ACUTE PANCREATITIS

ACUTE PANCREATITIS

At a glance

Domain	Practical point
Diagnosis (Revised Atlanta Classification 2012)	2 of 3: characteristic upper abdominal pain, Sr. Amylase/lipase ≥3× ULN, or compatible imaging.
Etiology	Gallstones and alcohol account for about two-thirds of cases; actively assess biliary, alcohol, metabolic, drug, structural and uncommon causes.
Severity	Persistent organ failure >48 h is the key determinant of severe disease; SIRS helps early severity prediction.
Fluids	RL goal-directed hydration; avoid indiscriminate aggressive fluid loading. In Hypercalcemia induced pancreatitis- Normal Saline preferred over RL
Nutrition	Feed early when tolerated; use enteral tube feeding when oral intake is not tolerated.
Antibiotics	No routine prophylaxis. Treat proven infection or strong suspicion of infected necrotizing pancreatitis.
Biliary disease	Early ERCP for acute cholangitis , therapeutic ERCP for persistent CBD obstruction. Not routine uncomplicated biliary pancreatitis.

Table of Contents

1. Definition and clinical spectrum

Acute pancreatitis (AP) is an acute inflammatory process of the pancreas caused due to the premature activation of pancreatic enzymes, leading to auto-digestion and inflammation of the pancreas. Diagnosis is based on Revised Atlanta Classification (2012) discussed in section

2. Differential diagnosis

Diagnosis	Helpful clue / why it matters
Acute coronary syndrome / MI	Epigastric discomfort may be an anginal equivalent; obtain ECG and high-sensitivity troponin when clinically appropriate
Perforated peptic ulcer	Sudden severe pain with peritonism/free intraperitoneal air
Acute cholecystitis	Persistent RUQ/epigastric pain with inflammatory gallbladder findings
Biliary colic	Discrete episodic RUQ/epigastric pain, often postprandial
Intestinal obstruction	Colicky pain, vomiting, and distension
Mesenteric ischemia	Severe pain out of proportion to examination; vascular risk factors
Aortic dissection/AAA	Sudden severe pain, pulse/BP abnormalities, or vascular risk factors
Renal colic	Flank radiation and hematuria
DKA	Hyperglycemia, ketones, and metabolic acidosis
Lower-lobe pneumonia/pleurisy	Respiratory symptoms or basal chest findings

3. Etiology

Common / Important Cause	Reason / pathology / important clinical point
Gallstones / biliary disease (30%-60%)	Most common cause; transient ampullary/CBD obstruction may trigger AP.
Alcohol (15%-30%)	2^nd MC; risk increases with cumulative exposure and individual susceptibility.
Severe hypertriglyceridemia	Usually when TG is >1,000 mg/dL; toxic free-fatty-acid injury contributes.
Post-ERCP	Papillary/ductal injury or edema; risk reduced by prophylactic rectal NSAID ± pancreatic-duct stent in selected high-risk cases.
Idiopathic	After initial evaluation, repeat USG and consider EUS/MRCP for occult biliary/structural causes.
Drugs	Examples: azathioprine/6-MP, valproate, tetracyclines, sulfonamides, estrogens, 5-ASA, DPP-4 inhibitors
Hypercalcemia	Consider primary hyperparathyroidism and malignancy; intracellular calcium promotes pancreatic enzyme activation.
Malignancy	IPMN(MC), Pancreatic adenocarcinoma
Autoimmune pancreatitis	Consider with IgG4-related disease, characteristic imaging or other-organ involvement.
Trauma / postoperative	Blunt trauma and abdominal surgery can cause pancreatic duct/acinar injury.
Genetic / structural	PRSS1, CFTR, SPINK1, CTRC and ductal abnormalities in selected recurrent/young-onset disease.

Note: A normal transabdominal ultrasound does not exclude microlithiasis or small CBD stones; in unexplained AP, repeat USG and proceed to EUS/MRI-MRCP when appropriate.
EUS can identify occult biliary disease in otherwise unexplained acute pancreatitis
Risk of pancreatitis in patients with smaller gallbladder stone or GV sludge is much higher as compared to larger GB stone.

