Cholangitis and pancreatitis diagnosis

Acute Ascending Cholangitis: Life-Threatening Biliary Sepsis

Acute cholangitis is a medical and surgical emergency arising from bacterial infection supervening upon an obstructed biliary tree. Elevated intraductal pressure ($> 20\text{ cmH}_2\text{O}$) breaches the hepatocyte tight junctions, driving bacteria and endotoxins directly into the hepatic venous sinusoids and systemic circulation (cholangiovenous reflux).

• Clinical Presentation:
  • Charcot's Triad (Present in 50% to 70%): (1) Right upper quadrant pain, (2) Jaundice, (3) High fevers with shaking rigors.
  • Reynolds' Pentad (Indicates Toxic, Suppurative Cholangitis): Charcot's triad PLUS (4) Septic shock (hypotension, tachycardia) and (5) Altered mental state / acute confusion. Carries a mortality $> 30\%$ without emergent biliary decompression.
• Emergency Management Protocol:
  1. Immediate Resuscitation: Aggressive intravenous balanced crystalloids to restore intravascular volume, oxygen therapy, and close monitoring in an intensive care or high-dependency unit.
  2. Antimicrobial Therapy: Take immediate blood cultures (positive in $> 50\%$ of cases), then commence prompt, broad-spectrum intravenous antibiotics active against enteric Gram-negative bacilli, enterococci, and anaerobes: piperacillin-tazobactam ($4.5\text{ g}$ IV 8-hourly) or ampicillin + gentamicin + metronidazole.
  3. Biliary source control: Arrange urgent ERCP/drainage according to severity, instability and local expertise, with immediate senior help in septic shock. Not every stable case has an identical hour deadline. Percutaneous or surgical approaches can be alternatives when endoscopy is unsuitable or fails; antibiotics alone may not control obstruction.

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Acute Pancreatitis: Diagnostic Criteria & Aetiology

Acute pancreatitis is an acute inflammatory process of the pancreas characterized by premature intracellular activation of digestive enzymes (trypsinogen converted to active trypsin within acinar cells), leading to autodigestion of the pancreatic parenchyma, microvascular leakage, necrosis, and a profound systemic inflammatory response syndrome (SIRS).

Diagnostic Criteria (Revised Atlanta Consensus)

A definitive diagnosis of acute pancreatitis requires the presence of at least 2 of the following 3 criteria:

1. Characteristic Abdominal Pain: Acute, severe, persistent, constant epigastric pain that frequently radiates directly through to the back, characteristically partially relieved by sitting upright and leaning forward, and aggravated by movement.
2. Biochemical Elevation: Serum lipase or amylase $\ge 3\text{ times}$ the upper limit of normal (ULN).
3. Characteristic Imaging Findings: Contrast-enhanced CT, MRI, or transabdominal ultrasound demonstrating features of acute pancreatitis (peripancreatic fluid stranding, interstitial oedematous pancreatitis, or non-enhancing areas of necrotizing pancreatitis).

Lipase vs. Amylase

• Serum Lipase is the Gold Standard Biomarker: Lipase sensitivity ($95-100\%$) and specificity ($95-98\%$) are significantly superior to amylase. Lipase remains elevated for 8 to 14 days (allowing late diagnosis), whereas amylase returns to normal within 3 to 5 days. Furthermore, serum amylase can be falsely elevated in numerous non-pancreatic conditions (macroamylasaemia, parotitis, perforated duodenal ulcer, mesenteric ischaemia, ectopic pregnancy, renal failure).
• Pancreatitis diagnosis/imaging: Typical pain plus lipase at least three times the upper limit meets two diagnostic criteria. Routine immediate CT is often unnecessary when diagnosis is clear, but uncertainty, deterioration or suspected complications can warrant imaging at any stage. Do not require waiting seventy-two hours in an unstable or worsening patient.

Aetiologies of Acute Pancreatitis

The two predominant causes account for over 80% of all cases:

• Gallstones (40% to 45%): A calculus transiently lodges at or passes through the ampulla of Vater, causing biliary-pancreatic ductal reflux and ductal hypertension.
• Alcohol Misuse (30% to 35%): Chronic alcohol consumption increases pancreatic ductal permeability, stimulates enzyme synthesis, and promotes protein plug precipitation.
• Hypertriglyceridaemia (3% to 5%): Fasting serum triglyceride levels $> 11.3\text{ mmol/L}$ ($> 1000\text{ mg/dL}$) undergo hydrolysis by pancreatic lipase into toxic free fatty acids, inducing capillary thrombosis and acinar injury.
• Post-ERCP (3% to 5%): Mechanical instrumentation or contrast injection into the pancreatic duct.
• Hypercalcaemia: Activates intra-acinar trypsinogen.
• Trauma: Blunt abdominal trauma (crushing against vertebral column, e.g., bicycle handlebar injury in children).
• Drugs: Azathioprine, 6-mercaptopurine, thiazide diuretics, sodium valproate, didanosine, tetracycline, corticosteroids.
• Infections: Mumps virus, Coxsackievirus, cytomegalovirus.
• Anatomical / Neoplastic: Pancreas divisum, intraductal papillary mucinous neoplasm (IPMN), pancreatic ductal adenocarcinoma.
• Autoimmune Pancreatitis: IgG4-related systemic fibro-inflammatory disease.

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Severity Stratification & Prognostic Scoring

While 80% of acute pancreatitis presentations are mild and self-limiting (resolving within 3 to 5 days), 20% progress to severe acute pancreatitis complicated by extensive pancreatic necrosis, infected collections, and multi-organ failure, with mortality reaching 20% to 30%.

Revised Atlanta Severity Classification

• Mild Acute Pancreatitis: Absence of organ failure and absence of local or systemic complications. Patients typically recover rapidly with oral re-feeding and crystalloids.
• Moderately Severe Acute Pancreatitis: Presence of transient organ failure (resolves within 48 hours) and/or local or systemic complications without persistent organ failure.
• Severe Acute Pancreatitis: Presence of persistent organ failure ($> 48\text{ hours}$) affecting one or more organ systems:
  • Respiratory: $PaO_2 / FiO_2 \le 300\text{ mmHg}$.
  • Renal organ failure: Revised Atlanta uses a modified Marshall assessment; creatinine around 170 micromol/L corresponds to about 2 mg/dL, not two times baseline. Organ failure persisting beyond forty-eight hours defines severe disease. Interpret renal findings with resuscitation and other organ systems.
  • Cardiovascular: Systolic blood pressure $< 90\text{ mmHg}$ refractory to intravenous fluid challenge.

Primary references (checked 7 October 2026): ASGE cholangitis guidance.