acute obstructive suppurative cholangitis
Introduction
Introduction to acute obstructive suppurative cholangitis Acute obstructive suppurative cholangitis is caused by acute obstruction of the bile duct and purulent infection. It is a serious type of biliary infection, also known as acute severe cholangitis. This disease is more common in China. Bile duct stones are the most common obstructive factors, and others include tumors, inflammatory stenosis, and aphids. Pathogenic bacteria causing purulent infections include Gram-negative bacilli such as Escherichia coli, Proteus, Aerogen, and Pseudomonas aeruginosa, and anaerobic bacteria are also common; if mixed infection, the condition is more serious. Clinical manifestations: Most patients have a history of biliary tract disease. Generally, the onset is rapid, and there is sudden pain or cramps under the xiphoid or upper right abdomen, followed by chills, high fever, nausea, and vomiting. The condition often develops rapidly, and sometimes symptoms such as indifference, lethargy, and coma have occurred before the jaundice has occurred. If it is not treated effectively, it will continue to develop, and there will be general purpura, hypotension shock, acute respiratory failure and acute renal failure. In severe cases, it can die in a short period of time. Check the patient's body temperature is usually up to 40 ° C or more, the pulse rate is 120 ~ 140 beats / min, blood pressure is reduced, breathing is shallow. There are tenderness and muscle tension under the xiphoid process, hepatomegaly, sputum pain in the liver area, and sometimes a swollen gallbladder. Laboratory tests for white blood cell counts and neutrophils were significantly elevated. Many patients developed metabolic acidosis and decreased blood oxygen partial pressure. basic knowledge The proportion of illness: 0.28% Susceptible people: no special people Mode of infection: non-infectious Complications: renal failure, diffuse intravascular coagulation
Cause
Causes of acute obstructive suppurative cholangitis
(1) Causes of the disease
The disease is characterized by acute pyogenic infection and empyema on the basis of biliary obstruction, biliary hypertension, a large amount of bacterial endotoxin into the blood, resulting in multiple strains, strong virulence, anaerobic and aerobic mixed septicemia , endotoxemia, azotemia, hyperbilirubinemia, toxic hepatitis, septic shock and multiple organ failure, etc., including septic shock, biliary liver abscess, sepsis Sepsis and multiple organ failure are the three main causes of death in patients. The etiology and pathogenesis are not fully understood, and are mainly related to the following links.
1. Bacterial infection in the bile duct
The tight junction between the Oddi sphincter at the distal end of the normal bile duct and the hepatocytes on both sides of the proximal capillary bifurcation constitutes an anatomical barrier between the intestinal tract and the biliary tract, bile flow and blood flow; physiological bile flow hinders the retention of bacteria on the bile duct mucosa; At physiological concentrations, bile salts can inhibit the growth of intestinal flora; liver Kupffer cells and immunoglobulins can form an immune defense barrier, so there is no bacteria in normal human bile, when lesions occur in the biliary system (such as stones, mites, stenosis) , tumor and cholangiography, etc., can cause a sharp increase in the number of bacteria in the bile, and excessive reproduction in the biliary tract, the formation of persistent biliary disease, it is currently believed that bacteria can also enter the biliary tract through the lymphatic, portal or hepatic artery, AOSC The positive rate of bile bacterial culture can be as high as 95.64%-100%. When the biliary acute suppurative infection is surgically removed, the bacteria in the bile still exist for a long time after the clinical cure. The cause and mechanism of the bile is difficult to purify. It is very clear that the majority of the bacteria are intestinal-derived bacteria, and the positive rate of aerobic gram-negative bacilli is the highest, of which the large intestine The most common bacterium is Escherichia coli, Escherichia coli, Escherichia coli, Aerogen, Pseudomonas aeruginosa, Proteus and Klebsiella, and Gram-positive cocci are Streptococcus faecalis, pneumococci And staphylococcus are more common, with the improvement of culture and separation technology, the detection rate of anaerobic bacteria in bile is significantly increased, the positive rate can reach 40% to 82%, and the strain is also consistent with the intestinal flora, mainly for the class. Bacillus, which is a common bacterium of the genus Bacteroides fragilis, Clostridium, aerobic and anaerobic mixed bacteria is a bacteriological feature of AFC. The bacteria produce a large number of strong toxins, which are caused by severe viral infection, shock and multiple organ failure. The important reason is that bacteria is an essential factor in the pathogenesis of acute cholangitis, but not in patients with bilirubin. Recently, many clinical and experimental studies have shown that the severity and mortality of sepsis are not completely dependent on The type and virulence of invading microorganisms.
