This is a disease with a relatively high mortality rate among surgical acute abdominal conditions, often secondary to bile duct stones and biliary ascariasis. However, conditions such as bile duct strictures and bile duct tumors can also sometimes lead to this disease. The aforementioned conditions cause bile duct obstruction, gallbladder stasis, and secondary bacterial infections. The pathogenic bacteria almost always originate from the intestines, entering the bile duct retrograde through the ampulla of Vater or via biliary-enteric anastomotic pathways. Bacteria can also enter the bile duct through the bloodstream or lymphatic channels. The primary pathogenic bacteria include Escherichia coli, Klebsiella, Enterococcus faecalis, and certain anaerobic bacteria.

bubble_chart Pathological Changes

On the basis of pre-existing obstructive diseases such as stones, biliary tract infection occurs, leading to congestion and edema of the bile duct mucosa, which exacerbates the obstruction of the bile duct. The bile gradually becomes purulent, and the pressure within the bile duct continuously increases, causing the proximal bile duct to gradually dilate. Under the high pressure of the bile duct containing purulent bile, the liver may enlarge, and the small intrahepatic bile ducts and surrounding liver parenchymal cells may also undergo inflammatory changes. Hepatocytes develop extensive necrosis, leading to the formation of multiple small abscesses within the liver. The bile ducts may also develop ulcers and biliary hemorrhage due to infection and suppuration. The high pressure within the bile duct causes rupture of intrahepatic bile capillaries, allowing purulent bile or even bile thrombi to enter the bloodstream through hepatic sinusoids, resulting in bacteremia and sepsis. In rare cases, pulmonary septic emboli may occur. In the late stage (third stage), a series of pathophysiological changes such as septic shock, hepatic and renal failure, or disseminated intravascular coagulation may occur, which is known as acute obstructive suppurative cholangitis or acute severe cholangitis. Once these pathological changes occur, even if surgical intervention relieves the bile duct hypertension, damage to the liver parenchyma and bile ducts will persist, which underscores the severity of this condition.

The onset is often abrupt, with sudden severe pain in the epigastrium or right upper abdomen, usually persistent. This is followed by shivering and remittent high fever, with body temperature possibly exceeding 40°C. It is often accompanied by nausea and vomiting. Most patients exhibit jaundice, though the severity of jaundice may not correlate with the severity of the condition. Nearly half of the patients show central nervous system depression symptoms such as dysphoria, restlessness, impaired consciousness, lethargy, or even unconsciousness, often accompanied by a drop in blood pressure. This usually indicates that the patient has developed sepsis and septic shock, a critical manifestation of the condition. The body temperature rises, and the pulse rate may exceed 120 beats per minute, with a weak pulse. There is marked tenderness and muscle rigidity in the epigastrium and right upper abdomen. In patients with an intact gallbladder, an enlarged and tender gallbladder and liver are often palpable. The white blood cell count is significantly elevated with a shift to the right, reaching 20,000 to 40,000/mm³, and toxic granules may appear. Serum bilirubin and alkaline phosphatase levels are elevated, and liver function impairment is often indicated by increased GPT and r-GT values. Blood cultures frequently show bacterial growth.

bubble_chart Diagnosis

【Treatment Measures】Based on the typical clinical manifestations of the triad of abdominal pain, chills with high fever, and jaundice—known as Charcot's sign—along with the progression of symptoms such as central nervous system depression and hypotension, the diagnosis of acute suppurative cholangitis is generally not difficult. However, in a minority of patients, such as those with acute suppurative cholangitis complicated by intrahepatic bile duct stones, atypical symptoms like the absence of abdominal pain or jaundice may sometimes lead to delayed diagnosis. In such cases, certain specialized diagnostic methods, such as non-invasive B-ultrasound examinations, can often reveal intrahepatic or extrahepatic bile duct dilation, multiple small liver abscesses, or the presence of bile duct stones. These findings help infer the existence of obstructive pathological changes in the bile ducts, which, combined with clinical manifestations, can aid in diagnosis. Occasionally, additional diagnostic tools like PTC or ERCP may also be employed to assist in the diagnosis.

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The treatment principle is surgical intervention to relieve biliary obstruction, decompress the bile ducts, and drain the biliary tract. However, in the early stages of the disease, such as acute simple cholangitis when the condition is not severe, non-surgical methods may be attempted first. Approximately 75% of patients can achieve stabilization of their condition and control of infection, while the remaining 25% who do not respond to non-surgical treatment and progress from simple cholangitis to acute obstructive suppurative cholangitis should promptly undergo surgical intervention. Non-surgical treatments include the use of antispasmodic, analgesic, and cholagogic medications. A 50% magnesium sulfate solution is often effective, administered at 30–50 ml in a single dose or 10 ml three times daily. Gastrointestinal decompression is also commonly employed. The combined use of high-dose broad-spectrum antibiotics is crucial. Although the antibiotic concentration in bile may not reach therapeutic levels during biliary obstruction, these drugs can effectively treat bacteremia and septicemia. Commonly used antibiotics include gentamicin, chloramphenicol, cephalosporins, and ampicillin. Ultimately, appropriate antibiotics should be adjusted based on blood or bile bacterial cultures and drug sensitivity tests. If shock is present, aggressive anti-shock therapy should be initiated. If the condition shows no significant improvement within 12–24 hours of non-surgical treatment, surgery should be performed immediately. Even if shock is difficult to correct, surgical drainage should still be pursued. For cases that are severe from the outset, particularly those with deep jaundice, timely surgery is essential. The surgical mortality rate remains as high as 25–30%. The surgical approach should aim for simplicity and effectiveness, primarily involving bile duct exploration and drainage. It is crucial to place the drainage tube proximal to the obstruction; drainage distal to the obstruction is ineffective and will not alleviate the condition. If the patient's condition permits, the inflamed gallbladder may also be removed. Once the patient has passed the critical phase, definitive treatment for the biliary lesions can be performed.