4. Clinical presentation

Feature	Typical findings
Pain	Acute, persistent, severe epigastric or upper abdomen ; often radiate to the back, chest, flank, or lower abdomen.
GI	Nausea, vomiting, abdominal distension, and ileus.
Hemodynamics	Tachycardia, hypotension, and shock in severe disease.
Abdominal examination	Tenderness; rigidity/peritonism when severe or when another abdominal emergency is present.
Respiratory	Pleural effusion, atelectasis, hypoxemia, and ARDS in severe disease.
Jaundice	Suggests CBD stone/obstruction, extrinsic compression, or another hepatobiliary process.
Cullen / Grey-Turner signs	Rare late hemorrhagic signs; absence does not exclude severe AP.

Absence of pain seen in 5% case, suggestive of bad prognosis

5. Diagnosis — Revised Atlanta Classification 2012

Criterion	Typical finding
Characteristic abdominal pain	Acute, persistent, severe epigastric pain; may radiate to the back
Enzyme elevation	Serum lipase and/or amylase ≥3 × ULN
Characteristic imaging	Characteristic pancreatic inflammation on abdominal imaging, usually ultrasound or CT, MRI appropriate ultrasound

for diagnosis, 2/3 variables should be present

6. Initial investigations

Investigation	Clinical use
Lipase	Preferred enzyme; ≥3× ULN
CBC / Hematocrit	Leukocytosis; hemoconcentration may indicate hypovolemia.
BUN / Creatinine	Assess renal perfusion and evolving organ dysfunction.
LFT + bilirubin	Identify biliary etiology and obstruction. Raised ALT/GGT – Biliary cause, SGOT- Alcohol
Triglycerides	Important etiologic test; severe hypertriglyceridemia is a major cause.
Calcium	Hypercalcemia can be an etiology; hypocalcemia may accompany severe AP.
CRP	Useful after the first 48 to 72 hours for severity assessment, trend with clinical status

7. Amylase vs lipase

Sr. Lipase is more specific as compared to Sr. Amylase
Sr. Lipase rises within 4 to 8 hours. Peaks at about 24 hours and remain elevated for 8 to 14 days.
There is no prognostic or severity assessment significance of Sr. Amylase/ Lipase. So do not use serial amylase/lipase levels to monitor recovery or determine severity.
Amylase can be falsely negative/normal i/c/o hypertriglyceridemia induced pancreatitis.

7.1 Causes of hyperamylasemia

Cause	Clinical clue
Acute pancreatitis	Compatible pain ± lipase/imaging
Salivary gland disease	Parotitis/sialadenitis
Renal dysfunction	Reduced clearance
Macroamylasemia	Persistent, isolated amylase elevation without pancreatitis
Peptic ulcer/perforation	Severe intra-abdominal disease
Bowel ischemia/obstruction	Abdominal catastrophe
Gynecologic pathology	Selected ovarian/tubal disorders
Malignancy	Some pancreatic/GI and other tumors
Drugs/systemic illness	Interpret in clinical context

8. Morphological features — Revised Atlanta Classification

8.1 Types of acute pancreatitis

Interstitial Pancreatits- 75%-80%, good prognosis
Necrotising pancreatitis- include both pancreatic and peri pancreatic necrosis

8.2 Morphological features of AP — Revised Atlanta Classification

	NO NECROSIS	NECROSIS
EARLY / <4 WEEKS	Acute peripancreatic fluid collection ( APFC) • Fluid only • No wall	Acute necrotic collection (ANC) • Fluid + necrotic material • No mature wall
LATE / >4 WEEKS	PSEUDOCYST • Fluid only • Well-defined wall	Walled-off necrosis (WON) • Fluid + necrotic material • Well-defined wall

9. Severity — Revised Atlanta Classification

Category	Definition
Mild AP	No organ failure and no local/systemic complications
Moderately severe AP	Transient organ failure <48 h and/or local/systemic complications without persistent organ failure
Severe AP	Persistent organ failure >48 h involving one or more organ systems

Note: Severity is dynamic; reassess organ function and clinical trajectory throughout the first 48 hours

10. Severity scores — Practical clinical role

System	When	What it does best	Current role
SIRS	Admission + serial	Indicates systemic inflammation; persistence predicts severe AP	HIGH / guideline-recommended
Modified Marshall	Any time organ dysfunction suspected	Defines organ failure	VERY HIGH / defines Atlanta severity
BISAP	First 24 h	Simple early risk stratification	HIGH. BISAP >/=3 suggest high risk and warrants closer monitoring
APACHE II	ICU Admission	Severity; mortality prediction	ICU-selective
Ranson	Admission + 48 h	Not routinely preferred now.	LOW routine;
Glasgow-Imrie	First 48 h	Historical ,severity prediction	LOW routine
CTSI	After appropriate CT	Morphology + necrosis	MODERATE; not early triage
mCTSI	After appropriate CT	Morphology + necrosis + extrapancreatic complications	MODERATE; adjunct

10.1 SIRS — bedside screen

Criterion	Positive if
Temperature	<36°C or >38°C
Heart rate	>90/min
Respiratory	RR >20/min OR PaCO₂ <32 mmHg
WBC	<4,000/mm³ or >12,000/mm³ or >10% immature bands

SIRS is present when ≥2 criteria are positive. Persistent SIRS at 48 h is more concerning and helps predict severe AP; SIRS alone do not define severe AP.

