Biliary infection

Introduction to biliary infection Biliary tract infections are common in clinical practice and are classified into cholecystitis and cholangitis according to the location of the disease. According to the onset of illness and the course of the disease, it is divided into acute, subacute and chronic inflammation. Biliary tract infection and cholelithiasis are causal relationships. Cholelithiasis can cause biliary obstruction, leading to bile stasis, bacterial reproduction, and biliary infection. Repeated episodes of biliary infection are important pathogenic factors and triggering factors for gallstone formation. Most patients have had gallbladder disease before the attack. The typical onset of an acute attack is a sudden onset of paroxysmal cramps in the right upper quadrant, often after a meal, after getting greasy food, or at night. The pain is often radiated to the right shoulder, shoulders and back. With nausea, vomiting, anorexia and other gastrointestinal symptoms. The ultimate treatment for acute calculous cholecystitis is surgery. The timing of surgery and the choice of surgical procedure should be based on the patient's specific circumstances. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: cholecystitis

Causes of biliary infection

Acute cholecystitis (35%):

(1) Acute calculous cholecystitis

The main cause of acute calculous cholecystitis.

1 cystic duct obstruction: stones can be suddenly blocked or incarcerated in the cystic duct or gallbladder neck, the incarcerated stones also directly damage the mucosa of the compression site caused by inflammation, resulting in obstruction of bile discharge, bile retention, bile concentration. High concentrations of bile salts are cytotoxic, causing damage, aggravating mucosal inflammation, swelling, and even necrosis.

2 bacterial infection: mostly secondary infection, pathogenic bacteria can retrograde into the gallbladder through the biliary tract, or enter the gallbladder through the blood circulation or lymphatic pathway. Bile or gallbladder wall bacteria culture positive accounted for 50% to 70%. The pathogenic bacteria are mainly Gram-negative bacilli, of which Escherichia coli is the most common, and other enterococcus, Pseudomonas aeruginosa and the like. Anaerobic infections are also more common. Recently, it has been reported that Helicobacter pylori (HP) DNA is detected in the bile of 30% gallstone patients, indicating that the digestive tract bacteria through the duodenal papillary countercurrent is an important way of biliary infection.

3 Other factors: Clinical and animal experiments have confirmed that simple gallbladder obstruction does not necessarily lead to acute cholecystitis, such as hydronephrosis. Animal experiments have confirmed that after the cystic duct obstruction, if there is pancreatic juice, gastric juice or concentrated bile sweat in the gallbladder cavity, it can cause acute inflammation.

Pathology of acute calculous cholecystitis

At the beginning of the lesion, cystic duct obstruction, gallbladder enlargement, increased pressure, mucosal congestion and edema, and increased exudation are called acute simple cholecystitis. If the obstruction is not relieved or the inflammation is not controlled at this time, the lesion spreads to the whole layer of the gallbladder wall, and the wall of the cyst is thickened, the blood vessels are dilated, and even the serosal surface has cellulose and purulent exudate, which becomes acute suppurative cholecystitis. If the gallbladder obstruction is still not relieved, the pressure in the gallbladder continues to rise, the wall tension of the gallbladder is increased, and the blood vessel is stressed, causing the gallbladder ischemic gangrene, which becomes gangrenous cholecystitis. Perforation of the gangrene gallbladder often occurs, and perforation occurs mostly at the bottom of the gallbladder and the neck. If the cystic duct obstruction is removed during the course of the disease, the inflammation can gradually subside, and most of the tissue restores the original structure. Such as repeated attacks, gallbladder wall fibrous tissue hyperplasia, scarring, gallbladder mucosa disappeared, showing chronic cholecystitis changes, and even atrophy. In acute cholecystitis, the pus in the gallbladder can be rushed to the bile duct and pancreatic duct, causing cholangitis or pancreatitis. Acute cholecystitis due to gallstone compression and inflammatory infiltration, can also break through to the surrounding organs such as the duodenum to form the gallbladder gastrointestinal tract sputum, and the acute inflammation symptoms quickly subsided.

