The document provides an in-depth overview of acute pancreatitis, including its anatomy, causes, symptoms, diagnosis, treatment, and complications. Key points include the dual function of the pancreas, the major etiological factors for acute pancreatitis, and diagnostic criteria using blood tests, ultrasounds, and CT scans. It also discusses both conservative and surgical treatment options along with dietary recommendations for managing the condition.

1. IVANO-FRANKIVSK NATIONAL MEDICAL
UNIVERSITY
DEPARMENT OF SURGERY № :1
TOPIC : ACUTE PANCREATITIS
B Y
V E L L A I C H A M Y R A J R A J K U M A R
5 4 + G R O U P, I V C O U R S E
0 6 / 0 7 / 2 0 1 5

2. • Anatomy
• DEFINITION
• ETIOLOGY
• CLASSIFICATION
• PATHOGENESIS
• PATHOMORPHOLOGY
• SIGNS AND SYMPTOMS
• Physical examination
• COMPLICATIONS
• DIFFERNTIAL DIAGNOSIS
• DIAGNOSITIC METHODS
• TACTICS OF TREATMENT

4.  The pancreas is situated in the retroperitoneum.
 It is divided into a head, body and tail.
 The head lies within the curve of the duodenum, overlying
the body of the second lumbar vertebra and the vena cava.
 The aorta and the superior mesenteric vessels lie behind the
neck of the gland.
 Coming off the side of the pancreatic head and passing to
the left and behind the superior mesenteric vein is the
uncinate process of the pancreas.
 Behind the neck of the pancreas, near its upper border, the
superior mesenteric vein joins the splenic vein to form the
portal vein.
 The tip of the pancreatic tail extends up to the splenic hilum.

5.  The pancreas is a dual-function gland, having
features of both endocrine and exocrine glands.
 The part of the pancreas with endocrine function is
made up of cell clusters called islets of Langerhans.
Four main cell types exist in the islets.
 α alpha cells secrete glucagon (increase glucose in
blood), β beta cells secrete insulin (decrease
glucose in blood), Δ delta cells secrete somatostatin
(regulates/stops α and β cells) and PP cells, or γ
(gamma) cells, secrete pancreatic polypeptide.

6.  The pancreas also functions as an exocrine
gland that assists the digestive system.
 Exocrine cells make and release pancreatic
juice. The juice travels through the pancreatic
duct into the duodenum. Enzymes in the
pancreatic juice help digest fat, carbohydrates
and protein in food.
 Pancreatic juice discharges into the duodenum
through ducts. It is alkaline as it
contains bicarbonate and chloride ions.

9.  The pancreas receives parasympathetic nerve fibers
from the posterior vagal trunk via its celiac branch.
Sympathetic supply comes from T6-T10 via the
thoracic splanchnic nerves and the celiac plexus

10.  Pancreatitis is inflammation of the gland
parenchyma of the pancreas.
 Acute pancreatitis is defined as an acute
condition presenting with abdominal pain
and is usually associated with raised
pancreatic enzyme levels in the blood or
urine as a result of pancreatic inflammation.
 Acute pancreatitis may recur.

11. ETIOLOGY
The two major causes of acute pancreatitis are
biliary calculi, which occur in 50–70 per cent of
patients, and alcohol abuse, which accounts
for 25 per cent of cases.

12. POSSIBLE CAUSES OF ACUTE PANCREATITIS
Gallstones
Alcoholism
Post-ERCP
Abdominal trauma
Following biliary, upper gastrointestinal or cardiothoracic
surgery
Ampullary tumour
Drugs (corticosteroids, azathioprine, asparaginase, valproic
acid, thiazides, oestrogens)
Hyperparathyroidism
Hypercalcaemia
Pancreas divisum
Autoimmune pancreatitis
Hereditary pancreatitis
Viral infections (mumps, Coxsackie B)

13. 
 Idiopathic acute pancreatitis
 Biliary acute pancreatitis (Gallstone pancreatitis)
 Alcohol-induced acute pancreatitis
 Drug-induced acute pancreatitis (Azathioprine,
Mesalazine, Valproate, Propofol, Enalapril and other
ACE inhibitors, Statins)
 Other acute pancreatitis
 Acute pancreatitis, unspecified
CLASSIFICATION
ICD-10

