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2025 PACUPrep BCCCP Preparatory Course Acute Pancreatitis Evidence-Based Management of Acute Pancreatitis

Lesson 28, Topic 2

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Evidence-Based Management of Acute Pancreatitis

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Diagnosis and Severity Stratification in Acute Pancreatitis

Learning Objective

Apply diagnostic and classification criteria to assess a patient with acute pancreatitis and guide initial management.

I. Clinical Presentation

Acute pancreatitis typically presents with severe epigastric pain and systemic signs of inflammation. Early recognition guides diagnostic testing and timely pharmacotherapy.

Case vignette: A 55-year-old man awakens at 2 AM with constant, severe epigastric pain radiating to his back. He has nausea, vomiting, tachycardia (110 bpm), and BP 100/60 mm Hg.

Characteristic pain: constant, intense epigastric discomfort, often worsened by eating and radiating to back
Associated symptoms: nausea, vomiting, anorexia
Physical exam: epigastric tenderness, voluntary guarding; Grey Turner’s (flank ecchymosis) or Cullen’s (periumbilical ecchymosis) are late and severe findings
Vital signs: low-grade fever, tachycardia; hypotension may reflect hypovolemia or SIRS

Key Pearl: Pain Presentation Variability

Absence of classic pain does not exclude AP in elderly or altered-mental-status patients.

II. Laboratory Evaluation

Diagnosis requires ≥2 of: clinical presentation, enzyme elevation (>3× ULN), or imaging. Additional labs stratify etiology and severity.

Serum lipase (>3× ULN): preferred marker (sensitivity ~90 %, specificity ~95 %); rises 4–8 h, peaks at 24 h, remains elevated up to 14 d
Serum amylase: rises 6–12 h, normalizes by day 3–5; less specific (other intra-abdominal processes)
Enzyme magnitude does not correlate with severity
Liver function tests: ALT >150 U/L suggests gallstone etiology
Triglycerides: fasting levels >1000 mg/dL indicate hypertriglyceridemia-induced AP
Calcium: hypocalcemia may occur in severe disease
Blood urea nitrogen (BUN): admission >20 mg/dL or rising at 24 h predicts necrosis and mortality
Hematocrit: >44 % (hemoconcentration) signals higher necrosis risk
C-reactive protein (CRP): >150 mg/L at 48 h predicts severe AP

Key Pearl: BUN as an Early Predictor

A rising BUN within the first 24 h is one of the strongest early predictors of severe disease.

III. Imaging Modalities

Ultrasound is first-line for etiology; contrast CT at 48–72 h confirms necrosis; MRI/MRCP and EUS refine ductal evaluation.

Transabdominal ultrasound: detect gallstones, biliary dilation; noninvasive, no radiation but limited by bowel gas
Contrast-enhanced CT (CECT): gold standard for necrosis and local complications; best performed ≥48 h after onset unless diagnosis is unclear
MRI/MRCP: ideal for patients with contraindications to iodinated contrast and for ductal imaging (stones, strictures)
Endoscopic ultrasound (EUS): highest sensitivity for microlithiasis and small tumors

Controversy: Routine Early CT

Routine early CT (<48 h) adds radiation and contrast risks without changing initial management in straightforward cases.

Key Pearl: CECT Timing

Reserve CECT for diagnostic uncertainty or clinical deterioration; otherwise defer until ≥48 h.

IV. Etiologic Work-Up

Identifying the cause prevents recurrence and guides interventions.

Gallstones: ALT >150 U/L, ultrasound evidence; MRCP/EUS if obstruction suspected but not visualized
Hypertriglyceridemia: confirm fasting TG >1000 mg/dL
Alcohol: history of heavy use; assess withdrawal risk and plan intervention
Medications: review for azathioprine, didanosine, valproate, tetracyclines
Other: hypercalcemia, autoimmune serologies, genetic testing in young idiopathic cases, neoplasm evaluation in patients >40 years

Key Pearl: Idiopathic AP and Neoplasm

In idiopathic AP, especially patients >40, consider imaging for pancreatic neoplasm.

V. Severity Assessment and Classification

Use the Revised Atlanta Classification and validated scoring systems (Ranson’s, APACHE II, BISAP) to stratify risk and direct triage.

1. Revised Atlanta Classification

Mild AP: no organ failure, no local/systemic complications
Moderately severe AP: transient organ failure (≤48 h) and/or local or systemic complications
Severe AP: persistent organ failure (>48 h), single or multiple

Organ failure assessed by modified Marshall score (respiratory, cardiovascular, renal).

2. Scoring Systems Comparison

Comparison of Scoring Systems for Acute Pancreatitis Severity
Score	Timing	Variables	Clinical Use
Ranson’s	Admission + 48 h	Age, WBC, glucose, LDH, AST; Hct fall, BUN rise, Ca, PaO₂, base deficit, fluid sequestration	Prognosis at 48 h
APACHE II	Any time	Age, chronic health, 12 physiologic variables	ICU triage, dynamic reassessment
BISAP	First 24 h	BUN >25 mg/dL, impaired mental status, SIRS, age >60, pleural effusion	Early mortality risk

Key Pearl: Persistent Organ Failure

Persistent organ failure (>48 h) is the single strongest predictor of mortality.

VI. Integration into Initial Management

Severity stratification informs ICU vs ward admission, monitoring intensity, fluid and nutrition strategies.

Triage: ICU for ≥2 organ failures or high APACHE II/BISAP; ward for mild cases
Fluid resuscitation: goal-directed moderate approach using lactated Ringer’s; avoid aggressive fixed-rate protocols to prevent overload
Nutrition: initiate early enteral feeding (within 24–72 h) as tolerated; nasogastric or nasojejunal routes acceptable
Consults: gastroenterology for ERCP in biliary AP with cholangitis; surgery for same-admission cholecystectomy in mild gallstone AP

Case decision point: BISAP score of 3 → ICU admission, invasive monitoring, aggressive supportive care.

Key Pearl: Score-Driven Triage

Score-driven triage and goal-directed fluids reduce complications and optimize resource use.

VII. Pearls, Pitfalls, and Controversies

Early false negatives: normal enzymes in delayed presentations or chronic pancreatitis
Overuse of early CT: contrast nephropathy risk, limited impact on management
Scoring variability: no system is perfect—repeat assessment and clinical judgment are essential
Electronic calculators: improve accuracy and efficiency of score computation

Controversy: Protocols vs. Individualized Assessment

Universal protocols vs individualized, dynamic assessment based on evolving clinical status.

Key Pearl: Clinical Acumen and Scores

Combine clinical acumen with validated scores for best patient outcomes.

References

de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis. N Engl J Med. 2022;387(11):989–1000.
Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN. AGA Institute Guideline on Initial Management of Acute Pancreatitis. Gastroenterology. 2018;154(4):1096–1101.
Tenner S, Baillie J, DeWitt J, Vege SS. ACG Guideline: Management of Acute Pancreatitis. Am J Gastroenterol. 2013;108(9):1400–1415.
Banks PA, Bollen TL, Dervenis C, et al. Revision of the Atlanta Classification for Acute Pancreatitis. Gut. 2013;62(1):102–111.
Wu BU, Bakker OJ, Papachristou GI, et al. Blood Urea Nitrogen in Early Assessment of Acute Pancreatitis. Arch Intern Med. 2011;171(7):669–676.
Sternby H, Bolado F, Canaval-Zuleta HJ, et al. Determinants of Severity in Acute Pancreatitis: A Multicenter Cohort Study. Ann Surg. 2019;270(3):348–355.

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