This document provides information about acute pancreatitis including its anatomy, pathogenesis, clinical presentation, diagnosis, severity assessment, complications and management. Some key points: - Acute pancreatitis can range from mild to severe and is commonly caused by gallstones or alcohol use. - Diagnosis involves elevated pancreatic enzymes and imaging such as CT scan which can also assess severity. Several scoring systems exist to evaluate prognosis. - Management of mild cases is usually conservative while severe cases require ICU monitoring, IV fluids, nutritional support and antibiotics if infected necrosis is present. - Complications include fluid collections, pancreatic necrosis, pseudocysts and vascular issues which may require drainage or surgical debridement.

1. ACUTE PANCREATITIS
Moderator : PROF.Dr.K.SRINIVASAN.
Presentor:Dr.S.SIVA SANKAR.
Post Graduate, General surgery

2. Pancreas
● The pancreas is an elongated, accessory digestive gland
that lies retroperitoneally, overlying and transversely
crossing the bodies of the L1 and L2 vertebra on the
posterior abdominal wall .
● It lies posterior to the stomach between the duodenum on
the right and the spleen on the left .
● The transverse mesocolon attaches to its anterior margin

3. ● The average gland weighs between 75 and
125 gm. and measures 10 to 20 cm
● lies in an oblique position, sloping upward from
the C-loop of the duodenum to the splenic hilum

6. 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

7. Pancreatic duct
● The main pancreatic duct begins in the tail of the
pancreas and runs through the parenchyma of the gland
to the pancreatic head
● The main pancreatic duct and bile duct usually unite to
form the short, dilated hepatopancreatic ampulla (of
Vater), which opens into the descending part of the
duodenum at the summit of the major duodenal papilla

8. ● The accessory pancreatic duct opens into the duodenum
at the summit of the minor duodenal papilla
● . Usually, the accessory duct communicates with the main
pancreatic duct.

9. Pancreas Divisum
Failure of the dorsal and ventral ducts to fuse during
embryogenesis leads to pancreas divisum.
Most pancreatic exocrine secretions exit through the dorsal duct, pancreas
divisum can lead to a condition of partial obstruction caused by a small minor
papilla, leading to chronic backpressure in the duct which causes relapsing acute
or chronic pancreatitis

10. 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
Acute pancreatitis

11. 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%

12. 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.

13. 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

14. 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

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

17. 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

20. Organ failure is scored using the Marshall or Sequential
Organ Failure
Assessment (SOFA) system
The 3 organ system most frequently involved are
Cardiovascular, Respiratory and Renal

22. A. Clinical presentation
B. Investigation

23. 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.
Tachypnea, tachycardia and hypotension may be
present
In gallstone pancreatitis mild icterus may be present

24. 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

25. Cullen sign

26. Grey-Turner sign – discoloration in the flanks

27. 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

28. Lipase is more specific marker of Acute
pancretitis
The degree of amylase/lipase elevation does
not correlate with severity of Acute pancretitis
In patients who do not present to the emergency
department within the first 24 to 48 hours after
the onset of symptoms,determination of lipase
levels is a more sensitive indicator to establish
the diagnosis

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

30. Nonspecific findings in patients in plain abdomen xray include
air-fluid levels suggestive of ileus,
cutoff colon sign as a result of colonic spasm at the splenic
flexure,
and widening of the duodenal C loop caused by severe
pancreatic head edema.

31. usefulness of ultrasound for diagnosis of pancreatitis is
limited by intra-abdominal fat and increased intestinal gas as
a result of the ileus.
Combined elevations of liver transaminase and pancreatic
enzyme levels and the presence of gallstones on ultrasound
have higher sensitivity (97%) and specificity (100%) for
diagnosing acute biliary pancreatitis.

32. Contrast-enhanced computed tomography (CT) is currently
the best modality for evaluation of the pancreas, especially if
thestudy is performed with a multidetector CT scanner.
The most valuable contrast phase in which to evaluate the
pancreatic parenchyma is the portal venous phase (65 to 70
seconds after injection of contrast material),

33. EUS has been proven to be sensitive for identifying
choledocholithiasis.
it allows examination of the biliary tree and pancreas with no
risk of worsening of the pancreatitis.
In patients in whom persistent choledocholithiasis is
confirmed by EUS,
ERCP can be used selectively as a therapeutic measure.

34. 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

35. 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

36. 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

37. 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%

39. 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%

41. 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

44. 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

45. 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

46. 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

47. 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

48. 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

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

50. 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

51. 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

54. Complications
● Sterile and Infected Peripancreatic Fluid Collections
● Pancreatic Necrosis and Infected Necrosis
● Pancreatic Pseudocysts
● Pancreatic Ascites and Pancreaticopleural Fistulas
● Vascular Complications
● Pancreatocutaneous Fistula

55. Sterile and Infected Peripancreatic Fluid Collections
The presence of acute abdominal fluid during an episode of
acute pancreatitis has been described in 30% to 57% of
patients.
Treatment is supportive
Fever, elevated white blood cell count, and abdominal pain
suggest infection of this fluid, and percutaneous aspiration is
confirmatory.
Percutaneous drainage and IV administration of antibiotics
should be instituted if infection is present.

