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Acute Pancreatitis
S K Sinha
Professor
Department of Gastroenterology
PGIMER, Chandigarh
Index Case
24May 2016
40 yrs old male, alcohol abuser presented with
â–șPain abdomen for 3 hours
Upper abd, non-colicky, severe, radiating to back
Associated vomiting, multiple time bilious
Associated abd distension +
â–șPast, Family History : Not significant
â–șPersonal History: 80-100 gms of alcohol/day for 15-16
yrs
GPE – Pulse 122 , BP 140/82 mmHg, RR 24/min
Abdomen
â–șLiver 3 cm, soft to firm
â–șSpleen not palpable
â–șDiffuse tenderness & guarding in whole abdomen
â–șBowel sound sluggish
Chest: reduced breath sound at bases
CVS, CNS – NS
Possibilities:
Index Case
Index case: Investigations
Hb -15.5 TLC – 14000 DLC – N 76 L 22 Platelets –
355
Urea : 55 Creatininine : 1.2
Bil – 1.5 SGOT – 55 SGPT – 62 ALP 130 (ULN – 128)
TP – 7.6 Albumin – 4.9
Amylase – 155 (40-140)
Lipase – 96 (0-50)
Abd X-ray: No evidence of pneumoperitoneum
USG abdomen – Bulky pancreas, GB sludge
Issue 1
What is the practically acceptable criteria
for diagnosis of acute pancreatitis?
Acute pancreatitis: Diagnosis
At least two of the following
â–șAbdominal pain consistent with the disease
â–șSerum amylase and / or lipase greater than three
times the upper limit of normal
â–șCharacteristic findings from abdominal imaging
CECT and / or MRI should be reserved for
â–șPatients in whom the diagnosis is unclear
â–șWho fail to improve clinically within the first 48 – 72 h
after hospital admission
â–șTo evaluate complications
ACG Guideline. Am J Gastroenterol 2013; 108:1400–1415
Issue 2
Which enzyme assay is preferable : amylase or
lipase or combination of two?
â–șRelative accuracy
â–șFalse negative and false positive
Pattern of rise
â–șRises within a few hours, may return to normal within 5
days
â–șSensitivity in AP – approx 80%
Acute pancreatitis with no rise in amylase
â–șHypertriglyceridemia
â–șAlcohol related AP
â–șAcute on chronic pancreatitis
High amylase but no pancreatitis
â–șMacroamylasemia
â–șRenal failure
â–șdiseases of the salivary glands
â–șExtrapancreatic abdominal conditions with inflammation
â–șGynaecological diseases
Serum amylase estimation: Pitfalls
Amylase vs Lipase
Barbieri JS. Journal of Hospital Medicine 2016;11 :366-68
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
Index case
Repeat Lipase at 24 hours : 480 IU
Diagnosis of Acute pancreatitis was made
Treatment
â–șIV fluid
â–șAnalgesia
Issue 3
Fluid for initial resuscitation/therapy of acute
pancreatitis?
â–șDoes initial aggressive fluid resuscitation matter?
â–șWhich the preferred or currently recommended
crystalloid fluid in initial management of acute of
pancreatitis?
â–șHow to monitor fluid resuscitation?
Non-invasively – clinical/lab parameter
Invasively
How frequently the fluid therapy should be
monitored?
Fluid therapy in acute pancreatitis
Aggressive hydration, defined as 250 – 500 ml per hour
of isotonic crystalloid solution unless contraindicated
Early aggressive intravenous hydration is most beneficial
during the first 12 – 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
Lactated Ringer ’ 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 – 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
IV line secured, started on RL
NPO
Injectable PPI – Pantoprazole 80 mg followed
by 40 mg BD
Inj Metoclopramide 10 mg IV stat
Analgesic: Buscopan + Diclofenac injection –
pain reduced in intensity but did not subside
Index case: Investigations
Issue 4
Which narcotic analgesic should be used
in acute pancreatitis?
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
Effect of narcotics on Sphincter of Oddi
pressure
Staritz M et al. Gut, 1986, 27, 567-569
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
Pain persisted in lower intensity – was put on Inj Tramadol
sos, Buprenorphine patch was given
Started having fever from Day 3 – Temp upto 38.5 degrees C
Bowel not moved
Tachypnea – RR 24-30, O2 – 0.30
Repeat Labs on day 4
â–șS/Electrolytes, RFT – N
â–șLFT – Bil – N, Mild rise of transaminases
â–șHb 12.9 gms TLC -13500 DLC – N 70 L 26
Index case: Course
Issue 5
How do we define severity of acute
pancreatitis?
â–șMild/moderate/severe
Revised Atlanta Definitions 2012
Interstitial oedematous pancreatitis
â–șAcute inflammation of the pancreatic parenchyma and
peripancreatic tissues, but without recognisable tissue
necrosis
â–șCECT criteria
Pancreatic parenchyma enhancement by intravenous
contrast agent
No findings of peripancreatic necrosis
Necrotizing pancreatitis
â–șInflammation associated with pancreatic parenchymal
necrosis and/or peripancreatic necrosis
â–șCECT criteria
Lack of pancreatic parenchymal enhancement by
intravenous contrast agent and/or
Presence of findings of peripancreatic necrosis
Mild acute pancreatitis
â–șNo organ failure
â–șNo local or systemic complications
Moderately severe acute pancreatitis
â–șOrgan failure that resolves within 48 h
â–șTransient organ failure and/or
â–șLocal or systemic complications without
persistent organ failure
Severe acute pancreatitis
â–șPersistent organ failure (>48 h)
Single organ failure
Multiple organ failure
Severity of acute pancreatitis
Parameters
Score
0 1 2 3 4
PaO2/ FiO2 ratio >400 301–400 201–300 101–
200
≀101
Serum creatinine,
mg/dl)
<1.4 1.4–1.8 1.9–3.6 3.6–4.9 >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.
Organ failure in acute pancreatitis
Shock
â–ș(systolic blood pressure < 90 mm Hg),
Pulmonary insufficiency
â–ș (PaO 2 < 60 mm Hg),
Renal failure
â–șcreatinine > 2 mg / dl after rehydration
Gastro intestinal bleeding
â–ș > 500 ml of blood loss/ 24 h
Bradley EL et al. Arch Surg 1993 ; 128 : 586 –
Local complications of AP
APFC (acute peripancreatic fluid
collection)
Pancreatic pseudocyst
Acute necrotic collection
Acute necrotic collection
Infected pancreatic necrosis
WON (walled-off necrosis)
Issue 6
Is this patient having severe acute pancreatitis
or likely to have severe acute pancreatitis?
How to identify patients with severe acute
pancreatitis?