2. Biliary obstruction and elevated bile pressure
There are many reasons for biliary obstruction. The common causes in China are: stones, parasitic infections (aphids, Chinese branch sinus), fibrous stenosis, and other rare causes of obstruction: anastomotic stoma after biliary anastomosis Stenosis, iatrogenic bile duct injury, congenital intrahepatic bile duct cystic dilatation, congenital pancreaticobiliary confluence, duodenal papillary diverticulum, primary sclerosing cholangitis, various biliary instruments, etc. Western countries have more common bile duct stones and tumors around the ampulla. The intraductal hypertension caused by biliary obstruction is the primary factor in the development, progression and deterioration of AFC. Animal experiments have shown that the common bile duct of the dog is ligated into the bile duct. Injecting Escherichia coli, the dog developed high fever within 24 hours and died within 2 days. If the same amount of Escherichia coli was injected into the bile duct of the unligated common bile duct, the animal did not develop symptoms. The experiment also proved that when the bile duct pressure> At 2.9 kPa (30cmH2O), bacteria and their toxins can flow back into the blood and cause clinical infection symptoms. The more complete the obstruction, the higher the intra-barial pressure, the incidence of bacteremia and endotoxemia. The more obvious, under the continuous high pressure of the bile duct, the damage of the gallbladder-blood barrier is the premise of the bacteria in the biliary tract to flow into the bacteremia of the blood. By retrograde injection of various tracer substances into the biliary tract, by means of light microscopy, electron microscopy and nuclides. Possible pathways for regurgitation of the biliary tract system under biliary hypertension have been shown:
1 Hepatocyte reflux: When biliary obstruction and bile stasis, hepatocytes can inhale the components of bile into the cytoplasm of hepatocytes by phagocytosis and transfer them to the gap of Disse.
2 by hepatocyte bypass reflux, clinical observation also found that many AFC patients for bile duct decompression, when the discharge of high-pressure bile, blood pressure quickly rebound and pulse rate slowed down, it is obviously difficult to use simple septic shock reasonable explanation, indicating There are neurological factors involved.
3. Endotoxemia and the role of cytokines
Endotoxin is a lipopolysaccharide component of the cell wall of Gram-negative bacteria. Its toxicity is present in lipid A. Endotoxin has complex physiological activities and plays an important role in the pathogenesis of AOSC.
(1) Endotoxin directly damages cells, causes white blood cells and platelets to aggregate, endotoxin mainly damages platelet membrane, and can damage the intima of the blood vessels, so that fibrin deposits on the intima of the blood vessels to increase vascular resistance, coupled with the release of hepatocyte necrosis. Tissue lectin, and thus the blood coagulation mechanism is seriously hindered, the thrombus can be released after the platelet is destroyed, it can strengthen vasoactive substances such as catecholamine, causing contraction of peripheral blood vessels and changes in pulmonary circulation, platelet aggregation leads to thrombosis in the microcirculation, blocking microvessels, Increases the permeability of capillaries, which can spread throughout vital organs of the body, causing focal necrosis and dysfunction of the lungs, kidneys and liver.
(2) Endotoxin stimulates the macrophage system to produce a polypeptide substance, tumor necrosis factor (TNF), which undergoes a series of harmful effects involving multiple mediators under the action of TNF:
1 TNF activates polynuclear leukocytes to form microthrombus. Thrombosis stimulates vascular endothelial cells to release interleukin and platelet activating factor, which agglutinates platelets and promotes disseminated intravascular coagulation (DIC).
2 Activated polynuclear leukocytes release a large number of oxygen free radicals and a variety of proteases. The former aggravates neutrophils and vascular endothelial cells and increases intravascular coagulation. It also damages tissue cell membranes, mitochondrial membranes and dissolved lysosomes, severely destroying cell structure. And biological function, the latter damages vascular endothelial cells and fibronectin and releases bradykinin, increases vasodilation and permeability, causes tissue edema and reduces blood volume.
