i have tried to answer most of the burning questions with regards to the controversies of Pancreatitis managemnt

1. ICU MANAGEMENT
OF
ACUTE PANCREATITIS
DR.GOWTHAM KRISHNA J.
GEM HOSPITALS

2. INTRODUCTION
• Acute pancreatitis (AP) is one of the most common diseases of the gastrointestinal tract,
leading to tremendous emotional, physical, and financial human burden .
• Recent studies show the incidence of AP varies between 4.9 and 73.4 cases per 100,000
worldwide.1
1-American college of gastroenterology guidelines-2013
Andersson, Bodil; et al.(2013).
Acute pancreatitis – costs for healthcare and loss of production.
Scandinavian Journal of Gastroenterology, 48(12), 1459–1465.
doi:10.3109/00365521.2013.843201

3. 95%
Death - 4(6%)
AMA – 1(1.5%)
5%
The Pancreatic burden (Apr 2019- Present day)
Total ICU census
Pancreatitis

4. Why worry……
: van Dijk SM, Hallensleben NDL, van Santvoort HC, et al. Gut 2017;66:2024–2032.

5. Diagnosis
Clinical upper abdominal pain
laboratory serum amylase or lipase >3x upper limit of normal
imaging CECT or MRI only
• if the diagnosis is unclear or
• if pt fail to improve clinically within the first 48 –
72 h of hospital admission or
• to evaluate complications
Atlanta/ASG/IAP/UK

6. Revised Atlanta clasification

7. In the ER
• UK guidelines 2003
(CRP/IL-6)

8. Into the ICU…….

9. Admission
• Every patient considered at high risk of rapid clinical deterioration, such as those with
• persistent SIRS,
• elderly,
• obese,
• patients requiring ongoing volume resuscitation,
• moderately severe acute pancreatitis as defined by the revised Atlanta classification
• The routine use of single markers, such as CRP, hematocrit, BUN or procalcitonin alone
to triage patients to an intensive care setting is not recommended.

10. Finding the cause
• USG abdomen if not done already
• If no gallstones or alcohol use then serum TGL should be done and considered the etiology if >
1,000 mg / dl.
• In a patient > 40 yrs, a pancreatic tumor should be considered as a possible cause of acute
pancreatitis.
• Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks
and benefits of investigation in these patients are unclear.-
• Genetic testing may be considered in young patients ( < 30 years old) if no cause is evident and a
family history of pancreatic disease is present.
• ASG-2013

11. Grading….(WSES)
Local complications are
• peripancreatic fluid collections,
• pancreatic and peripancreatic necrosis
(sterile or infected),
• pseudocyst and walled-off necrosis (sterile or
infected).

13. Risk stratification and prognostication –
Markers, scores and more markers

14. • Cytokines peak before acute phase proteins
• IL-6 – peaks after 72hrs of onset of clinical
disease
• CRP – cost effective(>150 cutoff)-peaks at 72hrs
of the onset of “symptoms”.
• Conclude that- IL-6 – day 1 f/b CRP on day
2(peak) to asses and stratify

15. • Hematocrit>44- independent indicator for necrosis
• Urea>20 – independent indicator for mortality
• Both amylase and lipase rise in AP. Lipase(preferred) remains raised for longer period of time(8-14
days)-can also be raised in other conditions.
• Newer marker –Resistin-more useful than CRP or WBC.1
• WSES-2019
• 1-Kibar YI, Albayrak F, Arabul M, Dursun H, Albayrak Y, Ozturk Y. Resistin: new serum
marker for predicting severity of acute pancreatitis. J Int Med Res. 2016;44:328–37.
https://doi.org/10.1177/0300060515605428

16. Management

17. Fluid Therapy
• Early fluid resuscitation associated with less SIRS and OF
• Preferred IVF- Inj.RL(if Ca inc.- pl A)
• Preferred infusion rate – goal directed with 5-10ml/kg/h
• Measuring response to fluid therapy
non-invasive clinical
targets
invasive clinical targets biochemical targets
• heart rate <120/min,
• mean arterial
pressure between 65
and 85 mmHg
• urinary output >0.5-1
ml/kg/h,
stroke volume variation,
and intrathoracic blood
volume determination
hematocrit 35-44%.

18. Pain Control
• No evidence or recommendation about any restriction in pain medication is available.
• Nonsteroidal anti-inflammatory drugs (NSAID) should be avoided in acute kidney injury (AKI).
• Epidural analgesia should be an alternative or an agonist with intravenous analgesia, in a
multimodal approach.
• Patient-controlled analgesia (PCA) should be integrated with every described strategy.
• Dilaudid(hydromorphone) is preferred over morphine(sphinter of oddi spasm) or fentanyl in the
nonintubated patient.
• WSES

19. Nutrition
• Acute pancreatitis is a hypercatabolic state resulting in rapid loss of body weight, fat and protein.
• Bowel rest is associated with intestinal mucosal atrophy and increased infectious complications
because of bacterial translocation from the gut.
• So the question now is
WHEN – WHAT - HOW

20. • Oral feed is preferred in mild AP
• Low fat, low residue soft diet preferred(traditional clear liquid start to upgradation not followed)-
Mild AP
• Enteral tube feeding should be the primary therapy in patients with predicted severe acute
pancreatitis who require nutritional support.(better to start<48 hrs)
• Nasojejunal vs Nasogastric?????