(2) acute acalculous cholecystitis

Acute acalculous cholecystitis refers to the obvious acute inflammation of the gallbladder without the presence of stones. It is rare in clinical practice, and the incidence rate accounts for 4% to 8% of acute cholecystitis. In recent years, its discovery rate has increased. The cause is not well understood and may be due to a variety of factors. The disease is prone to severe trauma, burns or surgery; it is also easy to occur in critically ill patients, such as sepsis, nodular polyarteritis, lupus erythematosus, multiple blood transfusions and after delivery; malignant tumors, etc. Compression of non-calculus factors causes cystic duct obstruction. Long-term TPN is easy to be complicated by this disease, and the lack of rheumatoid contraction of gallbladder caused by CCK stimulation causes gallbladder bile stasis to play an important role in the onset. Viscous bile and biliary mud can stimulate the gallbladder epithelium to secrete inflammatory mediators such as prostaglandins and interleukins, causing inflammation of the gallbladder, obstruction of venous and lymphatic drainage, ischemia and necrosis. In surgery, trauma, burns, severe infection, the patient may have hypotension and tissue hypoperfusion at different degrees and different times. The gallbladder may also be damaged by hypoperfusion, resulting in mucosal erosion, increased bile salt concentration, and gallbladder wall. Damaged. Bile stasis is also beneficial for bacterial reproduction and infection. Acute acalculous cholecystitis is the same as acute calculous cholecystitis. Acute acalculous cholecystitis, if not treated promptly, develops rapidly, and the incidence of gallbladder necrosis and perforation is high, which may be related to the inherent features or delay in diagnosis and treatment.

Chronic cholecystitis acute cholecystitis (25%):

Chronic cholecystitis due to repeated stimulation of inflammation, stones, etc., the gallbladder wall has different degrees of explosive cell infiltration, fibrous tissue hyperplasia, thickened wall, adhesion to surrounding tissues and other chronic inflammation. In severe cases, the scar of the gallbladder wall is formed, and different degrees of atrophy may occur. Even the gallbladder has only the size of the thumb, which is closely attached to the liver bed and completely loses its function.

Acute obstructive suppurative cholangitis acute cholecystitis (25%):

The basic pathological changes of acute obstructive suppurative cholangitis are complete obstruction of the bile duct and purulent infection of the bile duct. The obstruction site can be in the extrahepatic and/or intrahepatic bile duct. Under normal circumstances, a small amount of bacteria entering the liver through the portal vein can be swallowed by the mononuclear-phagocytic system of the liver. Occasionally, because the normal defense mechanism fails to prevent bacteria from entering the bile, or the bacteria flow back from the intestine into the biliary tract, such as the biliary system intact, the bile flow is sufficient to remove bacteria from the bile. Conversely, when the bile duct is obstructed, the bacteria in the bile will multiply and cause cholangitis. After biliary obstruction, the bile duct pressure increased, the bile duct expanded above the obstruction, the wall thickened, the bile duct mucosa congestion and edema, inflammatory cell infiltration, mucosal epithelial erosion and shedding, forming ulcers. Liver congestion is swollen. Under light microscopy, hepatocytes were swollen and degenerated, inflammatory cells infiltrated in the portal area, and cholestasis in the bile duct. A large piece of necrosis occurs in the liver cells at the end of the lesion, and the bile duct can be broken to form a bile duct portal vein, which can form multiple abscesses in the liver and cause biliary bleeding. Hepatic sinus expansion, endothelial cell swelling, containing bile pigment granule thrombus (or cholestasis thrombosis), a large number of bacteria and toxins can enter the systemic circulation through the hepatic vein to cause systemic suppurative infection and multiple organ dysfunction.

The flow of bacteria into the bloodstream is related to the pressure in the biliary tract. When the pressure in the biliary tract exceeds 1.96 kPa (20 cm H ₂ O), there is a possibility of bile blood reflux; when it exceeds 2.45 kPa (25 cm H ₂ O), the blood culture positive rate is significantly higher than the lower bile pressure. After the radiolabeled cells are injected into the biliary tract, the bacteria can appear in the peripheral blood when the intra-biliary pressure slightly exceeds the secretion of the liver and bile. The bacteria in the blood are mainly Gram-negative bacteria (Escherichia coli, Klebsiella, Proteus, Pseudomonas) and Gram-positive bacteria (Streptococcus faecalis, Enterococcus); common with anaerobic infections. Among the pathogenic bacteria, a single bacterial infection accounts for about 40%, two bacterial infections account for 40%, and three or more bacterial infections account for 20%.

Biliary infection prevention

(1) pay attention to strengthen nutrition, eat attention to high sugar, high protein, high vitamin, low fat, easy to digest diet.

(2) When taking non-surgical treatment, attention should be paid to the changes of the condition. If the body temperature exceeds 39 degrees, the upper abdominal cramps should be notified to the medical staff. When taking the Chinese medicine, pay attention to observe the presence or absence of stones in the feces.

