Lectrure By: DR.TARIK S. ALNOGOMI ER Chief. EMERGENCY MEDICINE SPECIALIST MEGAT GENERAL HOSPITAL

2. WHY PANCREATITIS…?

3. WHY PANCREATITIS…?

4. NOT UNCOMMON PATHOLOGY

5. SERIOUS CONDITION
POTENTIALLY

6. ACUTE PANCREATITIS
CAUSES
BILIARY
ALCOHOLIC
IDIOPATHIC

7. OTHER UNUSUALL CAUSES
HYPERLIPIDEMIA
HYPERCALCEMIA
CONGENITAL
VIRAL
DRUGS
TRAUMATIC OTHER
CAUSES

8. o Trans-abdominal ultrasound should be performed in ALL
patient with acute pancreatitis to assess gallstones as
etiology of acute pancreatitis.
o In absence of gallstones or significant alcohol use, obtain
serum triglycerides.
o If serum triglycerides > 1,000 mg/dL, consider as
etiology of acute pancreatitis.
o In patients > 40 years of age, consider pancreatic tumor
in absence of other causes.
o In patients < 30 years of age and +FH of acute pancreatitis
in absence of other causes, consider genetic testing for
hereditary pancreatitis.
Etiology

9. PATHOLOGY
OSTRUCTION - SECREATION
COMMON CHANNEL THEORY
DUODENAL REFLUX
INCREASED PANCREATIC DUCT
PERMEABILITY.
ENZYME AUTOACTIVATION

10. Acute Pancreatitis - Pathophysiology
Premature Activation of Trypsin →
Autodigestion of pancreatic tissue
ACTIVATION OF INFLAMMATORY RESPONSE
Inflammatory mediators
Vasodilation
SHOCK
ARDSMODSATN 10
Extravascular movement
of serum albumin
3rd spacing Panc. edema
SHOCK

11. 11

14. ACUTE OEDEMATOUS PANCREATITIS
ACUTE PERSISTENT UNRESOLVING .
ACUTE NECROTIZING , FULMINANT.
RECURRENT ACUTE PANCREATITIS

15. ACUTE PANCREATITIS IN INFANTS
AND CHILDRENS …???

16. PRESENTATION OF ACUTE
PANCREATITIS
ABDOMINAL PAIN
NAUSEA
VOMITING
RETCHING
HYPOTENTION

17. SIGNES OF ACUTE PANCREATITIS
FINDING OF ABD. EXAMINATION
CULLEN , S SIGNE
GREY TURNER , S SIGNE later
FINDING OF
COMPLICATIONS

18. Pain, Oh the pain
“Worse than childbirth” “Worse than being shot”
Starts fast within 10-20min reaches peak
–Third fastest pain onset in GI after perf and SMA
thromb
Does not usually undulate (not colicy)
Lasts days (if no underlying chronic damage)
–Longer than biliary colic which is hours
Radiate to back in 50%
Sometimes diagnosed at autopsy (painless)
Almost always causes ER visit/admission
Capsaicin, glutamate, vanilloid, ppar-gamma

19. ECG CHANGES ……???

20. Acute Pancreatitis
0 20 40 60 80 100
Presenting features

27. ???????????????

34. DIFFERANTIOAL DIAGNOSIS ?
REFERED PAIN FROM THE
CHEST
ABDOMINAL
CAUSES

42. LAPORATORY INVESTIGATION
CBC
UREA CREATININE
RBS
SERUM ELECTROLYTES
LFT
SERUM AMYLASE

44. IS THERE
OTHER CAUSES FOR
ELEVATED SERUM
AMYLASE….?

45. OTHER INVESTIGATIONS
URINARY AMYLASE : CREATININE CLEARANCE RATIO. TIMED
URINARY AMYLASE OUTPUT
AMYLASE CLEARANCE STUDIES
SERM LIPASE
IN NECROTISING PANCREATITIS
COMPLEMENT C3 AND C4 (INCREASE)
ALPHA2 MACROGLOBULIN (DECRAESES)
ALPHA2 PROTEASES (DECREASES)

46. Acute Pancreatitis: Time course of enzyme
elevations
Hours after onset
Fold
increase
over
normal
0 6 12 24 48 72 96
0
2
4
6
8
10
12
Lipase
Amylase
Amylase
half life 10
hrs

47. TO WHAT LEVEL IS DIAGNOSTIC….?

48. Serum Amylase (25-125 U/L)
>200 U/L for 24-72 hours
starts to rise 2-6 hr after onset
of pain
Peaks @ 24 hours
Return to normal @ 72 hr
Serum Lipase (3-19 U/dL)
used with amylase; rises later
than amylase (48 hours)
return to normal 5-7 days
  WBC’s
  glucose
  lipids
  calcium
  magnesium

50. Blood tests
 Amylase and lipase
 Plasma level peak within 24 hours
 t1/2 of amylase << lipase
Sensitivity Specificity
Amylase 67-100 85-98
Lipase 82-100 86-100
Gut 1997,41:431-35; Br J Surg 1998,84:1665-69.

