This document provides an overview of acute pancreatitis, including: - The epidemiology, with highest rates in the US and among males related to alcohol use. - The pathophysiology, involving premature activation of digestive enzymes within the pancreas. - Diagnosis is based on abdominal pain plus elevated pancreatic enzymes or imaging findings. Severity is assessed using scores like Ranson's criteria or CT severity index. - Treatment involves fluid resuscitation, nutritional support, pain management, and antibiotics only for proven or suspected infected pancreatic necrosis. The goals are to prevent complications and infections.

1. Acute pancreatitis
Dr.MANOJ ARYAL
RESIDENT
INTERNAL MEDICINE

2. Outline
• Introduction
• Epidemiology
• Pathophysiology
• Etiology
• Clinical Presentation
• Workup
• Severity Scoring
System
• Treatment
• Prognosis
• Complications

3. DEFINITION
An acute inflammatory process of the
pancreas with variable involvement
of other regional tissues or remote
organ systems.

4. Epidemiology
World wide incidence
ranges between 13 and 45 per 100,000 population
GEOGRAPHICAL
Highest incidence(worldwide) recorded in the United
States and

5. Epidemiology
Gender Predilection
Generally M>F
In males more often related to alcohol
In females more often related to biliary
tract disease
Idiopathic pancreatitis no clear
gender predilection

7. Pathogenesis

9. Mechanisms against Auto-digestion
of Pancreas
• Packing of enzyme in precursor form
• Synthesis of trypsin inhibitor
• Low calcium level inside acinar cell promote trypsin destruction

10. Gallstone pancreatitis
• Reflux of bile into the pancreatic duct due to
transient obstruction of the ampulla during
passage of gallstones
• Obstruction at the ampulla secondary to stone(s) or
edema resulting from the passage of a stone .

11. Pathogenesis of Acute
Pancreatitis

12. CLINICAL FEATURES
• Abdominal pain
• Other symptoms
• Physical Examination

13. Other Manifestations
• Subcutaneous fat necrosis
• Small(<1 cm), red, tender nodules on extensor skin
of legs
• Purtscher retinopathy(on fundoscopy)

14. 1
Grey Turner
sign
Cullen’s sign

15. DIFFERENTIAL DIAGNOSIS
ABDOMINAL CONDITONS
• Perforated peptic ulcer/gastroentritis
• Biliary colic/acute cholecystitis/
Cholangitis
• Mesentric Ischemia
• Ruptured Aortic Anuerysm
• Intestinal Obstruction
• Gastric/colon/pancreatic CA
• Viral Hepatitis
• IBS
SYSTEMIC CONDITIONS
• DKA
THORAX
CONDITIONS
• Pneumonia/ARDS
• Pleuritic pain
• MI
GYNECOLOGICAL
CONDITONS
• Ectopic pregnancy
• Salpingtis

16. DIAGNOSIS
AP established by the presence of 2 of
the 3 following criteria:
• 1. Abdominal pain consistent with the
disease
• 2. Serum amylase and / or lipase greater
than three times the upper limit of normal
• 3.Characteristic findings from abdominal
imaging

17. HEMATOLOGICAL
•Pancreatic Enzymes Assays

18. SERUM AMYLASE
• ONSET: almost immediately
• PEAK: within several hours
• 3-4 times upper limit of normal within 24 hrs (90%)
• RETURN to normal depends on severity(3-5 days)
• normal at time of admission in 20% cases
• Compared with lipase, returns more quickly to values below
the upper limit of normal.

20. • more sensitive/specific than amylase
• Remains elevated longer than amylase(12 days)
• Useful if late presentation
• Serum Lipase:

21. DIAGNOSIS
Contrast-enhanced computed tomography (CECT)
and / or magnetic resonance imaging (MRI) of the pancreas
should be reserved for patients in whom (3- 5 days later )
• The diagnosis is unclear
• Who fail to improve clinically within the first 48– 72 h after
hospital admission
• Evaluate complications

23. DIAGNOSIS
MRI is helpful in patients with :
• A contrast allergy
• Renal insufficiency where T2-weighted images
without gadolinium contrast can diagnose pancreatic
necrosis
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis

24. ETIOLOGICALINVESTIGATIONS
• Abdominal ultrasound should be performed in all patients with AP
• In the absence of gallstones and / or history of significant history of
alcohol use, serum triglyceride should be obtained and
considered the etiology if >1000 mg/dl
The American Journal of Gastroenterology , (30 July 2013) | doi:10.1038/ajg.2013.218
Guideline: Management of Acute Pancreatitis

25. • Alcohol-induced pancreatitis the diagnosis
should not be entertained unless a person has a
history of over 5 years of heavy alcohol
consumption ( > 50 g per day, but is often
much higher )
• In a patient > 40 years old, a pancreatic tumor
should be considered as a possible cause of AP

26. • Genetic testing may be considered in
young patients (< 30 years old) if no
cause is evident & a family history of
pancreatic disease is present

27. IDIOPATHIC AP
• IAP is defined as pancreatitis with no etiology
established after initial laboratory (including lipid and
calcium level) and imaging tests (transabdominal
ultrasound and CT in the appropriate patient)

28. A focal dilated proximal jejunal loop in the left upper quadrant.
A focal area of adynamic ileus close to an intraabdominal
inflammatory process The sentinel loop sign may aid in
localizing the source of inflammation.

