This document discusses pancreatitis, including its types, causes, pathophysiology, clinical presentation, diagnosis, and treatment. It notes that pancreatitis is an inflammatory process where pancreatic enzymes auto-digest the gland. The main causes are alcohol abuse and gallstones. Clinical features include epigastric pain radiating to the back, nausea, vomiting, and fever. Diagnosis involves blood tests showing elevated lipase and amylase levels. Treatment depends on severity but generally involves pancreatic rest, fluid resuscitation, nutritional support, and pain management.

1. PANCREATITIS
Dr. Aloo

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