3TNF activates arachidonic acid through the catalysis of cyclooxygenase to produce thromboxane and prostaglandins, the former causing vasoconstriction and platelet aggregation, the latter increasing vasodilation and permeability.
4TNF also acts as a lipoxygenase to cause arachidonic acid to produce histamine-effect leukotrienes, which aggravate vascular permeability. During the progression of shock, the tissue is severely ischemia-anoxia, structurally disrupted, and can release a variety of Toxic body fluid factors, such as histamine, serotonin, oxygen free radicals, various proteolytic enzymes, myocardial inhibitors, prostaglandins and endopeptides, further aggravate tissue damage, forming a bacterial toxin, which activates and activates the body. The mutual promotion of the vicious circle involved in the body fluid medium, the exotoxin produced by the intestinal positive cocci, is also involved in the contraction of blood vessels, the dissolution of blood cells and the aggregation of platelets.
(3) Endotoxin activates complement reaction: After complement activation and mass consumption, it loses its biological effects, including inflammatory cell chemotaxis, conditioning and lysing bacteria, thereby aggravating infection and spread, and complement degradation products stimulating basophilic granules. Cells and mast cells release histamine, which aggravates damage to the vessel wall.
(4) Production of immune complexes: The endotoxin produced by some bacteria is antigenic, and the immune complex formed by the action of the antibody is deposited on the endothelial cells of various organs, and a strong immune reaction can occur, causing the cells to undergo metamorphosis. Necrosis, aggravating multiple organ damage.
(5) Oxygen free radical damage to the body: The basic pathological processes of AFC (biliary obstruction, infection, endotoxin shock and organ failure, tissue ischemia/reperfusion) can cause the production of oxygen free radicals and peroxides. The lipid peroxidation of oxygen free radicals changes the flow and liquidity of biofilms, affects the activity of various enzymes embedded in biofilms, changes the ion channels of biofilms, and causes a large amount of extracellular calcium ions to flow in, causing mitochondria and The destruction of lysosomes, oxygen free radicals can also activate alipase, catalyzing the release of arachidonic acid and platelet activating factor, which are chemotactic for leukocytes, thereby causing a large accumulation of white blood cells and aggravating inflammatory reactions. A large number of oxygen free radicals form a vicious circle, causing serious damage to the body tissues and hepatobiliary system.
4. Hyperbilirubinemia
The normal liver secretes bile at a pressure of 3.1 kPa (32 cm H2O). When the bile duct pressure exceeds about 3.43 kPa (35 cm H 2 O), the hepatic capillary bile duct epithelial cells are necrotic and ruptured, and bile flows back into the blood via the hepatic sinus or lymphatic vessels, ie, the bile canal vein. Reflux, bile-binding and unconjugated bilirubin enter the blood circulation in a large amount, causing hyperbilirubinemia with elevated bilirubin. If the bile duct hypertension and severe suppurative infection are not controlled in time, the liver tissue is affected. The damage is more serious, the ability of hepatocyte uptake and binding to unbound bilirubin is drastically decreased, and unconjugated bilirubin is significantly increased. Hyperbilirubinemia is a factor that can aggravate AFC, and its harm is not completely clear. More definitely:
1 progressive increase in bilirubin, can lead to bilirubin deposition in various organs, forming a bile-plug, affecting the function of each major organ.
2 bile acid inhibits the growth of Escherichia coli in the intestine and eliminates endotoxin. When obstructive jaundice, the intestine lacks bile acid, Escherichia coli multiplies and releases a large amount of endotoxin, and the gastrointestinal mucosa of AFC is affected. The damage is aggravated, causing the absorption of bacteria and endotoxin to the portal vein. In addition, the function of removing the bacteria and toxins from the reticuloendothelial system of the liver during obstructive jaundice and bile duct infection is weakened, and the bacteria and toxins in the portal vein are easy to enter the systemic circulation, and the bile is more daring. The extent of endotoxemia.
