Acute pancreatitis is inflammation of the pancreas that ranges from mild to severe. Mild cases involve pancreatic edema while severe cases involve pancreatic necrosis and multi-organ failure. The main causes are gallstones and alcohol use. Diagnosis is based on abdominal pain and elevated pancreatic enzymes. Severity is assessed using criteria like Ranson score, CT severity index, and Atlanta criteria. Treatment of mild cases involves fluids and pain control while severe cases require intensive care monitoring, fluids, nutrition, and may involve ERCP or surgery for complications.

1. ACUTE
PANCREATITI
S
Dr. Priyadarshan Konar
1st year PGT
Department of Surgery
IMS & SUM Hospital
08.12.2016

2. Introduction
 The name ‘pancreas’ is derived from the greek ‘pan’ (all) and
‘kreas’ (flesh)
 The average gland weighs between 75 and 125 gm. and
measures 10 to 20 cm
 Retroperitoneal organ that lies in an oblique position, sloping
upward from the C-loop of the duodenum to the splenic hilum
 Due to its retroperitoneal location, pain associated with
pancreatitis often is characterized as penetrating through the
back

3.  Anatomically divided into 4 parts -
① Head
② neck
③ Body
④ Tail
 Head occupies 30% of the gland by
mass, whereas body and tail
comprises 70% of the whole organ
 Coming off the side of the pancreatic head and passing to the
left and behind the sup mesenteric vein is the Uncinate process
of the pancreas

4.  80-90% is composed of exocrine acinar tissue, which is organized
into lobules
 The main duct is lined by columnar epithelium, which becomes
cuboidal in the ductules
 The endocrine cells arrange in clusters, known as Islets of
Langerhans, are distributed throughout the pancreas, which
consists of ‘B’ cells (producing insulin), ‘A’ cells (producing
glucagon) and ‘D’ cells (producing somatostatin)

6.  Pancreatitis is inflammation of the gland parenchyma of the pancreas
 Acute pancreatitis is defined as an acute condition presenting with
abdominal pain and associated with raised pancreatic enzymes levels in the
blood or urine as a result of pancreatic inflammation

7. Acute pancreatitis may be categorised into..
 Mild acute pancreatitis
- characterised by interstitial edema of the gland and minimal
organ dysfunction.
- 80% of the patients will have a mild attack of pancreatitis
- mortality is around 1%
 Severe acute pancreatitis
- characterised by pancreatic necrosis, a severe systemic
inflammatory response and often multi-organ failure
- mortality varies from 20-50%
- death occurs in the early phase from multi-organ failure, while
deaths occuring after 1st week of onset are due to septic complication.

8. 1) Biliary or gallstone pancreatitis (40%)
2) Alcohol induced injury (35%)
3) Post ERCP
4) Anatomic obstruction (ampullary tumour, pancreas divisum)
5) Drug induced (corticosteroids, azathioprine, asparaginase, valproate,
thiazides, estrogens)
6) Metabolic factors (hypertriglyceridemia, hypercalcemia)
7) Abdominal trauma
8) Following biliary, upper GI and cardiothoracic surgery
9) Autoimmune pancreatitis
10)Viral infections (mumps, coxsackie B)
11)Scorpion bite
12)Idiopathic

9.  Exact mechanism of AP not completely known
 Most researchers believe that AP begins with the activation of
zymogens inside acinar cells, which causes acinar cell injury
 Severity of AP may be determined by the events that occur subsequent
to acinar cell injury, which include release of cytokines and other
chemical mediators of inflammation

10. Events of pathogenesis of Acute Pancreatitis include:
A. Precipitating Initial Events
B. Intrapancreatic Events
C. Systemic Events

11. A. Precipitating Initial Events
 Acinar Cell Events
 When acinar cells are pathologically stimulated, their
Lysosomal(L) & Zymogen(Z) contents colocalize,
consequently trypsinogen is activated to trypsin by
cathespin B
 Increased cytosolic Calcium is required
 Cathespin B and other contents of these colocalized
organelles are released
 Cathespin B activates apoptosis by causing
cytochrome c to be released from mitochondria

12. Schematic presentation of the
Acinar cell Events
 Activation of PKC results in a sudden
activation of NF Kappa beta
 Which triggers release of Cytokines
 Cytokines attract inflammatory
response cells which mediate local &
syst inflammation

13. B. Intrapancreatic Events
 After activation of superoxides (“Respiratory burst”) and release of
proteolytic enzymes (cathespin, elastase and collagenase), activated
neutrophils are attracted to focus of tissue injury
 Macrophages release TNF-alfa, IL-6 & IL-8 which mediate the local and
systemic inflammatory response
 The inflammatory mediators cause increased pancreatic vascular
permeability – leading to edema, hemorrhage & microthrombi
 Failure of pancreatic microcirculation resulting in pancreatic hypoperfusion
& necrosis