29. -Colon Cut-off Sign describes gaseous distension seen in
proximal colon
-Associated with narrowing of splenic flexure in cases
of Acute Pancreatitis
-This Appearance results from inflammatory process
extending from Pancreas into the phrenicolic ligament via
transverse mesocolon

30. Scoringsystems
• Ranson’s Criteria
• Glasgow-Imrie Score
• ComputedTomographySeverityIndex (CTSI)
• BedsideIndexfor SeverityinAcute
Pancreatitis(BISAP)Scoring

33. ComputedTomographySeverityIndex (CTSI)

34. Bedside index of severity in acute
pancreatitis (BISAP)score
•
•
BUN>25 mg/dL (8.9 mmol/L)
Impairment of mental status with aGlasgowcoma
score <15
SIRS(systemic inflammatory response syndrome) Age
>60 years old
Pleural effusion
•
•
•
Eachdeterminant is given one point
SIRSis defined as2 or more of the followingvariables;
• Fever of more than 38°C(100.4°F) or lessthan 36°C(96.8°F)
• Heart rate of more than 90 beats per minute
• Respiratory rate of >20 breaths per minute or PaCO2<32mm Hg
• Abnormal white blood cell count (>12,000/µL or <4,000/µL or >10%immature [band] forms)
Wu BU et al GUT 2008
Singh VK et al Am.J.Gastro 2009

36. BISAPScore
• 0
• 1
• 2
• 3
• 4
• 5
BISAPScoreObserved Mortality
0.1%
0.4%
1.6%
3.6%
7.4%
9.5%
Wu et al, Gut 2008

41. TREATMENT GUIDELINES
• Supportive
• Transfer to intensive care
• Nutritional support
• Use of prophylactic antibiotics
• Treatment of infected necrosis
• Treatment of sterile necrosis
• Role of ERCP and biliary
sphinchterotomy

42. INITIAL MANAGEMENT
• NPO
•Obtain vital signs at frequent intervals
(such as every 4-6 h)
• ABG should be performed when oxygen
saturation is ≤95% , hypoxemia or hypotension
refractory to a bolus of IV fluids

43. PAIN MANAGEMENT
• Parenteral analgesics usually needed.
• A number of parenteral narcotics are used
• In past, morphine avoided due to a concern it cause spasm of
the SOD and worsens although no evidence in humans .
• Meperidine with the accumulation of a neurotoxic
metabolite (normeperidine) ,relatively short duration of
action, and many hospitals have severely limited its use..
• Hydromorphine may thus be preferred.

44. INITIAL MANAGEMENT
ICU
Transfer to ICU should be considered If there are :
• Signs that suggest that the pancreatitis is severe
or is likely to be severe
• Need for very aggressive fluid resuscitation to
overcome hemoconcentration, especially in an
older person who may have underlying
cardiovascular disease
• If a patient does not have hypoxemia but is
showing signs of labored respiration, transfer
should be considered to monitor pulmonary status
carefully in anticipation

45. INITIAL MANAGEMENT
• Fluid therapy in acute pancreatitis:
Adequate prompt fluid resuscitation
- Fluids are given intravenously
- Aim to maintain urine output >0.5 ml/kg

46. INITIAL MANAGEMENT
• Aggressive hydration, defined as 250-500ml per hour of
isotonic crystalloid solution should be provided to all
patients, unless cardiovascular, renal, or other related
comorbid factors exist
• Early aggressive intravenous hydration is most
beneficial during the first 12 – 24 hr, and may have little
benefit beyond this time period
• In a patient with severe volume depletion, manifest as
hypotension and tachycardia, more rapid repletion
(bolus) may be needed

47. • Lactated Ringer solution may be the preferred
isotonic crystalloid replacement fluid
• Fewer patients developing SIRS as compared with
patients receiving normal (0.9% ) saline
• Normal saline given in large volumes may lead to the
development of a non-anion gap hyperchloremic
metabolic acidosis
INITIAL MANAGEMENT

49. INITIAL MANAGEMENT
• Fluid requirements should be
reassessed at frequent intervals within
6 hr of admission and for the next 24 –
48 hr
• The goal to decrease hematocrit
(demonstrating hemodilution) and
BUN (increasing renal perfusion)
and maintain a normal creatinine
during the first day of hospitalization

50. NUTRITION IN AP
• In mild AP, oral feedings can be started
immediately if there is no nausea and
vomiting, and the abdominal pain has
resolved
• In mild AP, initiation of feeding with a
low-fat solid diet appears as safe as a
clear liquid diet