14. CLASSIFICATION
V All-russian convention of surgeons, 1978
Clinico-anatomical forms:
• Arching form
• Fatty pancreatonecrosis
• Hemorrhagic pancreatonecrosis
Prevelence of necrosis:
• Local(focus) damage of gland
• Subtotal dmage of the gland
• Total damage of the gland
Accordng to progress:
• Abortive
• progressive
Periods of disease:
• Hemodynamic violations and pancreatogenic shock
• Functional insufficiency of parenchymatous organ
• Degenerative and suppuration complication

15. PATHOGENESIS OF ACUTE PANCREATITIS
Interstitial oedema
Impaired blood flow
Ischaemia
Acinar cell injury
Interstitial inflammation
oedema
Gallstone
Chronic alcoholism
Release of intracellular
proenzymes and
lysosomal hydrolases
Activation of enzymes
ACTIVATED ENZYMES
Delivery of proenzymes to
lysosomal compartment
Intracellular activation of
enzymes
Proteolysis
(proteases)
Fat necrosis
(lipase, phospholipase)
Haemorrhage
(elastase)
Alcohol, drugs
trauma, ischaemia,
viruses
Metabolic injury
(experimental)
Alcohol, duct obstruction
DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR
TRANSPORT

18. • Autodigestion is a currently accepted pathogenic theory; according
to it, pancreatitis results when proteolytic enzymes (e.g.,
trypsinogen, chymotrypsinogen, proelastase, and lipolytic enzymes
such as phospholipase A 2 ) are activated in the pancreas rather than
in the intestinal lumen. A number of factors (e.g., endotoxins,
exotoxins, viral infections, ischemia, anoxia, lysosomal calcium,
and direct trauma) are believed to facilitate activation of trypsin.
Activated proteolytic enzymes, especially trypsin, not only digest
pancreatic and peripancreatic tissues but also can activate other
enzymes, such as elastase and phospholipase A 2 .
• Spontaneous activation of trypsin also can occur.
• Activation of pancreatic enzymes in the pathogenesis of acute pancreatitis.
• Theory of “general duct” with the reflux of bile into the ducts of pancreas.
• Theory of blockade of outflow of pancreatic juice with the development of
intraductal hypertension and penetration of secret into the interstial tissue.
• Violation of blood flow of pancreatic juice (vasculitis, thrombophelibitis, and
embolism).
• Toxic and allergic damage of gland.

19. PATHOMORPHOLOGY
•The process of acute inflamation of pancreas passes through the
stages of edema,pancreatonecrosis and suppuration
•Edema : Hyperemia, increased in volume, with shallow nodes of
necrosis .
•Pancreatonecrosis can be fatty or hemorrhagic character (shows
whitish yellow necrosis).
•Dystrophy : its exposed microscopically .
•Necrosis: hemorrhages, thrombosis of vessels and signs of
inflammatory.

20. ACUTE PANCREATITIS; HEMORRHAGE
AND NECROSIS

21. NORMAL PANCREAS
ACUTE PANCREATITIS

22. SAPONIFICATION OF FAT
A SURGICAL SPECIMEN OF THE
TRANSVERSE COLON AND
GREATER OMENTUM

23. SIGNS AND
SYMPTOMS
Main symptoms :
• Upper abdominal pain that radiates into the back. It may
be aggravated by eating, especially foods high in fat.
• Swollen and tender abdomen
• Nausea and vomiting (coffee ground appearence)
• Fever
• Increased heart rate

24. Additional symptoms:
• Weight loss caused by poor absorption (malabsorption) of
food.
• This malabsorption happens because the gland is not
releasing enough enzymes to break down food.
• Also, diabetes may develop if the insulin-producing cells
of the pancreas are damaged.
• Severe intoxication

25. CULLEN SIGN – DISCOLOURATION AROUND
UMBILICUS
Grey-Turner sign- discolouration in the flanks

26. • The abdominal is distended, peristaltic sounds inaudible.
• The signs of paresis of stomach and intestine appears
early.
• On palpation tenderness in the epigastria area and in
right and some times in the left hypochondria also
marked.
*

27. Complication:
Early
• Shock
• Acute cardiac, pulmonary, hepatic insufficiency
Late
• Abscess of pancreas
• Subdiaphargmatic, interintestinal abscesses
• Pyogenic abscesses of omentum
• Phelgmons of retro peritoneal space.
• Erosive bleeding.