3 The lack of bile acid in the intestine makes the fat-soluble vitamins unable to be absorbed. Among them, vitamin K is an essential component in the synthesis of prothrombin in the liver, and thus can cause a disorder of blood coagulation.
5. Body response
(1) Abnormal response of the body: It is often noted in clinical practice that the biliary purulent infection of patients seen during surgery is often not exactly the same as the severity of clinical manifestations. It is often difficult to correct sepsis and improve the symptoms of bacterial infection. Prognosis of patients, the above phenomenon suggests that factors other than pathogenic microorganisms must play a dominant role in the pathogenesis of sepsis. In recent years, clinical and animal experimental research data accumulated gradually at the cellular and molecular levels are increasingly revealed. The clinicopathological manifestations of sepsis are the result of abnormal response of the host to various infections and non-infectious injury factors, resulting in acute physiological disorders in the body. The damage of organ tissues caused by serious diseases and secondary infections are important start-ups. Factors, but the multiple mediators of endogenous mediators triggered by various motility drivers are also important in the pathogenesis of sepsis and multiple organ dysfunction.
(2) weakened immune defense function: the damage of systemic and local immune defense system caused by this disease is an important factor affecting the deterioration of infection. Phagocytosis is the most important defense function in human body. Kupffer cells on the wall of hepatic sinus The systemic macrophage system, 70% of the reticuloendothelial system, has a strong ability to scavenge microorganisms, toxins, immune complexes and other macromolecular chemicals, preventing these foreign bodies from entering the blood from the bile duct or from the blood into the bile duct. Important barriers, bile duct obstruction, high pressure and infection can all attenuate the phagocytic function of Kupffer cells. Liver tissue of AFC can cause severe sinusitis and necrosis of liver sinus, plus liver fibrosis caused by repeated acute and chronic alternating infections. Atrophy or biliary cirrhosis, Kupffer cell structure and function are more impaired, plasma opsonin and fibronectin are the humoral mediators that promote the phagocytosis of macrophage system, their blood content decreases during infection It also indirectly reflects the decline of immune function. The cellular and humoral immune mechanisms of patients with obstructive jaundice are inhibited. The longer the jaundice is deepened, the more immune damage Weight, experiments have also demonstrated that cellular immune function in animals with obstructive impairment, mainly the ability to recognize an antigen is inhibited T lymphocytes, may mediate the cellular immune deficiency or related to some kind of inhibitor.
(two) pathogenesis
The location and extent of the lesion are related to the location, extent, completeness, duration, bacterial virulence, patient's constitution, nutritional status, complications, and timely treatment.
When the bile duct acute suppurative infection is not relieved in time, the inflammatory sensation is rapidly aggravated and spreads to the surrounding liver tissue, causing all the peribiliary septic hepatitis around the obstruction, and then forming multiple majority due to multiple focal necrosis and liquefaction. Sexual micro-hepatic abscess, hepatic bile ducts at all levels may also be severely degenerated due to tube wall, gangrene or perforation, high-pressure purulent bile directly into the liver tissue, accelerate the development of hepatitis and abscess formation.
The microabscess continues to develop or expand into an abscess of varying size within the liver. The superficial can often self-destruct and break into the adjacent body cavity or tissue to form a purulent infection or abscess outside the liver. , localized or diffuse suppurative peritonitis, can also break through the diaphragm and occur in pericardial empyema, empyema, pleural lung and bronchial purulent and abdominal wall abscess, bile duct obstruction caused by extrahepatic bile duct or gallbladder gangrene, perforation caused by biliary Peritonitis is also more common, and the pancreatic duct pressure is increased due to abdominal obstruction, which can be complicated by severe acute pancreatitis.
During the development of liver abscess, it can also corrode and damage the vessel wall (mostly portal vein or hepatic vein branch). If the abscess is connected with the bile duct, biliary bleeding, biliary wall erosion, ulcer, and blood vessel damage are also the cause of biliary bleeding. one.
