The document provides information on acute pancreatitis including its anatomy, definition, etiology, pathogenesis, clinical presentation, diagnosis, classification of severity, management, and intervention. Some key points: - The pancreas has a head, body, and tail and receives its blood supply primarily from the splenic artery and splenic vein. - Acute pancreatitis is defined as abdominal pain with elevated pancreatic enzymes and may be associated with acute swelling and inflammation of the pancreas. - Etiologies include systemic infections, trauma, anomalies of pancreaticobiliary ducts, drugs, metabolic abnormalities, and idiopathic causes. - Management involves fluid resuscitation, pain relief, prevention of infection typically

1. Acute Pancreatitis

2. ANATOMY
• The pancreas is divided into
•Head
•Body and
•Tail
• Most of the pancreas is extraperitoneal, with just a
portion of the tail coming through the mesenteric
folds.

3. • The head is to the right of L2,
• The body overlies L1,
• The tail rises up to the left of T12.

4. • The splenic artery provides most of the blood supply
to the pancreas and lies along its superior border with
the splenic vein.
• The blood supply is generally greatest to the head of
the pancreas.

5. • The head of the pancreas shares its blood supply with
the duodenum through the
• gastroduodenal artery and
• superior and inferior pancreaticoduodenal arteries,

7. • Blood from the pancreas drains in a posterior
direction into the
• superior mesenteric vein and
• splenic vein

8. DEFINITION
• Clinically, acute pancreatitis is defined as a
• single or recurrent episodes of abdominal pain associated
with elevated serum pancreatic enzyme levels

9. • The morphologic correlate is
• acute focal or diffuse swelling and inflammation of the
pancreas.
• Following an acute episode
• Resolution of symptoms and normalization of blood
biochemistry and anatomic abnormalities follows

10. ETIOLOGY
1. Systemic infection:
• Mumps
• Rubella
• Coxsackie B virus
2. Trauma:
• Blunt abdominal trauma
• Iatrogenic (e.g., surgery, ERCP)

11. 3. Anomalies of the pancreaticobiliary duct system:
• Pancreaticobiliary malunion
• Pancreas divisum
• Hypertensive sphincter of Oddi
• Choledochal cyst
• Choledocholithiasis

12. 4. Drugs:
• Azathioprine
• Tetracycline
• L-Asparaginase
• Immunosuppressants
• Valproic acid

13. 5. Metabolic abnormalities:
• Hypertriglyceridemia
• Hypercalcemia
• Cystic fibrosis
6. Hereditary:
• Alteration in the long arm of chromosome 7, which yields an aberrant
trypsinogen protein
7. Idiopathic.

14. PATHOGENESIS:

16. PANCREAS DIVISUM
•The adult pancreas is derived from
• ventral and dorsal pancreatic buds that fuse by the end of
the eighth week of gestation
• Most of the gland is derived from the dorsal bud
• it includes the superior anterior part of the head, body,
and tail it is drained by the duct of Santorini through the
minor papilla.
•The ventral bud becomes the
• posterior and inferior part of the head it is drained by the
duct of Wirsung into the major papilla of Vater

17. • Normally fusion of the
• Ventral and Dorsal pancreas and their duct system occurs
• The duct of Wirsung becomes the major duct, and the duct of
Santorini usually regresses
• Failure of the fusion of two ductal systems leads to Pancreas
Divisum
• In this disorder the duct of Wirsung is small, and the duct of
Santorini becomes the major ductal system and maintains
communication with the duodenum through the minor
papilla

19. • Pancreas divisum is suspected on MRCP or ERCP when the
duct of Wirsung fails to be visualized or when it is attenuated
and rudimentary
• MRCP is a useful and noninvasive diagnostic tool for
pancreas divisum
• ERCP can provide detailed information on the pancreatic
duct
• ERCP shows Santorini as the dominant duct and that it
extends the entire length of the body and tail of the
pancreas

20. • Neblett and O’Neill reported that pancreas divisum was
identified in 7.4% of all children with pancreatitis and 19.2%
of children with relapsing or chronic pancreatitis
• The primary goal of treatment of pancreas divisum
associated with pancreatitis is to establish adequate
drainage of the duct of Santorini
• Endoscopic sphincterotomy has been performed, but
restenosis and recurrence of symptoms have been reported

21. • If chronic pancreatitis has developed in the presence of a
dilated duct, longitudinal pancreaticojejunostomy should be
considered

22. CLINICAL PRESENTATION AND DIAGNOSIS
• The diagnosis of acute pancreatitis is based on two or more of the
following criteria
• severe abdominal pain
• serum amylase or lipase more than three times higher than the institution’s
upper limit and
• Contrast enhanced computed tomography (CECT) findings of acute
pancreatitis
• Usually, the first two criteria are present, and CECT is not required for
diagnosis

