2. Index Case
24May 2016
40 yrs old male, alcohol abuser presented with
âșPain abdomen for 3 hours
ï¶Upper abd, non-colicky, severe, radiating to back
ï¶Associated vomiting, multiple time bilious
ï¶Associated abd distension +
âșPast, Family History : Not significant
âșPersonal History: 80-100 gms of alcohol/day for 15-16
yrs
3. GPE â Pulse 122 , BP 140/82 mmHg, RR 24/min
Abdomen
âșLiver 3 cm, soft to firm
âșSpleen not palpable
âșDiffuse tenderness & guarding in whole abdomen
âșBowel sound sluggish
Chest: reduced breath sound at bases
CVS, CNS â NS
Possibilities:
Index Case
4. Index case: Investigations
Hb -15.5 TLC â 14000 DLC â N 76 L 22 Platelets â
355
Urea : 55 Creatininine : 1.2
Bil â 1.5 SGOT â 55 SGPT â 62 ALP 130 (ULN â 128)
TP â 7.6 Albumin â 4.9
Amylase â 155 (40-140)
Lipase â 96 (0-50)
Abd X-ray: No evidence of pneumoperitoneum
USG abdomen â Bulky pancreas, GB sludge
5. Issue 1
What is the practically acceptable criteria
for diagnosis of acute pancreatitis?
6. Acute pancreatitis: Diagnosis
At least two of the following
âșAbdominal pain consistent with the disease
âșSerum amylase and / or lipase greater than three
times the upper limit of normal
âșCharacteristic findings from abdominal imaging
CECT and / or MRI should be reserved for
âșPatients in whom the diagnosis is unclear
âșWho fail to improve clinically within the first 48 â 72 h
after hospital admission
âșTo evaluate complications
ACG Guideline. Am J Gastroenterol 2013; 108:1400â1415
7. Issue 2
Which enzyme assay is preferable : amylase or
lipase or combination of two?
âșRelative accuracy
âșFalse negative and false positive
8. Pattern of rise
âșRises within a few hours, may return to normal within 5
days
âșSensitivity in AP â approx 80%
Acute pancreatitis with no rise in amylase
âșHypertriglyceridemia
âșAlcohol related AP
âșAcute on chronic pancreatitis
High amylase but no pancreatitis
âșMacroamylasemia
âșRenal failure
âșdiseases of the salivary glands
âșExtrapancreatic abdominal conditions with inflammation
âșGynaecological diseases
Serum amylase estimation: Pitfalls
10. Pancreatic enzyme testing in AP
Amylase testing offers no additional value to
lipase testing
Dual testing is not superior to Lipase testing
alone
Neither have prognostic value
Pancreatic enzymes should not be repeated
after making the diagnosis of acute pancreatitis
Barbieri JS. Journal of Hospital Medicine 2016;11 :366-68
11. Index case
Repeat Lipase at 24 hours : 480 IU
Diagnosis of Acute pancreatitis was made
Treatment
âșIV fluid
âșAnalgesia
12. Issue 3
Fluid for initial resuscitation/therapy of acute
pancreatitis?
âșDoes initial aggressive fluid resuscitation matter?
âșWhich the preferred or currently recommended
crystalloid fluid in initial management of acute of
pancreatitis?
âșHow to monitor fluid resuscitation?
ï¶Non-invasively â clinical/lab parameter
ï¶Invasively
ï¶How frequently the fluid therapy should be
monitored?
13. Fluid therapy in acute pancreatitis
Aggressive hydration, defined as 250 â 500 ml per hour
of isotonic crystalloid solution unless contraindicated
Early aggressive intravenous hydration is most beneficial
during the first 12 â 24 hrs
In a patient with severe volume depletion, manifest as
hypotension and tachycardia, more rapid repletion
(bolus) may be needed
ACG Guideline. Am J Gastroenterology 2013
14. Lactated Ringer â s solution may be the preferred isotonic
crystalloid replacement fluid
Fluid requirements should be reassessed at frequent
intervals within 6 h of admission and for the next 24 â 48
h.