Bacteria, toxins, bile duct infections such as gallstones, aphids or eggs, can enter the blood circulation directly through the bile duct - hepatic sinus fistula, bile duct - liver abscess - vasospasm or bile duct - vasospasm, causing severe endotoxemia , multi-strain sepsis and sepsis sepsis, and cause acute suppurative damage of multiple system organs, more commonly found in acute suppurative pneumonia, lung abscess, interstitial pneumonia, pulmonary edema, nephritis, renal cortical and tubular epithelial degeneration Necrosis, myocarditis, pericarditis, splenitis, encephalitis, gastrointestinal mucosal congestion, erosion and hemorrhage, etc. These severe systemic infections are the pathological basis for severe illness, difficulty in reversing shock and multiple organ failure.
It should be noted that the pathological damage of the liver and biliary tract in acute cholangitis and biliary sepsis is varied, but the gross and microscopic pathological changes of the hepatobiliary system are not consistent with the severity of the patient's clinical manifestations, in the biliary tree. There was no constant difference in clinical manifestations between patients with or without purulent bile biliary obstruction. No significant correlation was found between liver histopathological changes and the etiology, clinical manifestations, and laboratory findings of biliary obstruction.
There is no unified classification of AOSC. For the actual needs of medical treatment, it can be classified according to the pathological characteristics, the disease process and clinical manifestation.
Pathological typing
(1) common bile duct obstructive cholangitis: AFC mainly due to obstruction of common bile duct, this type accounts for more than 80%, the pathological range affects the entire biliary system, early biliary hypertension and obstructive jaundice, the disease develops rapidly, very Become a full biliary cholangitis.
(2) intrahepatic biliary obstructive cholangitis: mainly intrahepatic bile duct stones with bile duct stricture cholangitis, because the lesion is often confined to a leaf or a section of the liver, although there is a serious infection, there may be no obvious abdominal pain, Astragalus membranaceus is also often less common. The clinical symptoms of this type of cholangitis are relatively concealed. At the same time, due to bile duct obstruction due to intrahepatic infection, unobstructed drainage, local bile duct dilatation, biliary hypertension and biliary blood barrier are destroyed. Bacterial endotoxin enters the bloodstream and sepsis occurs.
(3) pancreatic cholangitis: acute pancreatitis can occur when acute biliary tract infection, conversely, pancreatitis, pancreatic juice back into the bile duct caused by pancreatic cholangitis or cholecystitis, this type of patient is often pancreatitis and cholangitis At the same time, it increases the complexity and severity of pathology.
(4) biliary reflux cholangitis: after biliary tract or biliary drainage, especially after common bile duct duodenal anastomosis, due to intestinal contents and bacteria into the biliary tract, especially when the biliary tract is obstructed When it occurs, it can cause recurrent reflux cholangitis.
(5) Parasitic cholangitis: clinically common parasitic cholangitis, caused by biliary mites, accounting for 8% to 12% of biliary tract diseases. After the mites enter the biliary tract, the worms stimulate the common sphincter of the common bile duct. Paroxysmal pain occurs in the patient. Acute suppurative cholangitis can occur due to bacterial infection and obstruction caused by aphids. S. sinensis passes through the first host freshwater snail and the second host freshwater fish and shrimp, which are ingested by the human body during development. Parasitic in the bile duct and gallbladder, such as causing biliary obstruction and infection, acute cholangitis can occur, severe cases can occur obstructive jaundice and liver abscess, liver cysticercosis after breaking into the biliary tract, acute cholangitis can also occur, serious Biliary tract infections can cause toxic shock.
(6) iatrogenic cholangitis: the development of endoscopic techniques and interventional treatment, corresponding to some operations such as PTC, PTCD, ERCP, EST, cholangiography through T tube, stone removal through T tube sinus choledochoscopy, etc. The incidence of acute cholangitis is increasing, especially in the case of biliary obstruction or infection.
2. Clinical classification
(1) fulminant: Some AFC can rapidly develop into septic shock and biliary sepsis, and then turn into diffuse intravascular coagulation (DIC) or multiple organ system failure (MODS). The pathological changes of hepatobiliary system are acute cellular Inflammation, the patient quickly develops into a fatal complication.