10.2 Organ failure — Modified Marshall Score

Organ system	0	1	2 = organ failure	3	4
Respiratory (PaO2/FiO2)	>400	301–400	201–300	101–200	≤100
Renal(Sr.Creat mg/dl)	<1.4	1.4–1.8	1.9–3.5	3.6–4.9	≥5.0
Cardiovascular(SBP mmhg)	SBP >90	SBP <90, fluid responsive	SBP <90, not fluid responsive	SBP <90 + pH <7.30	SBP <90 + pH <7.20

A Modified Marshall score ≥2 in any one organ system constitutes organ failure. Persistence beyond 48 hours defines severe AP.

10.3 BISAP

Component	1 point if
BUN	>25 mg/dL
Impaired mental status	Present
SIRS	Present
Age	>60 years
Pleural effusion	Present

0-2: lower risk, >/= 3: high risk of severe disease

BISAP is useful for early risk stratification; it does not replace repeated organ-failure assessment.

10.4 CTSI (CT Severity Index)

Balthazar Grade	CT Finding	Points
A	Normal pancreas	0
B	Focal/diffuse enlargement	1
C	Pancreatic abnormality + peripancreatic inflammation	2
D	Single peripancreatic fluid collection	3
E	≥2 collections or gas in/adjacent to pancreas	4

Necrosis	Points
None	0
<30%	2
30–50%	4
>50%	6

CTSI = Balthazar grade + necrosis score; maximum 10. Traditionally: 0–3 mild, 4–6 moderate, 7–10 severe.

Current significance: MODERATE for describing CT morphology/necrosis; NOT a primary early severity tool. The 2025 IAP guideline states CT severity scores are not superior to clinical scoring systems and recommends severity CT only after ~72–96

10.5 Modified CT Severity Index (mCTSI)

Component	Finding	Points
Pancreatic inflammation	Normal	0
	Intrinsic pancreatic abnormality ± peripancreatic inflammation	2
	Pancreatic/peripancreatic fluid collection or fat necrosis	4
Necrosis	None	0
	≤30%	2
	>30%	4
Extrapancreatic complication	Any major extrapancreatic complication	2

Maximum 10. Traditional categories: 0–2 mild, 4–6 moderate, 8–10 severe.

Note: CTSI/MCTSI describe radiologic severity; clinical organ failure and trajectory remain more important for prognosis and ICU decisions.

11. Imaging strategy

Ultrasound —First-line assessment for gallstones, gallbladder pathology and biliary dilatation.

Limitation: pancreas may be poorly visualized because of bowel gas; a normal study does not exclude microlithiasis/small CBD stones.

CECT — Used i/c/o diagnostic uncertainty (to rule out other differentials like perforated ulcer, mesenteric ischemia, bowel obstruction, ruptured AAA) failure to improve, clinical deterioration, suspected complications, necrosis, or procedural planning.
Timing: for severity assessment, usually ≥72–96 h after symptom onset; avoid routine immediate CT in clearly diagnosed uncomplicated AP.

Modality	Best use	Indication	Not for
EUS	Occult CBD stones/ microlithiasis (Find)	Suspected CBD stone; idiopathic/recurrent AP	Routine diagnostic testing when no clinical question
MRCP	Non invasive duct evaluation (See)	Suspected obstruction; duct evaluation; selected idiopathic AP	Urgent decompression
ERCP	Therapy (Fix/treat)	Cholangitis; persistent biliary obstruction requiring drainage/stone extraction	Not routine diagnostic ERCP

12. Management algorithm

12.1 Confirm diagnosis

2 of 3 criteria: typical pain + Sr. Amylase / lipase >3× ULN +/- compatible imaging.

12.2 Establish etiology

History + LFT + triglycerides + calcium + trans abdominal ultrasound.