28. DIFFERNTIAL DIAGNOSIS:
Acute peritonitis, cholecystitis
Macroamylasemia
Macrolipasemia
Malabsorption syndromes/processes
Perforated viscus
Acute mechanical intestinal obstruction

29. predicting the severity of acute pancreatitis:
At admission
 age in years > 55 years
 white blood cell count > 16000 cells/mm3
 blood glucose > 11 mmol/L (> 200 mg/dL)
 serum AST > 250 IU/L
 serum LDH > 350 IU/L
At 48 hours
 Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
 Hematocrit fall > 10%
 Oxygen (hypoxemia PO2 < 60 mmHg)
 BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
 Base deficit (negative base excess) > 4 mEq/L
 Sequestration of fluids > 6 L

30. Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality Score 7 to 8 : 100%
mortality
 Hemorrhagic peritoneal fluid
 Obesity
 Indicators of organ failure
 Hypotension (SBP <90 mmHG) or tachycardia > 130
beat/min
 PO2 <60 mmHg
 Oliguria (<50 mL/h) or increasing BUN and creatinine
 Serum calcium < 1.90 mmol/L (<8.0 mg/dL)
 serum albumin <33 g/L (<3.2.g/dL)>

31. Balthazar Grade
Balthazar Grade Appearance on CT CT Grade Points
 Grade A Normal CT 0
points
 Grade B Focal or diffuse enlargement of the pancreas 1
point
 Grade C Pancreatic gland abnormalities and peripancreatic inflammation
2points
 Grade D Fluid collection in a single location 3
points
 Grade E Two or more fluid collections and / or gas bubbles in or adjacent to
pancreas4points
Necrosis Score
Necrosis Percentage Points
 No necrosis 0 points
 0 to 30% necrosis 2 points
 30 to 50% necrosis 4 points
 Over 50% necrosis 6 points
The numerical CTSI (Computed Tomography Severity Index) has a maximum of
ten points, it is the sum of the Balthazar grade points and pancreatic necrosis
grade points

32. Diagnostic criteria:
 Blood test
 Urine test
 Biochemical test (amylase, bilirubin, sugar)
 Ultrasound
 CT scan
 Cholecystocholangiography
 Endoscopic retrograde cholangiopancreatgraphy
 Laparoscopy
 Laprocentesis

33. BLOOD TEST:
 Acompletebloodcount(CBC)demonstratesleukocytosis(whitebloodcell
[WBC]counthigherthan12,000/µL)withthedifferentialbeingshifted
towardthesegmentedpolymorphonuclear(PMN)cells.Leukocytosismay
representinflammationorinfection.
 AC-reactiveprotein(CRP)valuecanbeobtained24-48hoursafter
presentationtoprovidesomeindicationofprognosis.Higherlevelshave
beenshowntocorrelatewithapropensitytowardorganfailure.ACRPvalue
indoublefigures(ie,≥10mg/dL)stronglyindicatesseverepancreatitis.CRP
isanacute-phasereactantthatisnotspecificforpancreatitis.

34. LIVER ENZYMES :
 Determine alkaline phosphatase, total bilirubin, aspartate aminotransferase (AST), and
alanine aminotransferase (ALT) levels to search for evidence of gallstone pancreatitis. An
ALT level higher than 150 U/L suggests gallstone pancreatitis and a more fulminant disease
course.
 Obtain measurements for blood urea nitrogen (BUN), creatinine, and electrolytes; a great
disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids.
Measure blood glucose level because it may be elevated from B-cell injury in the pancreas.
 Measure calcium, cholesterol, and triglyceride levels to search for an etiology of
pancreatitis (eg, hypercalcemia or hyperlipidemia) or complications of pancreatitis (eg,
hypocalcemia resulting from saponification of fats in the retroperitoneum). However, be
aware that baseline serum triglyceride levels can be falsely lowered during an episode of
acute pancreatitis.
 Elevated serum amylase and lipase levels, in combination with severe abdominal pain,
often trigger the initial diagnosis of acute pancreatitis.
 Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14
days after treatment.
 Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis
(depleted acinar cell mass) and hypertriglyceridemia.
 Reasons for false positive elevated serum amylase include salivary gland disease (elevated
salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.
 If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis
due to alcohol.[9]
 Decreased serum calcium

35. Ultrasound exam:
 Increase in size of pancreas, thickening
of walls and presence or absence of
calculus of gall bladder and common
bile duct.