Ranson’s Criteria for acute pancreatitis
Glasgow criteria for acute pancreatitis
APACHE II scoring system for acute
pancreatitis
Japanese society severity score
Variables
â–șBE level < -3 mEq/L or shock
â–șPaO2 < 60 mm Hg (room air) or respiratory failure
â–șBlood urea nitrogen level > 40 mg/dL or creatinine
level > 2 mg/dL
â–șLactate dehydrogenase level > 2 folds of upper normal
limit
â–șPlatelet count < 105/mm3
â–șCalcium level < 7.5 mg/dL
â–șC-reactive protein level > 15 mg/dL
â–șSystemic inflammatory response syndrome score > 3
â–șAge > 70 years old
Pancreas 2014, 43:487-89
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:
â–șTemperature of <36℃ or >38℃
â–șRespiratory rate >20 breaths/min or PaCO2<32 mmHg
â–șPulse>90 beats/min
â–șWBC<4×109 or >12×109/L or >10% immature bands
Age>60 yr
Pleural effusion detected on imaging
Clinical findings predicting a severe course
Patient characteristics
â–ș Age > 55 years, Obesity (BMI > 30 kg / m2
)
â–ș Altered mental status
Comorbid disease
The systemic infl ammatory response syndrome (SIRS)
â–șPresence of > 2 of the following criteria:
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
â–ș BUN > 20 mg/dl, Rising BUN, HCT > 44 %, Rising HCT, Elevated
creatinine
Radiology findings
â–ș Pleural effusions, Pulmonary infiltrates, Multiple or extensive
extrapancreatic collections
ACG Guideline 2013. Am J Gastroenterol 2013
Comparison of different scores
Park JY. Hepatobiliary Pancreat Dis Int 2013
Issue 7 – Imaging in AP
CECT of abdomen in acute pancreatitis
â–șWhat are the findings which should especially be
taken into consideration?
â–șWhat is accuracy of CT scan?
â–șShould all patients be subjected to CT scan
examination?
â–șWhen should CT scan be done?
â–șWhat is the ideal timing?
â–șDoes accuracy depend on timing and technique?
â–șWhat are the risks involved with CT scan
examination?
â–șWhat are the modalities to reduce the risk?
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 – 72 CECT or MRI
imaging is recommended to assess local complications
CT and MRI are comparable in the early assessment of
AP
â–șMRCP can detect CBD stones upto 3 mm
Timing of CT scan
â–șFor assessment of severity and local complications:
after 3-5 days
â–șWhen diagnosis in doubt: any time
ACG Guideline. Am J Gastroenterol 2013; 108:1400–1415
CT severity index of acute pancreatitis
Balthazar CT Score
â–șA -Normal
â–ș B -Focal or diffuse enlargement of the pancreas, including
irregularities of contour and inhomogeneous attenuation
â–ș C - Pancreatic gland abnormalities in grade B plus per
pancreatic inflammation
â–ș D - Grade C plus a single fluid collection
â–ș E - Grade C plus 2 or more fluid collections and/or the
presence of gas in or adjacent to the pancreas
Necrosis
â–șNone – score 0
â–șLess than 30% - score 2
â–ș30-50% - score 4
â–ș> 50% - score 6
Mortele KJ et al. AJR 2004;183:1261–1265
Modified CT Severity Index
CECT abdomen: CTSI – 8/10 MCTSI – 10/10
Patient having low grade fever - ? Start antibiotics
Nutritional support????
Index case: Course
Issue 8 – Antibiotic prophylaxis in AP
Antibiotics in acute panreatitis
â–șShould prophylactic antibiotics be given to all patients
with acute pancreatitis?
â–șShould prophylactic antibiotics be given to all patients
with severe acute pancreatitis?
â–șWhat are the commonly acceptable indications of
emperical use of antibiotics?
â–șWhat the antibiotics preferred for prophylactic or
emperical use?
â–șWhen to start and when to stop?
Prophylactic antibiotics in AP
“It is very difficult to study this very very challenging
question and it is likely to remain enigma for quite some
time”
Alphonso Brown, Gastroenterology 2004
Last 15 years
â–șMultiple trials
â–șIncluded mainly severe pancreatitis
â–șMany randomized trials, only one double blind
randomized trial
â–șVariable results
â–șAntibiotics : Imipenem, Cephalosporins,
Ciprofloxacin/Metronidazole
Prophylactic antibiotics in SAP
Gastroenterology 2004
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
Prophylactic antibiotics in AP
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 – 10 days of hospitalization.
â–ș In these patients, either (i) initial CT-guided fine-needle
aspiration (FNA) for Gram stain and culture to guide use
of appropriate antibiotics or
â–șEmpiric use of antibiotics after obtaining necessary
cultures for infectious agents, without CT FNA, should be
given
ACG Guideline . Am J Gastroenterology 2013
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
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) 22:405–432
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
Issue 9 – Nutrition in acute pancreatitis
Feeding in acute pancreatitis
â–șWhich is the preferred route – enteral or parenteral?
â–șWhen to start feeding”?
â–șMild to moderate pancreatitis
â–șSevere acute pancreatitis
â–șWhich is preferred feeding formula –
elemental/polymeric/Immune feeding?
â–șWhich is the preferred enteral feeding route –
nasogastric or nasoduodenal or nasojejunal?
Nutrition in acute pancreatitis
In mild AP, oral feedings can be started once there is no
nausea and vomiting, and abdominal pain
â–șlow-fat solid diet appears as safe as a clear liquid diet
In severe AP, enteral nutrition is recommended to
prevent infectious complications.
Parenteral nutrition
â–șenteral 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
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
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
Enteral feeding formula
Elemental
â–șComprising amino acids or oligopeptides,
maltodextrins, and medium—chain and long-chain
triglycerides;
Polymeric
â–șComprising nonhydrolyzed proteins, maltodextrins,
and oligofructosaccharides, as well as long-chain
triglycerides;
Immune-enhancing
â–șComprising 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.
Nutrition in Acute pancreatitis
Enteral nutrition –
â–șCurtails of acute inflammation of the pancreas
â–șReduces 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 – more information is
required
Petrov M et al. ISRN Inflammation 2013
Put on IV antibiotics – Piperacillin+ Tazobactum for 14
days
Nasojejunal tube placed – feeding attempted
â–șDistension of abdomen
â–șSOB
Feeding had to be stopped temporarily
O2 supplementation
CXR was unremarkable
IAP was measured
Index case: Course
Issue 10 : IAP monitoring in acute
pancreatitis
Role of intra-abdominal pressure monitoring in acute
pancreatitis?
â–șHow to define abdominal compartment syndrome?
â–șHow to monitor for abdominal compartment syndrome?
â–șHow to treat abdominal compartment syndrome?
Abdominal compartment syndrome
IAH – IAP> 12 mmHg ACS – IAP> 20 mmHg
Causes
â–șInflammatory fluid collection, inflammatory mass
â–șParalytic ileus and distension of bowel
â–șAscites
Consequences
â–șReduced renal and abd perfusion
â–șIschemic bowel complication
â–șRespiratory impairment
Remedial measure
â–șDecompression of stomach & bowel
â–șAscitic tap/ placement of drains
â–șMechanical ventilation with muscle relaxants
â–șRestrict fluid if possible
Mentula P et al. World Journal of Emergency Surgery 2014, 9:15
NJ feeding could be established after 5 days
NJ feeding was given for two weeks
Oral feeding in third week – gradually built up
â–șFullness and bloating – post meals
â–șNo vomiting
Palpable lump abdomen, No fever , No vomiting
Labs: normal RFT, LFT, Mild leucocytosis
Discharged in 5th
week
Index case: Course
Re-evaluation during 7 – 8 th week
â–șMild abdominal pain/discomfort, post prandial bloating
â–șNo fever
â–șTolerating oral diet, low fat
â–șExamination: large upper abdominal lump, mild
tenderness
Index case: Course
Issue 11 : Management of Non-Infected
Necrosis
Pancreatic necrosis without infection
â–șWhat are factors which determine the
outcome?
â–șWhat should be the preferred approach in
management?