51. IN ACUTE PANCREATITIS
IS SERUM AMYLASE ALWAYS
HIGHT……???

52. CXR
ABDOMINAL XRS
ERECT
SUPINE

53. ABDOMINAL ULTRASOUND
WHAT IS THE ROLE OF ABD
US IN ACUTE PANCREATITIS ……??
DIAGNOSTIC …..!!?
FOLLOW UP
…!!?

56. ABDOMINAL CT SCAN

57. CT Scan
 Normal
– Homogeneous enhancement of the whole
pancreas
 Abnormal
– Non-visualization of a part of the pancreas
 Sensitivity of 90-95%
 Specificity – 100%

58. CT scan
 Not necessary for the diagnosis
 Diagnostic doubt
– Atypical presentations
– Asymptomatic hyperamylasaemia or
hyperlipasemia
Gastroenterol Clin N Am 1990;19:811-42

59. Recommendation
 A dynamic CT scan should be performed
in all (predicted) severe cases between 3
and 10 days after admission
(Evidence grade B)

61. http://dbwmpns0f8ewg.cloudfront.net/imag
es/a_panc/ct_apanc.jpg

65. Magnetic Resonance
Cholangio-Pancreatography
(MRCP)
 Sensitivity of > 90%

67. Endoscopy Ultrasound
(EUS)
 EUS
– Sensitivity of > 95%
– Specificity of > 95-
100%

69. IPMN

70. Clinical indices of severity

71. Multiple Factors Scoring
System
 Ranson
– Separate for alcohol and gallstone etiology
– Score > 3 = severe acute pancreatitis
 Glasgow
– valid in all types of pancreatitis
Both of these systems require 48 hours from
the admission for full assessment
Can J Gastroent 2003 325-328

72. Ranson
At presentation
Age >55
White blood cell count
>16
Blood glucose >200
mg/dL
LDH >350 U/L
AST >250 U/L
At 48 hours
Hematocrit Fall by ≥10%
BUN Increase by ≥5
mg/dL despite fluids
Serum calcium <8 mg/dL
pO2 <60 mmHg
Base deficit >4 MEq/L
Fluid sequestation >6 L
1-2 criteria - > <1% mortal
3-5 cirteria - > 15% mortal
6-8 criteria- > 60% mortal
9-11 -> >75% mortal

73. APACHE II
 Acute Physiology and Chronic Health Evaluation
 as good as the Ranson or Glasgow at 24 and
48 hours of the admission
 APACHE II score > 8 = Severe acute pancreatitis
 Cumbersome to use if one does not use a pc or
palm - where the formula is easily downloaded
Br J Surg 1997,84:1665-69

74. APACHE II
•Temp high or low
•MAP high or low
•HR high or low
–(HR 60 gets 2pts!)
•Na high or low
•K high or low
•Creat elev
•Age over 44
•APACHE-O
–BMI>25 1 pt
–BMI>30 2pts
•WBC high or low
•Glasgow coma (low)
•pH or HCo3
–High or low
•PaO2
•Nonsurgical and
emergency surgery
–More points
Score <8 Mortal <4%
Score >8 8-18%

75. Grading of pancreatitis (Balthazar score)
•A: normal pancreas: 0
•B: enlargement of pancreas: 1
•C: inflammatory changes in pancreas and peripancreatic fat: 2
•D: ill-defined single peripancreatic fluid collection: 3
•E: two or more poorly defined peripancreatic fluid collections: 4
Pancreatic necrosis
•none: 0
•≤30%: 2
•>30-50%: 4
•>50%: 6
The maximum score that can be obtained is 10.
Treatment and prognosis
The CTSI is the sum of the scores obtained with the Balthazar
score and those obtained with the evaluation of pancreatic necrosis:
•0-3: mild acute pancreatitis
•4-6: moderate acute pancreatitis
•7-10: severe acute pancreatitis

76. Desirable features of Markers
of Severity
 Accuracy - High Sensitivity
 Predictability within 24 hours of
admission
 Easy to use

77. BISAP
•SIRS
–T >38.5°C or <35.0°C, HR>90,
–RR >20 or PaCO2 <32 mm Hg
–WBC >12,000, <4000 or >10 percent immature
(band) forms
•BUN>25
•Age>60
•Pleural effusion
•Altered mental status (glasgow CS < 15)
0-2 pts: <2% mortal
3-5pts: 22% mortal

