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

Acute Pancreatitis

S K Sinha

ProfessorDepartment of Gastroenterology

PGIMER, Chandigarh

Index Case

24May 201640 yrs old male, alcohol abuser presented with►Pain abdomen for 3 hours

Upper abd, non-colicky, severe, radiating to back

Associated vomiting, multiple time biliousAssociated abd distension +

►Past, Family History : Not significant

►Personal History: 80-100 gms of alcohol/day for 15-16 yrs

GPE – Pulse 122 , BP 140/82 mmHg, RR 24/minAbdomen►Liver 3 cm, soft to firm►Spleen not palpable►Diffuse tenderness & guarding in whole abdomen►Bowel sound sluggish

Chest: reduced breath sound at basesCVS, CNS – NS

Possibilities:

Index Case

Index case: Investigations

Hb -15.5 TLC – 14000 DLC – N 76 L 22 Platelets – 355

Urea : 55 Creatininine : 1.2Bil – 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 pneumoperitoneumUSG 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 ►Abdominal pain consistent with the disease►Serum amylase and / or lipase greater than three

times the upper limit of normal►Characteristic findings from abdominal imaging

CECT and / or MRI should be reserved for ►Patients in whom the diagnosis is unclear ►Who fail to improve clinically within the first 48 –

72 h after hospital admission ►To 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?►Relative accuracy►False negative and false positive

Pattern of rise ►Rises within a few hours, may return to normal within 5

days►Sensitivity in AP – approx 80%

Acute pancreatitis with no rise in amylase►Hypertriglyceridemia►Alcohol related AP►Acute on chronic pancreatitis

High amylase but no pancreatitis►Macroamylasemia►Renal failure►diseases of the salivary glands►Extrapancreatic abdominal conditions with inflammation►Gynaecological 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 testingDual testing is not superior to Lipase testing aloneNeither have prognostic valuePancreatic 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►IV fluid►Analgesia

Issue 3

Fluid for initial resuscitation/therapy of acute pancreatitis?►Does initial aggressive fluid resuscitation matter?►Which the preferred or currently recommended

crystalloid fluid in initial management of acute of pancreatitis?

►How to monitor fluid resuscitation?Non-invasively – clinical/lab parameterInvasivelyHow 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


IV line secured, started on RLNPOInjectable PPI – Pantoprazole 80 mg followed by 40 mg BDInj Metoclopramide 10 mg IV statAnalgesic: 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


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 pressureTramadol and Buprenorphine increase SO pressure minimallyTramadol has the same analgesic effect as morphine. But it has little effect on the respiratory system and circulation system


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 CBowel not movedTachypnea – RR 24-30, O2 – 0.30

Repeat Labs on day 4►S/Electrolytes, RFT – N►LFT – Bil – N, Mild rise of transaminases►Hb 12.9 gms TLC -13500 DLC – N 70 L 26

Index case: Course

Issue 5

How do we define severity of acute pancreatitis?►Mild/moderate/severe

Revised Atlanta Definitions 2012

Interstitial oedematous pancreatitis►Acute inflammation of the pancreatic parenchyma

and peripancreatic tissues, but without recognisable tissue necrosis

►CECT criteriaPancreatic parenchyma enhancement by

intravenous contrast agentNo findings of peripancreatic necrosis

Necrotizing pancreatitis► Inflammation associated with pancreatic

parenchymal necrosis and/or peripancreatic necrosis►CECT criteria

Lack of pancreatic parenchymal enhancement by intravenous contrast agent and/or

Presence of findings of peripancreatic necrosis

Mild acute pancreatitis►No organ failure►No local or systemic complications

Moderately severe acute pancreatitis►Organ failure that resolves within 48 h►Transient organ failure and/or ►Local or systemic complications without

persistent organ failure

Severe acute pancreatitis►Persistent organ failure (>48 h)

Single organ failureMultiple organ failure

Severity of acute pancreatitis

ParametersScore

0 1 2 3 4PaO2/ 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 ►(systolic blood pressure < 90 mm Hg),

Pulmonary insufficiency► (PaO 2 < 60 mm Hg),

Renal failure ►creatinine > 2 mg / dl after rehydration

Gastro intestinal bleeding ► > 500 ml of blood loss/ 24 h

Bradley EL et al. Arch Surg 1993 ; 128 : 586 – 90

Local complications of AP

APFC (acute peripancreatic fluid collection)