Management of local complication of AP
Japanese Guideline 2015
Sterile pancreatic necrosis
Debridement for sterile necrosis is recommended if
â–șAssociated with gastric outlet obstruction
â–șBile duct obstruction
Asymptomatic pancreatic and / or extrapancreatic
necrosis does not mandate intervention regardless of
size, location, and extension.
10th
week of illness
â–șGradual increase in upper abdominal pain over 3-4
days
â–șFever – High grade
â–șVomitng off and on
â–șShortness of breath
â–șExamination
Palpable upper abominal lump, tender
Reduced breath sound at lung bases
â–șLabs
RFT, LFT – N
HMG – Hb 10.5 gm, TLC – 24000, DLC – N88%, L
12
PCT – 3.9
Index case: Course
Issues 12: Infected Pancreatic Necrosis
Pancreatic necrosis - With evidence of infection
â–șShould all patients be referred for surgery?
â–șWhat are the factors which determine the outcome?
â–șHow to select the cases for non-surgical
management?
â–șWhat is the optimum timing for surgery?
Issue
Infections in acute pancreatits
â–șWhat are the common sites of infection in patients
with acute pancreatitis?
â–șWhat are the risk factors for infected pancreatic
necrosis?
â–șTiming of pancreatic infection
â–șMethods of diagnosis
â–șOrganisms
â–șWhat are the common organisms?
â–șWhat is the source of these organisms
â–șHow common are the anaerobes?
â–șHow common is fungal infection ?
Risk of pancreatic infection
Risk depends upon
â–șSeverity of pancreatitis
Ranson’s score < 3 : 5.3%
Ranson’s score > 5 : 58%
â–șExtent of necrosis
<30% : 5-10%
30 – 50% : 10-20%
> 50% : 30 – 70%
â–șBacterial colonization of gut
Br J Surgery 1999
Surgical
necrosectomy
Medical series
Guided FNA
First week 11.1% 22.2%
Second week 17.7% 33.3%
Third week 22.2% 22.2%
Fourth week 48% 22.2%
Timing of pancreatic infection
Gastroenterology 1986, 1987
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
Fungal infection in pancreatic
necrosis
Risk factors
â–șBroad spectrum antibiotics
â–șAbdominal surgery
â–șMale sex, Age > 40 years
â–șCentral venous access , Hypotension at admission
â–șHigh APACHE II score
â–șRenal failure , TPN, Respiratory failure at admission
â–șMechanical ventilation
â–șERCP/ Pancreatic stenting
â–șDiabetes mellitus
â–șPercutaneous drainage
â–șDuration of hospital stay > 4 weeks
Kochhar R, JGH 2013
Fungal infection in pancreatic
necrosis
Impact of pancreatic infection
Increased mortality
Increased morbidity
â–șIncreased risk of renal failure
â–șIncreased risk of GI bleed
â–șIncreased risk of respiratory failure
â–șIncreased cardiovascular complication
Longer hospital stay
Increased probability of surgery
Increased cost of therapy
Infected
necrosis
Sterile
necrosis
Cardiovascular
complication
31.0% 7.3%
Pulmonary
insufficiency
40.0% 14.3%
Renal
insufficiency
42.2% 21.7%
Sepsis/SIRS 35.6% 8.7%
G I bleeding 17.8% 5.8%
Gastroenterology 1996
Impact of pancreatic infection
Infection in pancreatic necrosis
When to suspect
â–șTiming : second or third week
â–șClinical feature
Recurrence of pain abdomen
Worsening of organ system function
Increasing temperature
Increasing TLC
New onset ileus
Am Surgeon 2000
Methods of diagnosis
â–șPlain X-Ray
â–șUltrasonography, CT
â–șBlood culture
â–șGallium scan
â–șIn111 labelled leucocyte scan
â–șUSG/CT guided FNA
â–șPET CT
Infection in pancreatic necrosis
Gut 2005, Gastroenterology2004
Methods of diagnosis
â–șPlain X-Ray
â–șUltrasonography, CT
â–șBlood culture
â–șGallium scan
â–șIn111 labelled leucocyte scan
â–șUSG/CT guided FNA
â–șPET CT
Infection in pancreatic necrosis
Gut 2005, Gastroenterology2004
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 gram’s stain, aerobic & anaerobic bacterial
culture, fungal smear & culture
Rapid inoculation, use of transport medium
USG/ CT guided FNA
Complications : rare
Results : High PPV, high NPV
â–șTotal patients : 60
â–șTotal aspirations : 92
Grams stain + : 41
Culture + : 42
â–șFinal diagnosis
Infected : 42
Uninfected : 50
Gastroenterology 1997
Infected pancreatic necrosis
Antibiotics alone can lead to resolution of infection and,
in select patients, avoid surgery altogether
â–ș16/28 pts improved with antibiotics
Unstable patients with infected necrosis needs
consideration for urgent debridement
â–șa course of antibiotics before intervention to allow the
inflammatory reaction to become better organized
â–șIf pt fails to improve : Necrosectomy
Endoscopic/radiologic/video-assisted
retroperitoneal/ laparoscopic approach/
combination
Cochrane review
â–șThe 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
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
â–șHigh risk of hemorrhage
â–șIncreased organ dysfunction and death.
Necrosectomy within the first two weeks - 75% mortality
Necrosectomy after 6-8 weeks – Mortality 5%
Multiple organ dysfunction increases mortality
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
â–șRole of percutaneous drain – single or multiple
â–șMinimally invasive surgery/ endoscopic procedure
Infected pancreatic necrosis
Infected pancreatic necrosis
Supportive care for organ failure
Nutrition
Antibiotics : as per sensitivity and local data
Drainage and necrosectomy
â–șOpen surgical
â–șLaparoscopic
â–șRadiological
â–șEndoscopic
USG guided aspiration
â–șPus culture – E coli sensitive to Imipenem,
Meropenem and Colistin
Was started on Meropenem
PCD was places – upgraded to 16 F
Percutaneous endoscopic necrosectomy – 2 sessions
Patient became afebrile after first session
ERCP – Disrupted MPD, stented
Index case: Course
Necrosectomy for infected
necrosis
Best surgical method not defined
â–șNo 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
Percutaneous drainage of
necrosis/collection
Endoscopic drainage/necrosectomy
Baron & Kozarek. Clin Gastro Hepatol 2012
Endoscopic necrosectomy
Baron & Kozarek. Clin Gastro Hepatol 2012
Issue 13
ERCP in acute biliary pancreatitis
â–șWhat are the indications for ERCP in acute biliary
pancreatitis?
Urgent indications
Semi-elective indications
â–șDoes timing of ERCP matter?
â–șWhat is the preferred ERCP intervention – stent or
NBD or sphincterotomy or CBD clearance?
â–șPatient taken up for ERCP but no stone on
cholangiogram – what to do next?