78. ATLANTA (1992)
Mild vs severe (necrosis or organ failure)
APACHE≥8 or RANSON≥3
Organ failure
Systolic blood pressure <90 mmHg
Pulmonary insufficiency PaO2 ≤ 60 mmHg
Renal failure Creatinine ≥2 mg/dl after rehydration
Gastrointestinal bleeding 500 ml in 24 h
DIC: Platelets ≤100 fibrinogen <1·0 g/l and fibrin-split
products >80 μg/l
Calcium ≤7·5 mg/dl

79. ATLANTA REVISED (2008)
Early severity->organs fail
Late severity->Structural (necrosis), esp
infect
PERSISTANT ORGAN FAILURE (>48
hrs)
NEW DEFs of Radiographic/structural
features of severity

80. Current Recommendations
 Mild to moderate
Ranson < 3
APACHE II < 8
 Severe
Ranson >3
APACHE II >10
Organ failure
Pancreatic necrosis

81.  If a multiple factor scoring system is to
be used, the best choice at present
appears to be APACHE II calculated at
24 hours - Evidence category A

83. Is It Possible to Predict Severity
Early in Acute Pancreatitis?
 Good clinical judgment
– Specificity - 80%
– Sensitivity - 40%
 Scoring
 Specificity – 60%
– Sensitivity – 95%

84.  CRP is currently the gold standard
 Amylase and lipase of no value
 High likelihood that IL-6/ TAP will
replace the CRP
Recommendations

85. Advantage
 Used to monitor the clinical course of the
disease
Disadvantage
 Not always present on admission
 Lack specificity
C-reactive protein (CRP)

86. C-reactive protein (CRP)
 Gold standard for the prediction of the
necrotizing course of the disease
 Accuracy of 86%
 Readily available

87. C-reactive protein (CRP)
 Acute phase reactant
 Synthesized by the hepatocytes
 Synthesis is induced by the release of
interleukin 1 and 6
 Peak in serum is three days after the onset
of pain
 Most popular single test severity marker
used today
Isenmann et al Pancreas 1993;8:358-61

88. Management of Acute Pancreatitis
Not Recommended
Antibiotics
CT scan
PPI
Recommended (All pts.)
Admit to general ward
Refeed when pain subsides
Mild AP
80% of cases
< 5% of mortality
Necrosis
Sterile- observe
If infection suspected - FNA
Necrosectomy in infected necrosis
Recommended
Admit to ICU
Antibiotics
CT scan - day 3
Severe AP
20% of cases
> 95% of mortality
Not Recommended
Antibiotics
CT scan
PPI
Recommended (All pts.)
Admit to general ward
Refeed when pain subsides
Mild AP
80% of cases
< 5% of mortality
Necrosis
Sterile- observe
If infection suspected - FNA
Necrosectomy in infected necrosis
Recommended
Admit to ICU
Antibiotics
CT scan - day 3
Severe AP
20% of cases
> 95% of mortality

89. Treatment Of Acute Pancreatitis
UNCOMPLICATED PANCREATITIS …. MEDICAL
SELF LIMITED IN MOST CASES
AIM
FLUIDS AND ELECTROLYTES
PANCREATIC
SECRETION

90. KEEP PATIENT …… NPO
UNTILL WHEN …???
NASOGASTRIC SUCTION ……..???
AGGRESSIVE FLUIDS REPLACEMNT
MANGEMENT OF HYPO. K ,Ca ,CL,Mg.
OXYGEN

91. WHAT IS ABOUT…??

92. ANTICHOLINERGICS…..???
ANTIACIDES …….
???

93. UCAGON ……???
MATOSTATIN .. ??
ACYLOL ……. ???

94. ANTIBIOTICS …..????

95. Antibiotics
 Sepsis
– Accounts for > 80% of deaths
 Intestinal flora
– Gram negative bacteria
 Mechanism – translocation of the
bacteria across the gut wall

96. Antibiotics - Rationale
 Early (1 week) Sterile necrosis
– Massive inflammatory response – multi-system
organ failure (SIRS)
 Late –
– Infected necrosis

97. Why the controversy ?
 Early trials in 1970’s did not show the
benefit of antibiotics
 Antibiotics that did not penetrated the
pancreatic tissue

98. Evidence
 8 clinical trials
 Five of these trials showed a significant reduction
in the incidence of pancreatic infections
 1 trial showed a significant reduction in mortality
 Limitations
– Small sample size
– None were double blinded randomized placebo
controlled trials