(2) relapsing type: if the bile duct is formed by stone or aphid with piston-like obstruction or incomplete obstruction, the infection of bile is not smooth, acute, subacute and chronic pathological changes of the hepatobiliary system may alternately occur and continue to develop, and the bile duct hypertension causes the capillary bile duct Inflammation, focal necrosis and diffuse biliary hepatic abscess around the bile duct, the infection can also spread to the larger liver, the outer bile duct wall, causing bile duct wall ulcer and full-thickness necrosis, forming an axillary or perihepatic Abscess, intrahepatic or perihepatic abscess may be a potential lesion of purulent bacteria, causing acute cholangitis to have multiple recurrent pathological processes, gastrointestinal bile duct fistula in the infected foci, which can lead to biliary infection and periodic major bleeding.
(3) Prolonged type: In the case of incomplete obstruction of the bile duct and chronic inflammation, inflammatory granuloma and fibrotic healing occur in the bile duct wall, and then develop into pathological changes such as scar bile duct stricture, biliary cirrhosis and focal hepatic atrophy. These changes are often associated with occult purulent lesions in the liver. In the case of progressive decompensation of liver function, the clinical course of acute suppurative cholangitis is prolonged, eventually developing multiple irreversible pathological lesions of the entire hepatobiliary system. Poor prognosis.
(4) diffuse type: AOSC infection becomes systemic sepsis, due to the spread of infected blood, causing acute suppurative inflammation or abscess formation in organs such as liver, lung, kidney, spleen and meninges, in acute suppurative bile duct Multiple organs and systemic failure occur under recurrent inflammation.
Each of the above types may occur alternately or in combination in the onset of individual patients. Each episode may have individual differences due to urgency, severity, and pathological characteristics. Therefore, each time the patient visits, the individual should be based on the specific circumstances at the time. Processing.
Prevention
Acute obstructive suppurative cholangitis prevention
1. Primary prevention of acute suppurative cholangitis is a serious complication of hepatolithiasis and biliary ascariasis. Therefore, the primary prevention of this disease is mainly for the prevention and treatment of hepatolithiasis and biliary mites. 1 The key to prevention and treatment of hepatolithiasis is to prevent and eliminate pathogenic factors. Patients who have been diagnosed with hepatolithiasis should be highly alert to the occurrence of this disease, especially in the case of concurrent biliary infections. Early use of high-dose sensitive antibiotics to fight infection, pay attention to water, electrolytes and acid-base balance, strengthen systemic support for the treatment of biliary tract infections. Surgery as soon as possible under conditions of the whole body, removing stones and smooth drainage, thus preventing the occurrence of AFC. 2 prevention and treatment of biliary ascariasis. When the mites enter the biliary tract, they cause different degrees of obstruction of the biliary tract. Increases biliary pressure and induces AFC when concurrent bacterial infections occur. In addition, biliary ascariasis is also an important factor in the formation of hepatolithiasis. Therefore, prevention and treatment of biliary ascariasis is an extremely important aspect of preventing AFC, mainly paying attention to drinking water, food hygiene, and prevention and treatment of intestinal ascariasis. Once the diagnosis is diagnosed, if it is diagnosed as biliary ascariasis, it should be treated as soon as possible. Give analgesia, relieve phlegm, control infection, and prompt the mites to withdraw from the biliary tract. In addition, duodenal endoscopy can be performed, and a part of the mites entering the common bile duct can be pulled out of the body by a snare. Surgical treatment is considered when treatment is ineffective.
2. Secondary prevention of AFC The disease develops rapidly and toxic shock can occur soon. Therefore, the secondary prevention of the disease is mainly early diagnosis and early treatment. According to the history of recurrent biliary tract disease, there are high fever, chills, jaundice, systemic poisoning symptoms and signs of peritonitis. Combined with B-ultrasound examination, the diagnosis is not difficult. Once diagnosed, it should actively fight against infection, anti-shock, use sufficient amount of sensitive antibiotics, supplement blood volume, correct acidosis, prevent and treat biliary sepsis, and prepare for emergency surgery. The principle of surgery is to relieve obstruction, decompression biliary tract, and smooth drainage, and strive to be simple and fast. For patients with advanced age and poor general condition, PTCD or transnasal bile duct drainage can be performed first, and surgery should be performed after the general condition is improved. Active systemic supportive and anti-infective measures should still be performed after surgery.
