Welcome To The

Morning Session

Dr. Sadia Afrin

Intern Doctor
Department of Medicine
TMMC&H
Acute pancreatitis
 INCIDENCE

• Acute pancreatitis accounts for

3% of all cases of abdominal
pain admitted to hospital.
• It affects 2-28 per 100000 of the
population.
• Second most common inpatient GI
diagnosis.
– After cholelithiasis and acute
cholecystitis.
– Ahead of acute appendicitis.
• Overall mortality rate less than 5%
 DEFINITION

– It is an acute abdominal condition

presenting with abdominal pain
and usually associated with raised
pancreatic enzyme levels as a
result of inflammation of
pancreas.
 CLINICALLY
Presenting with 2 of the following 3
criteria:
• Symptoms (e.g, Epigastric
pain) consistent with
pancreatitis.
• Serum amylase or lipase level
greater than 3 times the
laboratory’s upper limit of
normal.
• Radiologic imaging
consistent with pancreatitis.
₋ (Usually using CT or MRI)
 CAUSES OF ACUTE PANCREATITIS
1 COMMON

• Gall stones.
• Alcohol.
• Idiopathic.
• Post- ERCP.
2 RARE

• Post- surgical (abdominal, cardiopulmonary

bypass).
• Trauma.
• Drugs(thiazide diuretics, sodium valproate).
• Metabolic- hypercalcaemia,
hypertryglyceridaemia.
• Pancreas divisum.
• Infections- mumps, coxsackie virus.
• Hereditary.
• Renal failure.
• Organ transplantation.
• Severe hypothermia.
• Petrochemical exposure.
 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 rxn.

The third phase of pancreatitis is due to

the effects of activated proteolytic
enzymes and cytokines, released by the
inflamed pancreas, on distant organs.
• Conversion of trypsinogen to trypsin,
within acinar cells.
• Trypsin catalyzes conversion of
proenzymes, including trypsinogen and
inactive precursors of elastase,
phospholipase A2 (PLA2), and
carboxypeptidase, to active enzymes.
• Trypsin also may activate the
complement and kinin systems.
• Active enzymes autodigest the
pancreas and initiate a cycle of
releasing more active enzymes.
• Pancreatic secretory trypsin inhibitor
(PSTI, now called SPINK1) binds and
inactivates about 20% of the trypsin
activity.
• Low intraacinar calcium
concentrations also prevent further
autoactivation of trypsin.
 Management
History

• Alcohol intake.
• Gallstone disease.
• ERCP.
• Drug : Thiazide diuretics, sodium
valproate.
• Abdominal surgery.
• Trauma to the abdomen.
 Clinical features
Symptoms

1.Upper abdominal pain.

• Severe
• Constant
• Increasing intensity over 15-60 minutes
• Radiates to the back

2. Nausea and vomiting.

 Signs
• Marked epigastric tenderness.

• Bowel sound become quiet or absent as

paralytic ileus develops.

• In severe cases patient becomes

hypoxic & develops hypovolaemic
shock with oliguria.

• Grey Turner’s sign or Cullen’s sing.

 Investigations
 Serum amylase: significant if there is
more than 3 times of normal level
within 24 hours of onset of pain.

 Serum lipase: Remain elevated for a

longer period of time than amylase.

 Urinary amylase.
 CRP: For severity & prognosis.

 WBC count: Leukocytosis.

 Serum calcium: Hypocalcaemia.

 Blood glucose level: May be elevated.

 Blood urea, s. electrolytes, s. ALT.

Radiology

• USG of W\A.
• Plain X-ray of abdomen.
• MRCP.
• ERCP.
 TREATMENT
1. Hospitalization.

2. Analgesics & anti-emetics: Opiate

analgesics should be given.

3. Correction of hypovolaemia: By N\S or

other crystalloids.

4. Oxygen should be given to hypoxic

patients.
5. Nasogastric aspiration : if paralytic ileus
present.

6. Ventilatory support: Who develops SIRS.

7. Hyperglycaemia: corrected by using insulin.

8. Hypocalcaemia: by intravenous calcium

injection.
9. Enteral feeding.

10. Prophylaxis of thromboembolism with

LMW heparin.

11. Prophylactic broad spectrum IV

antibiotic [Imipenem, Cefuroxime].

12. Treatment of cause.

• Patient who presents with cholangitis
or jaundice in association with severe
acute pancreatitis should undergo
urgent ERCP to diagnose and treat
choledocolithiasis.
Cholecystectomy should be undertaken
within two weeks of resolution of
pancreatitis.
Patient with necrotising pancreatitis or
pancreatic abscess require urgent
endoscopic or minimally invasive
retroperitoneal pancreatic (MIRP)
necrosectomy to debride all cavities of
necrotic material.
• Pancreatic pseudocyst can be treated by
drainage into stomach , duodenum or
jejunum.
• This is usually performed after an interval
of at least 6 weeks once a pseudo capsule
has matured, by surgical or endoscopic
cystogastrostomy.
Adverse Prognostic Factor
1. Age > 55 years .
2. PO2 < 8 kPa[ 60mmHg].
3. WBC > 15000/cmm.
4. Albumin < 32 g/l.
5. Serum Calcium < 2mmol/L.
6. Glucose > 10 mmol/L.
7. Urea > 16mmo/L.
8. ALT > 200 U/L.
9. LDH > 600 U/L.
Complication of Acute Pancreatitis.
A. Systemic
1. SIRS.
2. Hypoxia.
3. Hyperglycaemia.
4. Hypocalcaemia.
5. Reduce S.albumin concentration.

B. Pancreatic
1. Necrosis.
2. Abscess.
3. Pseudocyst.
4. Pancreatic ascites or pleural effusion.

C. GIT
1. Upper GI bleeding.
2. Variceal Haemorrhage.
3. Erosion into colon.
4. Duodenal obstruction.
5. Obstructive jaundice.
 Prognosis
• The vast majority of patients with a
mild to moderate episodes of acute
pancreatitis will make a full recovery
with no long term sequelae.
• Recurrent episodes of pancreatitis may
occur,particularly if there has been any
long term pancreatic ductular damage.
• Patients with more severe acute
pancreatitis may develop pancreatic
insufficiency with respect to both
exocrine (Malabsorption) and
endocrine function(Diabetes).
• Both of these carry their own significant
life long morbidity.
 REFERENCES
1. DAVIDSONS PRINCIPLES AND PRACTICE
OF MEDICINE. (23rd Edition)
THANK YOU