(3) Emergency patients should receive fasting and intravenous infusion, and pay attention to the location and nature of abdominal pain, whether there is chills, high fever, shock and so on. Cooperate with preoperative skin preparation, blood matching, etc.

(4) When itching, pay attention to keep the skin clean, bathe and change clothes, and receive intramuscular vitamin K1.

(5) Actively treat diseases of the biliary system and eat less high-fat and high-cholesterol foods.

Biliary tract infection complications Complications cholecystitis

The main causes of death in patients with acute severe cholangitis are severe development of sepsis, toxic shock, biliary liver abscess, biliary bleeding, and multiple organ failure.

At the beginning of the lesion, cystic duct obstruction, gallbladder enlargement, increased pressure, mucosal congestion and edema, and increased exudation are called acute simple cholecystitis. If the obstruction is not relieved or the inflammation is not controlled at this time, the lesion spreads to the whole layer of the gallbladder wall, and the wall of the cyst is thickened, the blood vessels are dilated, and even the serosal surface has cellulose and purulent exudate, which becomes acute suppurative cholecystitis.

If the gallbladder obstruction is still not relieved, the pressure in the gallbladder continues to rise, the wall tension of the gallbladder is increased, and the blood vessel is stressed, causing the gallbladder ischemic gangrene, which becomes gangrenous cholecystitis. Perforation of the gangrene gallbladder often occurs, and perforation occurs mostly at the bottom of the gallbladder and the neck.

Such as repeated attacks, gallbladder wall fibrous tissue hyperplasia, scarring, gallbladder mucosa disappeared, showing chronic cholecystitis changes, and even atrophy.

Symptoms of biliary tract infections Common symptoms Acute abdomen high fever chills jaundice abdominal pain sudden upper right abdominal cramps

First, acute cholecystitis

Clinical manifestations of acute calculous cholecystitis

More common in women, the incidence of men and women in the north changes with age, the ratio of men to women before the age of 50 is 1:3, after the age of 50 is 1:1.5. Most patients have had gallbladder disease before the attack. The typical onset of an acute attack is a sudden onset of paroxysmal cramps in the right upper quadrant, often after a meal, after getting greasy food, or at night. The pain is often radiated to the right shoulder, shoulders and back. With nausea, vomiting, anorexia and other gastrointestinal symptoms. If the lesion develops, the pain can turn into persistence and paroxysmal aggravation. Almost every acute attack has pain, and if there is no pain, the disease can be basically ruled out. Patients often have mild fever, usually without chills. If there is obvious chills and high fever, it indicates that the condition is aggravated or complications have occurred, such as gallbladder effusion, perforation, etc., or combined with acute cholangitis. 10% to 25% of patients may have mild jaundice, which may be due to biliary pigment entering the circulation through the damaged gallbladder mucosa, or Oddi sphincter spasm caused by inflammation. Or jaundice is heavier and persistent, indicating that there is a common bile duct stone and obstruction may be.

Clinical manifestations of acute acalculous cholecystitis

Acute acalculous cholecystitis is more common in men, with a male to female ratio of 1.5:1. The clinical manifestations are similar to those of acute calculous cholecystitis, but the symptoms and signs such as pain are often in patients with acute acalculous cholecystitis, and only 50% of those diagnosed correctly before surgery. A full meal or greasy food can induce an acute attack of the disease. Improving awareness and vigilance against acute acalculous cholecystitis is the key to early diagnosis of this disease. In patients with acute illness, patients with severe trauma, post-operative and long-term TPN have right upper quadrant pain, and this disease should be considered when fever is unknown.

Second, chronic cholecystitis

Chronic cholecystitis is often not typical. Most patients have a history of biliary colic. Afterwards, they have gastrointestinal symptoms such as oily food, abdominal distension, and belching. They have pain in the right upper abdomen and shoulder and back, but less chills, high fever and jaundice. At the time of physical examination, there was mild tenderness and discomfort in the gallbladder area of the right upper quadrant, and the Murphy sign was positive.