12.3 Assess severity

SIRS, hypovolemia and organ dysfunction; persistent organ failure >48 h = severe AP. Reassess dynamically during first 24-48 hours.

12.4 Fluid resuscitation

Lactated Ringer’s + moderate goal-directed fluid therapy (WATERFALL TRIAL). Use 10ml/kg bolus over 2 hours if hypovolemic f/b maintenance @ 1.5- 3 mL/kg/hr with frequent assessment , analgesia, early oral/enteral nutrition, close monitoring.

Fluid targets: MAP 65–85 mmHg, urine output ≥0.5 mL/kg/h and hematocrit <44% can support assessment of adequate fluid status

12.4.1 Reassessment targets

12.5 Analgesia

Option	Adult reference approach	Important cautions
Paracetamol	maximum 4 g/day in adults without hepatotoxicity risk	Reduce dose in significant liver disease/alcohol-related risk
Morphine	Small IV titrated doses, commonly 2.5–5 mg IV initially in adults	Respiratory depression, hypotension; titrate to effect
Fentanyl	Short-acting IV titration in ICU settings	Potent; requires airway/respiratory monitoring
NSAID	Can be considered in selected mild/moderate pain	Avoid in AKI, GI bleeding/ulcer disease, severe renal dysfunction, or other contraindications

12.6 Nutrition

Current 2025 IAP/APA/EPC/IPC/JPS guidance strongly favors early oral feeding when tolerated and enteral tube feeding when oral intake is inadequate.

Clinical setting	Recommended approach
Predicted mild/moderate AP	Oral feeding as soon as appetite is present and vomiting/ileus are absent
Diet	A regular low-fat solid diet is acceptable; clear liquids are not mandatory
Unable to tolerate oral intake	Early enteral tube feeding, preferably within 72 h
Predicted severe / necrotizing AP with insufficient oral intake	Nasoenteric feeding; NG and NJ routes are both acceptable
Parenteral nutrition	Use only when enteral nutrition cannot meet nutritional needs or is contraindicated

12.7 Antibiotics

Situation	Action
Uncomplicated sterile AP	No antibiotics
Sterile pancreatic necrosis	No prophylactic antibiotics
Proven extrapancreatic infection	Treat according to source
Strongly suspected infected necrosis	Start broad-spectrum IV therapy promptly while arranging multidisciplinary assessment/source control
Gas in necrotic collection	Strong radiologic evidence supporting infected necrosis
Positive cultures	Treat and narrow according to susceptibility
CRP/WBC alone	Not sufficient to start antibiotics
Prophylactic antifungal therapy	Not recommended routinely

12.8 Identify emergencies

Cholangitis → early ERCP.

Deterioration → CT.

Suspected infected necrosis → antibiotics + multidisciplinary evaluation.

12.9 Prevent recurrence

Mild biliary AP → index-admission cholecystectomy; address alcohol, triglycerides, drugs and other causes.

12.10 Necrotizing disease

Conservative treatment initially; when intervention is needed, favor delayed minimally invasive step-up management.

Delay intervention when clinically feasible until the collection becomes organised/ walled off usually ~3 to 4 weeks.

13. Etiology-specific management

13.1 Gallstone pancreatitis

Situation	Management
AP + cholangitis	Urgent/early ERCP for biliary drainage.
Persistent CBD obstruction / choledocholithiasis	ERCP when obstruction is established, if suspicion remains without cholangitis, use EUS/MRCP to confirm choledocholithiasis before ERCP
Gallstone AP without cholangitis/obstruction	No routine urgent ERCP.
Mild biliary AP	Same-admission laparoscopic cholecystectomy, preferably before discharge.

The 2025 IAP guideline specifically recommends against early ERCP in biliary AP without cholangitis and supports ERCP for acute cholangitis or documented persistent CBD obstruction.

13.2 Hypertriglyceridemia-associated AP

TG level	Interpretation
≥500 mg/dL	Risk increases; search for secondary causes
≥1000 mg/dL	Strongly consider HTG as the cause
>2000 mg/dL	Very high risk of pancreatitis

Standard AP care: fluid management, analgesia, nutrition, and organ support remain the foundation.
Diabetes: insulin is recommended to reduce TG in diabetic HTG-associated AP.
Non-diabetic patient: insulin may be considered to lower TG in selected cases.
Plasmapheresis: not routine first-line therapy; reserve for selected severe/refractory situations particularly with acute renal failure.
Long-term prevention: fibrate/statin therapy according to lipid phenotype, glycemic control, weight management and elimination of secondary causes.