3. Stage-prevention of AFC Early toxic shock and biliary sepsis can occur, if not treated in time, the prognosis is very poor, and the mortality rate is extremely high.
Complication
Complications of acute obstructive suppurative cholangitis Complications, renal failure, diffuse intravascular coagulation
AFC often complicated with multiple system organ failure. The incidence of major complications was highest in renal failure (referred to as renal failure) (23.14%), followed by respiratory failure (referred to as respiratory failure) (14.88%), liver failure (13.22). %), circulatory failure (9.92%) and disseminated intravascular coagulation (DIC) (3.31%). The mortality rate of multiple organ failure was 94.4%, which was significantly higher than the mortality rate of single organ failure (33.3%). The mortality rate of AFC complicated with organ failure was 79.2%. Multiple systemic organ failure associated with AFC is the leading cause of death in AFC. The level of serum total bilirubin is an important factor affecting the occurrence of multiple system organ failure. When serum total bilirubin is >160 mol/L, single organ failure tends to develop into multiple system organ failure.
Symptom
Acute obstructive suppurative cholangitis symptoms common symptoms abdominal pain jaundice biliary obstruction relaxation heat microcirculation disorder abscess oligosperemia blood pressure drop shock
Severe acute cholangitis is a pathological process in which hepatobiliary surgical diseases develop to a serious stage. Its pathogenesis is complicated. The patient's age is different from that of past biliary diseases or surgery. The clinical manifestations are not exactly the same, so you can't simply pursue the so-called typical Symptoms, such as triad or five-link, in order to avoid delay in diagnosis and treatment, the basic clinical manifestations of severe acute cholangitis are consistent with its main pathological process, the first stage has a history of biliary tract disease or biliary tract surgery, on the basis of biliary obstruction and infection Abdominal pain, fever, jaundice and other acute symptoms, but because of the intrahepatic and extrahepatic differences in the biliary obstruction, the degree of abdominal pain and jaundice is very different, and the symptoms of acute biliary tract infection are common to all types of cholangitis, the second Stage due to severe biliary septic inflammation, biliary hypertension, endotoxemia, sepsis, patients with persistent relaxation of heat, or jaundice is increasing, indicating liver function damage, changes in mind, pulse fast and weak, poisoning Symptoms, stage 3 disease progresses to severe stage, microcirculatory disorders, water, electrolytes and acid-base Disorder, the patient showed septic shock, blood pressure decreased, oliguria, internal environment steady state gradually lost compensation, major organ function disorders, the fourth stage was mainly multiple organ system failure, liver, kidney, heart, lung, Gastrointestinal, coagulation, etc. are successively or alternately functionally impaired, which constitutes a serious combination. If the disease progresses further, biliary obstruction and biliary hypertension are not relieved, which endangers the patient's life.
Examine
Examination of acute obstructive suppurative cholangitis
In addition to the old and weak and the body's resistance is very poor, many white blood cell counts are significantly increased, often up to 20 × l09 / L, the degree of rise is directly proportional to the severity of infection, classification see nuclear left shift; biliary obstruction and hepatocyte necrosis Can cause serum bilirubin, urinary bilirubin, urinary bilirubin, alkaline phosphatase, serum aminotransferase, -glutamyl transpeptidase, lactate dehydrogenase, etc., such as elevated serum amylase, Indicates that accompanied by pancreatitis, decreased platelet count and prolonged prothrombin time, suggesting a tendency to DIC, in addition, often hypoxemia, metabolic acidosis, hypokalemia, hypoglycemia, etc., blood culture positive, bacteria The type was consistent with the culture in bile, and the endotoxin concentration in the portal vein and peripheral venous blood was 10 times higher than the normal number (normal value was less than 50 pg/ml).
Patients with severe acute cholangitis were examined for peripheral venous blood platelet count and platelet aggregation rate (AGG). The results showed that platelet count and AGG were significantly decreased in patients with severe acute cholangitis, indicating that platelet volume and aggregation changes are closely related to pathological degree and prognosis. Determination of platelet volume and AGG is important for determining the extent of disease and prognosis.