The goal of aggressive hydration should be to decrease
the BUN
CVP/USG monitoring of IVC
Fluid therapy in acute pancreatitis
ACG Guideline. Am J Gastroenterology 2013
15. IV line secured, started on RL
NPO
Injectable PPI â Pantoprazole 80 mg followed
by 40 mg BD
Inj Metoclopramide 10 mg IV stat
Analgesic: Buscopan + Diclofenac injection â
pain reduced in intensity but did not subside
Index case: Investigations
17. Effect of narcotics on Sphincter of Oddi
pressure
Sphincter
pressure at base
line
Sphincter
pressure 20 min
after inj
Morphine 8.90±9.11 20.51±13.46
Pethidine 7.06±5.07 6.68±4.32
Tramadol 7.01±5.50 6.39±5.37
Pentazocine 6.42±5.10 11.34±8.40
Wu SD. World J Gastroenterol 2004;10(19):2901-2904
18. Effect of narcotics on Sphincter of Oddi
pressure
Staritz M et al. Gut, 1986, 27, 567-569
19. Morphine and pentazocine increase SO and
CBD pressure
Pethidine does not increase SO or bile duct
pressure
Tramadol and Buprenorphine increase SO
pressure minimally
Tramadol has the same analgesic effect as
morphine. But it has little effect on the
respiratory system and circulation system
Effect of narcotics on Sphincter of Oddi
pressure
Wu SD. World J Gastroenterol 2004;10(19):2901-2904
20. Pain persisted in lower intensity â was put on Inj Tramadol
sos, Buprenorphine patch was given
Started having fever from Day 3 â Temp upto 38.5 degrees C
Bowel not moved
Tachypnea â RR 24-30, O2 â 0.30
Repeat Labs on day 4
âșS/Electrolytes, RFT â N
âșLFT â Bil â N, Mild rise of transaminases
âșHb 12.9 gms TLC -13500 DLC â N 70 L 26
Index case: Course
21. Issue 5
How do we define severity of acute
pancreatitis?
âșMild/moderate/severe
22. Revised Atlanta Definitions 2012
Interstitial oedematous pancreatitis
âșAcute inflammation of the pancreatic parenchyma and
peripancreatic tissues, but without recognisable tissue
necrosis
âșCECT criteria
ï¶Pancreatic parenchyma enhancement by intravenous
contrast agent
ï¶No findings of peripancreatic necrosis
Necrotizing pancreatitis
âșInflammation associated with pancreatic parenchymal
necrosis and/or peripancreatic necrosis
âșCECT criteria
ï¶Lack of pancreatic parenchymal enhancement by
intravenous contrast agent and/or
ï¶Presence of findings of peripancreatic necrosis
23. Mild acute pancreatitis
âșNo organ failure
âșNo local or systemic complications
Moderately severe acute pancreatitis
âșOrgan failure that resolves within 48 h
âșTransient organ failure and/or
âșLocal or systemic complications without
persistent organ failure
Severe acute pancreatitis
âșPersistent organ failure (>48 h)
ï¶Single organ failure
ï¶Multiple organ failure
Severity of acute pancreatitis
24. Parameters
Score
0 1 2 3 4
PaO2/ FiO2 ratio >400 301â400 201â300 101â
200
â€101
Serum creatinine,
mg/dl)
<1.4 1.4â1.8 1.9â3.6 3.6â4.9 >4.9
Cardiovascular
(systolic blood
pressure, mm)
>90 <90, fluid
responsive
<90, not
fluid
responsive
<90,
pH<7.3
<90,
pH<7.
2
Modified Marshall scoring system for organ
dysfunction
A score of 2 or more in any system defines the presence of organ failure.
25. Organ failure in acute pancreatitis
Shock
âș(systolic blood pressure < 90 mm Hg),
Pulmonary insufficiency
âș (PaO 2 < 60 mm Hg),
Renal failure
âșcreatinine > 2 mg / dl after rehydration
Gastro intestinal bleeding
âș > 500 ml of blood loss/ 24 h
Bradley EL et al. Arch Surg 1993 ; 128 : 586 â
33. Issue 6
Is this patient having severe acute pancreatitis
or likely to have severe acute pancreatitis?
How to identify patients with severe acute
pancreatitis?
37. Japanese society severity score
Variables
âșBE level < -3 mEq/L or shock
âșPaO2 < 60 mm Hg (room air) or respiratory failure
âșBlood urea nitrogen level > 40 mg/dL or creatinine
level > 2 mg/dL
âșLactate dehydrogenase level > 2 folds of upper normal
limit
âșPlatelet count < 105/mm3
âșCalcium level < 7.5 mg/dL
âșC-reactive protein level > 15 mg/dL
âșSystemic inflammatory response syndrome score > 3
âșAge > 70 years old
Pancreas 2014, 43:487-89
38. BISAP: Bedside index for severity in acute
pancreatitis
Blood urea nitrogen >25 mg/dL
Impaired mental status (Glasgow coma scale score<15)
SIRS : SIRS is defined as two or more of the following:
âșTemperature of <36â or >38â
âșRespiratory rate >20 breaths/min or PaCO2<32 mmHg
âșPulse>90 beats/min
âșWBC<4Ă109 or >12Ă109/L or >10% immature bands
Age>60 yr
Pleural effusion detected on imaging
39. Clinical findings predicting a severe course
Patient characteristics
âș Age > 55 years, Obesity (BMI > 30 kg / m2
)
âș Altered mental status
Comorbid disease
The systemic infl ammatory response syndrome (SIRS)
âșPresence of > 2 of the following criteria:
ï¶pulse > 90 beats / min, respirations > 20 / min, PaCO 2 > 32 mm
Hg, temperature > 38 ° C or < 36 ° C, WBC count > 12,000 or
< 4,000 cells / mm3
, 10 % immature neutrophils (bands)
Laboratory findings
âș BUN > 20 mg/dl, Rising BUN, HCT > 44 %, Rising HCT, Elevated
creatinine
Radiology findings
âș Pleural effusions, Pulmonary infiltrates, Multiple or extensive
extrapancreatic collections
ACG Guideline 2013. Am J Gastroenterol 2013
41. Issue 7 â Imaging in AP
CECT of abdomen in acute pancreatitis
âșWhat are the findings which should especially be
taken into consideration?