23. LABORATORY INVESTIGATION
• CBC
• Serum amylase and serum lipase
• Liver function tests, calcium and triglyceride levels.
• Hypercalcemia (usually related to hyper
parathyroidism) and
• Hypertriglyceridemia (arbitrarily >15 mmol/L) are
both well-documented causes and represent easily
treatable causes of acute pancreatitis

24. IMAGING
• The most important imaging modality at admission is
transabdominal ultrasound in order to detect
gallstones or sludge in the gallbladder or in the
common bile duct

25. • CECT is used to diagnose
• peripancreatic collections and pancreatic parenchymal or
peripancreatic fat necrosis.
• A CECT scan has to be performed in patients who do not
improve after the first week of symptoms.
• CECT cannot discriminate solid components (necrosis) within
a predominantly fluid collection

26. • Magnetic resonance imaging (MRI) or ultrasonography are
the only modalities capable of demonstrating the presence
or absence of necrosis in such collections
• The absence of necrosis is a prerequisite for the collection to
be called a Pseudocyst.
• A true Pseudocyst in the initial 4 weeks of acute pancreatitis
is very rare.

27. CLASSIFICATION OF SEVERITY
• The clinical course of acute pancreatitis is highly unpredictable
and ranges from recovery within a single day to multiorgan
failure and mortality within hours or a few days
• Although predictive scores have been designed to guide
clinicians in the initial management and the level of care or
observation needed in each patient, their value for day-to-day
clinical practice is only limited

28. • If a patient meets a certain cutoff value, this only means that
a patient can at that stage of disease, temporarily, be
classified as having “predicted severe pancreatitis.”
• The positive predictive value (the chance of truly developing
severe pancreatitis) is generally in the order of 50% to70%.
• These classifications are most useful in excluding patients at
risk for severe pancreatitis, because with a negative
predictive value of 85% to 90

31. EARLY AND LATE ORGAN FAILURE:
Acute pancreatitis typically runs a biphasic course.
• The first phase is characterized by a systemic inflammatory
response syndrome (SIRS) and lasts about 2 weeks.
• The second phase is characterized by a counteractive anti-
inflammatory response syndrome (CARS), characterized by a
state of immunosuppression.

32. • Organ failure in the SIRS phase is considered not to be related to
infection but rather to severe systemic inflammation.
• Organ failure in the CARS phase is related to secondary infections,
such as infected necrosis.
• Organ failure may affect all organ systems, but the pulmonary and the
cardiovascular systems are dominant.
• Organ failure in the SIRS phase is diagnosed at a median of 2 days
after admission but may already be present at admission
• Half of the patients who die from acute pancreatitis suffer from organ
failure but not from infected necrosis.

33. Treatment:
CONSERVATIVE
MANAGEMENT
SIRS Phase or
Wks 1-2
1.Fluid resuscitation
(Goal 1ml/kg/hr
urine production)
2.Pain relief
CARS Phase
(wks 3)
and thereafter
Pancreatic Necrosis
and Peripancreatic
collection has to be
ruled out
Prevention of
infection

34. Prevention of infection:
• Infection is associated with increased mortality in
acute pancreatitis, numerous prophylactic strategies
have been explored in the past two decades.
• Enteral bacteria are considered responsible for the
majority of these infections, and the current concept
is that these bacteria pass through the mucosal
barrier in the first 24 hours of disease.

35. • Bacteremia increased the risk of infection of necrosis
from 38% to 65%.
• Persistent organ failure and bacteremia were the
strongest predictors of mortality.
• Enteral nutrition, systemic intravenous antibiotics,
selective bowel decontamination, and enteral
probiotics all have been tried to lower the rate of
infection.

36. ENTERAL NUTRITION:
• Enteral nutrition
• reduces small bowel bacterial overgrowth and
• improves intestinal mucosal barrier function thereby reducing
bacterial translocation and resultant infectious complications
• In patients with mild pancreatitis, oral feeding can be
started as early as the day of admission or the day
thereafter.

37. • In predicted severe pancreatitis
• It is now generally advised to start enteral nutrition by
nasojejunal feeding tube within approximately 3 days, if
the patient is not expected to quickly resume a normal
diet.
• The optimal route for the administration of enteral
feeding through a nasojejunal or a nasogastric feeding
tube—is not yet known

38. Systemic Intravenous Antibiotics:
• A recent updated meta-analysis clearly demonstrated
no beneficial effect in the routine use of systemic
antibiotic prophylaxis
• There is no longer support for the routine prophylactic
use of antibiotics.

