This document provides an overview of acute pancreatitis including its anatomy, etiology, pathophysiology, diagnosis, severity assessment, treatment, and complications. Some key points: - The pancreas is located in the retroperitoneum and has a head, neck, body and tail supplied by various arteries and veins. - Acute pancreatitis is defined as inflammation of the pancreas with abdominal pain and elevated pancreatic enzymes. Common causes include gallstones, alcohol use, and hyperlipidemia. - Inflammation occurs when pancreatic enzymes prematurely activate within the pancreas, causing injury. Systemic complications can develop depending on severity. - Diagnosis involves history, exam, and lab tests

1. Acute pancreatitis
Dr Lalit K Shah
Resident 1st year
General Surgery

2. Anatomy
• Pancreas is derived from Greek word ‘pan’ (all) and
‘kreas’ (flesh)
• Pancreas is situated in the retroperitoneum
• The average pancreas weighs beween 75 g to 125 g and
measures 10 cm to 20 cm
• Anatomically divided into five sections, the head;
uncinate; neck; body and tail

3. • The head, which occupies 30%
of the gland by mass lies to
right of midline within the C
loop of the duodenum,
overlying the body of second
lumbar vertebra and vencava
• Uncinate process extends from
the head of the pancreas
behind the SMV and terminates
adjacent to the SMA

4. • Behind the neck of the
pancreas, near its upper
border, the SMV joins splenic
vein to form the portal vein
• The body and tail of the
pancreas extend across the
midline slightly cephald
terminating within the splenic
hilum

5. Arterial Supply
• The head and uncinate process
are supplied by the
pancreaticoduodenal arteries
(superior and inferior)
• The neck, body, and tail receive
arterial supply from the splenic
arterial system (several small
branches, including the dorsal
pancreatic artery and greater
pancreatic artery)

6. Venous Drainage
• Head of the pancreas draining into the anterior
and posterior pancreaticoduodenal veins
• The posterosuperior pancreaticoduodenal vein
enters the SMV laterally at the superior border
of the neck of the pancreas.
• The anterior superior pancreaticoduodenal
vein enters the right gastroepiploic vein just
before its confluence with the SMV at the
inferior border of the pancreas
• The body and tail are drained through the
splenic venous system

7. Lymphatic Drainage

9. Definition
• Pancreatitis is inflammation of the pancreatic parenchyma
• Acute pancreatitis is defined as an acute condition
presenting with abdominal pain, a threefold or greater rise
in the serum levels of the pancreatic enzymes amylase or
lipase, and/or characteristic findings of pancreatic
inflammation on contrast-enhanced CT

10. Classification
• Two classification system have been proposed : on the
basis of severity
1. Three grades (mild, moderately severe and severe ) of
Revised Atlanta classification
2. Four catagories(mild, moderate severe and critical) of
Determinant based classification
Schwartz 11th ed

12. Epidemiology
• In context of Nepal, incidence of AP ranges from 10 to 50
per 100,000 per annum
• Overall mortality of approximately 4-6% and increases to
17-39 %in severe cases
• In Nepal exact data are yet to be discovered
• But study claims alcoholic pancreatitis as the leading
cause,accounting for 66 % of all causes

14. Etiology

15. Gallstones:
• Are the most common
cause (worldwide)
• Accounts for 40 to 70% of
cases
• However only 3 -7 % of
patients with gallstones
develop pancreatitis

16. • Three possibilities have been suggested
1. Common channel hypothesis : Reflux of bile into the
pancreatic duct due to transient obstruction of ampulla
during passage of stone
2. Edema resulting from the passage of a stone
3. Obstruction of pancreatic duct and leading to ductal
hypertension
• Small gallstones are associated with increase risk of pancreatitis

17. Alcohol : responsible for approximately 25 to 35 % of cases of acute
pancreatitis ,worldwide
1. Act by increasing the synthesis of enzymes by pancreatic acinar
cells to synthesize the digestive and lysosomal enzymes
2. Sensitization of acinar cells to cholecystokinin induced premature
activation of zymogens
3. Ethanol induces ductal permeability which cause prematurely
activated enzyme to cause damage to the pancreatic parenchyma
4. Decreases the level of trypsin inhibitor concentration

18. Hyper lipidemia :
• Lipase liberates toxic fatty acid into pancreatic micro
circulation
• Leads to impairment of pancreatic microcirculation and
ischemia

19. • Hereditary pancreatitis : Autosomal dominant disease
related to mutation of trypsinogenic gene
• Drugs : Thaizides diuretics, frusemide, Estrogen
replacement therapy,steroid therapy , propofol

20. Pathophysiology
Pancreatitis begins with :
Premature activation of pancreatic enzymes within
pancreas
Activation of digestive zymogen inside acinar cells
Causes injury to acinar cells

21. • Events subsequent to acinar cell injury :
Inflammatory cell activation and recruitment
Generation and release of cytokines and other chemical
mediators
That causes systemic inflammation and multiple organ
dysfunction