Pancreatic pseudocyst

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►BE level < -3 mEq/L or shock►PaO2 < 60 mm Hg (room air) or respiratory failure►Blood urea nitrogen level > 40 mg/dL or creatinine

level > 2 mg/dL►Lactate dehydrogenase level > 2 folds of upper

normal limit►Platelet count < 105/mm3►Calcium level < 7.5 mg/dL►C-reactive protein level > 15 mg/dL►Systemic inflammatory response syndrome score >

3►Age > 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: ►Temperature of <36℃ or >38℃ ►Respiratory rate >20 breaths/min or PaCO2<32

mmHg ►Pulse>90 beats/min ►WBC<4×109 or >12×109/L or >10% immature

bandsAge>60 yrPleural effusion detected on imaging

Clinical findings predicting a severe course

Patient characteristics► Age > 55 years, Obesity (BMI > 30 kg / m2 )► Altered mental status

Comorbid diseaseThe systemic infl ammatory response syndrome (SIRS)►Presence 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► BUN > 20 mg/dl, Rising BUN, HCT > 44 %, Rising HCT, Elevated

creatinine Radiology findings► 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►What are the findings which should especially be

taken into consideration?►What is accuracy of CT scan?►Should all patients be subjected to CT scan

examination?►When should CT scan be done?►What is the ideal timing?►Does accuracy depend on timing and technique?►What are the risks involved with CT scan

examination?►What 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 unwarrantedIf 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►MRCP can detect CBD stones upto 3 mm

Timing of CT scan►For assessment of severity and local complications:

after 3-5 days►When diagnosis in doubt: any time

ACG Guideline. Am J Gastroenterol 2013; 108:1400–1415

CT severity index of acute pancreatitis

Balthazar CT Score►A -Normal► B -Focal or diffuse enlargement of the pancreas, including

irregularities of contour and inhomogeneous attenuation► C - Pancreatic gland abnormalities in grade B plus per

pancreatic inflammation► D - Grade C plus a single fluid collection► E - Grade C plus 2 or more fluid collections and/or the

presence of gas in or adjacent to the pancreasNecrosis►None – score 0►Less than 30% - score 2►30-50% - score 4►> 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

►Should prophylactic antibiotics be given to all patients with acute pancreatitis?

►Should prophylactic antibiotics be given to all patients with severe acute pancreatitis?

►What are the commonly acceptable indications of emperical use of antibiotics?

►What the antibiotics preferred for prophylactic or emperical use?

►When 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►Multiple trials► Included mainly severe pancreatitis►Many randomized trials, only one double blind

randomized trial►Variable results►Antibiotics : Imipenem, Cephalosporins, Ciprofloxacin/Metronidazole

Prophylactic antibiotics in SAP

Gastroenterology 2004

Author Agent Duration

Panrcreatic infection

Mortality

Antibiotics

Control Antibiotics

Control

Pederzoli Imipenem 14 12.1 30.3 7.3 12.1

Sainio Cefuroxime 14 30.0 40.0 3.3 23.3

Delcenserie

Ceftazidime, Amika, Metro

10 0 25 9.1 25

Schwarz Ofloxacin, Metro

10 61.5 53.8 0 23

Nordback Imipenem/cilastatin

Not stated

8.0 42.4 8.0 15.1

Isenman Cipro, metro 14 12.0 8.9 5.1 7.1


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.► In these patients, either (i) initial CT-guided fine-needle

aspiration (FNA) for Gram stain and culture to guide use of appropriate antibiotics or

►Empiric use of antibiotics after obtaining necessary cultures for infectious agents, without CT FNA, should be given

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


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►Which is the preferred route – enteral or

parenteral?►When to start feeding”?►Mild to moderate pancreatitis►Severe acute pancreatitis►Which is preferred feeding formula –

elemental/polymeric/Immune feeding?►Which 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 ► low-fat solid diet appears as safe as a clear liquid

dietIn severe AP, enteral nutrition is recommended to prevent infectious complications.

