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Pancreatitis - Complete Overview


Definition

Inflammation of the pancreas due to autodigestion by its own activated enzymes. Comes in two major forms:
  • Acute pancreatitis - reversible if the cause is removed
  • Chronic pancreatitis - irreversible destruction of exocrine (and eventually endocrine) pancreas

Anatomy Recap

The pancreas is a retroperitoneal organ with head (within the duodenal C-loop), body (posterior to stomach), and tail (at splenic hilum). The main duct (duct of Wirsung) joins the common bile duct at the ampulla of Vater, draining via the sphincter of Oddi.

ACUTE PANCREATITIS

Epidemiology

  • Incidence: 33-74 per 100,000 globally; 5-35 per 100,000 in the West
  • Overall mortality ~5%; up to 30% in severe cases
  • Incidence rising due to obesity epidemic and gallstone disease

Causes (mnemonic: GET SMASHED)

CategoryCauses
Gallstones#1 cause (40-70%) - impaction at ampulla of Vater
Ethanol/Alcohol#2 cause (25-35%)
TraumaBlunt abdominal injury
Steroids / DrugsThiazides, azathioprine, anticonvulsants, estrogens, chemotherapy
Mumps / InfectionsMumps, coxsackievirus, Ascaris, Clonorchis
AutoimmuneIgG4-related disease
Scorpion venomTityus trinitatis
Hypercalcemia / HypertriglyceridemiaTG >1000 mg/dL (5-10% of cases); hyperparathyroidism
ERCP5-10% incidence post-procedure
Divisum / Duct obstructionPancreatic cancer, pancreas divisum, biliary sludge
  • Idiopathic: 10-20% (many due to occult microlithiasis or CFTR/PRSS1/SPINK1 mutations)
  • Smoking and diabetes are independent risk factors

Pathophysiology

  1. Inciting event (duct obstruction, toxin) → disrupts normal membrane trafficking
  2. Inappropriate activation of trypsinogen → excess trypsin
  3. Trypsin activates other digestive enzymes → autodigestion of pancreatic tissue
  4. Macrophage/neutrophil recruitment, cytokine release → increased vascular permeability
  5. Edema, hemorrhage, necrosis
  6. If severe: SIRS → sepsis, shock, multiorgan failure
  7. Bacterial translocation from intestinal flora → bacteremia

Clinical Features

Symptoms:
  • Persistent, moderate-to-severe epigastric or LUQ pain radiating to the back (classic)
  • Pain relieved by leaning forward/sitting up
  • Nausea, vomiting, anorexia
  • Oral intake worsens pain
Signs:
  • Fever, tachycardia
  • Epigastric tenderness ± guarding
  • Diminished bowel sounds (ileus)
  • Jaundice if obstructive cause
  • Cullen sign - periumbilical bruising (hemoperitoneum) - rare, poor prognosis
  • Grey Turner sign - flank bruising (retroperitoneal bleeding) - rare, poor prognosis
  • Murphy sign if gallstone cause
Complications:
LocalSystemic
Pancreatic necrosisSIRS/Sepsis/Shock
Pseudocyst formationARDS (hypoxemia)
AbscessPleural effusion (left >> right, 50% of patients)
Bowel necrosisRenal failure
Portal/splenic vein thrombosisDIC/Coagulopathy
Gastric outlet obstructionHypocalcemia (fat saponification)

Diagnosis

Lab tests:
TestKey Points
LipaseMore sensitive AND specific than amylase; peaks early, stays elevated 1-2 weeks. Preferred test.
AmylaseRises in hours, normalizes in 3-5 days. False-negative in alcohol/hypertriglyceridemia pancreatitis.
Cutoff≥3x upper limit of normal for both
ALTElevated → biliary cause (PPV 95% for gallstone pancreatitis)
CBC, BMPSIRS, organ failure assessment
Calcium, TGIdentify metabolic causes
  • Degree of enzyme elevation does NOT correlate with severity
Imaging:
  • NOT routinely needed for diagnosis
  • CT with IV contrast indicated for:
    1. Diagnostic uncertainty
    2. Rule out other pathology
    3. Assess complications if not improving after 48-72 hours
  • CT findings of necrosis often not seen early - most useful at 3-7 days
  • CT is normal in 15% of acute pancreatitis cases
  • MRI/MRCP: better for duct anatomy, preferred in renal failure or contrast allergy
Atlanta Classification (Severity):
ClassFeatures
MildNo organ failure, no local complications
Moderately severeTransient organ failure (<48h) or local complications
SeverePersistent organ failure (>48h), single or multiorgan
Scoring Systems:
  • Ranson criteria (on admission and 48h)
  • BISAP score (BUN, Impaired mental status, SIRS, Age >60, Pleural effusion)
  • APACHE II
  • CT Severity Index (Balthazar score)