âșWhat is accuracy of CT scan?
âșShould all patients be subjected to CT scan
examination?
âșWhen should CT scan be done?
âșWhat is the ideal timing?
âșDoes accuracy depend on timing and technique?
âșWhat are the risks involved with CT scan
examination?
âșWhat are the modalities to reduce the risk?
42. Contrast CT scan of abdomen
CECT provides over 90 % sensitivity and specificity for
the diagnosis of AP ( 20 ).
Routine use of CECT in patients with AP is unwarranted
If a patient fails to improve after 48 â 72 CECT or MRI
imaging is recommended to assess local complications
CT and MRI are comparable in the early assessment of
AP
âșMRCP can detect CBD stones upto 3 mm
Timing of CT scan
âșFor assessment of severity and local complications:
after 3-5 days
âșWhen diagnosis in doubt: any time
ACG Guideline. Am J Gastroenterol 2013; 108:1400â1415
43. CT severity index of acute pancreatitis
Balthazar CT Score
âșA -Normal
âș B -Focal or diffuse enlargement of the pancreas, including
irregularities of contour and inhomogeneous attenuation
âș C - Pancreatic gland abnormalities in grade B plus per
pancreatic inflammation
âș D - Grade C plus a single fluid collection
âș E - Grade C plus 2 or more fluid collections and/or the
presence of gas in or adjacent to the pancreas
Necrosis
âșNone â score 0
âșLess than 30% - score 2
âș30-50% - score 4
âș> 50% - score 6
44. Mortele KJ et al. AJR 2004;183:1261â1265
Modified CT Severity Index
48. Issue 8 â Antibiotic prophylaxis in AP
Antibiotics in acute panreatitis
âșShould prophylactic antibiotics be given to all patients
with acute pancreatitis?
âșShould prophylactic antibiotics be given to all patients
with severe acute pancreatitis?
âșWhat are the commonly acceptable indications of
emperical use of antibiotics?
âșWhat the antibiotics preferred for prophylactic or
emperical use?
âșWhen to start and when to stop?
49. Prophylactic antibiotics in AP
âIt is very difficult to study this very very challenging
question and it is likely to remain enigma for quite some
timeâ
Alphonso Brown, Gastroenterology 2004
50. Last 15 years
âșMultiple trials
âșIncluded mainly severe pancreatitis
âșMany randomized trials, only one double blind
randomized trial
âșVariable results
âșAntibiotics : Imipenem, Cephalosporins,
Ciprofloxacin/Metronidazole
Prophylactic antibiotics in SAP
Gastroenterology 2004
51. Author Agent Durat
ion
Panrcreatic
infection
Mortality
Antibi
otics
Control Antibi
otics
Control
Pederzoli Imipenem 14 12.1 30.3 7.3 12.1
Sainio Cefuroxime 14 30.0 40.0 3.3 23.3
Delcenseri
e
Ceftazidime,
Amika, Metro
10 0 25 9.1 25
Schwarz Ofloxacin,
Metro
10 61.5 53.8 0 23
Nordback Imipenem/cila
statin
Not
state
d
8.0 42.4 8.0 15.1
Isenman Cipro, metro 14 12.0 8.9 5.1 7.1
Prophylactic antibiotics in AP
53. Antibiotics in acute pancreatitis
Routine use of prophylactic - not recommended
Prophylactic antibiotic in necrotizing pancreatitis - not
recommended
Antibiotics should be given for an extra-pancreatic infection
Infected necrosis should be considered in patients with
pancreatic or extrapancreatic necrosis who deteriorate or
fail to improve after 7 â 10 days of hospitalization.
âș In these patients, either (i) initial CT-guided fine-needle
aspiration (FNA) for Gram stain and culture to guide use
of appropriate antibiotics or
âșEmpiric use of antibiotics after obtaining necessary
cultures for infectious agents, without CT FNA, should be
given
ACG Guideline . Am J Gastroenterology 2013
54. In patients with infected necrosis, antibiotics known to
penetrate pancreatic necrosis, such as carbapenems,
quinolones, and metronidazole, may be useful in delaying
or sometimes totally avoiding intervention, thus
decreasing morbidity and mortality
Duration of antibiotics : ??