36.  Inhomogeneous swollen pancreas and dilatated bile duct

37.  Edematous swollen tail and extrapancreatic soft tissue
edema

38. CT scan:
 Intrapancreatic-diffuseorsegmentalenlargement,edema,gas
bubbles,pancreaticpseudocystsandphlegmons/abscesses(which
present4to6wksafterinitialonset)
 Peripancreatic/extrapancreatic-irregularpancreaticoutline,
obliteratedperipancreaticfat,retroperitonealedema,fluidinthe
lessarsac,fluidintheleftanteriorpararenalspace
 Locoregional-Gerota'sfasciasign(thickeningofinflamedGerota's
fascia,whichbecomesvisible),pancreaticascites,pleuraleffusion
(seenonbasalcutsofthepleuralcavity),adynamicileus,etc.

39.  Axial CT in a patient with acute exudative pancreatitis
showing extensive fluid collections surrounding the
pancreas.

40. Endoscopic retrograde
cholangiopancreatgraphy
 Endoscopic retrograde
cholangiopancreatogram
of a young woman with
gallbladder stones.

41.  Conservative treatment
 Surgical treatment
 Diet therapy

42. CONSERVATIVE TREATMENT:
 Fluid replacement:
Aggressive hydration at a rate of
5 to 10 mL/kg per hour of isotonic
crystalloid solution (e.g., normal
saline or lactated Ringer’s
solution) to all patients with acute
pancreatitis.
 Pain control:
1. Opioids are safe and effective
at providing pain control in
patients with acute
pancreatitis.
2. Hydromorphone or fentanyl (I
ntravenous) may be used for
pain relief in acute pancreatitis

43.  Etiological treatment:
1. Antibiotic, antiviral drugs in
case of etiology is bacteria or
virus.
2. Carbapenems 0.5 gram
intravenously every eight
hours for two weeks.
 Anticholinergic
drug(atropine sulphate,
methacin)
 H2-histamine
drug(cimetidine, ranisan,
ranitidine)

44. SURGICALTREATMENT:
 Superior-middle
laparotomy
 Cholecystectomy
 Pancreatectomy
 Transduodenal
papillotomy with
sphincteroplasty
 Indications:
1. Infected pancreatic necrosis
2. Diagnostic uncertainty
3. Complications

45.  Sphincterotomy. Using a small wire on the endoscope, the doctor
finds the muscle that surrounds the pancreatic duct or bile ducts and
makes a tiny cut to enlarge the duct opening. When a pseudocyst is
present, the duct is drained.
 Gallstone removal. The endoscope is used to remove pancreatic or
bile duct stones with a tiny basket. Gallstone removal is sometimes
performed along with a sphincterotomy.
 Stent placement. Using the endoscope, the doctor places a tiny piece
of plastic or metal that looks like a straw in a narrowed pancreatic or
bile duct to keep it open.
 Balloon dilatation. Some endoscopes have a small balloon that the
doctor uses to dilate, or stretch, a narrowed pancreatic or bile duct. A
temporary stent may be placed for a few months to keep the duct
open.
 People who undergo therapeutic ERCP are at slight risk for
complications, including severe pancreatitis, infection, bowel
perforation, or bleeding. Complications of ERCP are more common in
people with acute or recurrent pancreatitis. A patient who experiences
fever, trouble swallowing, or increased throat, chest, or abdominal pain
after the procedure should notify a doctor immediately.

46. DIET THERAPY:
1. Diet №:5 ( avoid
oily, spicy fatty
foods, fast foods )

47. AVOID FAST FATTY FOODS