Diagnosis of Biliary Pancreatitis
ERCP in acute biliary pancreatitis
Indications
â–șSuspected bile-duct stones as the cause of
pancreatitis established clinically, and one of the
following:
Cholangitis (fever, jaundice, sepsis)
Persistent biliary obstruction (conjugated bilirubin
level >5 mg/dl
Clinical deterioration (worsening pain, increasing
white-cell count, worsening vital signs)
Stone detected in the common bile duct on imaging
ACG Guideline. Am J Gastroenterology 2013
Contraindications
â–șAbsolute
Unstable medical condition precluding safe
administration of moderate sedation or general
anesthesia
Decision by competent patient not to provide consent
for the procedure
Endoscopist with inadequate training in ERCP
â–șRelative (may be overcome)
Anatomical condition (gastroduodenal disease or
surgical alteration) that would impede endoscopic
access to the major papilla;
Clinically significant or uncorrectable coagulopathy
ERCP in acute biliary pancreatitis
ACG Guideline. Am J Gastroenterology 2013
UK guideline 2005
â–șEarly ERCP (within 72 hours after admission to the
hospital) in all patients with predicted or actual severe
biliary pancreatitis
AGA 2007
â–șUrgent ERCP (within 24 hours after admission) if
cholangitis
â–șEarly ERCP (within 72 hours after admission) if suspicion
of persistent bile-duct stones
ACG 2013
â–șPatients with AP and concurrent acute cholangitis should
undergo ERCP within 24 h of admission
â–șERCP 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
ERCP in acute pancreatitis
Sphincterotomy and CBD clearance
â–șEvidence of CBD stone, biliary obstruction : at any
time during course
â–șSuspicion or evidence of cholangitis : at any time
during course
â–șPersistent biliary obstruction
â–ș? Any case of biliary pancreatitis taken up for ERCP
ERCP in acute pancreatitis
“While 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
surgery”
Gut 2005
Issue 14
Timing of cholecystectomy after an episode of acute
biliary pancreatitis?
â–ș What is the risk of recurrence over time?
Risk of delayed cholecystectomy
Jee SL. Asian Journal of Surgery 2016
Summary
AP – 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
Open surgical necrosectomy
Various techniques
â–șOpen packing
â–șPlanned re-laparotomies
â–șClosed packing
â–șClosed continuous lavage
Author No. of
patients
Pts with
infected
necrosis
Mortality Re-
laparotomy
Bradley
1993
71 100% 15% 1-5/pt
Branum
1998
50 84% 12% 2-13/pt
Bosscha
1998
28 100% 39% 17/pt
Nieuwenh
uijs 2003
38 47%
Surgical necrosectomy : Open
packing
Author No. of
patients
Pts with
infected
necrosis
Mortality Re-
laparotomy
Beger
1988
95 39% 8% 27%
Farkas
1996
123 100% 7%
Buchler
2000
29 93% 24% 22%
Buchler
2001
42 93% 21% 17%
Nieuwenh
uijs 2003
21 33%
Surg. necrosectomy : closed continuous
lavage
AP: Magnitude of problem
Incidence : 4.9 – 73.4 cases per lac population
Incidence is increasing
Mortality: minimal decrease over years
Severity of pancreatitis
â–șMild : 70 -80%
No local or systemic complication Usually no
necrosis
Recovery in 3 – 7 days
â–șSevere : 20 -30 %
Local or systemic complications
Necrosis usual
Infection : 20 – 70%
Gut 2005, Am J Gastro 2013
Course of acute pancreatitis
Overall mortality: 5 – 10%
Almost all mortality in severe cases
Two phases of illness
â–șEarly phase - within 7 days: largely unrelated to
infection, mostly cytokine mediated
SIRS
Organ failure
â–șLate phase – after 7 days, largely related to infection
and consequences of organ failure
Local complications
Fluid collections, necrosis – sterile or infected
Acute pseudocyst
Walled off pancreatic necrosis
Organ failure - persistent
Tanner S et al. Am J Gastroenterol 2013
Cochior D et al. Chirurgia (2013) 108: 631-642
Course of acute pancreatitis
Initial assessment and risk stratification
Hemodynamic status be assessed immediately upon
presentation
â–șAggressive hydration, defined as 250-500 ml per hour of
isotonic crystalloid solution preferably Ringer Lactate
Exceptions: Cardiovascular and renal comorbidity
â–șHigher infusion rate in those with hypotension or
tachycardia
â–șAssess fluid requirement every 6 hours for 48 hours –
aim to decrease BUN
Risk assessment :
â–șStratify patients into higher- and lower-risk categories to
assist triage, such as admission to an intensive care
setting
Patients with organ failure:
â–șadmitted to an ICU or HDU
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
â–șOccurs in the setting of interstitial oedematous
pancreatitis
â–șHomogeneous collection with fluid density
â–șConfined by normal peripancreatic fascial planes
â–șNo definable wall encapsulating the collection
â–șAdjacent to pancreas (no intrapancreatic extension)
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
â–șWell circumscribed, usually round or oval
â–șHomogeneous fluid density
â–șNo non-liquid component
â–șWell defined wall; that is, completely encapsulated
â–șMaturation usually requires >4 weeks after onset of
acute pancreatitis; occurs after interstitial oedematous
pancreatitis
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
â–șOccurs only in the setting of acute necrotizing
pancreatitis
â–șHeterogeneous and non-liquid density of varying
degrees in different locations (some appear
homogeneous early in their course)
â–șNo definable wall encapsulating the collection
â–șLocation—intrapancreatic and/or extrapancreatic
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
â–șHeterogeneous with liquid and non-liquid density with
varying degrees of loculations (some may appear
homogeneous)
â–șWell defined wall, that is, completely encapsulated
â–șLocation—intrapancreatic and/or extrapancreatic
â–șMaturation usually requires 4 weeks after onset of
acute necrotising pancreatitis
Etiology work up
Initial work up:
â–șAlcohol, Gall stones, Hypercalcemia,
hypertriglyceridemia
idiopathic acute pancreatitis,
â–șEUS - to assess for occult microlithiasis, neoplasms
and chronic pancreatitis.
â–șIf 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
Abdominal compartment syndrome
IAH – IAP> 12 mmHg ACS – IAP> 20 mmHg
Causes
â–șInflammatory fluid collection, inflammatory mass
â–șParalytic ileus and distension of bowel
â–șAscites
Consequences
â–șReduced renal and abd perfusion
â–șIschemic bowel complication
â–șRespiratory impairment
Remedial measure
â–șDecompression of stomach & bowel
â–șAscitic tap/ placement of drains
â–șMechanical ventilation with muscle relaxants
â–șRestrict fluid if possible
Mentula P et al. World Journal of Emergency Surgery 2014, 9:15
Interventions in local complications
Acute pancreatitis
Antibiotics prophylaxis for
prevention of infection in
necroting pancreatitis
EUS and acute pancreatitis
Fusaroli P et al. World J Gastroenterol 2012; 18(32): 4243-4256
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 – fluid collection, FNA,
necrosectomy, pseudocyst drainage
Hypertriglyceridemia induced acute
pancreatitis
Tsuang W et al. Am J Gastroenterol 2009
Hypertriglyceridemia induced acute
pancreatitis
Tsuang W et al. Am J Gastroenterol 2009
Management of Acute Pancreatitis
Da Cost DW et al. BJS 2014;101:65-79
Da Cost DW et al. BJS 2014;101:65-79
Management of Acute Pancreatitis
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
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
â–șexcessive fluid infusion, high severity,
â–șrenal and respiratory complications,
â–șfluid accumulation in multiple areas as observed by CT,
Japanese Guideline 2015
When there is persistent or recurrent IAP≧12mmHg,
â–șgastrointestinal decompression,
â–șintra-abdominal decompression,
â–șimprovement of abdominal wall compliance,
â–șappropriate 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
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
Japanese Guideline 2015
Japanese Guideline 2015
Japanese Guideline 2015
Author No. of
patients
Pts with
infected
necrosis
Mortality Re-
laparotomy
Planned re-
laparotomies
Sarr 1991 23 75% 17% 2-5/pt
Tsiotos 1998 72 79% 25% 1-7/pt
Closed
packing
Fernandez
1998
64 56% 6% 17%
Surgical necrosectomy
Surgical method Author No. of
pts
Fistula
(pancreatic/
enteric)
Bleeding
Open packing Bradley 1993 71 46 7%
Branum 1998 50 88%
(72%/16%)
Bosscha 1998 28 25% 50%
Planned re-lap Sarr 1991 23 26%/52% 26%
Tsiotos 1998 72 19% 27% 18%
Closed packing Fernandez
1998
64 53%/16% 3%
Closed cont.
lavage
Farkas 1996 123 13%/1% 2%
Buchler 2001 42 19% 5%
Open necrosectomy : complications
Author No
.