Routine administration of antifungal agents along with
prophylactic or therapeutic antibiotics is not
recommended
Antibiotics in acute pancreatitis
ACG Guideline . Am J Gastroenterology 2013
55. Prophylactic antibiotics in AP
Mild pancreatitis : Not recommended
SAP: The prophylactic administration of
antibiotics may improve the prognosis, if
carried out in the early phases of pancreatitis
(within 72 h of onset). (2B)
Prophylactic antifungals are not recommended.
(1C)
Japanese Guideline. J Hepatobiliary Pancreat Sci (2015) 22:405â432
56. Antibiotics Efficacy factor
Imipenem 0.98%
Ofloxacin 0.87%
Ciprofloxacin 0.86%
Ceftriaxone 0.79%
Cefotaxime 0.78%
Tobramycin 0.22%
Netilmycin 0.21%
Efficacy factor of antibiotics in SAP
Trop GE 1998
57. Issue 9 â Nutrition in acute pancreatitis
Feeding in acute pancreatitis
âșWhich is the preferred route â enteral or parenteral?
âșWhen to start feedingâ?
âșMild to moderate pancreatitis
âșSevere acute pancreatitis
âșWhich is preferred feeding formula â
elemental/polymeric/Immune feeding?
âșWhich is the preferred enteral feeding route â
nasogastric or nasoduodenal or nasojejunal?
58. Nutrition in acute pancreatitis
In mild AP, oral feedings can be started once there is no
nausea and vomiting, and abdominal pain
âșlow-fat solid diet appears as safe as a clear liquid diet
In severe AP, enteral nutrition is recommended to
prevent infectious complications.
Parenteral nutrition
âșenteral route is not available, not tolerated, or not
meeting caloric requirements
Nasogastric delivery and nasojejunal delivery of enteral
feeding appear comparable in efficacy and safety
59. Nutrition in acute pancreatitis
Petrov M et al. ISRN Inflammation 2013
Reduced risk of infective complications and possibly
reduced mortality with enteral feeding in severe acute
pancreatitis
60. Nutrition in acute pancreatitis
Petrov M et al. ISRN Inflammation 2013
Most of the patients with SAP are able to tolerate enteral
feeding and nutritional goal is achieved in most patients
61. Enteral feeding formula
Elemental
âșComprising amino acids or oligopeptides,
maltodextrins, and mediumâchain and long-chain
triglycerides;
Polymeric
âșComprising nonhydrolyzed proteins, maltodextrins,
and oligofructosaccharides, as well as long-chain
triglycerides;
Immune-enhancing
âșComprising substrates that have been hypothesised to
modulate the activity of the immune system, for
example, immunonutrition (glutamine, arginine, and
omega-3 fatty acids), probiotics, fibre-enriched
formulation.
62. Nutrition in Acute pancreatitis
Enteral nutrition â
âșCurtails of acute inflammation of the pancreas
âșReduces septic complications
Nasojejunal tube feeding improves outcomes in SAP
Safety and efficacy of nasogastric tube feeding in SAP
Early NG feeding may have benefits even in mild-to-
moderate acute pancreatitis
Optimal enteral feeding formulations â more information is
required
Petrov M et al. ISRN Inflammation 2013
63. Put on IV antibiotics â Piperacillin+ Tazobactum for 14
days
Nasojejunal tube placed â feeding attempted
âșDistension of abdomen
âșSOB
Feeding had to be stopped temporarily
O2 supplementation
CXR was unremarkable
IAP was measured
Index case: Course
64. Issue 10 : IAP monitoring in acute
pancreatitis
Role of intra-abdominal pressure monitoring in acute
pancreatitis?
âșHow to define abdominal compartment syndrome?
âșHow to monitor for abdominal compartment syndrome?
âșHow to treat abdominal compartment syndrome?
65. Abdominal compartment syndrome
IAH â IAP> 12 mmHg ACS â IAP> 20 mmHg
Causes
âșInflammatory fluid collection, inflammatory mass
âșParalytic ileus and distension of bowel
âșAscites
Consequences
âșReduced renal and abd perfusion
âșIschemic bowel complication
âșRespiratory impairment
Remedial measure
âșDecompression of stomach & bowel
âșAscitic tap/ placement of drains
âșMechanical ventilation with muscle relaxants
âșRestrict fluid if possible
Mentula P et al. World Journal of Emergency Surgery 2014, 9:15
66. NJ feeding could be established after 5 days
NJ feeding was given for two weeks
Oral feeding in third week â gradually built up
âșFullness and bloating â post meals
âșNo vomiting
Palpable lump abdomen, No fever , No vomiting
Labs: normal RFT, LFT, Mild leucocytosis
Discharged in 5th
week
Index case: Course
67. Re-evaluation during 7 â 8 th week
âșMild abdominal pain/discomfort, post prandial bloating
âșNo fever
âșTolerating oral diet, low fat
âșExamination: large upper abdominal lump, mild
tenderness
Index case: Course
68.
