Acute obstructive suppurative cholangitis (AOSC) represents a severe stage of acute cholangitis and is also referred to as acute cholangitis of severe type (ACST). The condition arises from a combination of biliary obstruction and bacterial infection. If biliary obstruction is not resolved and the bacterial infection in the bile duct remains uncontrolled during acute cholangitis, AOSC may develop, posing a significant threat to the patient's life.
Etiology
The common causes include malignant tumors and benign biliary conditions causing strictures. In recent years, there has been a growing incidence of cases due to biliary-enteric anastomosis strictures, percutaneous transhepatic cholangiography (PTC), endoscopic retrograde cholangiopancreatography (ERCP) with stent placement, and other interventional procedures.
Pathology
Studies have shown that when the pressure within the bile duct exceeds 15 cmH2O, bacteria labeled with radionuclides can appear in peripheral blood. Bile and lymph cultures are typically negative when ductal pressure is below 20 cmH2O but turn positive rapidly if the pressure exceeds 25 cmH2O. While most bacteria entering the liver along with bile are engulfed by the mononuclear phagocyte system in cases of obstruction, approximately 10% may reverse into the bloodstream, causing bacteremia.
The presence of bile crystals in portal blood and lymphatic vessels indicates that bile, containing bacteria, may directly regurgitate into the bloodstream. This phenomenon, known as "cholehemia," can occur via pathways such as bile canaliculi-hepatic sinusoid fistulas into hepatic veins, pyogenic liver abscess rupture into blood vessels, inflamed biliary ductal mucosa eroding into nearby portal vein branches, or via intrahepatic lymphatic vessels. Bacteria or infected bile entering circulation leads to systemic suppurative infections. Large quantities of bacterial toxins may trigger a systemic inflammatory response syndrome (SIRS), hemodynamic changes, and multiple organ dysfunction syndrome (MODS).
Clinical Manifestations
The condition affects both men and women equally and occurs most frequently in young and middle-aged adults. Many patients have a history of recurrent biliary infections and/or biliary surgeries. In addition to the classic Charcot's triad of acute cholangitis (fever, right upper quadrant pain, and jaundice), patients may present with signs of shock and central nervous system depression, forming Reynolds' pentad.
The onset is often abrupt, and the disease progresses rapidly. It can be categorized into extrahepatic and intrahepatic obstruction. Extrahepatic obstruction is often accompanied by severe abdominal pain, chills with high fever, and noticeable jaundice, while intrahepatic obstruction is characterized mainly by chills with high fever, sometimes with abdominal pain, but relatively mild jaundice. Gastrointestinal symptoms such as nausea and vomiting are common. Neurological symptoms may include lethargy, drowsiness, confusion, and even coma. Shock-associated symptoms may include restlessness, agitation, and delirium.
Physical examination findings often reveal a fever with a remitting or continuous pattern, frequently exceeding 39–40°C. Patients may have rapid, weak pulses and low blood pressure. Cyanosis of the lips and bluish discoloration of nail beds may be observed. Petechiae and subcutaneous ecchymosis may be present on the skin. Tenderness in the epigastric region or the right upper quadrant is often observed, along with signs of peritoneal irritation. Hepatomegaly is common, accompanied by tenderness and percussion pain. Gallbladder enlargement may occur in cases of common bile duct obstruction.
Auxiliary Examinations
Laboratory Tests
White blood cell counts are elevated, often exceeding 20×109/L, with an increased proportion of neutrophils exhibiting toxic granules in their cytoplasm. Liver function is variably impaired, and prothrombin time is prolonged. Arterial blood gas analysis may reveal reduced PaO2 and oxygen saturation, along with metabolic acidosis and water-electrolyte imbalances such as dehydration and hyponatremia.
Imaging Studies
Simple, practical, and convenient imaging methods should be selected based on the clinical situation. Ultrasound, which can be performed bedside, is useful for identifying the site of biliary obstruction, assessing intrahepatic and extrahepatic bile duct dilation, and determining the nature of the lesion. If the patient is stable, CT or magnetic resonance cholangiopancreatography (MRCP) can be utilized. For patients requiring decompressive interventions, such as percutaneous transhepatic biliary drainage (PTBD) or endoscopic naso-biliary drainage (ENBD), PTC or ERCP examinations may be performed.
Treatment
The primary approach is to promptly relieve biliary obstruction and ensure effective drainage. Reducing biliary pressure can temporarily stabilize the patient’s condition, allowing time for further treatment planning.
Non-Surgical Treatment
Non-surgical options serve both as therapeutic measures and as preoperative preparation. The main aspects include:
- Establishing fluid replacement and volume restoration: Replenishment of blood volume is necessary. In addition to using crystalloids for volume expansion, colloid solutions should also be included.
- Antibiotic therapy: Broad-spectrum antibiotics targeting Gram-negative bacilli and anaerobic bacteria are commonly initiated. Empirical therapy typically determines dosage and dosing intervals based on the antibiotic's half-life.
- Correction of water, electrolyte, and acid-base disturbances: Restoring balance in fluid and electrolytes and managing acid-base imbalances is prioritized.
- Management of coagulation dysfunction: Administering vitamin K₁ or fresh frozen plasma can improve coagulation in cases of clotting abnormalities.
- Symptomatic and supportive care: Interventions like temperature control, vitamin supplementation, and general supportive treatments may be utilized.
- Escalation of therapy in the absence of improvement: If the patient does not improve after short-term treatment, measures such as vasopressors to stabilize blood pressure may be necessary, along with corticosteroids to protect cellular membranes, counteract bacterial toxins, and modulate inflammatory responses. Oxygen therapy may also be applied to address hypoxia.
- Emergency biliary drainage if non-surgical methods fail: If the condition does not improve despite the above steps, immediate biliary decompression and drainage are essential alongside ongoing anti-shock management.
Emergency Biliary Decompression and Drainage
Rapid reduction in biliary pressure is critical to preventing further deterioration by halting the reflux of bile or bacteria into the bloodstream. The decompression methods aim to be straightforward and effective, including:
- Common bile duct (CBD) incision and T-tube drainage: This technique can stabilize the condition immediately after decompression. However, in cases of higher intrahepatic bile duct obstruction, this approach may not effectively decrease pressure. For large abscesses encountered during surgery, drainage can be performed, while small multiple abscesses may be addressed through bile duct drainage. Gallbladder fistulization is generally not recommended as it often fails to provide effective drainage.
- Endoscopic nasobiliary drainage (ENBD): ENBD involves a minimally invasive approach that effectively reduces intrabiliary pressure. The catheter can be left in place for two weeks or longer, depending on the patient’s condition. For high-level biliary obstructions, however, the efficacy of ENBD in managing cholangitis is unclear.
- Percutaneous transhepatic cholangial drainage (PTCD): PTCD is technically straightforward and provides timely decompression, offering better outcomes in non-stone-related or proximal bile duct obstructions. However, there is a risk of the drainage tube dislodging or becoming blocked by stones, and coagulation function must be carefully monitored during the procedure.
Follow-Up Treatment
Emergency biliary decompression and drainage alone rarely address the underlying cause of the obstruction, leading to the potential for recurrence. Once the patient’s general condition stabilizes, definitive surgical treatment should be considered within 1–3 months, depending on the etiology.