14. C. Systemic Events
 Organ failure can develop at any stage of acute pancreatitis, associated
with an overwhelming proinflammatory response early, or secondary to the
development of infected local complications
 The development pancreatic necrosis, the breakdown of the interstitial
barrier and suppression of immune response contribute to the
development of infected pancreatic necrosis
 This may associated with late development of SIRS or MODS
 Organ failure is scored using the Marshall or Sequential Organ Failure
Assessment (SOFA) system
 The 3 organ system most frequently involved are Cardiovascular,
Respiratory an Renal

17. Pathogenesis

18. Normal Pancreas
Acute Pancreatitis

19. A. Clinical presentation
B. Investigation

20. Clinical presentation:
 The cardinal symptom of AP is epigastric or periumbilical pain that
radiates to the back
 Some patients may gain relief by sitting or leaning forward
 Nausea, repeated vomiting and retching are usually marked
accompaniments
 Tachypnea, tachycardia and hypotension may be present
 In gallstone pancreatitis mild icterus may be present
 Bleeding into fascial planes can produce bluish discoloration of the
flanks (GreyTurner sign) or umbilicus (Cullen sign)
 Usually muscle guarding in the upper abdomen
 Pleural effusion is present in 10-20% patients

21. Cullen sign – discoloration around umbilicus

22. Cullen sign

23. Grey-Turner sign – discoloration in the flanks

25.  Cornerstone of diagnosis of AP is the clinical findings plus elevation
of pancreatic enzyme levels in serum
 3 folds or higher elevation of amylase and lipase level confirms the
diagnosis.
 Serum half life of amylase is shorter than that of lipase, thus lipase
level is more sensitive indicator to establish the diagnosis
 Lipase is more specific marker of AP, because amylase an be
elevated in PUD, mesentric ischemia, salpingitis and
macroamylasemia
 The degree of amylase/lipase elevation does not correlate with
severity of AP

26.  CBC: Leukocytosis
 Blood sugar: Hyperglycemia in severe cases
 Electrolyte imbalance: Hypokalemia and hypocalcaemia
 Elevated LDH in biliary disease
 Glycosuria in 10% cases
 CT Scan
 MRI
 EUS

27. CT scan showing well perfused interstitial edematous
acute pancreatitis of the neck and tail of pancreas with
confluent area of necrosis of the pancreatic body

28. A. Ranson Prognostic criteria
B. Acute Physiology And Chronic Health Evaluation
(APACHE II)score
C. Computed Tomography Severity Index (CTSI)
D. Atlanta Criteria for Acute Pancreatitis

29. Ranson Prognostic Criteria for Non-Gallstone Pancreatitis
At presentation
 Age > 55 yrs
 Blood glucose level > 200 mg/dl
 White blood cell count > 16,000 cells/ mm3
 Lactate dehydrogenase level > 350 IU/L
 Aspartate Aminotransferase level > 250 IU/L
After 48 hours of admission
 Hematocrit : decrease > 10%
 Serum calcium level < 8mg/dl
 Base deficit > 4 mEq/L
 Blood urea nitrogen level : increase > 5 mg/dl
 Fluid requirement > 6 L
 PaO2 < 60 mm Hg
** Ranson score ≥ 3 defines severe pancreatitis

30. Ranson Prognostic Criteria for Gallstone Pancreatitis
At presentation
 Age > 70 yrs
 Blood glucose level > 220 mg/dl
 White blood cell count > 18,000 cells/ mm3
 Lactate dehydrogenase level > 400 IU/L
 Aspartate Aminotransferase level > 250 IU/L
After 48 hours of admission
 Hematocrit : decrease > 10%
 Serum calcium level < 8mg/dl
 Base deficit > 5 mEq/L
 Blood urea nitrogen level : increase > 2 mg/dl
 Fluid requirement > 4 L
 PaO2 : Not available
** Ranson score ≥ 3 defines severe pancreatitis

31. Acute Physiology and Chronic Health Evaluation
(APACHE II) Score :
 APACHE II provides a general measure of the severity of the
disease
 Based on patient’s age, previous health status and 12 routine
physiologic measurements
 The main advantage is that it can be used on admission and
repeated at any time
 APACHE II score of 8 or higher defines severe pancreatitis
 APACHE II has a positive predictive value of 43% and a negative
predictive value of 89%

32. Computed Tomography Severity Index (CTSI)
FEATURE POINTS
Pancreatic inflammation
• Normal pancreas 0
• Focal / diffuse pancreatic enlargement 1
• Intrinsic pancreatic alterations with peripancreatic fat 2
inflammatory changes
• Single fluid collection / phlegmon 3
• 2 or more fluid collection or gas, in or adjacent to the 4
Pancreas
Pancreatic necrosis
• None 0
• ≤ 30% 2
• 30% - 50% 4
• > 50% 6
** CTSI 0-3, mortality 3%, morbidity 8%
CTSI 4-6, mortality 6%, morbidity 35%
CTSI 7-10, mortality 17%, morbidity 92%