69.
70. Issue 11 : Management of Non-Infected
Necrosis
Pancreatic necrosis without infection
âșWhat are factors which determine the
outcome?
âșWhat should be the preferred approach in
management?
72. Sterile pancreatic necrosis
Debridement for sterile necrosis is recommended if
âșAssociated with gastric outlet obstruction
âșBile duct obstruction
Asymptomatic pancreatic and / or extrapancreatic
necrosis does not mandate intervention regardless of
size, location, and extension.
73. 10th
week of illness
âșGradual increase in upper abdominal pain over 3-4
days
âșFever â High grade
âșVomitng off and on
âșShortness of breath
âșExamination
ï¶Palpable upper abominal lump, tender
ï¶Reduced breath sound at lung bases
âșLabs
ï¶RFT, LFT â N
ï¶HMG â Hb 10.5 gm, TLC â 24000, DLC â N88%, L
12
ï¶PCT â 3.9
Index case: Course
74.
75.
76. Issues 12: Infected Pancreatic Necrosis
Pancreatic necrosis - With evidence of infection
âșShould all patients be referred for surgery?
âșWhat are the factors which determine the outcome?
âșHow to select the cases for non-surgical
management?
âșWhat is the optimum timing for surgery?
77. Issue
Infections in acute pancreatits
âșWhat are the common sites of infection in patients
with acute pancreatitis?
âșWhat are the risk factors for infected pancreatic
necrosis?
âșTiming of pancreatic infection
âșMethods of diagnosis
âșOrganisms
âșWhat are the common organisms?
âșWhat is the source of these organisms
âșHow common are the anaerobes?
âșHow common is fungal infection ?
78. Risk of pancreatic infection
Risk depends upon
âșSeverity of pancreatitis
ï¶Ransonâs score < 3 : 5.3%
ï¶Ransonâs score > 5 : 58%
âșExtent of necrosis
ï¶<30% : 5-10%
ï¶30 â 50% : 10-20%
ï¶> 50% : 30 â 70%
âșBacterial colonization of gut
Br J Surgery 1999
80. Bacteriology of pancreatic infection
Organism Frequenc
y
E coli 35%
K pneumoniae 24%
Enterococcus 24%
Staphylococcus 14%
Pseudomonas 11%
Proteus 8%
Aerobic
streptococci
7%
Enterobacter 7%
Bacteroides 6%
Compiled data
No of series : 45
Total patients > 1100
Am Surgeon 2000
81. Fungal infection in pancreatic
necrosis
Risk factors
âșBroad spectrum antibiotics
âșAbdominal surgery
âșMale sex, Age > 40 years
âșCentral venous access , Hypotension at admission
âșHigh APACHE II score
âșRenal failure , TPN, Respiratory failure at admission
âșMechanical ventilation
âșERCP/ Pancreatic stenting
âșDiabetes mellitus
âșPercutaneous drainage
âșDuration of hospital stay > 4 weeks
Kochhar R, JGH 2013
83. Impact of pancreatic infection
Increased mortality
Increased morbidity
âșIncreased risk of renal failure
âșIncreased risk of GI bleed
âșIncreased risk of respiratory failure
âșIncreased cardiovascular complication
Longer hospital stay
Increased probability of surgery
Increased cost of therapy
85. Infection in pancreatic necrosis
When to suspect
âșTiming : second or third week
âșClinical feature
ï¶Recurrence of pain abdomen
ï¶Worsening of organ system function
ï¶Increasing temperature
ï¶Increasing TLC
ï¶New onset ileus
Am Surgeon 2000
86. Methods of diagnosis
âșPlain X-Ray
âșUltrasonography, CT
âșBlood culture
âșGallium scan
âșIn111 labelled leucocyte scan
âșUSG/CT guided FNA
âșPET CT
Infection in pancreatic necrosis
Gut 2005, Gastroenterology2004
87. Methods of diagnosis
âșPlain X-Ray
âșUltrasonography, CT
âșBlood culture
âșGallium scan
âșIn111 labelled leucocyte scan
âșUSG/CT guided FNA
âșPET CT
Infection in pancreatic necrosis
Gut 2005, Gastroenterology2004
88. USG/CT guided FNA
Needle should not pass through a bowel
Each suspected area should be sampled, multiple passes
may be required
Multiple sessions may be required
Samples for gramâs stain, aerobic & anaerobic bacterial
culture, fungal smear & culture
Rapid inoculation, use of transport medium
90. Infected pancreatic necrosis
Antibiotics alone can lead to resolution of infection and,
in select patients, avoid surgery altogether
âș16/28 pts improved with antibiotics
Unstable patients with infected necrosis needs
consideration for urgent debridement
âșa course of antibiotics before intervention to allow the
inflammatory reaction to become better organized
âșIf pt fails to improve : Necrosectomy
ï¶Endoscopic/radiologic/video-assisted
retroperitoneal/ laparoscopic approach/
combination
91. Cochrane review
âșThe minimally invasive step-up approach resulted in
fewer adverse events, serious adverse events, less
organ failure, and lower costs compared to open
necrosectomy.
