This document provides information on acute pancreatitis including: 1. The epidemiology, causes, pathophysiology, clinical presentation, investigations, management, and complications of acute pancreatitis are summarized. Gallstones and alcohol are the most common causes. 2. Laboratory markers like lipase and amylase are used to diagnose, while CT, MRI, and ultrasound can identify complications like fluid collections and necrosis. Treatment involves fluid resuscitation, pain management, and treating any organ dysfunction. 3. Complications include pancreatic and extra-pancreatic complications like fluid collections, necrosis, infection, and vascular or bowel issues. Infected necrosis requires antibiotics while severe cases may require drainage procedures or surgery.

1. ACUTE
PANCREATITIS
D R K T D P R I YA D A R S H A N I
R E G I S T R A R - E M E R G E N C Y M E D I C I N E

2. SCOPE
• Anatomy & Physiology
• Epidemiology
• Pathophysiology
• Clinical presentation
• Investigation
• Treatment
• Complication
• Disposition

3. ANATOMY & PHYSIOLOGY

5. EPIDEMIOLOGY
• Incidence*
– Acute pancreatitis 13-45 per 100,000
• Most have only one episode
• 15-30% at least one recurrence
• 5-25% chronic pancreatitis*
– Chronic pancreatitis 5-12 per 100,000
• Gender
– Acute pancreatitis- both genders equal
– Chronic pancreatitis- More common among men than women
• Age
– Acute- increases with age
– Chronic- primarily affects middle aged patients
• Yadav D, Lowenfels AB. The epidemiology of pancreatitis & pancreatic cancer. Gastroenterology 2013
• Tintinal’s Emergency Medicine 9th edition

6. • Mortality among all admissions 1%
– 15% in pancreatic necrosis
– 30% in infected pancreatic necrosis
• Up to 15% will develop necrosis
Heckler, M., Hackert, T., Hu, K. et al. Severe acute pancreatitis: surgical indications and treatment. Langenbecks Arch Surg 406, 521–535 (2021)

7. CAUSES
1. Gall stones (40-50%)
2. Alcohol (20%)
3. Hypertriglyceridemia ( triglycerides >1000 mg/dL/ 11.30 mmol/L)
4. Medication ( over 500 drugs- but <2% cases)
5. Infection
6. Metabolic
7. Autoimmune
8. Iatrogenic (post ERCP- 5% with in 30 days)
9. Hereditary
10. Malignancy
10-25% of acute pancreatitis cases the etiology is unclear despite workup*
Idiopathic pancreatitis, >40yrs or with prolonged or recurrent disease- consider pancreatic malignancy *
*Waller A, Long B, Koyfman A, Gottlieb M. Acute pancreatitis :updates for emergency clinicians. J Emerg Med. 2018
* Tanner S, Baillie J, DeWitt J, Vege SS: American college of Gastroenterology. American college of gastroenterology guideline: Management of acute
pancreatitis- 2014

8. Medications
• Analgesics
– Acetaminophen
– Codeine (& other opiates)
• CVS drugs
– Amiodarone
– ACEI/ARB
– Diuretics
• Steroids
– Dexamethasone
• Antibiotics
– Erythoromycin
– Metronidazole
– Tetracycline
– TB antibiotics ( dapsone, isoniazid,
rifampin)
• Antiepileptic
– Carbamazepine
– Valporic acid
• Endocrine drugs
– Estrogens
– Methimazole
– Simvastatin
• Cannabis
• Antiretrovirals
– 2-3 dideoxyinosine
• Chemotherapy
• Immune suppressants

9. PATHOPHYSIOLOGY
• An inflammatory process caused by pancreatic autodigestion
– Cell damage
– Activate trypsinogen & inflammatory mediators
– Potentiate feedback loop
• Chronic pancreatitis-
– progressive inflammatory changes
– Leads to structural damage
– Impaired endocrine & exocrine function
– significant fibrosis- enzymes are not elevated

10. CLINICAL PRESENTATION
• Persistent epigastric upper abdominal pain
– Often radiates to back, chest or flanks
– Associated with nausea & vomiting (90%)
– Worsen with lying supine & improve with sitting up with the knees flexed.
• May have anorexia- pain worsen with oral
• Risk factors
– Alcohol
– Past hx of pancreatitis
– Medications
– Positive family history