21. Subjective……..
• Clinical observation of gastric ileus – many prefer NJ over NG
• Also tolerance to a NG tube is less
• In addition, the use of NJ tube feeds is intuitively more consistent
with the concept of pancreatic rest (area of ongoing investigation.)
• However, hard data showing the advantage of NJ over NG routes has
not yet been established
• Mykoniatis, A. (2016). Nutritional Support in Acute Necrotizing Pancreatitis. Difficult Decisions in
Hepatobiliary and Pancreatic Surgery, 411–420. doi:10.1007/978-3-319-27365-5_37

22. Types of TF
• Elemental or semi elemental(expensive)-
• simple amino acids, carbohydrates chains, and free fatty acids
• (pancreatic enzymes not required for digestion)
• Polymeric(cheaper)-
• complex lipids, carbohydrates, and proteins
• Immunonutrition-
• specific amino acid complexes though to be beneficial for inflammatory conditions
• No clear advantage

23. Parentral nutrition- role or no role….
• Parenteral nutrition should only be started if the nutritional goals cannot be reached with oral
orenteral feeding.
• A delay up to 5 days in initiation of parenteral nutrition may be appropriate to allow for restarting of
oral or enteral feeding

24. Kanthasamy, K. A., Akshintala, V. S., & Singh, V. K. (2020).
Nutritional Management of Acute Pancreatitis. Gastroenterology
Clinics of North America. doi:10.1016/j.gtc.2020.10.014

25. Identifying the enemy/Diagnosing the sepsis…
Battling an illusion or are we???

26. The happening of an infection
Hematogenous Pathway
Biliary system/From
duodenum through MPD
Transmural
translocation
of colonic
bacteria

27. When should we turn suspicious……
SW Schmidt et all , 1999
Infected necrosis –
• a late complication of acute pancreatitis;
>2 weeks after the onset of disease
• But have also been documented earlier.

28. Sr.PCT raise
D.R.J. Wolbrink et al. / Clinical Microbiology and
Infection 2019

30. Antibiotics- Damned if you do –damned if you
don’t……

31. The Septic diversity of pancreatic infections…

32. SW Schmidt et all , 1999

33. D.R.J. Wolbrink et al. / Clinical Microbiology and
Infection 2019

34. Our antibiotic protocol
• It involves a carbapenem in case of suspicion of sepsis(Preferred-Merpenam)
• Antifungal – If duration of disease is more/multiple hospital admissions/previous antibiotic
administartions- (Preferred Azole antifungal-Flucanozole(candida)
Occhionorelli S, Morganti L, Cultrera R, Andreotti D, Maccatrozzo S, Cappellari L, Stano R, Vasquez G. Acute necrotizing pancreatitis: can
tigecycline be included in a therapeutic strategy?. Il Giornale di chirurgia. 2015 Jan;36(1):15.
Occhionorelli et
al.2015(Italy)

35. Summary
1. Routine use of prophylactic antibiotics in patients with severe AP or sterile necrosis is not
recommended.
2. However antibiotics should be given for any extrapancreatic infection, such as cholangitis,
catheter-acquired infections, bacteremia, urinary tract infections, pneumonia
3. Infected necrosis should be considered in patients with pancreatic/extrapancreatic necrosis
who deteriorate or fail to improve after 7 – 10 days of hospitalization.

36. • In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, can
delay or avoid intervention, thus decreasing morbidity and mortality
• Routine administration of antifungal agents along with prophylactic or therapeutic
antibiotics is not recommended.
• Probiotics and selective digestive decontamination are not recommended.(PROPATRIA
trial.)

37. Steroids and Pancreatitis
• Corticosteroids are potent non-specific anti-inflammatory drugs
utilized in a variety of inflammatory diseases.
• Several case reports have suspected steroids of being the etiology to
iatrogenic AP but a definitive relationship has not been established

38. The hypothesis of a steroid benefit
• Yang et al (1999) found in SAP rats a positive correlation between the TNF-α concentrations in pancreatic tissue and
plasma and the level of pancreatic injury and inflammation.
• PLA2 plays an important role in SAP onset,-Benefits of PLA2 antagonists demonstrated in animal models(Caronna R et all
2003,2005)
• Bhatia M et al(2002) - Contibution of Il-6 in pancreatitis
Zhang XP, Chen L, Hu QF, Tian H, Xu RJ, Wang ZW, Wang KY, Cheng QH, Yan W, Li Y, Li QY, He
Q, Wang F. Effects of large dose of dexamethasone on inflammatory mediators and
pancreatic cell apoptosis of rats with severe acute pancreatitis. World J Gastroenterol 2007;
13(41): 5506-5511

39. Dong LH, Liu ZM, Wang SJ, Zhao SJ, Zhang D, Chen Y, Wang YS. Corticosteroid therapy for severe acute pancreatitis: a meta-
analysis of randomized, controlled trials. International journal of clinical and experimental pathology. 2015;8(7):7654.
• Cortisone and its analogs have been shown to be life-saving in the "malignant" type. Its usefulness in the severe forms of
the benign disease remains to be evaluated. (Kaplan et al.1957)
• Dexamethasone may reduce the serum concentration of 6-keto-PGI1alpha, TXB2, and IL-6, and the severity of acute
pancreatitis while increasing the survival rate of rats with acute pancreatitis.(Wang et al. 2003)

40. Steroids –to do or not to do
• Unresolved - Not enough evidence to use it routinely

41. Thank you all…..