56. Pancreatic necrosis
Presence of non viable pancreatic parenchyma or
peripancreatic fat.
CECT is the most reliable investigation.
Complication of pancreatic necrosis is infection.
Caused by enteric flora,such as
E.coli,klebsiella,pseudomonas spp and Enterococcus spp.
Clinically presented with prolonged fever,progressive clinical
deterioration.

58. If infected necrosis is suspected,
FNAC may be performed if the diagnosis is equivocal; from
the aspirate, a positive Gram stain or culture establishes the
diagnosis.
Carbapenems are the first option of treatment.
Alternative therapy includes quinolones, metronidazole,
thirdgeneration cephalosporins, and piperacillin.

59. ● Definitive treatment is surgical debridement with
necrosectomy,closed continuous irrigation or open
packing.
● Currently endoscopic drainage with a large bore stent and
endoscopic debridement with or without percutaneous
drainage may avoid open operations in some patients.

60. The overall mortality rate after open necrosectomy has been
as high as 25% to 30%
Outcomes are time dependent;
patients who undergo surgery in the first 14 days have a
mortality rate of 75%,
and those who undergo surgery between 15 and 29 days and
after 30 days have mortality rates of 45% and 8%,
respectively

61. The longer a patient can be medically optimized and
managed with enteral nutrition and antibiotics (if indicated),
the more mature a fluid collection (with or without necrosis),
and therefore the extent of an endoscopic or operative
débridement (if needed) will be better delineated and
tolerated.

62. 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

64. Pancreatic pseuocysts
● occur in 5% to 15% of patients who have peripancreatic
fluid collections.
● the capsule of a pseudocyst is composed of collagen and
granulation tissue,and it is not lined by epithelium.
● Persistent pain, early satiety, nausea, weight loss, and
elevated pancreatic enzyme levels in plasma suggest this
diagnosis.
● The diagnosis is corroborated by CT or MRI.
● EUS with FNA is indicated for patients in whom the
diagnosis of pancreatic pseudocyst is not clear

66. Management
● spontaneous regression in up to 70% of cases,with
pseudocyst smaller than 4cm in diameter.
● Invasive therapies are indicated for symptomatic patients
or when the differentiation between a cystic neoplasm and
pseudocyst is not possible
● Surgical drainage has been the traditional approach for
pancreatic pseudocysts
● transgastric and transduodenal endoscopic drainage are
safe and effective approaches for patients with pancreatic
pseudocysts in close contact (defined as <1 cm) with the
stomach and duodenum.

68. Pancreatic pseudocysts closely attached to the stomach
should be treated with a cystogastrostomy
Pancreatic pseudocysts located in the head of the pancreas
that are in close contact with the duodenum are treated with a
cystoduodenostomy
pseudocysts not in contact with the stomach or duodenum-
Roux-en-Y cystojejunostomy.

71. Complications of pancreatic pseudocysts include
● Bleeding( secondary to vascular erosion)
● pancreaticopleural fistula (secondary to pleural erosion)
● bile duct and duodenal obstruction;
● Rupture into the abdominal cavity
● infection

72. Pancreatic Ascites
complete disruption of the pancreatic duct can lead to
significant accumulation of fluid -pancreatic Ascites
Diagnostic paracentesis typically demonstrates elevated
amylase and lipase levels.
Treatment consists of abdominal drainage combined with
endoscopic placement of a pancreatic stent across the
disruption.
Failure of this therapy requires surgical treatment; it consists
of distal resection and closure of the proximal stump.

73. Pancreaticopleural Fistulas
Posterior pancreatic duct disruption into the pleural space
leads to pancreaticopleural fistula
Symptoms include dyspnea, abdominal pain, cough, and
chest pain.
The diagnosis is confirmed with chest radiography,
thoracentesis, and CT scan.
Amylase levels above 50,000 IU in the pleural fluid confirm
the diagnosis.

74. Initial treatment requires chest drainage, parenteral nutritional
support, and administration of octreotide.
Persistent drainage should also be treated with endoscopic
sphincterotomy and stent placement.
Patients who do not respond to these measures require
surgical treatment.

75. Vascular Complications
● The most common vessel affected is the splenic artery.
● Pancreatic elastase damages the vessels, leading to
pseudoaneurysm formation.
● Clinical manifestations include sudden onset of abdominal
pain, tachycardia, and hypotension.
● Arterial embolization should be attempted to control the
bleeding.
● Refractory cases require ligation of the vessel affected.
● The mortality ranges from 28% to 56%.

76. ● Pancreatic inflammation can also produce vascular
thrombosis;
● splenic vein thrombosis -most common
● can extend into the portal venous system in severe cases.
● Imaging demonstrates splenomegaly, gastric varices, and
splenic vein occlusion.
● Thrombolytics have been described in the acute early
phase
● Recurrent episodes of upper gastrointestinal bleeding
caused by venous hypertension should be treated with
splenectomy.

77. Pancreatocutaneous Fistula
● 0.4% of patients after an acute episode of pancreatitis will
develop Pancreatocutaneous Fistula ,
● 4.5% in patients with pancreatic pseudocysts
● 40% in patients with infected necrosis after surgical
débridement.
● Treatment is conservative