Management

Supportive (mainstay):
  1. IV fluid resuscitation - aggressive early hydration (Lactated Ringer preferred over normal saline in some studies)
  2. Pain control - IV opioids (morphine/hydromorphone)
  3. NPO initially - restart oral feeding early (within 24-48h if tolerated); enteral nutrition via NG/NJ tube preferred over TPN in severe disease
  4. Antiemetics for nausea
  5. Monitoring for organ failure
Specific interventions:
  • Gallstone pancreatitis: early ERCP if cholangitis or persistent biliary obstruction; cholecystectomy during same admission (mild disease) or after recovery
  • ERCP pancreatitis prevention: rectal indomethacin, prophylactic pancreatic stent in high-risk patients
  • Infected pancreatic necrosis: IV antibiotics (imipenem or meropenem) ± image-guided drainage or surgical necrosectomy
  • Pseudocyst: most resolve spontaneously; endoscopic cystgastrostomy/cystduodenostomy if symptomatic
  • Hypertriglyceridemia: insulin infusion, plasmapheresis in severe cases
What NOT to do:
  • Routine antibiotics (no benefit in sterile necrosis)
  • Nasogastric decompression routinely
  • Early CT (first 24-48h rarely changes management)

CHRONIC PANCREATITIS

Definition

Long-standing inflammation causing irreversible destruction of exocrine pancreas, eventually destroying islets of Langerhans (endocrine).

Causes

  • Alcohol - most common (especially middle-aged men)
  • Idiopathic (up to 40%) - many have CFTR, PRSS1, SPINK1 mutations
  • Autoimmune pancreatitis (IgG4-related) - responds to steroids/anti-B cell therapy
  • Duct obstruction, hyperparathyroidism, cystic fibrosis

Pathology (Morphology)

  • Grossly: hard gland, dilated ducts, calcific concretions
  • Microscopically:
    • Parenchymal fibrosis
    • Reduced/absent acini
    • Dilated ducts with ductal concretions
    • Relative sparing of islets early → eventual islet loss
    • Ductal epithelium: atrophy, hyperplasia, or squamous metaplasia
  • Autoimmune type: lymphocyte + IgG4+ plasma cell infiltration, "swirling" fibrosis, venulitis

Clinical Features

  • Recurrent epigastric/back pain - most common symptom
  • Repeated bouts of jaundice
  • Steatorrhea (exocrine insufficiency) - foul, greasy stools
  • Diabetes mellitus (endocrine insufficiency - late)
  • Weight loss, malabsorption
  • May be silent until pancreatic insufficiency develops
  • Increased risk of pancreatic adenocarcinoma

Diagnosis

  • Plain X-ray/CT: pancreatic calcifications (pathognomonic)
  • MRCP or ERCP: "chain of lakes" ductal appearance
  • EUS: excellent for early/subtle changes
  • Labs: lipase/amylase may be normal (burned-out gland)
  • Fecal elastase: low in exocrine insufficiency
  • Secretin stimulation test: most sensitive for exocrine function

Management

  • Pain: analgesics, pancreatic enzyme supplements (reduce secretion), celiac plexus block, surgery
  • Exocrine insufficiency: pancreatic enzyme replacement therapy (PERT) with meals
  • Endocrine insufficiency: insulin for diabetes
  • Alcohol cessation - mandatory
  • Autoimmune pancreatitis: corticosteroids (dramatic response)
  • Surgery/Endoscopy: duct decompression (Puestow procedure), partial resection for refractory pain or obstruction

Quick Comparison

FeatureAcuteChronic
ReversibilityReversibleIrreversible
Main causeGallstones > AlcoholAlcohol > Idiopathic
EnzymesElevated (lipase >amylase)May be normal
CalcificationsNo (except late)Yes (pathognomonic)
DiabetesTransientPermanent (late)
Key complicationNecrosis, pseudocyst, MOFExocrine insufficiency, Ca risk

Sources: Robbins & Kumar Basic Pathology; Rosen's Emergency Medicine; Sleisenger and Fordtran's GI and Liver Disease
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