic Health
Examination (APACHE)-II Scoring
• Computed Tomography Severity
Index (CTSI)
• Bedside Index for Severity in Acute
Pancreatitis (BISAP) Scoring
 Bedside index of severity in acute
pancreatitis (BISAP) score
Evaluates the following Clinical Criteria:
• BUN >25 mg/dL (8.9 mmol/L)
• Impairment of mental status with a Glasgow coma
score <15
• SIRS (systemic inflammatory response syndrome)
• Age >60 years old
• Pleural effusion

Each determinant is given one point

SIRS is defined as 2 or more of the following variables;
• Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F)
• Heart rate of more than 90 beats per minute
• Respiratory rate of >20 breaths per minute or PaCO2 <32mm Hg
• Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms)
Wu BU et al GUT 2008
Management
 Acute pancreatitis

Management
• Severe pancreatitis carries a mortality of 80%
• Interventions in the first 24hrs can help to minimise the
morbidity and mortality.
Management Points:

• IV fluids

• Relief of pain

• Role of antibiotics

• Nutritional support

• Role of endoscopy
 Acute pancreatitis Managment
• The patient is made NPO to rest the pancreas and is
given intravenous narcotic analgesics to control pain
and supplemental oxygen (2 L) via nasal cannula.

• Intravenous fluids of lactated Ringer’s or normal saline

are initially bolused at 15–20 mL/kg (1050–1400 mL),
followed by 2–3 mL/kg per hour (200–250 mL/h), to
maintain urine output >0.5 mL/kg per hour.

• Lactated Ringer’s solution has been shown to decrease

systemic inflammation and may be a better crystalloid
than normal saline
• A decrease in hematocrit and BUN during the first 12–24
h is strong evidence that sufficient fluids are being
administered.

• A rise in hematocrit or BUN during serial measurement

should be treated with a repeat volume challenge with a
2-L crystalloid bolus followed by increasing the fluid rate
by 1.5 mg/kg per hour.

• If the BUN or hematocrit fails to respond (i.e., remains

elevated or does not decrease) to this bolus challenge and
increase in fluid rate, consideration of transfer to an
intensive care unit is strongly recommended for
hemodynamic monitoring.
 Acute pancreatitis
Relief of pain
• Narcotic analgesics
• Non narcotic analgesics
 Acute pancreatitis
Role of prophylactic Antibiotics
• Debatable
• SIRS v/s Infection
• Infection is unlikely in the first week
• No role of prophylatic antibiotics
 Role of Endoscopy

• Biliary pancreatitis – ERCP plus sphincterotomy

• Pancreatic Necrosis – Video Assisted Retroperitoneal

Debridement and Endoscopic Transgastric
Necrosectomy

• Ductal Disruption – Pancreatic duct Stenting

 Take Home Points
• The cornerstone in the diagnosis of acute pancreatitis is elevation in
amylase and lipase, but these enzymes are not useful in assessing disease
severity.
• At 24 hours of admission BISAP score is accurate, less cumbersome for
early identification of patients at risk for in-hospital mortality.
• Several simple and easy to obtain risk factors, including BMI, age,
hematocrit, BUN, and presence of pleural effusions on a chest x-ray, should
be documented to assist in severity assessment.
• C-reactive protein is the most heavily utilized, easy to employ, readily
available, and inexpensive acute phase reactant, and it remains the gold
standard for predicting severity of AP beyond 48 hrs of symptom onset.
The development of persistent or multiorgan failure during acute
• pancreatitis is associated with the highest risk of death.
Managing pancreatitis is NOT just starving a patient, giving IV fluids
• and analgesics. It’s about vigilantly observing for complications,
timely diagnosing and appropriate action.
Thank you