Acute pancreatitis

Reading File

Finding Sources

Reading File

Loading Image

I now have comprehensive content from multiple authoritative sources. Let me synthesize a complete clinical overview of acute pancreatitis.

Acute Pancreatitis

Definition & Epidemiology

Acute pancreatitis (AP) is a sudden inflammatory disease of the pancreas that ranges from mild, self-limited illness to a life-threatening emergency. Hospital admissions in the USA appear to be increasing. The clinical diagnosis requires two of three criteria:

Abdominal pain strongly suggestive of AP
Serum amylase and/or lipase ≥ 3× the upper limit of normal
Characteristic imaging findings

— Grainger & Allison's Diagnostic Radiology

Etiology (Mnemonic: GET SMASHED)

Category	Examples
Gallstones	Most common cause in adults (~40%)
Ethanol	Second most common (~30%)
Trauma	Blunt abdominal trauma
Steroids	Corticosteroids, azathioprine
Mumps / infections	EBV, CMV, Coxsackievirus, Mycoplasma
Autoimmune	IgG4-related disease
Scorpion venom / Spider bite	Rare
Hyperlipidaemia / Hypercalcaemia	Metabolic causes
ERCP	Post-procedural pancreatitis
Drugs	Valproate, L-asparaginase, 6-mercaptopurine, furosemide, tetracyclines

Additional causes: pancreas divisum, genetic mutations (SPINK1, CFTR, PRSS1), malignancy, vasculitis (SLE, Kawasaki disease). ~5% remain idiopathic.

Pathogenesis

The final common pathway is premature intracellular activation of trypsinogen to trypsin within acinar cells, triggering auto-digestion. This releases inflammatory mediators (IL-1, IL-6, TNF-α), leading to a local inflammatory cascade that, in severe cases, progresses to systemic inflammatory response syndrome (SIRS) and multi-organ dysfunction.

Clinical Features

Pain: Sudden-onset, severe, constant epigastric pain radiating to the back or left scapular region; patients are more comfortable leaning forward
Nausea, vomiting, anorexia, fever
Examination: Tachycardia, tachypnoea, epigastric tenderness, hypoactive bowel sounds, abdominal rigidity (variable)
Rare signs of haemorrhagic pancreatitis:
- Grey-Turner sign: flank ecchymosis
- Cullen sign: periumbilical ecchymosis
Extremities may be cool and cyanotic from underperfusion

— Sleisenger and Fordtran's GI and Liver Disease

Laboratory Findings

Test	Findings
Serum amylase	Elevated within hours; non-specific (also elevated in other abdominal conditions)
Serum lipase	More sensitive and specific; stays elevated longer
WBC	12,000–20,000/mm³ typical
CRP	Marker of severity (>150 mg/L at 48h suggests severe disease)
LFTs	Elevated ALT >3× normal suggests gallstone etiology
Serum calcium	Hypocalcaemia (saponification of fat)
Blood glucose	Hyperglycaemia (transient or persistent)
Triglycerides	Check if hypertriglyceridaemia is suspected cause
ABG	Hypoxaemia in severe cases

Severity Classification — Revised Atlanta 2012

Category	Definition
Mild	No organ failure; no local/systemic complications
Moderately severe	Transient organ failure (<48 h) or local complications without persistent organ failure
Severe	Persistent organ failure (>48 h), single or multi-organ

Morphological types (Revised Atlanta):

Interstitial oedematous pancreatitis — pancreatic parenchyma enhances normally on contrast CT; peripancreatic oedema present
Necrotising pancreatitis — non-enhancing areas indicating parenchymal necrosis; may involve peripancreatic tissue

Severity Scoring Systems

Ranson Criteria (1974)

At admission (5 criteria): Age >55, WBC >16,000, glucose >200 mg/dL, LDH >350 IU/L, AST >250 IU/L

At 48 hours (6 criteria): Haematocrit fall >10%, BUN rise >5 mg/dL, Ca²⁺ <8 mg/dL, PaO₂ <60 mmHg, base deficit >4 mEq/L, fluid sequestration >6 L

Score ≥3 = severe disease.

BISAP Score

Each criterion = 1 point:

BUN > 25 mg/dL
Impaired mental status
SIRS present
Age > 60 years
Pleural effusion

Score ≥3 correlates with increased mortality.

CT Severity Index (CTSI / Modified Balthazar)

A radiological scoring system (max 10 points):

Parameter	Points
Normal pancreas	0
Intrinsic pancreatic abnormality ± peripancreatic fat changes	2
Pancreatic/peripancreatic fluid collection or fat necrosis	4
Necrosis ≤30%	+2
Necrosis >30%	+4
Extrapancreatic complications (pleural effusion, ascites, vascular/GI involvement)	+2

Mild: 0–2 | Moderate: 4–6 | Severe: 8–10

— Grainger & Allison's Diagnostic Radiology

Imaging

CT (Investigation of Choice for Severity)

Contrast-enhanced CT (CECT) is the gold standard for:

Confirming diagnosis when uncertain
Assessing extent of pancreatic necrosis
Identifying fluid collections and complications

Important timing caveat: CT performed within 12–24 hours may underestimate the degree of necrosis, which takes 2–3 days to fully develop. CECT is best performed after 72 hours if clinical deterioration warrants it.