Parenteral nutrition ►enteral 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


Petrov M et al. ISRN Inflammation 2013

Reduced risk of infective complications and possibly reduced mortality with enteral feeding in severe acute

pancreatitis



Most of the patients with SAP are able to tolerate enteral feeding and nutritional goal is achieved in most patients

Enteral feeding formula

Elemental►Comprising amino acids or oligopeptides,

maltodextrins, and medium—chain and long-chain triglycerides;

Polymeric►Comprising nonhydrolyzed proteins,

maltodextrins, and oligofructosaccharides, as well as long-chain triglycerides;

Immune-enhancing►Comprising 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 –►Curtails of acute inflammation of the pancreas ►Reduces septic complications

Nasojejunal tube feeding improves outcomes in SAPSafety 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


Put on IV antibiotics – Piperacillin+ Tazobactum for 14 daysNasojejunal tube placed – feeding attempted►Distension of abdomen►SOB

Feeding had to be stopped temporarilyO2 supplementationCXR was unremarkable

IAP was measured

Index case: Course

Issue 10 : IAP monitoring in acute pancreatitis

Role of intra-abdominal pressure monitoring in acute pancreatitis?

►How to define abdominal compartment syndrome?

►How to monitor for abdominal compartment syndrome?

►How to treat abdominal compartment syndrome?

Abdominal compartment syndromeIAH – IAP> 12 mmHg ACS – IAP> 20 mmHgCauses► Inflammatory fluid collection, inflammatory mass►Paralytic ileus and distension of bowel►Ascites

Consequences►Reduced renal and abd perfusion► Ischemic bowel complication►Respiratory impairment

Remedial measure►Decompression of stomach & bowel►Ascitic tap/ placement of drains►Mechanical ventilation with muscle relaxants►Restrict fluid if possible

Mentula P et al. World Journal of Emergency Surgery 2014, 9:15

NJ feeding could be established after 5 daysNJ feeding was given for two weeksOral feeding in third week – gradually built up►Fullness and bloating – post meals►No vomiting

Palpable lump abdomen, No fever , No vomitingLabs: normal RFT, LFT, Mild leucocytosisDischarged in 5th week

Index case: Course

Re-evaluation during 7 – 8 th week►Mild abdominal pain/discomfort, post prandial

bloating►No fever►Tolerating oral diet, low fat►Examination: large upper abdominal lump, mild

tenderness

Index case: Course

Issue 11 : Management of Non-Infected Necrosis

Pancreatic necrosis without infection

►What are factors which determine the outcome?

►What 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 ►Associated with gastric outlet obstruction ►Bile duct obstruction

Asymptomatic pancreatic and / or extrapancreatic necrosis does not mandate intervention regardless of size, location, and extension.

10th week of illness►Gradual increase in upper abdominal pain over 3-4

days►Fever – High grade►Vomitng off and on►Shortness of breath►Examination

Palpable upper abominal lump, tenderReduced breath sound at lung bases

►LabsRFT, LFT – NHMG – Hb 10.5 gm, TLC – 24000, DLC – N88%, L 12PCT – 3.9

Index case: Course

Issues 12: Infected Pancreatic Necrosis

Pancreatic necrosis - With evidence of infection►Should all patients be referred for surgery?►What are the factors which determine the

outcome?►How to select the cases for non-surgical

management?►What is the optimum timing for surgery?

Issue

Infections in acute pancreatits►What are the common sites of infection in

patients with acute pancreatitis?►What are the risk factors for infected pancreatic

necrosis?►Timing of pancreatic infection ►Methods of diagnosis►Organisms ►What are the common organisms?►What is the source of these organisms►How common are the anaerobes?►How common is fungal infection ?

Risk of pancreatic infection

Risk depends upon►Severity of pancreatitis

Ranson’s score < 3 : 5.3%Ranson’s score > 5 : 58%

►Extent of necrosis<30% : 5-10%30 – 50% : 10-20%> 50% : 30 – 70%

►Bacterial colonization of gut

Br J Surgery 1999

Surgical necrosectomy

Medical seriesGuided 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 Frequency

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►Broad spectrum antibiotics ►Abdominal surgery ►Male sex, Age > 40 years ►Central venous access , Hypotension at admission ►High APACHE II score ►Renal failure , TPN, Respiratory failure at admission►Mechanical ventilation ►ERCP/ Pancreatic stenting ►Diabetes mellitus ►Percutaneous drainage ►Duration of hospital stay > 4 weeks