Infected
(%)
Mort
ality
Succes
sful
Sepsis Complic
ation
Percut
aneous
Geeinwiese
r 1997
29 100 27% 69% 86% Fistula
7%
Freeny
1998
34 100 12% 47% 74% None
Echenique
1998
20 100 0% 20% Fistula
50%
Gouzi 1999 32 81 15% 65% Fistula
52%
Endos
copic
Baron 1996 11 27 0% 81% Bleeding
9%,
Fistula
36%
Percutaneous or endoscopic drainage
Author No. Infected(%) Mortality Bleeding/
Fistula
Fagniez
1989
40 97% 33% 45% /
45%
Villazan
1991
18 100% 22% 6% /32%
Van
Vyve
1993
20 20% 25%
Nakasaki
1999
8 100% 25% 13% / ?
Retroperitoneal laparotomy
Decontamination
group (n=50)
Control
group (n=55)
Mortality 22% 35%
Infected
necrosis
18% 38%
Laparotomy 32% 46%
Laparotomy/pt 0.9 3.1
Selective decontamination in SAP
Ann Surgery 1995
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

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Gastrocon 2016 - Dr S.K Sinha's observation on Acute Pancreatitis

  • 1. Acute Pancreatitis S K Sinha Professor Department of Gastroenterology PGIMER, Chandigarh
  • 2. Index Case 24May 2016 40 yrs old male, alcohol abuser presented with â–șPain abdomen for 3 hours Upper abd, non-colicky, severe, radiating to back Associated vomiting, multiple time bilious Associated abd distension + â–șPast, Family History : Not significant â–șPersonal History: 80-100 gms of alcohol/day for 15-16 yrs
  • 3. GPE – Pulse 122 , BP 140/82 mmHg, RR 24/min Abdomen â–șLiver 3 cm, soft to firm â–șSpleen not palpable â–șDiffuse tenderness & guarding in whole abdomen â–șBowel sound sluggish Chest: reduced breath sound at bases CVS, CNS – NS Possibilities: Index Case
  • 4. Index case: Investigations Hb -15.5 TLC – 14000 DLC – N 76 L 22 Platelets – 355 Urea : 55 Creatininine : 1.2 Bil – 1.5 SGOT – 55 SGPT – 62 ALP 130 (ULN – 128) TP – 7.6 Albumin – 4.9 Amylase – 155 (40-140) Lipase – 96 (0-50) Abd X-ray: No evidence of pneumoperitoneum USG abdomen – 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 â–șAbdominal pain consistent with the disease â–șSerum amylase and / or lipase greater than three times the upper limit of normal â–șCharacteristic findings from abdominal imaging CECT and / or MRI should be reserved for â–șPatients in whom the diagnosis is unclear â–șWho fail to improve clinically within the first 48 – 72 h after hospital admission â–șTo evaluate complications ACG Guideline. Am J Gastroenterol 2013; 108:1400–1415
  • 7. Issue 2 Which enzyme assay is preferable : amylase or lipase or combination of two? â–șRelative accuracy â–șFalse negative and false positive
  • 8. Pattern of rise â–șRises within a few hours, may return to normal within 5 days â–șSensitivity in AP – approx 80% Acute pancreatitis with no rise in amylase â–șHypertriglyceridemia â–șAlcohol related AP â–șAcute on chronic pancreatitis High amylase but no pancreatitis â–șMacroamylasemia â–șRenal failure â–șdiseases of the salivary glands â–șExtrapancreatic abdominal conditions with inflammation â–șGynaecological diseases Serum amylase estimation: Pitfalls
  • 9. Amylase vs Lipase Barbieri JS. Journal of Hospital Medicine 2016;11 :366-68
  • 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 â–șIV fluid â–șAnalgesia
  • 12. Issue 3 Fluid for initial resuscitation/therapy of acute pancreatitis? â–șDoes initial aggressive fluid resuscitation matter? â–șWhich the preferred or currently recommended crystalloid fluid in initial management of acute of pancreatitis? â–șHow to monitor fluid resuscitation? Non-invasively – clinical/lab parameter Invasively How frequently the fluid therapy should be monitored?
  • 13. Fluid therapy in acute pancreatitis Aggressive hydration, defined as 250 – 500 ml per hour of isotonic crystalloid solution unless contraindicated Early aggressive intravenous hydration is most beneficial during the first 12 – 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 ’ 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 – 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 – Pantoprazole 80 mg followed by 40 mg BD Inj Metoclopramide 10 mg IV stat Analgesic: Buscopan + Diclofenac injection – pain reduced in intensity but did not subside Index case: Investigations
  • 16. Issue 4 Which narcotic analgesic should be used in acute pancreatitis?
  • 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 – was put on Inj Tramadol sos, Buprenorphine patch was given Started having fever from Day 3 – Temp upto 38.5 degrees C Bowel not moved Tachypnea – RR 24-30, O2 – 0.30 Repeat Labs on day 4 â–șS/Electrolytes, RFT – N â–șLFT – Bil – N, Mild rise of transaminases â–șHb 12.9 gms TLC -13500 DLC – N 70 L 26 Index case: Course
  • 21. Issue 5 How do we define severity of acute pancreatitis? â–șMild/moderate/severe
  • 22. Revised Atlanta Definitions 2012 Interstitial oedematous pancreatitis â–șAcute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognisable tissue necrosis â–șCECT criteria Pancreatic parenchyma enhancement by intravenous contrast agent No findings of peripancreatic necrosis Necrotizing pancreatitis â–șInflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis â–șCECT criteria Lack of pancreatic parenchymal enhancement by intravenous contrast agent and/or Presence of findings of peripancreatic necrosis
  • 23. Mild acute pancreatitis â–șNo organ failure â–șNo local or systemic complications Moderately severe acute pancreatitis â–șOrgan failure that resolves within 48 h â–șTransient organ failure and/or â–șLocal or systemic complications without persistent organ failure Severe acute pancreatitis â–șPersistent organ failure (>48 h) Single organ failure Multiple organ failure Severity of acute pancreatitis
  • 24. Parameters Score 0 1 2 3 4 PaO2/ FiO2 ratio >400 301–400 201–300 101– 200 ≀101 Serum creatinine, mg/dl) <1.4 1.4–1.8 1.9–3.6 3.6–4.9 >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 â–ș(systolic blood pressure < 90 mm Hg), Pulmonary insufficiency â–ș (PaO 2 < 60 mm Hg), Renal failure â–șcreatinine > 2 mg / dl after rehydration Gastro intestinal bleeding â–ș > 500 ml of blood loss/ 24 h Bradley EL et al. Arch Surg 1993 ; 128 : 586 –
  • 27. APFC (acute peripancreatic fluid collection)
  • 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?