11. • Abnormal vital signs
– Tachycardia
– Tachypnea
– Fever
– Hypotension
• Abdominal examination
– Guarding
– Reduced bowel sounds +/-
– Occasionally- jaundice, pale, sweaty
• Grey Turner’s sign (0.96%), Cullen’s sign(0.77%) & erythematous skin nodules from
focal subcutaneous fat necrosis and purtscher retinopathy are rare & occur very late in
the disease*
* Wallwe A, Long B, Koyfman A, Gottlieb M. Acute pancreatitis :updates for emergency clinicians. J Emerg Med. 2018

13. DIAGNOSIS
• 2/3 Atlanta criteria (1992-2012)
1. Upper abdominal pain consistent with pancreatitis
2. Serum lipase or amylase at more than 3 time ULN
3. Imaging shows pancreatic inflammation on CT with IV contrast, MRI or USS

14. Severity
• Mild acute- no local or systemic complications
• Moderate acute-
– local or systemic complications or
– transient (<48h) organ failure
• Severe acute-
– persistent organ failure (>48h),
– pancreatic necrosis,
– persistent systemic inflammatory response syndrome
• Pulse >90
• RR >20 or partial pressure of CO2 <32mmHg
• Temperature >38 or <36
• WBC >12,000 or <4000
• Chronic-
– classic pain without laboratory abnormalities,
– accompanied by fibrotic changes or calcification on imaging

15. INVESTIGATIONS
Laboratory studies
• Amylase (3* ULN) sensitivity 70%- 80% PPV (15%-
72%)
– Rise with in few hours, peak with in 48 hrs,
normalizes in 3-5 days
– 20% (alcohol & Hypertriglyceridemia related
disease)- Normal amylase
– Elevate in multiple non pancreatic related disease
(Mnemonic: AMyLASE)
• Aortic aneurysm, appendicitis
• Macroamylasemia
• LOBE tumors (Lung, Ovary, Breast, Esophagus
cancers)
• Acidosis (DKA), Acute renal failure
• Salivary gland disease
• Ectopic rupture, Esophageal perforation
Test Rise Peak
Return
to
baseline
Lipase
4-6
hours
48
8-14
days
Amylase
2-4
hours
24-48 5-7 days

16. • Lipase (3* ULN) 100% Sensitive 99% Specific
– Remains elevated for longer
– Elevated in DM, Renal disease- less associated than amylase
– Mnemonic: LIPASE
• Lipasemia (Macrolipasemia)
• Inflammatory bowel disease
• Perforated duodenum
• Acute cholecystitis
• Embolism (Fat), Extrahepatic biliary obstruction
– More sensitive in delayed presentation & pancreatitis associated with alcohol &
hypertriglyceridemia
• Limitations
– Amylase *3ULN & Lipase *2 ULN
– Any elevation above normal is consistent with diagnosis
– Cutoffs for older with co-morbidities
– Amylase or lipase- level does not correlate severity or prognosis

17. • Urine trypsinogen 2 dipstick (sensitivity 82% & specificity 94%)
– Rapid, non invasive test
– Not widely available
• Alanine aminotransferase >150 U/L within the first 48 hrs
– Predict gallstone pancreatitis (>85% PPV)
• CRP may be useful in predicting disease severity*
• Procalcitonin may be a better marker of pancreatic necrosis than CRP at 24 h
• BUN- a prognostic indicator in acute pancreatitis- initial value & change within 24 hrs
can predict mortality*
• Chemokine monocyte chemotactic protein-1 (MCP-1) polymorphism- predict severity
• Majidi S, Golembioski A, Wilson SL, Thompson EC, Acute pancreatitis; Etiology, pathology, diagnosis & treatment. South Med J 2017
• Wu BU, Hwang JQ, Gardner TH et al; Lactated ringer’s solution reduces syatemic inflammation compared with saline in patients with acute
pancreatitis, Clin Gastroenterol Hepatol 2011

18. • Assess other organ involvement
– Renal
– Liver
– Electrolytes
– Glucose
– WBC
– Hb/HCT

19. Imaging-
• TAS
– Look for gallstones
• Endoscopic USS*
– In both acute & chronic pancreatitis
– Useful information regarding
pancreatic function, micro lithiasis
& periampullary lesions
– But needs highly skilled
gastroenterologist
*Tanner S, Baillie J, DeWitt J, Vege SS: American college of Gastroenterology. American college of gastroenterology guideline: Management of acute
pancreatitis- 2014