Kochhar R, JGH 2013

Fungal infection in pancreatic necrosis

Impact of pancreatic infection

Increased mortalityIncreased morbidity► Increased risk of renal failure► Increased risk of GI bleed► Increased risk of respiratory failure► Increased cardiovascular complication

Longer hospital stayIncreased probability of surgeryIncreased 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%


Impact of pancreatic infection

Infection in pancreatic necrosis

When to suspect►Timing : second or third week►Clinical feature

Recurrence of pain abdomenWorsening of organ system functionIncreasing temperatureIncreasing TLCNew onset ileus

Am Surgeon 2000

Methods of diagnosis►Plain X-Ray►Ultrasonography, CT►Blood culture►Gallium scan► In111 labelled leucocyte scan►USG/CT guided FNA►PET CT

Infection in pancreatic necrosis

Gut 2005, Gastroenterology2004

USG/CT guided FNA

Needle should not pass through a bowelEach suspected area should be sampled, multiple passes may be requiredMultiple sessions may be requiredSamples for gram’s stain, aerobic & anaerobic bacterial culture, fungal smear & cultureRapid inoculation, use of transport medium

USG/ CT guided FNA

Complications : rareResults : High PPV, high NPV►Total patients : 60►Total aspirations : 92

Grams stain + : 41Culture + : 42

►Final diagnosis Infected : 42Uninfected : 50



Antibiotics alone can lead to resolution of infection and, in select patients, avoid surgery altogether►16/28 pts improved with antibiotics

Unstable patients with infected necrosis needs consideration for urgent debridement►a course of antibiotics before intervention to

allow the inflammatory reaction to become better organized

► If pt fails to improve : NecrosectomyEndoscopic/radiologic/video-assisted

retroperitoneal/ laparoscopic approach/ combination

Cochrane review

►The 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


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►High risk of hemorrhage► Increased organ dysfunction and death.

Necrosectomy within the first two weeks - 75% mortalityNecrosectomy 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►Role of percutaneous drain – single or multiple►Minimally invasive surgery/ endoscopic procedure



Supportive care for organ failureNutritionAntibiotics : as per sensitivity and local dataDrainage and necrosectomy►Open surgical►Laparoscopic►Radiological►Endoscopic

USG guided aspiration►Pus culture – E coli sensitive to Imipenem,

Meropenem and ColistinWas started on Meropenem

PCD was places – upgraded to 16 F

Percutaneous endoscopic necrosectomy – 2 sessionsPatient became afebrile after first sessionERCP – Disrupted MPD, stented

Index case: Course

Necrosectomy for infected necrosis

Best surgical method not defined►No direct comparison available

Open surgical necrosectomy is the gold standard and standard of carePercutaneous and endoscopic necrosectomy are emerging modalitiesLocal 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►What are the indications for ERCP in acute biliary

pancreatitis?Urgent indicationsSemi-elective indications

►Does timing of ERCP matter?►What is the preferred ERCP intervention – stent or

NBD or sphincterotomy or CBD clearance?

►Patient taken up for ERCP but no stone on cholangiogram – what to do next?

Diagnosis of Biliary Pancreatitis

ERCP in acute biliary pancreatitis

Indications►Suspected 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/dlClinical deterioration (worsening pain,

increasing white-cell count, worsening vital signs)

Stone detected in the common bile duct on imaging


Contraindications►Absolute

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►Relative (may be overcome)

Anatomical condition (gastroduodenal disease or surgical alteration) that would impede endoscopic access to the major papilla;

Clinically significant or uncorrectable coagulopathy



UK guideline 2005►Early ERCP (within 72 hours after admission to the

hospital) in all patients with predicted or actual severe biliary pancreatitis

AGA 2007►Urgent ERCP (within 24 hours after admission) if

cholangitis►Early ERCP (within 72 hours after admission) if

suspicion of persistent bile-duct stonesACG 2013►Patients with AP and concurrent acute cholangitis

should undergo ERCP within 24 h of admission►ERCP is not needed early in most patients with

gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction


ERCP in acute pancreatitis

Sphincterotomy and CBD clearance►Evidence of CBD stone, biliary obstruction : at

any time during course►Suspicion or evidence of cholangitis : at any time

during course►Persistent biliary obstruction►? 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?► 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►Open packing►Planned re-laparotomies►Closed packing►Closed 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