1.B Ultra
It is the most convenient, quick and non-invasive auxiliary diagnosis method. It can show the extent and extent of bile duct enlargement to estimate the obstruction site. It can be found in stones, aphids, liver abscess larger than lcm diameter, underarm abscess.
2. chest and abdomen X-ray film
Helps to diagnose empyema, pneumonia, lung abscess, pericardial empyema, underarm abscess, pleurisy, etc., patients with reflux cholangitis after biliary anastomosis surgery, abdominal X-ray film can be seen biliary tract gas, upper digestive tract sputum meal Intestinal biliary reflux, abdominal X-ray film can also provide differential diagnosis, such as exclusion of intestinal obstruction and digestive tract perforation.
3.CT scan
AFC CT images can not only see signs of hepatic bile duct dilatation, stones, tumors, liver enlargement, atrophy, etc. There are fashions that can detect liver abscesses. If acute severe pancreatitis is suspected, CT examination can be performed.
4. Endoscopic retrograde biliary drainage (ERBD), percutaneous transhepatic drainage (PTCD) can determine the cause and location of biliary obstruction, but also can be used for emergency decompression drainage, but there are bile juices that aggravate biliary infection or cause infection. The danger of spilling into the abdominal cavity.
5. Magnetic resonance cholangiopancreatography (MRCP)
It can display the whole picture of the intrahepatic biliary tree, the location and extent of the obstruction, and the image is not restricted by the obstruction. It is a non-invasive biliary imaging technique, which has become an ideal imaging examination method. MRCT is better than PTC. Clearer, it can be used for multi-angle and different angle scan observation through 3D angiography (3D MRC), to make up for the deficiency caused by overlapping of tissue images on the plan, the diagnosis rate of obstruction is 100%, and the diagnosis rate of obstruction is up to 95.8%.
Diagnosis
Diagnosis and differentiation of acute obstructive suppurative cholangitis
Diagnostic criteria
According to the typical Charcot triad and Reynold five-link, the diagnosis of AFC is not difficult, but it should be noted that even if the Reynold five-link is not fully established, the clinical situation cannot completely exclude the possibility of this disease. For this reason, in 1983 in Chongqing The Hepatolithiasis Symposium was held to establish the diagnostic criteria in China:
1.Reynold five joints + shock.
2. For those who are not shocked, they should be diagnosed by satisfying 2 of the following 6 items:
1 mental symptoms;
2 pulse > 120 times / min;
3 white blood cell count> 20 × 109 / L;
4 body temperature > 39 ° C or < 36 ° C;
5 bile is purulent or accompanied by a significant increase in biliary pressure;
6 blood culture positive or endotoxin elevation, the application of this diagnostic criteria in clinical can solve the early diagnosis of most patients, but for some patients with atypical clinical performance, when there is shock or blood culture positive results, the condition is extremely serious, The mortality rate is greatly increased. Therefore, the diagnostic criteria of Reynold's five joints and AFC can only reflect the certain development stage of AFC. The clinical manifestations are also related to the number and virulence of bacteria and the immune status of the organism and whether it is timely and appropriate treatment. According to the pathophysiological development stage, the disease is divided into 4 grades: 1 grade: simple AOSC, the lesions are mostly confined to the bile duct, mainly toxemia; grade 2: AOSC with shock, cholangitis aggravated, bile duct purulent Hepatitis development, bile duct, capillary bile duct and hepatic sinus barrier are further impaired, the incidence of sepsis and sepsis is increased; grade 3: AOSC with biliary hepatic abscess; grade 4: AOSC with multiple organ failure, is the late stage of serious infection Performance, this classification is conducive to the choice of disease and treatment options, due to the pathology of acute suppurative cholangitis and acute suppurative hepatic cholangitis Clinical manifestations are different, attention should be identified.
Differential diagnosis
In the differential diagnosis, after detailed information on the history, symptoms, signs, etc., according to the actual characteristics of the patient, it should be done with acute cholecystitis, peptic ulcer perforation or hemorrhage, acute gangrenous appendicitis, esophageal varices bleeding, severe Acute pancreatitis, as well as right pleurisy, right lower lobar pneumonia, etc., in these diseases, it is difficult to have the basic characteristics of ACFC, careful analysis, it is not difficult to draw correct conclusions.