20. Computed Tomography
• Routine CT with IV/O contrast- not recommended
– Most have uncomplicated disease
– No evidence that early CT improves clinical outcome- probably CT findings are delayed &
may underestimate disease severity
– Early detection of peripancreatic fluid collection or pancreatic necrosis with in first few days-
require no Rx
– Complete extent of local complications is usually not appreciated until at least 3 days after
onset of symptoms (false negative in too early disease)
– IV contrast- allergic reactions, nephrotoxicity & worsening of pancreatitis
• If clinical diagnosis is in doubt- consider further evaluation with IV contrast abdominal
CT
– Pancreatic parenchymal inflammation +/- peripancreatic fat inflammation
– Pancreatic parenchymal necrosis or peripancreatic necrosis
– Peripancreatic fluid collection
– Pancreatic pseudocyst

22. • Non contrast MRI (MRCP)
– Can identify complications of pancreatitis & choledocholithiasis
– Alternative for renal failure, allergic for IV contrast, pregnancy

23. SCORING!
• Scoring systems- all have high false positive rates
1. Ranson’s criteria
2. Acute physiology & chronic health examination –II (APACHE)
3. Modified Glasgow score
4. Bedside index for severity in acute pancreatitis (BISAP)
5. Balthazar CT severity index

24. RANSON’S CRITERIA
• Require both admission & 48 h data
• >2 at presentation- severe illness require
admission
• Predict severity & mortality

25. GLASGOW SCORE
• Prognostic score
• >3- severe pancreatitis likely
• Refer to HDU/ICU
• <3- severe pancreatitis
unlikely

26. BISAP
• More sensitive & specific
than Ranson’s criteria &
APACHE II
• Allows for early
identification of patients at
increased risk for in hospital
mortality

27. BALTHAZAR SCORE

28. MANAGEMENT
• Goals
1. Limit the severity of pancreatic inflammation & necrosis
2. Provide supportive treatment

29. TREATMENT
1. Aggressive crystalloid therapy ( decreases morbidity & mortality)
– Vomiting, third spacing of fluids
– Large volumes of NS- hyperchloremic metabolic acidosis- further activate trypsinogen, AKI
& immune dysfunction*
– RL- reduces SIRS but contains Ca
– 20ml/kg bolus over 30 min, then 1.5-3 ml/kg/h for 12-24 hrs
2. Monitor
– Vital signs
– Pulse oximetry
3. Pain-
– IV Opioids
– Ketorolac may induce or worsen existing pancreatitis*
*de- Madaria E, Herrera- Marante I, Gonzalez- Camacho V et al. fluid resuscitayion with lactated Ringer’s solution vs normal saline in acute pancreatitis: a
triple blind, randomized, controlled trial 2018
*Majidi S, Golembioski A, Wilson SL, Thompson EC, Acute pancreatitis; Etiology, pathology, diagnosis & treatment. South Med J 2017

30. 1. Nausea /Vomiting
– Antiemetics
– NBM
– No benefit to NG tube ( exception ileus)
– Early initiation of a low fat diet is beneficial (24-48 hr) vs TPN
2. Electrolyte imbalance –
– Low Ca, Mg,
– Hyperglycemia
3. Antibiotics
– No prophylaxis
– If known or strongly suspect an infection only
– For septic patients give antibiotics until infected pancreatic necrosis excluded*
• Imipenem/cilastatin 500mg 6h
• Naser JY, Papachiristou GI, Early fluid resuscitation I acute pancreatitis: a lot more than just fluids. Clin Gastroenterol Hepatol 2011
• Waller A, Long B, Koyfman A, Gottlieb M. Acute pancreatitis :updates for emergency clinicians. J Emerg Med. 2018

31. 1. Other organ support
– CVS
– Respi
– Renal
2. Surgical management
1. GE referral if
• Liver dysfunction
• Cholangitis
• Dilated CBD
2. Biliary obstruction/ choledocholithiasis- urgent ERCP + sphincterotomy
3. Gallstone pancreatitis- Cholecystectomy
3. Preventive measures
– Counselling & cessation of alcohol*
*Yadav D, Lowenfels AB. The epidemiology of pancreatitis & pancreatic cancer. Gastroenterology 2013