No evidence to suggest that early open necrosectomy is
superior or inferior to peritoneal lavage or delayed open
necrosectomy
Endoscopic minimally invasive step-up approach
resulted in fewer adverse events than the video-assisted
minimally invasive step-up approach but increased the
number of procedures required for treatment
Infected pancreatic necrosis
92. Treatment of Infected pancreatic necrosis
Before demarcation of necrosis develops (< 4 weeks), it
is almost impossible to remove all necrotic tissue without
causing hemorrhage.
Early surgical debridement
âșHigh risk of hemorrhage
âșIncreased organ dysfunction and death.
Necrosectomy within the first two weeks - 75% mortality
Necrosectomy after 6-8 weeks â Mortality 5%
Multiple organ dysfunction increases mortality
93. Because high mortality is associated with early surgery ,
it is recommended that surgery for infected necrosis
should be postponed as late as possible, preferable later
than four week from disease onset
âșRole of percutaneous drain â single or multiple
âșMinimally invasive surgery/ endoscopic procedure
Infected pancreatic necrosis
94. Infected pancreatic necrosis
Supportive care for organ failure
Nutrition
Antibiotics : as per sensitivity and local data
Drainage and necrosectomy
âșOpen surgical
âșLaparoscopic
âșRadiological
âșEndoscopic
95. USG guided aspiration
âșPus culture â E coli sensitive to Imipenem,
Meropenem and Colistin
Was started on Meropenem
PCD was places â upgraded to 16 F
Percutaneous endoscopic necrosectomy â 2 sessions
Patient became afebrile after first session
ERCP â Disrupted MPD, stented
Index case: Course
96. Necrosectomy for infected
necrosis
Best surgical method not defined
âșNo direct comparison available
Open surgical necrosectomy is the gold standard and
standard of care
Percutaneous and endoscopic necrosectomy are
emerging modalities
Local expertise and quality of ICU care matters
100. Issue 13
ERCP in acute biliary pancreatitis
âșWhat are the indications for ERCP in acute biliary
pancreatitis?
ï¶Urgent indications
ï¶Semi-elective indications
âșDoes timing of ERCP matter?
âșWhat is the preferred ERCP intervention â stent or
NBD or sphincterotomy or CBD clearance?
âșPatient taken up for ERCP but no stone on
cholangiogram â what to do next?
102. ERCP in acute biliary pancreatitis
Indications
âșSuspected bile-duct stones as the cause of
pancreatitis established clinically, and one of the
following:
ï¶Cholangitis (fever, jaundice, sepsis)
ï¶Persistent biliary obstruction (conjugated bilirubin
level >5 mg/dl
ï¶Clinical deterioration (worsening pain, increasing
white-cell count, worsening vital signs)
ï¶Stone detected in the common bile duct on imaging
ACG Guideline. Am J Gastroenterology 2013
103. Contraindications
âșAbsolute
ï¶Unstable medical condition precluding safe
administration of moderate sedation or general
anesthesia
ï¶Decision by competent patient not to provide consent
for the procedure
ï¶Endoscopist with inadequate training in ERCP
âșRelative (may be overcome)
ï¶Anatomical condition (gastroduodenal disease or
surgical alteration) that would impede endoscopic
access to the major papilla;
ï¶Clinically significant or uncorrectable coagulopathy
ERCP in acute biliary pancreatitis
ACG Guideline. Am J Gastroenterology 2013
104. UK guideline 2005
âșEarly ERCP (within 72 hours after admission to the
hospital) in all patients with predicted or actual severe
biliary pancreatitis
AGA 2007
âșUrgent ERCP (within 24 hours after admission) if
cholangitis
âșEarly ERCP (within 72 hours after admission) if suspicion
of persistent bile-duct stones
ACG 2013
âșPatients with AP and concurrent acute cholangitis should
undergo ERCP within 24 h of admission
âșERCP is not needed early in most patients with gallstone
pancreatitis who lack laboratory or clinical evidence of
ongoing biliary obstruction
ERCP in acute biliary pancreatitis
105. ERCP in acute pancreatitis
Sphincterotomy and CBD clearance
âșEvidence of CBD stone, biliary obstruction : at any
time during course
âșSuspicion or evidence of cholangitis : at any time
during course
âșPersistent biliary obstruction
âș? Any case of biliary pancreatitis taken up for ERCP
106. ERCP in acute pancreatitis
âWhile laparoscopic cholecystectomy is the gold
standard to avoid recurrence in patients with gall
stone related pancreatitis, ERCP and sphincterotomy
are accepted alternatives in patients who are unfit for
surgeryâ
Gut 2005
107. Issue 14
Timing of cholecystectomy after an episode of acute
biliary pancreatitis?