CT Timing in Acute Pancreatitis — Panel A (12 hours) shows minimal signs; Panel B (day 3) reveals much more severe inflammation and necrosis

Fig. Appropriate timing of CT in acute pancreatitis: (A) CT at 12 hours shows only minimal signs; (B) follow-up CT on day 3 demonstrates much more severe inflammation. — Grainger & Allison's Diagnostic Radiology

A single venous-phase CT (70s delay; ~1.5–2 mL/kg contrast at 4 mL/s) is sufficient to stage AP. Arterial phase is not routinely needed.

If CECT is contraindicated (e.g. renal failure), contrast-enhanced ultrasound (CEUS) is an alternative to assess necrosis.

Ultrasound

First-line initial investigation
Limited pancreatic visualisation due to overlying bowel gas
Excellent for identifying gallstones as the cause
Useful for guiding drainage of fluid collections

MRI / MRCP

Superior to CT for characterising fluid collections and ductal disruption
MRCP useful to detect choledocholithiasis without ERCP risk
Preferred in pregnancy and young patients requiring serial imaging

Fluid Collections (Revised Atlanta Terminology)

Collection	Timing	Contents	Wall
Acute peripancreatic fluid collection (APFC)	<4 weeks, oedematous AP	Fluid	None
Pseudocyst	>4 weeks, oedematous AP	Fluid	Defined wall
Acute necrotic collection (ANC)	<4 weeks, necrotising AP	Fluid + necrosis	None
Walled-off necrosis (WON)	>4 weeks, necrotising AP	Fluid + necrosis	Defined wall

Complications

Local:

Pancreatic necrosis (sterile or infected)
Pseudocyst formation
Pancreatic duct disruption
Splenic vein thrombosis, pseudoaneurysm
Colonic infarction (middle colic or right colic artery thrombosis — presents with rapid haemodynamic collapse)

Systemic:

Hypovolaemia and shock
Acute kidney injury
Acute respiratory distress syndrome (ARDS) / pleural effusion
Hepatic failure
Hypocalcaemia
Hyperglycaemia/diabetes

Management

Initial Resuscitation

IV fluid resuscitation is the cornerstone: aggressive early resuscitation with Lactated Ringer's solution is preferred over normal saline (lower incidence of acidosis/SIRS); rate typically 250–500 mL/h adjusted to urine output, BUN, and haematocrit
Oxygen supplementation; intubation for ARDS if needed
Urinary catheter to monitor hourly urine output (target >0.5 mL/kg/h)
Analgesia: IV opioids (morphine, hydromorphone) — older concerns about morphine causing sphincter of Oddi spasm are not clinically significant; meperidine is no longer preferred due to toxic metabolite accumulation

Monitoring

Serial vital signs, fluid balance
Monitor BUN, creatinine, haematocrit, calcium every 6–12 hours initially
APACHE II or SOFA scores to guide ICU transfer

Nutrition

Mild AP: early oral feeding (soft, low-fat diet) as soon as tolerated — no need for NPO/bowel rest
Severe AP: enteral nutrition (via nasojejunal tube) is preferred over total parenteral nutrition (TPN); reduces infectious complications and mortality
TPN is reserved for patients who cannot tolerate enteral feeds

Specific Interventions

Gallstone AP (biliary pancreatitis):

Early ERCP with sphincterotomy within 24–72 hours if concurrent cholangitis or persistent biliary obstruction
Cholecystectomy should be performed during the same admission or early after recovery to prevent recurrence

Infected pancreatic necrosis:

Suspected when clinical deterioration occurs after initial improvement or fever/rising WBC at >1 week
CT-guided fine needle aspiration (FNA) with Gram stain and culture can confirm
Step-up approach: antibiotics (imipenem, meropenem, or ciprofloxacin + metronidazole) → percutaneous catheter drainage → minimally invasive necrosectomy → open surgery as last resort
Prophylactic antibiotics are not recommended routinely in sterile necrotising AP

Hypertriglyceridaemia-induced AP:

Insulin infusion, plasmapheresis in severe cases; fibrates for long-term prevention

Medications to Avoid

NSAIDs (worsen renal perfusion in hypovolaemia)
Prophylactic antibiotics in uncomplicated AP

Prognosis

~80% of AP cases are mild and self-limiting, resolving in 3–5 days
~20% have severe disease with local or systemic complications
Mortality: ~3–5% overall; up to 20–30% in severe necrotising pancreatitis with multiorgan failure
Colonic infarction from colic artery thrombosis carries an extremely high mortality and requires emergent laparotomy

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease | Grainger & Allison's Diagnostic Radiology | Textbook of Family Medicine, 9e

This is a shared conversation. Sign in to Orris to start your own chat.