32. ERCP
• ERCP + Sphincterotomy and stone extraction
– Reduce length of hospital stay
– Reduce complication rate
– Reduce mortality
• Biliary pancreatitis + dilated obstructed CBD + Elevated plasma bilirubin level
– ERCP is warranted with in first 72 hrs

33. COMPLICATIONS
Pancreatic Peri pancreatic Extra-pancreatic
• Fluid collection
• Necrosis
• Sterile or infected
• Acute or walled
off
• Abscess
• Ascites
• Fluid collection
• Necrosis
• Intra abdominal or
retroperitoneal
hemorrhage
• Pseudoaneurysm
• Bowel inflammation,
infarction or necrosis
• Biliary obstruction
with jaundice
• Splenic or portal vein
thrombosis
• CVS
• Pulmonary
• Hematologic
• GI
• Renal
• Metabolic

34. PERI PANCREATIC FLUID
• 30-57% of patient
– Resolve
– Progress to encapsulation of fluid ( pseudocyst) 4 wks
– Necrotic tissue ( walled off necrosis)- 4-6 wks
• Sterile vs infected- clinical challenge
• Intervention
– Infected pancreatic necrosis
– 33%*
– Mortality rate 15%
* Van Dijk SM, Hallenslebn NDL, van Santvoort HC, et al. Acute pancreatitis, recent advances through randomized trials 2017

35. • Infection can be confirmed by*
– Gas within a necrotic collection on imaging
– Positive result of fine needle aspiration
– Clinical suspicion based on signs of infection or new or persistent organ failure
• Antibiotics
– E coli 26%
– Pseudomonas species 16%
– Staphylococcus species 15%
• Delay intervention until walled off necrosis occurs*
– Follows a step up approach
• Catheter drainage first, then necrosectomy only when indicated
• Minimally invasive techniques are preferred over open surgery
*Van Dijk SM, Hallenslebn NDL, van Santvoort HC, et al. Acute pancreatitis, recent advances through randomized trials 2017

36. CHRONIC PANCREATITIS
• Classic triad- pancreatic calcifications, steatorrhea, DM
• Not seen until the patient develops very advanced disease*
• Amylase & lipase are often normal
• Home pain control- amitriptyline, pregabalin & chronic opiates
• Symptoms can be controlled by
– Alcohol cessation
– Small- low fat meals
– Smoking cessation
– Enzyme supplements

37. • Pseudocysts
– (10% ) Of chronic pancreatitis
• Often asymptomatic
• Depend on size & location- pain, duodenal or biliary obstruction, fistula formation, vascular
occlusion

38. DISPOSITION & FOLLOW-UP
• Discharge- young, non biliary pancreatitis, pain controlled, tolerate oral, no evidence
of gallstones
– Refer for follow-up to prevent recurrence
• Admission
– 1st bout of acute pancreatitis, biliary pancreatitis
– Pain not controlled
– Not tolerating oral
– Persistent abnormal vital signs
– Signs of other organ insufficiency

39. • Consider ICU if
– Elevated BUN
– >2 SIRS criteria
– Sign of persistent organ insufficiency
– BISAP score >2
– Abnormal vitals

40. REFERENCES
• Tintinali’s Emergency Medicine 9th
• Yadav D, Lowenfels AB. The epidemiology of pancreatitis & pancreatic cancer. Gastroenterology 2013
• Waller A, Long B, Koyfman A, Gottlieb M. Acute pancreatitis :updates for emergency clinicians. J Emerg Med.
2018
• Tanner S, Baillie J, DeWitt J, Vege SS: American college of Gastroenterology. American college of
gastroenterology guideline: Management of acute pancreatitis- 2014
• Szucs A, Marjai T, Szentesi A et al; chronic pancreatitis: multicenter prospective data collection and analysis
by the Hungarian pancreatic study group. PLoS One 2017
• Majidi S, Golembioski A, Wilson SL, Thompson EC, Acute pancreatitis; Etiology, pathology, diagnosis &
treatment. South Med J 2017
• de- Madaria E, Herrera- Marante I, Gonzalez- Camacho V et al. fluid resuscitayion with lactated Ringer’s
solution vs normal saline in acute pancreatitis: a triple blind, randomized, controlled trial 2018
• Van Dijk SM, Hallenslebn NDL, van Santvoort HC, et al. Acute pancreatitis, recent advances through
randomized trials 2017