99. Antibiotics ?
 Increased risk of fungal infections
 Associate with mortality as high as 85%

100. Recommendations
 Prophylactic antibacterial treatment is strongly
recommended in severe pancreatitis (Evidence B)
 No evidence when to start prophylactic treatment or
how long to continue therapy
 Appropriate antibiotics are those that are active
against in particular gram-negative organisms
 Commence as early as possible after the
identification of a severe attack

101. Therapy
 Treatment
– Antifungal therapy – definite role

102. Fungal Infection
 Antibiotics predispose to candida
infection of the pancreatic tissue which
increases the mortality substantially

103. Fungal infection
 92 patients with infected pancreatic necrosis
 22 patients (24%) with Candida infection
 Patients with Candida infections
– Suffered higher mortality (64% vs. 19%, p=.0001)
– More systemic complications
– Were given preoperative antibiotics for a longer
period (19 vs 6 days; p=.0001)
World J. Surg. 25,372-76

104. Fungal Infection
 Candida
 Torulopsis
 Commensal organism found in
human gastrointestinal tract
 Incidence 10-40%

105. KEEP PATIENT …… NPO
UNTILL WHEN …???
NASOGASTRIC SUCTION ……..???
AGGRESSIVE FLUIDS REPLACEMNT
MANGEMENT OF HYPO. K ,Ca ,CL,Mg.
OXYGEN

106. Evolution in Nutrition
Fasting
TPN is better
Early jejunal feeding is safe
Early jejunal feeding is superior
Gastric feeding is as good as jejunal
feeding

107. Current Recommendations
 Jejunal feeding should be started within 48
hours
 The optimal feeding formulae is unknown
 Ensure the jejunal placement of the tube
 Monitor for
– Hypertryglyceridemia/ hyperglycemia
 TPN in patients who do not tolerate
enteral feeding

109. IPMN

113. ERCP AND ES
INDICATION ....?
WHEN …..?

115. LOCAL …
GENERAL
…

116. LOCAL COMPLICATIONS
PANCREATIC
EXTRAPANCREATIC

117. PANCREATIC
PANCRATIC NECROSIS
PANCREATIC INFECTION
PANNCREATIC ABSCESS
PANCREATIC FISTULA
PANCREATIC ASCITES
PSUDOCYST

119. EXTRAPANCREATIC
INTRABDOMINAL HAEMORRHAGE
GASTROINTESTINAL HAEMORRHAGE
PORTAL VEIN THROMBOSIS
BILIARY OBSTRUCTION
DUODENAL OBSTRUCTION

120. Acute Pancreatitis
Complications
Pulmonary Cardiovascular Coagulation Renall Immunological
Pleural Effusion
(enzyme induced
Inflammation of
Diaphragm)
Atelectasis
Abdominal distention
&  diaphragmatic
movement
3rd spacing
BP, HR
Vasoconstriction d/t
SNS activation
Trypsin activates
both clotting
& lysing factors
 DIC & PE
Hypovolemia
GFR
Renal perfusion
Clots in renal
circulation
ATN
ARF
GI motility
bacteria outside GI
Pancreatic abscess
Necrosis
infection
120

121. Markers of Inflammation
 TNF-alpha
– Major role in mediating inflammatory response
– Conflicting reports as a predictor of severity
 Interleukin-6 and 8.
– Principal cytokine mediator
– Measured in serum and urine
– Discriminate severe from mild cases on day 1

122. GENERAL COMPLICATIONS
RESPIRATORY INSUFFICIENCY
ADRS
RENAL FAILURE
DEPRESSED MYOCARDIAL FUNCTION
( MULTIPLE ORGAN FAILURE )

123. MECHANISMS OF GENERAL COMPLICATION
PANCREATIC INFECTION
COLON …..???
RLEASE OF ACTIVE INFLAMATORY MEDIATORS

124. INDICATION OF LAPAROTOMY…??

125. ACCEPTED INDICATIONS
DIAGNOSIS IN DOUBT
PERSISTENT BILIARY PANCREATITIS
INFECTIVE PANCREATIC NECROSIS
PANCREATIC ABSCESS

126. CONTROVERSIAL INDICATIONS
> 50% STERILE PANCREATIC NECROSIS
STABLE BUT PERSISTENT DISEASE
DETERIORATION IN CLINICAL COURSE
ORGAN SYSTEMIC
FAILURE

127. WHAT IS THE OPERATION..?

130. UNDER
SURGICAL
OR
MEDICAL !!??

136. PROGNOSIS
RANSON,S CRITERIA
APACHE II SCORING SYSTEM
GLASCO CRITERIA
< 3 RANSONS ,S CR. MORTALITY RATE
0.9 % . 3-4
….19 % …..5-6 50% ….. > 6 ….90 %