The 2025 IAP guideline recommends insulin in diabetic patients and allows consideration in non-diabetic patients as first-line TG-lowering therapy in HTG-associated AP.

13.3 Hypercalcemia-associated AP

Search for primary hyperparathyroidism, malignancy, and other causes.
Use isotonic saline for volume expansion rather than calcium-containing LR when clinically significant hypercalcemia is present.
Avoid unnecessary calcium/vitamin D supplementation.
Definitive treatment of the underlying hyperparathyroidism reduces recurrence risk.

The 2025 IAP guideline specifically describes isotonic saline rather than LR in hypercalcemia-associated AP and emphasizes definitive management of primary hyperparathyroidism after the acute episode

14. Complications

System	Complications
Respiratory	Pleural effusion, ARDS, hypoxemia
Renal	AKI, oliguria
Cardiovascular	Hypovolemia, shock
Metabolic	Hypocalcemia, hyperglycemia
Vascular	Splenic/portal vein thrombosis, pseudoaneurysm, hemorrhage
Abdominal	Ileus, intra-abdominal hypertension, abdominal compartment syndrome

14.1 Exocrine pancreatic insufficiency after severe/recurrent AP

Think of EPI when: steatorrhea, weight loss, bloating, fat-soluble vitamin deficiency or malnutrition develops after recurrent/severe pancreatitis.
Testing: fecal elastase is commonly used as a noninvasive test, interpreted with stool consistency and clinical context.
Treatment: pancreatic enzyme replacement therapy with meals/snacks when EPI is confirmed or strongly suspected.
Nutrition: avoid unnecessary severe fat restriction; optimize calories, protein and micronutrients.

14.2 Post pancreatitis diabetes & metabolic complications

Monitor glucose during acute illness, especially with severe/necrotizing disease.
Recurrent or necrotizing AP can lead to pancreatogenic/type 3c diabetes.
After recovery, reassess glycemic status in patients with extensive pancreatic injury or recurrent disease.
Address obesity, dyslipidemia and alcohol exposure to reduce recurrence.

15. What NOT to do

Avoid	Reason
Routine prophylactic antibiotics	No benefit for sterile disease
Routine early ERCP in biliary AP without cholangitis/obstruction	No routine benefit
Routine immediate CT in clearly diagnosed uncomplicated AP	May not change management and can underestimate early necrosis
Serial lipase to judge recovery	Does not track clinical recovery reliably
Prolonged NPO	Delays enteral nutrition
Routine TPN	Enteral route is preferred when feasible
Blind aggressive fluid loading	Fluid overload can worsen respiratory/abdominal compartment physiology
Early necrosectomy in stable necrotizing disease	Organized collections are safer to manage
Routine antifungal prophylaxis	Not recommended
Calling AP idiopathic after only a normal ultrasound	Occult biliary disease may be missed

16. Evidence-based updates that improve on older bedside algorithms

Older/common approach	Current evidence-based refinement
Aggressive fixed-rate fluid resuscitation	Moderate, reassessment-driven LR strategy
Routine prophylactic antibiotics in severe/necrotizing AP	Do not give in sterile necrosis
Routine early ERCP for biliary AP	ERCP for cholangitis or selected persistent CBD obstruction
Prolonged NPO	Early oral feeding when tolerated
Routine TPN in severe AP	Enteral feeding preferred; PN only when EN cannot meet needs/is contraindicated
Early open necrosectomy	Conservative-first + step-up minimally invasive strategy
FNA routinely to prove infected necrosis	Usually unnecessary; combine clinical/radiologic/microbiologic evidence
CRP/WBC alone to start antibiotics	Do not use alone
Early intervention at around 4 weeks in every patient	Timing individualized; delay when feasible, intervene for deterioration/complications

17.REFERENCES — ACUTE PANCREATITIS

1. Harrison’s Principles of Internal Medicine. 22nd ed. Chapter 359: Acute and Chronic Pancreatitis.

2. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 12th ed.

3. International Association of Pancreatology. Revised Guidelines on Acute Pancreatitis 2025: Supported and Endorsed by the American Pancreatic Association, European Pancreatic Club, Indian Pancreas Club, and Japan Pancreas Society. Pancreatology. 2025;25:770–814.

4. Tenner S, Vege SS, Sheth SG, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis. Am J Gastroenterol. 2024;119(3):419–437.