  • 34. Ranson’s Criteria for acute pancreatitis
  • 35. Glasgow criteria for acute pancreatitis
  • 36. APACHE II scoring system for acute pancreatitis
  • 37. Japanese society severity score Variables â–șBE level < -3 mEq/L or shock â–șPaO2 < 60 mm Hg (room air) or respiratory failure â–șBlood urea nitrogen level > 40 mg/dL or creatinine level > 2 mg/dL â–șLactate dehydrogenase level > 2 folds of upper normal limit â–șPlatelet count < 105/mm3 â–șCalcium level < 7.5 mg/dL â–șC-reactive protein level > 15 mg/dL â–șSystemic inflammatory response syndrome score > 3 â–șAge > 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: â–șTemperature of <36℃ or >38℃ â–șRespiratory rate >20 breaths/min or PaCO2<32 mmHg â–șPulse>90 beats/min â–șWBC<4×109 or >12×109/L or >10% immature bands Age>60 yr Pleural effusion detected on imaging
  • 39. Clinical findings predicting a severe course Patient characteristics â–ș Age > 55 years, Obesity (BMI > 30 kg / m2 ) â–ș Altered mental status Comorbid disease The systemic infl ammatory response syndrome (SIRS) â–șPresence of > 2 of the following criteria: 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 â–ș BUN > 20 mg/dl, Rising BUN, HCT > 44 %, Rising HCT, Elevated creatinine Radiology findings â–ș Pleural effusions, Pulmonary infiltrates, Multiple or extensive extrapancreatic collections ACG Guideline 2013. Am J Gastroenterol 2013
  • 40. Comparison of different scores Park JY. Hepatobiliary Pancreat Dis Int 2013
  • 41. Issue 7 – Imaging in AP CECT of abdomen in acute pancreatitis â–șWhat are the findings which should especially be taken into consideration? â–șWhat is accuracy of CT scan? â–șShould all patients be subjected to CT scan examination? â–șWhen should CT scan be done? â–șWhat is the ideal timing? â–șDoes accuracy depend on timing and technique? â–șWhat are the risks involved with CT scan examination? â–șWhat 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 – 72 CECT or MRI imaging is recommended to assess local complications CT and MRI are comparable in the early assessment of AP â–șMRCP can detect CBD stones upto 3 mm Timing of CT scan â–șFor assessment of severity and local complications: after 3-5 days â–șWhen diagnosis in doubt: any time ACG Guideline. Am J Gastroenterol 2013; 108:1400–1415
  • 43. CT severity index of acute pancreatitis Balthazar CT Score â–șA -Normal â–ș B -Focal or diffuse enlargement of the pancreas, including irregularities of contour and inhomogeneous attenuation â–ș C - Pancreatic gland abnormalities in grade B plus per pancreatic inflammation â–ș D - Grade C plus a single fluid collection â–ș E - Grade C plus 2 or more fluid collections and/or the presence of gas in or adjacent to the pancreas Necrosis â–șNone – score 0 â–șLess than 30% - score 2 â–ș30-50% - score 4 â–ș> 50% - score 6
  • 44. Mortele KJ et al. AJR 2004;183:1261–1265 Modified CT Severity Index
  • 45.
  • 46.
  • 47. CECT abdomen: CTSI – 8/10 MCTSI – 10/10 Patient having low grade fever - ? Start antibiotics Nutritional support???? Index case: Course
  • 48. Issue 8 – Antibiotic prophylaxis in AP Antibiotics in acute panreatitis â–șShould prophylactic antibiotics be given to all patients with acute pancreatitis? â–șShould prophylactic antibiotics be given to all patients with severe acute pancreatitis? â–șWhat are the commonly acceptable indications of emperical use of antibiotics? â–șWhat the antibiotics preferred for prophylactic or emperical use? â–șWhen to start and when to stop?
  • 49. Prophylactic antibiotics in AP “It is very difficult to study this very very challenging question and it is likely to remain enigma for quite some time” Alphonso Brown, Gastroenterology 2004
  • 50. Last 15 years â–șMultiple trials â–șIncluded mainly severe pancreatitis â–șMany randomized trials, only one double blind randomized trial â–șVariable results â–șAntibiotics : 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 – 10 days of hospitalization. â–ș In these patients, either (i) initial CT-guided fine-needle aspiration (FNA) for Gram stain and culture to guide use of appropriate antibiotics or â–șEmpiric 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) 22:405–432
  • 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 – Nutrition in acute pancreatitis Feeding in acute pancreatitis â–șWhich is the preferred route – enteral or parenteral? â–șWhen to start feeding”? â–șMild to moderate pancreatitis â–șSevere acute pancreatitis â–șWhich is preferred feeding formula – elemental/polymeric/Immune feeding? â–șWhich is the preferred enteral feeding route – 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 â–șlow-fat solid diet appears as safe as a clear liquid diet In severe AP, enteral nutrition is recommended to prevent infectious complications. Parenteral nutrition â–șenteral 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 â–șComprising amino acids or oligopeptides, maltodextrins, and medium—chain and long-chain triglycerides; Polymeric â–șComprising nonhydrolyzed proteins, maltodextrins, and oligofructosaccharides, as well as long-chain triglycerides; Immune-enhancing â–șComprising 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–șCurtails of acute inflammation of the pancreas â–șReduces 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 – more information is required Petrov M et al. ISRN Inflammation 2013
  • 63. Put on IV antibiotics – Piperacillin+ Tazobactum for 14 days Nasojejunal tube placed – feeding attempted â–șDistension of abdomen â–șSOB 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? â–șHow to define abdominal compartment syndrome? â–șHow to monitor for abdominal compartment syndrome? â–șHow to treat abdominal compartment syndrome?
  • 65. Abdominal compartment syndrome IAH – IAP> 12 mmHg ACS – IAP> 20 mmHg Causes â–șInflammatory fluid collection, inflammatory mass â–șParalytic ileus and distension of bowel â–șAscites Consequences â–șReduced renal and abd perfusion â–șIschemic bowel complication â–șRespiratory impairment Remedial measure â–șDecompression of stomach & bowel â–șAscitic tap/ placement of drains â–șMechanical ventilation with muscle relaxants â–șRestrict 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 – gradually built up â–șFullness and bloating – post meals â–șNo 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 – 8 th week â–șMild abdominal pain/discomfort, post prandial bloating â–șNo fever â–șTolerating oral diet, low fat â–șExamination: large upper abdominal lump, mild tenderness Index case: Course
  • 68.
  • 69.
  • 70. Issue 11 : Management of Non-Infected Necrosis Pancreatic necrosis without infection â–șWhat are factors which determine the outcome? â–șWhat should be the preferred approach in management?
  • 71. Management of local complication of AP Japanese Guideline 2015
  • 72. Sterile pancreatic necrosis Debridement for sterile necrosis is recommended if â–șAssociated with gastric outlet obstruction â–șBile duct obstruction Asymptomatic pancreatic and / or extrapancreatic necrosis does not mandate intervention regardless of size, location, and extension.