âș What is the risk of recurrence over time?
108. Risk of delayed cholecystectomy
Jee SL. Asian Journal of Surgery 2016
109. Summary
AP â disease with unpredictable severity
Significant morbidity and mortality in severe disease
Team approach is crucial in management
Enteral nutrition is preferable to parenteral nutrition
Radiological interventions may play a crucial role in
stabilizing a critically ill patient
Endoscopic interventions are indicated in a select group
of patient
Early surgery is associated with higher complication rate
compared with late surgery
Specific treatment should be instituted when applicable
114. AP: Magnitude of problem
Incidence : 4.9 â 73.4 cases per lac population
Incidence is increasing
Mortality: minimal decrease over years
Severity of pancreatitis
âșMild : 70 -80%
ï¶No local or systemic complication Usually no
necrosis
ï¶Recovery in 3 â 7 days
âșSevere : 20 -30 %
ï¶Local or systemic complications
ï¶Necrosis usual
ï¶Infection : 20 â 70%
Gut 2005, Am J Gastro 2013
115. Course of acute pancreatitis
Overall mortality: 5 â 10%
Almost all mortality in severe cases
Two phases of illness
âșEarly phase - within 7 days: largely unrelated to
infection, mostly cytokine mediated
ï¶SIRS
ï¶Organ failure
âșLate phase â after 7 days, largely related to infection
and consequences of organ failure
ï¶Local complications
Fluid collections, necrosis â sterile or infected
Acute pseudocyst
Walled off pancreatic necrosis
ï¶Organ failure - persistent
Tanner S et al. Am J Gastroenterol 2013
116. Cochior D et al. Chirurgia (2013) 108: 631-642
Course of acute pancreatitis
117. Initial assessment and risk stratification
Hemodynamic status be assessed immediately upon
presentation
âșAggressive hydration, defined as 250-500 ml per hour of
isotonic crystalloid solution preferably Ringer Lactate
ï¶Exceptions: Cardiovascular and renal comorbidity
âșHigher infusion rate in those with hypotension or
tachycardia
âșAssess fluid requirement every 6 hours for 48 hours â
aim to decrease BUN
Risk assessment :
âșStratify patients into higher- and lower-risk categories to
assist triage, such as admission to an intensive care
setting
Patients with organ failure:
âșadmitted to an ICU or HDU
118. APFC (acute peripancreatic fluid
collection)
Peripancreatic fluid associated with interstitial
oedematous pancreatitis with no associated
peripancreatic necrosis.
This term applies only to areas of peripancreatic fluid
seen within the first 4 weeks after onset of interstitial
oedematous pancreatitis and without the features of a
pseudocyst.
CECT criteria
âșOccurs in the setting of interstitial oedematous
pancreatitis
âșHomogeneous collection with fluid density
âșConfined by normal peripancreatic fascial planes
âșNo definable wall encapsulating the collection
âșAdjacent to pancreas (no intrapancreatic extension)
119. Pancreatic pseudocyst
An encapsulated collection of fluid with a well defined
inflammatory wall usually outside the pancreas with
minimal or no necrosis.
This entity usually occurs more than 4 weeks after onset
of interstitial oedematous pancreatitis to mature.
CECT criteria
âșWell circumscribed, usually round or oval
âșHomogeneous fluid density
âșNo non-liquid component
âșWell defined wall; that is, completely encapsulated
âșMaturation usually requires >4 weeks after onset of
acute pancreatitis; occurs after interstitial oedematous
pancreatitis
120. ANC (acute necrotic collection)
A collection containing variable amounts of both fluid and
necrosis associated with necrotising pancreatitis;
the necrosis can involve the pancreatic parenchyma
and/or the peripancreatic tissues
CECT criteria
âșOccurs only in the setting of acute necrotizing
pancreatitis
âșHeterogeneous and non-liquid density of varying
degrees in different locations (some appear
homogeneous early in their course)
âșNo definable wall encapsulating the collection
âșLocationâintrapancreatic and/or extrapancreatic
121. WON (walled-off necrosis)
A mature, encapsulated collection of pancreatic and/or
peripancreatic necrosis that has developed a well defined
inflammatory wall.