22. Diagnosis
• Modalities of diagnosis
1.Detailed history
2.Thorough examination
3.Appropriate investigations

23. Detailed History
Clinical Presentation
• Pain is the cardinal symptom
• Characteristically develops quickly, reaching maximum
intensity within minutes
• Pain is severe , constant and refractory to the usual dose
of analgesics
• Usually experienced in the epigastrium, but may be
localized to the upper quadrant or diffused throughout
abdomen

24. • Radiates to back in 50% of the patient
• In some ,relieved by leaning forward
• Nausea ,repeated vomiting and retching are marked
• Retching may persists even if stomach is kept empty by
nasogastric aspiration

26. Thorough Examination
• Can be fair looking or at the extreme, gravely ill look with
profound shock toxicity and confusion
• Tachypnea and tachycardia is usual, hypotension can be
present
• Body temperature is often normal, but rises as
inflammation develops
• Mild icteric due to biliary obstruction in gall stone
pancreatitis

27. • Bleeding into fascial plane can produce bluish
discoloration Flanks (Grey turner’s sign) or umbilicus
(cullen’s sign)
• Usually muscle guarding in upper abdomen
• Pleural effusion present in 10-20% of patients
• Another rare sign is tetany due to hypocalcemia

28. Appropriate Investigations
• Investigations of acute pancreatitis must be based on :
1. Is a diagnosis of acute pancreatitis correct ?
2. How severe is the attack ?
3. What is the etiology ?

29. Laboratory
Serum amylase or lipase (> 3 times upper limit of normal)
• Serum amylase concentrates rises immediately with onset
of disease
• Peaks within several hours and remains elevated for 3-5
days
• No correlation between extent of serum amylase elevation
and severity
• Serum lipase if available, is more sensitive and specific
then amylase

30. Imaging
• Non specific sign on abdominal radiographs :
Colon cut off sign
Generalised or localized illeus (sentinel loop)
Renal halo sign
Chest radiograph may reveal a pleural effusion

32. • USG doesnot establish the diagnosis of acute pancreatitis
• Should be performed :
To detect gallstone,as a potential cause
To rule out acute cholecystitis

33. • CECT is indicated in following :
1. If there is diagnostic uncertainty.
2. In patients with severe acute pancreatitis, to distinguish
interstitial from necrotising pancreatitis
3. Severity of pancreatitis detected on CT be staged a/c to
balthazar score
4. In patients with organ failure, signs of sepsis and clinical
deterioration
5.When localized collection is suspected, fluid collection,
psuedocyst

35. • MRI and MRCP ,are used increasingly to diagnose and
assess severity
• MRI appears to be comparable to CT :
As effective as CT in demonstrating presence and extent of
pancreatic necrosis and fluid collection
Regarding the severity of the disease
Probably superior for indicating the suitability of collections
for non surgical drainage

37. Severity scoring system
• Ranson’s criteria
• Glass gow score
• SOFA score
• CT severity index (balthazar score)
• Apache II score
• Systemic inflammatory response syndrome score
• BISAP score
• Harmless acute pancreatitis score

41. Harmless Acute Pancreatitis Score
• Assess for the following features :
. No sign of peritonitis
Normal serum creatinine
Normal Hematocrit
If all three features are present ,it is 98% accurate at
identifying patients with a non severe disease

42. CT severity index :
23 % mortality with any degree of pancreatic necrosis
0 % with no necrosis

43. Treatment
• After initial assessment if a patient is considered to have mild
acute pancreatitis
A conservative approach is indicated with IV fluids and
frequent observation
Brief period of fasting for patient who is nauseated, prolonged
Nil by mouth has got little physiological justification
Antibiotics are not indicated
Apart from analgesic and anti emetics ,No drugs and
intervention are warranted

44. Early Management of Severe acute Pancreatitis
• Admission to HDU/ICU
• Analgesia
• Aggressive fluid rehydration
• Supplemental oxygen
• Invasive monitoring of vital signs, central venous
pressure, urine output, blood gases
• Frequent monitoring of haematological and biochemical
parameters (including liver and renal function, clotting, serum calcium,
blood glucose)

45. • Nasogastric drainage (only initially)
• Antibiotics if cholangitis suspected; prophylactic antibiotics can be
considered
• CT scan essential if organ failure, clinical deterioration or signs of
sepsis develop
• ERCP within 72 hours for severe gallstone pancreatitis or signs of
cholangitis
• Supportive therapy for organ failure if it develops (inotropes,
ventilatory support, haemofiltration,)

46. Local complications
• Acute (< 4 weeks, No defined walls)
 Acute pancreatic fluid collection
 Acute necrotic collection
• Chronic ( > 4 weeks, Defined walls)
 Pancreatic pseudocyst
 Walled of necrosis

48. Systemic complications
1.Cardiovascular
Shock, Arrhythmias
2. Pulmonary
ARDS ,Pulmonary Effusion
3.Renal failure
4.Haematological

49. 5. Metabolic
Hypocalcaemia
Hyperglycaemia
Hyperlipidaemia
6. Gastrointestinal
Ileus ,GI hemmorrhage
7. Neurological
Visual disturbances
Confusion, irritability
Encephalopathy
8. Miscellaneous
Subcutaneous fat necrosis, Arthralgia