Third, acute obstructive suppurative cholangitis

In the past, patients had a history of biliary tract disease and a history of biliary tract surgery. The disease has a rapid onset and the disease progresses rapidly. In addition to the Charcot triad (abdominal pain, chills, fever, jaundice) with general biliary tract infection, this disease can also show signs of shock and nervous system depression, namely the Reynolds five-link. At the beginning of the onset, there is chills and fever, and in severe cases, there is a significant chill, and the body temperature continues to rise. The pain varies according to the obstruction site, the extrahepatic obstruction is obvious, and the intrahepatic obstruction is lighter. The vast majority of patients may have more obvious jaundice, but if only one side of the hepatic bile duct obstruction may not appear jaundice, the patient after biliary drainage is less jaundice. Nervous system symptoms are mainly manifested as apathy, lethargy, unconsciousness, and even coma; when combined with shock, it can also be expressed as agitation, paralysis, and so on. The patient's body temperature often continues to rise by 39 to 40 C or higher during physical examination. The pulse is fast and weak, up to 120 beats / min, lower blood pressure, acute acute illness, subcutaneous ecchymosis or generalized hair loss. There are different ranges and degrees of tenderness or peritoneal irritation under the xiphoid and right upper abdomen; there may be hepatomegaly and pain in the liver area; sometimes the enlarged gallbladder can be seen.

Examination of biliary infection

First, acute cholecystitis

Examination of acute calculous cholecystitis

Physical examination: There are different degrees and different ranges of tenderness, rebound tenderness and muscle tension in the right upper abdomen, and the Murphy sign is positive. Some patients may have swollen and tender gallbladder. If the development of gallbladder lesions is slow, the omentum can adhere to the gallbladder, forming a painful mass with unclear borders and fixation; if the lesion develops rapidly, the gallbladder is necrotic and perforated, and diffuse peritonitis can occur.

Laboratory tests: 85% of patients have mild leukopenia (1.2 to 1.5 × 10 ⁹ /L). Elevated serum aminotransferase, AKP elevation is more common, 1/2 patients have elevated serum bilirubin, and 1/3 of patients have elevated serum amylase.

Imaging examination: B-ultrasound examination can show enlargement of the gallbladder, thickening of the cyst wall and even "bilateral" signs, as well as stones in the gallbladder. The diagnostic accuracy of the diagnosis of acute cholecystitis is 65% to 90%.

In addition, such as Tc-EHIDA examination, acute cholecystitis due to cystic duct obstruction, gallbladder is not developed, its sensitivity is almost 100%; conversely, if there is gallbladder development, 5% of patients can rule out acute cholecystitis.

Acute acalculous cholecystitis

If there is tenderness and peritoneal irritation in the right upper abdomen, or if the gallbladder is swollen, it will help early diagnosis. B-ultrasound, radionuclide hepatobiliary scanning and CT examination are helpful for early diagnosis.

Second, chronic cholecystitis

B-ultrasound can show that the gallbladder shrinks, the gallbladder wall thickens, and the emptying function can be reduced or disappeared. If the appearance of the stone shadow is more helpful for diagnosis. Oral gallbladder angiography showed that the gallbladder was developed with little or no development and the contractile function was reduced. If the contrast-enhanced gallbladder angiography is still not developed, the diagnosis can be confirmed. However, it needs to be differentiated from peptic ulcer and gastritis. Fiber gastroscopy and upper gastrointestinal barium meal examination are helpful for differential diagnosis.

Third, the examination of acute obstructive suppurative cholangitis

Laboratory examination: white blood cell count increased, more than 20 × 10 ⁹ / L, neutrophils increased, poisoning particles may appear in the cytoplasm. Decreased platelet count, the lowest (10 ~ 20) × 10 ⁹ / L, indicating a serious prognosis; prolonged prothrombin time, liver function is impaired to varying degrees. Impaired renal function, hypoxemia, loss of water, acidosis, and electrolyte imbalance are also common, especially in the elderly and those with shock.

Imaging examination: B-ultrasound is the most practical, can be carried out at the bedside, can understand the location of biliary obstruction and the nature of the lesion, as well as the expansion of the bile duct inside and outside the liver, which is very helpful for diagnosis. If the patient's condition permits, a CT scan may be performed if necessary.

Diagnosis and diagnosis of biliary tract infection

diagnosis

According to the typical clinical manifestations, combined with laboratory imaging examination, the diagnosis is generally no difficulty.

Differential diagnosis

Attention should be paid to the identification of peptic ulcer perforation, acute pancreatitis, high appendicitis, liver abscess, colonic hepatic carcinoma or diverticulum perforation, as well as right pneumonia, pleurisy and hepatitis.

Chronic cholecystitis needs to be differentiated from peptic ulcer and gastritis.

Diagnosis of acute obstructive suppurative cholangitis: Diagnosis can often be made in combination with clinically typical five-link manifestations, laboratory and imaging examinations. For those who do not have a typical five-link, when the body temperature continues to be above 39C, the pulse is >120 beats/min, and the white blood cells are >20×10E9/L. When the platelets are lowered, it should be considered as acute obstructive suppurative cholangitis.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.