WON usually occurs >4 weeks after onset of necrotising
pancreatitis.
CECT criteria
âșHeterogeneous with liquid and non-liquid density with
varying degrees of loculations (some may appear
homogeneous)
âșWell defined wall, that is, completely encapsulated
âșLocationâintrapancreatic and/or extrapancreatic
âșMaturation usually requires 4 weeks after onset of
acute necrotising pancreatitis
122. Etiology work up
Initial work up:
âșAlcohol, Gall stones, Hypercalcemia,
hypertriglyceridemia
idiopathic acute pancreatitis,
âșEUS - to assess for occult microlithiasis, neoplasms
and chronic pancreatitis.
âșIf EUS is negative, (secretin-stimulated) MRCP is
advised
For rare morphologic abnormalities - CT of the abdomen
If etiology remains unidentified, especially after a second
attack of idiopathic pancreatitis - genetic counseling (not
necessarily genetic testing)
ACG Guideline. Am J Gastroenterology 2013
123. Abdominal compartment syndrome
IAH â IAP> 12 mmHg ACS â IAP> 20 mmHg
Causes
âșInflammatory fluid collection, inflammatory mass
âșParalytic ileus and distension of bowel
âșAscites
Consequences
âșReduced renal and abd perfusion
âșIschemic bowel complication
âșRespiratory impairment
Remedial measure
âșDecompression of stomach & bowel
âșAscitic tap/ placement of drains
âșMechanical ventilation with muscle relaxants
âșRestrict fluid if possible
Mentula P et al. World Journal of Emergency Surgery 2014, 9:15
126. EUS and acute pancreatitis
Fusaroli P et al. World J Gastroenterol 2012; 18(32): 4243-4256
127. Role of EUS in acute pancreatitis
EUS may prevent ERCP in 71% of patients with AP and
offers a complication-free alternative
EUS seems superior to MRCP (51% vs 20%) in the
evaluation of AP
Cholelithiasis and biliary sludge (24%) are the most
frequent EUS diagnoses, and pancreas divisum (8%) is
the most frequent MRCP diagnosis
EUS can diagnose underlying chronic pancreatitis
Treatment of local complication â fluid collection, FNA,
necrosectomy, pseudocyst drainage
131. Da Cost DW et al. BJS 2014;101:65-79
Management of Acute Pancreatitis
132. Japanese Guideline 2015
Urinary trypsinogen-2 dipstick may be useful for
minimally invasive method and rapid diagnosis of acute
pancreatitis.
The prophylactic administration of antibiotics in severe
acute pancreatitis and necrotizing pancreatitis may
improve the prognosis, if carried out in the early phases
of pancreatitis (within 72 h of onset). (2B)
Intravenous hyperalimentation is not recommended for
mild cases. (1B)
In severe cases, it is more significant as a measure to
prevent infection rather than as a route of nutrition
support.
If initiated in the early phase, enteral nutrition can reduce
133. In principle, it is recommended that enteral feeding tubes
be inserted into the jejunum through the Treitz ligament.
However, if a feeding tube cannot be inserted into the
jejunum, nutrients can be infused into the duodenum or
stomach instead. (2B)
No life-saving effect has been observed from peritoneal
lavage for acute pancreatitis
The sequential measurement of IAP is recommended for
cases with
âșexcessive fluid infusion, high severity,
âșrenal and respiratory complications,
âșfluid accumulation in multiple areas as observed by CT,
Japanese Guideline 2015
134. When there is persistent or recurrent IAPâ§12mmHg,
âșgastrointestinal decompression,
âșintra-abdominal decompression,
âșimprovement of abdominal wall compliance,
âșappropriate fluid infusion and circulation management
Surgical decompression should be considered only when
internal treatment is not effective for patients with
IAP>20mmHg and where the additional complication of
organ failure is of concern
Routine use of FNA is not required for diagnosis, and
clinical signs and CT should be used for a
comprehensive determination.
Japanese Guideline 2015
135. If possible, therapeutic intervention for infected
pancreatic necrosis should be performed after 4 weeks of
onset, when the necrosis has been sufficiently walled off,
or in other words, during WON period
for infected pancreatic necrosis, percutaneous
(retroperitoneal) drainage or endoscopic transluminal
drainage should be first given, and if no improvement is
achieved, necrosectomy should then be performed
Japanese Guideline 2015
145. Probiotics in acute pancreatitis
Four RCTs (n=428) were included in the review. Sample
size ranged from 25 to 296 participants.
The present study showed that enteral feeding with
probiotics could not reduce rates of infected necrosis
and mortality. Future studies were required
Langenbeck's Archives of Surgery 2009; 394(1): 171-177