Nieuwenhuijs 2003

38 47%

Surgical necrosectomy : Open packing



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%

Nieuwenhuijs 2003

21 33%

Surg. necrosectomy : closed continuous lavage

AP: Magnitude of problem

Incidence : 4.9 – 73.4 cases per lac populationIncidence is increasingMortality: minimal decrease over years Severity of pancreatitis►Mild : 70 -80%

No local or systemic complication Usually no necrosis

Recovery in 3 – 7 days►Severe : 20 -30 %

Local or systemic complicationsNecrosis usualInfection : 20 – 70%

Gut 2005, Am J Gastro 2013

Course of acute pancreatitis

Overall mortality: 5 – 10%Almost all mortality in severe casesTwo phases of illness►Early phase - within 7 days: largely unrelated to

infection, mostly cytokine mediatedSIRSOrgan failure

►Late phase – after 7 days, largely related to infection and consequences of organ failureLocal complications

Fluid collections, necrosis – sterile or infectedAcute pseudocystWalled 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 ►Aggressive hydration, defined as 250-500 ml per hour

of isotonic crystalloid solution preferably Ringer LactateExceptions: Cardiovascular and renal comorbidity

►Higher infusion rate in those with hypotension or tachycardia

►Assess fluid requirement every 6 hours for 48 hours – aim to decrease BUN

Risk assessment :►Stratify patients into higher- and lower-risk categories

to assist triage, such as admission to an intensive care setting

Patients with organ failure:►admitted 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►Occurs in the setting of interstitial oedematous

pancreatitis►Homogeneous collection with fluid density►Confined by normal peripancreatic fascial planes►No definable wall encapsulating the collection►Adjacent 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►Well circumscribed, usually round or oval►Homogeneous fluid density►No non-liquid component►Well defined wall; that is, completely encapsulated►Maturation 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 tissuesCECT criteria►Occurs only in the setting of acute necrotizing

pancreatitis►Heterogeneous and non-liquid density of varying

degrees in different locations (some appear homogeneous early in their course)

►No definable wall encapsulating the collection►Location—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►Heterogeneous with liquid and non-liquid density

with varying degrees of loculations (some may appear homogeneous)

►Well defined wall, that is, completely encapsulated►Location—intrapancreatic and/or extrapancreatic►Maturation usually requires 4 weeks after onset of

acute necrotising pancreatitis

Etiology work upInitial work up: ►Alcohol, Gall stones, Hypercalcemia,

hypertriglyceridemia idiopathic acute pancreatitis, ►EUS - to assess for occult microlithiasis, neoplasms

and chronic pancreatitis. ► If 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)


Abdominal compartment syndromeIAH – IAP> 12 mmHg ACS – IAP> 20 mmHgCauses► Inflammatory fluid collection, inflammatory mass►Paralytic ileus and distension of bowel►Ascites

Consequences►Reduced renal and abd perfusion► Ischemic bowel complication►Respiratory impairment

Remedial measure►Decompression of stomach & bowel►Ascitic tap/ placement of drains►Mechanical ventilation with muscle relaxants►Restrict 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 alternativeEUS seems superior to MRCP (51% vs 20%) in the evaluation of APCholelithiasis 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

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


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 the incidence of complications

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 pancreatitisThe sequential measurement of IAP is recommended for cases with ►excessive fluid infusion, high severity, ►renal and respiratory complications,►fluid accumulation in multiple areas as observed by

CT,


When there is persistent or recurrent IAP≧12mmHg, ►gastrointestinal decompression,► intra-abdominal decompression,► improvement of abdominal wall compliance, ►appropriate fluid infusion and circulation

managementSurgical 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 concernRoutine use of FNA is not required for diagnosis, and clinical signs and CT should be used for a comprehensive determination.


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 periodfor 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




Mortality

Re-laparotomy

Planned re-laparotomiesSarr 1991 23 75% 17% 2-5/pt

Tsiotos 1998

72 79% 25% 1-7/pt

Closed packingFernandez 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(%)

Mortality

Successful

Sepsis

Complication

Percutaneous

Geeinwieser 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%

Endoscopic

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

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

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