  • 73. 10th week of illness â–șGradual increase in upper abdominal pain over 3-4 days â–șFever – High grade â–șVomitng off and on â–șShortness of breath â–șExamination Palpable upper abominal lump, tender Reduced breath sound at lung bases â–șLabs RFT, LFT – N HMG – Hb 10.5 gm, TLC – 24000, DLC – N88%, L 12 PCT – 3.9 Index case: Course
  • 74.
  • 75.
  • 76. Issues 12: Infected Pancreatic Necrosis Pancreatic necrosis - With evidence of infection â–șShould all patients be referred for surgery? â–șWhat are the factors which determine the outcome? â–șHow to select the cases for non-surgical management? â–șWhat is the optimum timing for surgery?
  • 77. Issue Infections in acute pancreatits â–șWhat are the common sites of infection in patients with acute pancreatitis? â–șWhat are the risk factors for infected pancreatic necrosis? â–șTiming of pancreatic infection â–șMethods of diagnosis â–șOrganisms â–șWhat are the common organisms? â–șWhat is the source of these organisms â–șHow common are the anaerobes? â–șHow common is fungal infection ?
  • 78. Risk of pancreatic infection Risk depends upon â–șSeverity of pancreatitis Ranson’s score < 3 : 5.3% Ranson’s score > 5 : 58% â–șExtent of necrosis <30% : 5-10% 30 – 50% : 10-20% > 50% : 30 – 70% â–șBacterial colonization of gut Br J Surgery 1999
  • 79. Surgical necrosectomy Medical series Guided FNA First week 11.1% 22.2% Second week 17.7% 33.3% Third week 22.2% 22.2% Fourth week 48% 22.2% Timing of pancreatic infection Gastroenterology 1986, 1987
  • 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 â–șBroad spectrum antibiotics â–șAbdominal surgery â–șMale sex, Age > 40 years â–șCentral venous access , Hypotension at admission â–șHigh APACHE II score â–șRenal failure , TPN, Respiratory failure at admission â–șMechanical ventilation â–șERCP/ Pancreatic stenting â–șDiabetes mellitus â–șPercutaneous drainage â–șDuration of hospital stay > 4 weeks Kochhar R, JGH 2013
  • 82. Fungal infection in pancreatic necrosis
  • 83. Impact of pancreatic infection Increased mortality Increased morbidity â–șIncreased risk of renal failure â–șIncreased risk of GI bleed â–șIncreased risk of respiratory failure â–șIncreased cardiovascular complication Longer hospital stay Increased probability of surgery Increased cost of therapy
  • 84. Infected necrosis Sterile necrosis Cardiovascular complication 31.0% 7.3% Pulmonary insufficiency 40.0% 14.3% Renal insufficiency 42.2% 21.7% Sepsis/SIRS 35.6% 8.7% G I bleeding 17.8% 5.8% Gastroenterology 1996 Impact of pancreatic infection
  • 85. Infection in pancreatic necrosis When to suspect â–șTiming : second or third week â–șClinical feature Recurrence of pain abdomen Worsening of organ system function Increasing temperature Increasing TLC New onset ileus Am Surgeon 2000
  • 86. Methods of diagnosis â–șPlain X-Ray â–șUltrasonography, CT â–șBlood culture â–șGallium scan â–șIn111 labelled leucocyte scan â–șUSG/CT guided FNA â–șPET CT Infection in pancreatic necrosis Gut 2005, Gastroenterology2004
  • 87. Methods of diagnosis â–șPlain X-Ray â–șUltrasonography, CT â–șBlood culture â–șGallium scan â–șIn111 labelled leucocyte scan â–șUSG/CT guided FNA â–șPET 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 gram’s stain, aerobic & anaerobic bacterial culture, fungal smear & culture Rapid inoculation, use of transport medium
  • 89. USG/ CT guided FNA Complications : rare Results : High PPV, high NPV â–șTotal patients : 60 â–șTotal aspirations : 92 Grams stain + : 41 Culture + : 42 â–șFinal diagnosis Infected : 42 Uninfected : 50 Gastroenterology 1997
  • 90. Infected pancreatic necrosis Antibiotics alone can lead to resolution of infection and, in select patients, avoid surgery altogether â–ș16/28 pts improved with antibiotics Unstable patients with infected necrosis needs consideration for urgent debridement â–șa course of antibiotics before intervention to allow the inflammatory reaction to become better organized â–șIf pt fails to improve : Necrosectomy Endoscopic/radiologic/video-assisted retroperitoneal/ laparoscopic approach/ combination
  • 91. Cochrane review â–șThe 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 â–șHigh risk of hemorrhage â–șIncreased organ dysfunction and death. Necrosectomy within the first two weeks - 75% mortality Necrosectomy after 6-8 weeks – 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 â–șRole of percutaneous drain – single or multiple â–șMinimally 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 â–șOpen surgical â–șLaparoscopic â–șRadiological â–șEndoscopic
  • 95. USG guided aspiration â–șPus culture – E coli sensitive to Imipenem, Meropenem and Colistin Was started on Meropenem PCD was places – upgraded to 16 F Percutaneous endoscopic necrosectomy – 2 sessions Patient became afebrile after first session ERCP – Disrupted MPD, stented Index case: Course
  • 96. Necrosectomy for infected necrosis Best surgical method not defined â–șNo 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
  • 98. Endoscopic drainage/necrosectomy Baron & Kozarek. Clin Gastro Hepatol 2012
  • 99. Endoscopic necrosectomy Baron & Kozarek. Clin Gastro Hepatol 2012
  • 100. Issue 13 ERCP in acute biliary pancreatitis â–șWhat are the indications for ERCP in acute biliary pancreatitis? Urgent indications Semi-elective indications â–șDoes timing of ERCP matter? â–șWhat is the preferred ERCP intervention – stent or NBD or sphincterotomy or CBD clearance? â–șPatient taken up for ERCP but no stone on cholangiogram – what to do next?
  • 101. Diagnosis of Biliary Pancreatitis
  • 102. ERCP in acute biliary pancreatitis Indications â–șSuspected bile-duct stones as the cause of pancreatitis established clinically, and one of the following: Cholangitis (fever, jaundice, sepsis) Persistent biliary obstruction (conjugated bilirubin level >5 mg/dl Clinical deterioration (worsening pain, increasing white-cell count, worsening vital signs) Stone detected in the common bile duct on imaging ACG Guideline. Am J Gastroenterology 2013
  • 103. Contraindications â–șAbsolute Unstable medical condition precluding safe administration of moderate sedation or general anesthesia Decision by competent patient not to provide consent for the procedure Endoscopist with inadequate training in ERCP â–șRelative (may be overcome) Anatomical condition (gastroduodenal disease or surgical alteration) that would impede endoscopic access to the major papilla; Clinically significant or uncorrectable coagulopathy ERCP in acute biliary pancreatitis ACG Guideline. Am J Gastroenterology 2013
  • 104. UK guideline 2005 â–șEarly ERCP (within 72 hours after admission to the hospital) in all patients with predicted or actual severe biliary pancreatitis AGA 2007 â–șUrgent ERCP (within 24 hours after admission) if cholangitis â–șEarly ERCP (within 72 hours after admission) if suspicion of persistent bile-duct stones ACG 2013 â–șPatients with AP and concurrent acute cholangitis should undergo ERCP within 24 h of admission â–șERCP 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 â–șEvidence of CBD stone, biliary obstruction : at any time during course â–șSuspicion or evidence of cholangitis : at any time during course â–șPersistent biliary obstruction â–ș? Any case of biliary pancreatitis taken up for ERCP
  • 106. ERCP in acute pancreatitis “While 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 surgery” Gut 2005
  • 107. Issue 14 Timing of cholecystectomy after an episode of acute biliary pancreatitis? â–ș What is the risk of recurrence over time?