51. INITIAL MANAGEMENT
Oral intake of limited amounts of calories is usually
initiated in:-
1) Abdominal pain has subsided
2) Parenteral narcotics are no longer required
3) Abdominal tenderness has markedly decreased
4) Nausea and vomiting have ceased
5) Bowel sounds are present
6) Overall assessment of the physician is that the patient
has improved

52. NUTRITION IN AP
• In severe AP, enteral nutrition is recommended to
prevent
infectious complications.
• Parenteral nutrition should be avoided, unless the
enteral route is
- - Not available
- - Not tolerated
- - Not meeting caloric requirements
• Nasogastric delivery and Nasojejunal delivery of
enteral feeding appear comparable in efficacy and
safety

54. NUTRITION IN AP
Enteral Feeding
• Stabilizes gut barrier function,
prevent systemic complications and
improve morbidity and mortality
• Enteral feeding is safer and less expensive
than TPN, but there is not major
improvements in morbidity and mortality of
acute pancreatitis

55. NUTRITION IN AP
• Role of immediate oral feeding versus
fasting in 60 patients with AP
• The orally fed group had a significant 2-day shorter
length of hospital stay without differences in
recurrent attacks of pancreatitis in a follow-up of 3
months.

57. ROLE OF ANTIBIOTICS INAP
• Routine use of prophylactic antibiotics in
patients with severe AP is not recommended
• The use of antibiotics in patients with sterile
necrosis to prevent the development of
infected necrosis is not recommended
• Antibiotics should be given for an extra-
pancreatic infection, such as cholangitis,
catheter-acquired infections, bacteremia,
urinary tract infections, pneumonia

58. ROLE OF ANTIBIOTICS INAP
• Infected necrosis should be considered in
patients with pancreatic or extrapancreatic necrosis who
deteriorate or fail to improve after 7– 10 days of
hospitalization
(ii
)
(i) Initial CT-guided (FNA) for Gram stain and culture to guide
use of appropriate antibiotics or
Empiric use of antibiotics after obtaining necessary
cultures for infectious agents, without CT FNA, should
be given

59. THE ROLE OF ANTIBIOTICSIN
AP
• Once blood and other cultures are found to be
negative and no source of infection is identified,
antibiotics should be discontinued.
• In patients with infected necrosis, antibiotics
known to penetrate pancreatic necrosis, such
as carbapenems, quinolones, and
metronidazole
• Routine administration of antifungal agents along
with prophylactic or therapeutic antibiotics is not
recommended

63. ERCP IN AP
• Patients with AP and concurrent acute
cholangitis should undergo ERCP
within 24 hr of admission
• ERCP is not needed early in most
patients with gallstone pancreatitis who
lack laboratory or clinical evidence
of ongoing biliary obstruction

64. ERCP IN AP
ERCP is indicated for clearance of bile duct
stones in patients with :
- Severe worsening biliary pancreatitis
- Cholangitis
- Poor candidates for cholecystectomy
- Post cholecystectomy
- Strong evidence of persistent biliary
obstruction

65. TREATMENT OF INFECTED
NECROSIS
• Treatment of choice in infected necrosis is surgical
debridement
(NOW minimal invasive procedure preferred )
• 33% of patients with necrotizing pancreatitis develop
infected necrosis, usually after 10 days of illness
• 48% of patients with infected necrosis have persistent
organ failure, either documented initially at admission
or sometime after admission

66. • In stable patients with infected necrosis,
surgical, radiologic, and/ or endoscopic drainage
should be delayed by preferably 4 weeks to allow the
development of a wall around the necrosis (walled-
off pancreatic necrosis).

67. TREATMENT OF
STERILE NECROSIS
• Sterile necrosis is best managed medically during the
first 2–3
wk
• After this interval, if abdominal pain persists and
prevents oral intake, debridement should be
considered.
• This is usually accomplished surgically, but
percutaneous or endoscopic debridement is a
reasonable choice in selected circumstances with
the appropriate expertise.

70. When to Discharge
Pain is well controlled with oral analgesia
Able to tolerate an oral diet that maintains their caloric needs,
and all complications have been addressed adequately

71. Follow up
• Routine clinical follow-up care (typically including physical
examinationand amylase and lipase assays) is needed to monitor
for potential complications of the pancreatitis, especially
pseudocysts Within 7-10 days

72. Prognosis
TYPE OF AP MORTALITY
Overall 10-15 %
(Biliary>alcholic)
Mild Acute Pancreatitis(80 % cases) 1 %
Severe Acute Pancreatitis(20 %
cases)
Severe  20-50 %
<1 week 1/3 cases MOF
>1 week 2/3 cases Sepsi
s
(+MO
F)

73. THANK YOU

74. REFERENCES:
Harrison principal of internal medicine 20th edition
The American Journal of Gastroenterology , Guideline:
Management of Acute Pancreatitis
Meta-analysis of parenteral nutrition versus enteral nutrition in
patients with acute pancreatitis BMJ 2004; 328