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GI & hepatology

Pancreatitis & pancreatic mass

2 of 3: typical pain, lipase ≥3× ULN, imaging. Gallstones #1 women; alcohol #1 men. TG, drugs, ERCP, hyperCa, post-op, idiopathic.

Lucas Cofer5 min6 questions2 trials

Two of three makes the diagnosis

Need 2 of 3: typical pain, lipase ≥3× ULN, characteristic imaging (revised Atlanta, ; ; ). Band-like epigastric / LUQ pain to the back in half; nausea/vomiting in 90%; ileus, jaundice, Grey-Turner / Cullen if necrotizing and late.

  • Do not trend lipase to decide discharge. False positives in CKD and DKA.
  • Every patient gets RUQ ultrasound for stones. CT (~90% sensitive) if the diagnosis is uncertain or for complications at 48–72 h. MRI/MRCP if necrosis, stricture, or a missed stone.
  • Labs: lipase, CBC (often high hematocrit), BMP including calcium, LFTs, triglycerides.
EtiologyWho / clue
Gallstones / sludge (40–75%)#1 in women
Alcohol (25–35%)#1 in men
Hypertriglyceridemia (~10%)Suspect if TG >1000
ERCP (1–30%)Rectal NSAIDs cut the risk
Hypercalcemia, anatomic, autoimmune, genetic, drugs, toxins, infection, ischemia, traumaIgG4 (type 1 AIP); CFTR / PRSS1 / SPINK1; ACEi, furosemide, valproate, AZA/6-MP, mesalamine, estrogen, propofol; scorpion; mumps / Coxsackie; vasculitis /
Idiopathic (10–25%)Repeat RUQUS and TG as outpatient; second idiopathic attack → cholecystectomy ± genetics

Atlanta severity — organ failure is the plot

Revised Atlanta classification
  1. Mild

    No organ failure, no local or systemic complications

    The dischargeable majority. Same-stay cholecystectomy if gallstone disease.

  2. Moderate

    Organ failure that resolves within 48 h, or a local / systemic complication

    Fluid collections, exacerbation of comorbidity. Watch the clock on organ failure.

  3. Severe

    Organ failure lasting >48 h

    ~22% mortality. Use a modified Marshall score. Necrosis is sterile until proven otherwise.

Risk flags for severe disease: abnormal vitals, age >55, BMI >30, BUN >20, Hct >44, pleural effusion / infiltrate, extra-pancreatic collections. BISAP is the practical score; Ranson and APACHE II are not.

WATERFALL fluids, early food, targeted ERCP

Moderately aggressive lactated Ringer’s in the first 6–12 h — not a flood (, ; ). Aggressive resuscitation increased overload without improving necrosis.

  • Pain: IV opioids. No prophylactic antibiotics.
  • Nutrition: low-fat solids within 24–48 h as hunger allows. If still NPO at 5–7 days, NG feeding (NG > NJ). Enteral beats TPN. Early feeding cuts infected necrosis.
  • Gallstone pancreatitis: urgent ERCP within 24 h only for cholangitis or persistent CBD obstruction — not for every stone pancreatitis. Cholecystectomy this admission if mild (); delayed CCY raises biliary complications.
  • Reverse precipitants: stop culprit drugs; treat calcium and triglycerides.

Collections, necrosis, chronic disease, masses

Morphology<4 weeks>4 weeks
Interstitial edematousAcute peripancreatic fluid collection — no wall; usually resolve, do not drainPseudocyst — well-defined wall. EUS-FNA (high amylase) if diagnosis unclear. Drain if symptomatic, rapidly growing, or infected
NecrotizingAcute necrotic collection (intra- or extra-pancreatic)Walled-off necrosis. Drain at >2–4 weeks if symptomatic or infected (endoscopic preferred to percutaneous)
  • Infected necrosis: ~1/3, suspect day 7–10. Gas on CT or positive blood culture. Do not routinely FNA necrosis (). Antibiotics: (cefepime or cipro) + metronidazole, or pip-tazo. Unstable → urgent drainage; stable on antibiotics → delay >4 weeks, step-up endoscopic / percutaneous (PANTER). No routine antifungal prophylaxis.
  • Vascular: splenic / portal / SMV thrombosis — anticoagulate if portal vein or bowel ischemia. Pseudoaneurysm (GDA / splenic artery) into a pseudocyst: falling Hb, expanding collection, unexplained GIB. Arterial-phase CT; IR embolize before draining the collection.
  • Systemic: abdominal compartment (bladder pressure >20 + new organ failure), ARDS (phospholipase vs surfactant), hypocalcemia, hyperglycemia, hyperTG, GIB, AKI, DIC.

Chronic pancreatitis (ACG: )

Repeated attacks (especially alcohol and smoking) → fibrosis, pain, exocrine failure (steatorrhea, fat-soluble vitamin deficiency), brittle diabetes. Lipase may be high early and normal/low later. Fecal fat positive, elastase low. CT/MRI: calcifications, duct dilation, atrophy. Cancer risk is up. Pancrelipase, replete ADEK, pain control, genetics when young or idiopathic.

Pancreatic masses (; )

  • Solid: adenocarcinoma 85–90%, AIP, neuroendocrine 1–5%, lymphoma, mets (melanoma, RCC).
  • Cystic: inflammatory (pseudocyst) vs neoplastic — main-duct IPMN >> side-branch IPMN > mucinous cystic ≈ solid pseudopapillary > serous cystadenoma.
  • Pancreatic-protocol CT; EUS-FNA if >2–3 cm (Sn 87%, Sp 96%); MRI for <2 cm or vascular questions. CA 19-9 positive in ~80% of pancreatic CA; CEA for mucinous cysts; ANA / IgG4 if autoimmune.