  • 108. Risk of delayed cholecystectomy Jee SL. Asian Journal of Surgery 2016
  • 109. Summary AP – 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
  • 110.
  • 111. Open surgical necrosectomy Various techniques â–șOpen packing â–șPlanned re-laparotomies â–șClosed packing â–șClosed continuous lavage
  • 112. Author No. of patients Pts with infected necrosis Mortality Re- laparotomy Bradley 1993 71 100% 15% 1-5/pt Branum 1998 50 84% 12% 2-13/pt Bosscha 1998 28 100% 39% 17/pt Nieuwenh uijs 2003 38 47% Surgical necrosectomy : Open packing
  • 113. Author No. of patients Pts with infected necrosis Mortality Re- laparotomy Beger 1988 95 39% 8% 27% Farkas 1996 123 100% 7% Buchler 2000 29 93% 24% 22% Buchler 2001 42 93% 21% 17% Nieuwenh uijs 2003 21 33% Surg. necrosectomy : closed continuous lavage
  • 114. AP: Magnitude of problem Incidence : 4.9 – 73.4 cases per lac population Incidence is increasing Mortality: minimal decrease over years Severity of pancreatitis â–șMild : 70 -80% No local or systemic complication Usually no necrosis Recovery in 3 – 7 days â–șSevere : 20 -30 % Local or systemic complications Necrosis usual Infection : 20 – 70% Gut 2005, Am J Gastro 2013
  • 115. Course of acute pancreatitis Overall mortality: 5 – 10% Almost all mortality in severe cases Two phases of illness â–șEarly phase - within 7 days: largely unrelated to infection, mostly cytokine mediated SIRS Organ failure â–șLate phase – after 7 days, largely related to infection and consequences of organ failure Local complications Fluid collections, necrosis – sterile or infected Acute pseudocyst Walled off pancreatic necrosis 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 â–șAggressive hydration, defined as 250-500 ml per hour of isotonic crystalloid solution preferably Ringer Lactate Exceptions: Cardiovascular and renal comorbidity â–șHigher infusion rate in those with hypotension or tachycardia â–șAssess fluid requirement every 6 hours for 48 hours – aim to decrease BUN Risk assessment : â–șStratify patients into higher- and lower-risk categories to assist triage, such as admission to an intensive care setting Patients with organ failure: â–șadmitted 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 â–șOccurs in the setting of interstitial oedematous pancreatitis â–șHomogeneous collection with fluid density â–șConfined by normal peripancreatic fascial planes â–șNo definable wall encapsulating the collection â–șAdjacent 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 â–șWell circumscribed, usually round or oval â–șHomogeneous fluid density â–șNo non-liquid component â–șWell defined wall; that is, completely encapsulated â–șMaturation 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 â–șOccurs only in the setting of acute necrotizing pancreatitis â–șHeterogeneous and non-liquid density of varying degrees in different locations (some appear homogeneous early in their course) â–șNo definable wall encapsulating the collection â–șLocation—intrapancreatic 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 â–șHeterogeneous with liquid and non-liquid density with varying degrees of loculations (some may appear homogeneous) â–șWell defined wall, that is, completely encapsulated â–șLocation—intrapancreatic and/or extrapancreatic â–șMaturation usually requires 4 weeks after onset of acute necrotising pancreatitis
  • 122. Etiology work up Initial work up: â–șAlcohol, Gall stones, Hypercalcemia, hypertriglyceridemia idiopathic acute pancreatitis, â–șEUS - to assess for occult microlithiasis, neoplasms and chronic pancreatitis. â–șIf 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 – IAP> 12 mmHg ACS – IAP> 20 mmHg Causes â–șInflammatory fluid collection, inflammatory mass â–șParalytic ileus and distension of bowel â–șAscites Consequences â–șReduced renal and abd perfusion â–șIschemic bowel complication â–șRespiratory impairment Remedial measure â–șDecompression of stomach & bowel â–șAscitic tap/ placement of drains â–șMechanical ventilation with muscle relaxants â–șRestrict fluid if possible Mentula P et al. World Journal of Emergency Surgery 2014, 9:15
  • 124. Interventions in local complications
  • 125. Acute pancreatitis Antibiotics prophylaxis for prevention of infection in necroting pancreatitis
  • 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 – fluid collection, FNA, necrosectomy, pseudocyst drainage
  • 128. Hypertriglyceridemia induced acute pancreatitis Tsuang W et al. Am J Gastroenterol 2009
  • 129. Hypertriglyceridemia induced acute pancreatitis Tsuang W et al. Am J Gastroenterol 2009
  • 130. Management of Acute Pancreatitis Da Cost DW et al. BJS 2014;101:65-79
  • 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 â–șexcessive fluid infusion, high severity, â–șrenal and respiratory complications, â–șfluid accumulation in multiple areas as observed by CT, Japanese Guideline 2015
  • 134. When there is persistent or recurrent IAP≧12mmHg, â–șgastrointestinal decompression, â–șintra-abdominal decompression, â–șimprovement of abdominal wall compliance, â–șappropriate 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
  • 139. Author No. of patients Pts with infected necrosis Mortality Re- laparotomy Planned re- laparotomies Sarr 1991 23 75% 17% 2-5/pt Tsiotos 1998 72 79% 25% 1-7/pt Closed packing Fernandez 1998 64 56% 6% 17% Surgical necrosectomy
  • 140. Surgical method Author No. of pts Fistula (pancreatic/ enteric) Bleeding Open packing Bradley 1993 71 46 7% Branum 1998 50 88% (72%/16%) Bosscha 1998 28 25% 50% Planned re-lap Sarr 1991 23 26%/52% 26% Tsiotos 1998 72 19% 27% 18% Closed packing Fernandez 1998 64 53%/16% 3% Closed cont. lavage Farkas 1996 123 13%/1% 2% Buchler 2001 42 19% 5% Open necrosectomy : complications
  • 141. Author No . Infected (%) Mort ality Succes sful Sepsis Complic ation Percut aneous Geeinwiese r 1997 29 100 27% 69% 86% Fistula 7% Freeny 1998 34 100 12% 47% 74% None Echenique 1998 20 100 0% 20% Fistula 50% Gouzi 1999 32 81 15% 65% Fistula 52% Endos copic Baron 1996 11 27 0% 81% Bleeding 9%, Fistula 36% Percutaneous or endoscopic drainage
  • 142. Author No. Infected(%) Mortality Bleeding/ Fistula Fagniez 1989 40 97% 33% 45% / 45% Villazan 1991 18 100% 22% 6% /32% Van Vyve 1993 20 20% 25% Nakasaki 1999 8 100% 25% 13% / ? Retroperitoneal laparotomy
  • 143.
  • 144. Decontamination group (n=50) Control group (n=55) Mortality 22% 35% Infected necrosis 18% 38% Laparotomy 32% 46% Laparotomy/pt 0.9 3.1 Selective decontamination in SAP Ann Surgery 1995
  • 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