39. Selective Bowel Decontamination
• If the gut is indeed the source of bacteria responsible for the
infectious complications in acute pancreatitis, it might seem
a rational approach to administer antibiotics enterally
• Effect of SBD (norfloxacin, colistin etc) has been studied.
• A reduction in mortality in the SBD group, caused mostly by
a reduction of gram-negative infections of pancreatic
necrosis, was found
• Has not gained wide acceptance

40. INTERVENTIONAL TREATMENT
Systemic Inflammatory Response Syndrome Phase (First and Second
Weeks)
• Intervention in this phase of the disease should aim at
1. Treatment of acute life-threatening complications or
2. Prevention of further deterioration.

41. The only acute complications justifying very early
intervention are
• abdominal compartment syndrome,
• bowel ischemia or perforation, and
• severe bleeding unresponsive to angiographic coiling.

42. Abdominal compartment syndrome
• Percutaneous drainage can be used as an initial step if
intraabdominal drainable fluid is present
• If drainage does not immediately lower the pressure
or if there is no (more) drainable fluid, laparotomy for
decompression is advised.
The pancreas should not be explored because it is too
early to remove necrosis safely, and there is a risk to
introduce infection into the necrosis.

43. • Percutaneous drainage of noninfected collections is not indicated as
sterile collections may become iatrogenically contaminated by the
percutaneous drains

44. Intervention to Prevent Further Deterioration
• Early Endoscopic Retrograde Cholangiopancreatography
and Sphincterotomy in Biliary Pancreatitis
• Theoretically, early relief by ERCP with endoscopic biliary
sphincterotomy may stop disease process at an early phase
and reduce the risk of progression to complications.

45. Intervention in the Second Counteractive
Antiinflammatory Response Syndrome Phase:
Intervention for Treatment of Infected Necrosis:
• During the CARS phase or second phase, the patient is
threatened by yet another episode of systemic infection or
sepsis, caused most often by secondary infection of
(peri)pancreatic necrosis.
• Documented or suspected infection of pancreatic or
peripancreatic necrosis with signs of sepsis therefore is the
most accepted indication for intervention, radiologically,
endoscopically, or surgically.

46. Timing of Intervention for Infected Necrosis:
• Timing and choice of the type of intervention are best
guided by an experienced multidisciplinary team.
• Postponing intervention until the intra- and/or
extrapancreatic collections have become
encapsulated, a process that usually takes 4 weeks, is
beneficial

47. • If clinical deterioration occurs, administration of
antibiotics to allow for further encapsulation, under
close guidance of the clinical developments and CECT
scan, performed at regular intervals to prevent
bacteraemia or sepsis, is a valid option to postpone
surgical intervention
• The length of the interval is mainly determined by the
completeness of encapsulation and the clinical
condition of the patient.

48. Types of Intervention:
Catheter Drainage :
• Least invasive technique
• Recent systematic review suggested that in approximately
55% of patients with necrotizing pancreatitis, percutaneous
catheter drainage can be the only intervention needed for
cure
• In patients who do not improve after technically adequate
drainage, necrosectomy should be performed as the next
step.

49. Minimally Invasive Necrosectomy
• In the United States and the Netherlands, the most frequently used
minimally invasive surgical intervention is the video-assisted
retroperitoneal debridement (VARD) procedure.
• It is not the goal to remove all necrosis.
• In contrast to purely percutaneous necrosectomy techniques, VARD
allows for the removal of large pieces of necrosis.
• In general, the more complete the encapsulation, the easier the
necrosectomy can be performed.

50. • Following near-complete debridement, two large-bore surgical drains
are placed into the empty cavity, one at the deepest point and one
more shallow.
• Postoperatively, the drains are continuously lavaged with increasing
amounts (2, 4, then 6 L) of 0.9% saline per day in the first 3 days.

51. Endoscopic Transluminal Necrosectomy.
• endoscopic transluminal/ transgastric necrosectomy
• Results are promising, with success rates ranging from 80% to 93%
and mortality from 0% to 6%
Advantages
• No abdominal incision
• External pancreatic fistula will not occur
• Incisional hernia is also avoided.
The need for repeated, multiple procedures to remove sufficient
amounts of necrosis is a distinct disadvantage

52. Open Necrosectomy
• the most frequently used techniques of open necrosectomy for
infected necrosis is laparotomy with placement of a retroperitoneal
lavage system after complete necrosectomy has been performed
• These drains are continuously lavaged with increasing amounts (2, 4,
then 6 L) of saline per day
• The mortality of this technique is approximately 25%

53. • Another open approach is open necrosectomy and closed packing
with gauze stuffed penrose drains

57. Thank You