2. Objectives
• Identify different types of pancreatitis.
• List various causes of pancreatitis as biliary stones, alcohol, and the
mechanism of their action.
• Clinical presentation of pancreatitis
• Understand how to diagnose a case of pancreatitis with the help of
clinical presentation, histopathologic changes, and imaging studies
and differentiate it from other causes of acute abdomen.
• complications of pancreatitis.
3. Introduction
• Pancreatitis is an inflammatory process in which pancreatic enzymes
auto-digest the gland.
• Can be: Acute, Chronic, Recurrent acute, and Acute on chronic
• Acute pancreatitis - May heal without any loss of function or
morphologic changes.
• Recurrent pancreatitis - recurs intermittently, contributing to the
functional and morphologic loss of the gland.
• Chronic pancreatitis-persistent low grade inflammations.
4. Epidemiology
• One of the commonest conditions that a physician or a surgeon comes
across
• Associated morbidity is high
• The cost of treatment is high
• In severe cases the mortality maybe 20-30%
• 40 cases per year per 100,000 adults.[International]
• Ranges between 5 and 80 per 100,000 population
• The highest incidence recorded in the United States and Finland
• In 80% of cases: mild and resolves without serious problem
• Sex No predilection exists.
5. Pathophysiology
• located in the retroperitoneal space No capsule, inflammation can spread easily.
Local effects:
• Acute edematous pancreatitis: When Parenchyma edema and peripancreatic fat necrosis occur first
• Haemorrhagic or narcotizing pancreatitis: When necrosis involves the parenchyma, accompanied by
hemorrhage and dysfunction of the gland
• pancreatic abscesses and Pseudocysts: due to necrotizing pancreatitis because enzymes can be walled off
by granulation tissue
systemic effects ;
• Due to cytokines: bradykinins and phospholipase A.
• Cytokines cause Vasodilatation, increase in vascular permeability, pain, and leukocyte accumulation in the
vessel walls.
• Fat necrosis may cause hypocalcemia. Pancreatic B-cell injury may lead to hyperglycemia.
• in its most severe form: Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression,
hemorrhage, and hypotensive shock
6. Causes
Alcohol abuse - 44% of patients
• At the cellular level – ethanol leads to intracellular accumulation of
digestive enzymes and their premature activation and release.
• At the ductal level - increases the permeability of ductules, enzymes
reach the parenchyma, resulting in pancreatic damage.
• Formation of protein plugs increases the protein content of the
pancreatic juice and decreases bicarbonate levels and trypsin
inhibitor concentrations.
• This leads to blocking the pancreatic outflow and obstruction.
7. Cont.
• Biliary calculi cholelithiasis, choledocholithiasis
calculi lodge in the pancreatic duct or ampulla of Vater and obstruct
the pancreatic duct, leading to the extravasation of enzymes into the
parenchyma.
• Medications, including azathioprine, corticosteroids, sulfonamides,
thiazides, furosemides, NSAID”S
• Viral infections
• Trauma
8. Clinical Presentation
The main presentation - Epigastric pain or right upper quadrant pain radiating through,
rather than around, to the back.
• Pain is frequently acute in onset, occurring 24 to 48 hours after a very heavy meal or
alcohol ingestion, and it may be diffuse and difficult to localize. It is generally more
severe after meals and is unrelieved by antacids.
• Nausea and/or vomiting, Fever
• History of previous biliary colic
• Palpitations
• Muscular spasm –in extremities may be noted secondary to hypocalcemia.
Ask the patient about ;
• Recent surgery or invasive procedure e.g. ERCP
• Family history of hypertriglyceridemia.
• Alcohol consumption
9. Cont.
• Patients are acutely ill
• Tachypnea
• Hypotension
• Fever
• Abdominal tenderness, distension, guarding, and rigidity
• Mild jaundice
• Diminished or absent bowel sounds
• Basilar rales, especially in the left lung.
• Pleural effusion: Because of the contiguous spread of inflammation from the pancreas
Severe cases may have;
• Grey Turner sign (ie, bluish discoloration of the flanks)
• Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak
of blood from the pancreas in hemorrhagic pancreatitis.
10. Laboratory Findings
• Elevation of white count- 20,000-50,000.
• Elevated serum lipase and amylase(5 to 40 times)
• (lipase is generally considered a better indicator).
• Abnormal low serum Ca due to Binding of Ca in areas of fat necrosis.
• Abdominal ultrasound is generally performed first, for detecting
gallstones, diagnosing alcoholic fatty liver (combined with history of
alcohol consumption).
11. Histopathologic Changes
• In mild acute pancreatitis: changes frequently include interstitial
edema and infiltration by inflammatory cells with relatively little
necrosis.
• In severe acute pancreatitis: extensive necrosis, thrombosis of
intrapancreatic vessels, vascular disruption, and intraparenchymal
hemorrhage can be seen.
• In chronic pancreatitis: there is loss of pancreatic acini, islets of
Langerhans and fibrosis.
12. Treatment
Mild Pancreatitis Pancreatic: rest Supportive care
• fluid resuscitation
• watch BP and urine output
• Pain Control
• NG tubes and H 2 blockers or PPIs are usually not helpful
• Refeeding (usually 3 to 7 days) If: – Bowel Sounds Present – Patient Is
Hungry – Nearly Pain-free (Off IV Narcotics)
13. Cont.
Severe Pancreatitis: Pancreatic Rest & Supportive Care
• Fluid Resuscitation – may require 5-10 liters/day –
• Careful Pulmonary & Renal Monitoring – ICU
• Maintain Hematocrit Of 26-30%
• Pain Control
• Correct Electrolyte Derangements (K +, Ca ++, Mg ++ )
• Contrasted CT scan at 48-72 hours
• Prophylactic antibiotics if present
• Nutritional support – May be NPO for weeks – TPN 15