33. Atlanta Criteria for Acute Pancreatitis
Organ Failure, as Defined by
 Shock (SBP <90mm Hg)
 Pulmonary insufficiency (PaO2 <60 mm Hg)
 Renal failure (creatinine level >2 mg/dl after fluid resuscitation)
 Gastrointestinal bleeding (>500 ml/24 hrs)
Systemic Complication
 DIC ( platelet ≤10,000)
 Fibrinogen <1 g/L
 Fibrin split products >80 mcg/dl
 Metabolic disturbance (calcium level ≤7.5 mg/dl)
Local Complications
 Necrosis
 Abscess
 Pseudocyst

35. A. Management of mild acute pancreatitis
B. Management of severe acute pancreatitis

36. A. Management of mild acute pancreatitis:
 Conservative approach
 Intravenous fluid administration
 Frequent, but non invasive observation
 Brief period of fasting in nauseating patients
 But no justification for prolonged NPM
 Analgesics and antiemetics
 Antibiotics are not indicated

37. B. Management of severe acute pancreatitis:
 Admission to HDU / ICU
 Analgesia
 Aggressive fluid rehydration
 Oxygenation
 Invasive monitoring of vital signs, CVP, urine output, ABG
 Frequent monitoring of haematological and biomedical parameters
(including LFT, RFT, Clotting, sr. calcium & bl. Glucose)
 Nasogastric drainage
 Antibiotics (imipenem, cefuroxime)
 CT scan essential if sign of organ failure
 ERCP within 72 hrs for severe gallstone pancreatitis / signs of
cholangitis
 Supportive therapy for organ failure (inotropes, ventilatory support,
hemofiltration etc.)
 Consider enteral(nasogastric) feeding, if nutritional support is required

38. 1. Resuscitation and monitoring:
 Patients with AP require management strategies specifically tailored to
disease severity
 Aggressive fluid resuscitation is important in order to replenish
extravascular or “third space” fluid losses
 I.V fluid at rates of greater than 200ml/h are often necessary to restore
and maintain intravascular volume
 Fluid resuscitation is important to avoid systemic complications,
particularly acute renal insufficiency
 Inadequate resuscitation pose a significant risk for further pancreatic
injury
 Banks and others have shown that while aggressive fluid resuscitation
does not necessarily prevent the progression of pancreatic necrosis,
patients with inadequate resuscitation have an increased risk of
developing necrosis

39.  Close monitoring of respiratory, cardiovascular and renal function is
essential
 Close assessment of fluid balance is required including a Foley catheter
 Patient with severe disease should be admitted to ICU with capacity for
continuous BP and SpO2 monitoring
 Intravenous narcotics are often essential for pain control
 Nasogastric tubes to avoid pancreatic stimulation was a common
practice previously, but no clinical data support this
 But in paralytic ileus which is quite common in AP, nasogastric tube
should be used to prevent emesis and aspiration pneumonia

40. 2. Nutritional support:
 “Rest the pancreas” by avoiding enteral nutrition is no longer acceptable
 There are evidences for nutritional support in acute pancreatitis
 Enteral nutrition should be commenced after initial fluid resuscitation and
within the first 24 hrs of admission
 Can be introduced through NG tube and increased in stepwise fashion in
2-3 days
 Delay in commencing enteral nutrition may contribute to the development
of intestinal ileus and feeding intolerance

41. 3. The role of ERCP:
 ERCP is used as a diagnostic as well as therapeutic modality in acute
pancreatitis
 Randomized trials have demonstrated that early ERCP reduces
complications, but not mortality
 Recent evidences suggested that early ERCP confers no benefit in the
absence of concomitant cholangitis

42. 4. Antibiotics:
 Controversy surrounding the use of prophylactic antibiotics
 Overuse of antibiotics has been associated with a documented rise in
fungal infections and resistant organisms
 Most recent studies do not support the use of prophylactic antibiotics

43. 5. Surgical management:
 In majority of AP patients, process is limited to parenchymal edema
without necrosis – they require surgical therapy for limited indications
 Intervention may be needed to address the etiology or complications of
pancreatitis
 Interventions may be either surgical or endoscopic
 Between 10-30% of patients develop severe illness, with pancreatic and
peripancreatic illness – these patients require pancreatic debridement as
standard of care

44.  In patients with severe pancreatitis or pancreatic necrosis, indications
for surgical intervention are:
①Diagnostic uncertainty
②Intra-abdominal catastrophe unrelated to necrotizing
pancreatitis such as perforated viscus
③Severe sterile necrosis
④Symptomatic organized pancreatic necrosis

46. Conclusion:
 Acute Pancreatitis is a complex , life threating disease
that requires diligent and comprehensive medical and
nursing care.

47. Thank you