Primary peritonitis

　　1. Etiology

　　The etiology of primary peritonitis is mainly bacterial infection, so the cause is easy to find. The main pathogenic bacteria are mostly Gram-negative bacteria. Commonly seen are Escherichia coli, Streptococcus pneumoniae, Streptococcus, Klebsiella pneumoniae, and a few are Staphylococcus aureus and anaerobic bacteria.

　　The routes of bacterial spread:

　　1. Blood-borne infection accounts for the majority. Streptococci and pneumococci may come from the blood-borne transmission of respiratory or urinary tract infections.

　　2. Ascending infection, such as female genital inflammation, can directly spread upwards through the fallopian tube to the peritoneal cavity.

　　3. Direct diffusion to the peritoneal cavity from adjacent tissues or organs infected, such as lung, pancreas, or urinary system infections, where bacteria can spread through the visceral peritoneum into the peritoneal cavity.

　　4. Bacterial spread through the intestinal wall into the peritoneal cavity.

　　Second, Pathogenesis

　　The causes and mechanisms of why patients with liver cirrhosis and ascites are prone to SBP are as follows:

　　1. Patients with liver cirrhosis have low liver function and weakened defense mechanisms, making it easier for invasive bacteria to cause disease. It is manifested as:

　　(1) Low function of the liver reticuloendothelial system, with reduced activity of phagocytes.

　　(2) Low and disordered immune status, with a decrease in opsonins such as complement and fibronectin in the blood, and a decrease in the concentration of IgG, IgM, and complement in the ascites.

　　(3) Weakening of the abdominal defense mechanism: In patients with liver cirrhosis and ascites, the protein content of the ascites is low, opsonins are scarce, and a large amount of ascites also reduces the opportunity for phagocytes to contact bacteria, resulting in a decreased ability to kill bacteria.

　　(4) The formation of ascites restricts diaphragmatic movement and reduces its elimination capacity.

　　2. Patients with liver cirrhosis may develop collateral circulation due to portal hypertension, portal-systemic shunting, allowing bacteria in the blood to enter the systemic circulation without passing through the liver or being eliminated by the reticuloendothelial system.

　　3. Patients with liver cirrhosis may develop portal hypertension-related enteropathy due to portal hypertension, intestinal mucosal congestion and edema, leading to the destruction of the intestinal mucosal barrier and increased permeability. Moreover, there is excessive bacterial proliferation in the small intestine, which leads to the easy penetration of bacteria from the intestinal mucosa into the peritoneal cavity or through submucosal lymphatics into the peritoneal lymph nodes and blood circulation. This enteric infection is currently considered to be the main bacterial source for the occurrence of SBP.

　　4. Other factors such as variceal bleeding in patients with liver cirrhosis, bleeding from portal hypertension-related gastric disease, and emergency endoscopic examination for bleeding all increase the opportunity for bacterial infection.

　　Primary peritonitis has a widespread abdominal cavity infection, which can affect the entire abdomen. Pus can spread between intestinal loops, with the intestinal wall congested and edematous, losing its luster. In long-standing cases, pus crusts may appear on the intestinal wall. Infections with Staphylococcus aureus or Escherichia coli tend to have localized peritoneal inflammation, with thick, yellow pus without an odor. In infections with hemolytic streptococcus, no纤维素 formation occurs between the intestines, and the pus is thin, odorless. Pneumococcal infection results in the formation of more纤维素 between the intestines, with thick, pale yellow-green pus, leaving intestinal adhesions after cure.

　　A portion of patients may experience deterioration in liver function, leading to hepatic encephalopathy, and even death. If peritonitis is not treated promptly and effectively, multiple organ failure will occur rapidly. The loss of fluid into the peritoneal cavity and intestines can lead to severe dehydration and electrolyte imbalance, causing the patient to exhibit a mask-like expression (Hippocratic facies), and may result in death within a few days. Adult respiratory distress syndrome may also appear rapidly, followed by renal failure, liver failure, and disseminated intravascular coagulation.

　　Pus in the abdominal cavity occurs in the pelvic cavity, subdiaphragmatic space, left or right colonic pericolic space, subhepatic space, and between intestinal loops. It must be found through clinical examination, ultrasound (useful for examining pelvic or subhepatic abscesses), CT (most effective for examining subdiaphragmatic abscesses), and sometimes laparotomy. Percutaneous catheter drainage under the guidance of ultrasound or CT is often possible.

　　The formation of adhesions or bands is a late complication, often causing obstruction in the future.

　　The main symptom is sudden onset of acute abdominal pain, the location is not fixed. Women are more common with lower abdominal pain due to bacteria from the reproductive organs, and the spread is generally fast. Some can reach the whole abdomen, and some are always limited to the lower abdomen. The pain is generally bearable. It is often accompanied by gastrointestinal irritation symptoms, such as nausea and vomiting, and there are also cases of intestinal paralysis, but the bowel sounds do not disappear completely. Examination may find elevated body temperature, rapid pulse, and generally not very serious poisoning symptoms. The abdomen is often bloated, with muscle tension in the abdomen, but not rigid, significant tenderness and rebound pain, and the percussion sound is often positive for abdominal effusion. The number of blood leukocytes increases, and the percentage of neutrophils is almost always elevated.

　　1. Clinical characteristics

　　The clinical characteristics of this disease are fever, abdominal pain, peritoneal irritation sign, and elevated white blood cell count. However, about half of the patients have hidden clinical manifestations. Some patients with liver cirrhosis may have a sudden increase in ascites in a short period of time, resistance to diuretics, occurrence of hepatorenal syndrome, hepatic encephalopathy, and other early manifestations, which should be paid attention to.

　　(1) There is often an upper respiratory tract infection before the onset, or it occurs in kidney disease, scarlet fever, liver cirrhosis ascites, and low immunity;

　　(2) The main symptom is sudden onset of acute abdominal pain, the initial location is not clear, and it quickly spreads to the whole abdomen;

　　(3) Accompanied by nausea and vomiting, fever, rapid pulse, systemic symptoms of poisoning;

　　(4) Abdominal distension, general muscle tension of the abdomen, tenderness and rebound pain, decreased or absent bowel sounds.

　　2. Clinical typing

　　(1) The disease is divided into mild and severe types according to the severity of the disease. The mild type has a slow progression of the disease, mild abdominal pain, body temperature of 37.5～38.5℃, no obvious signs of poisoning, mild muscle tension in the abdomen, mild abdominal distension, tenderness, decreased bowel sounds, white blood cell count of 12×109～20×109/L. The severe type has an acute onset, body temperature above 39℃, abdominal distension, marked tenderness and rebound pain, white blood cell count of 20×109～60×109/L, obvious systemic poisoning, which can lead to death.

　　(2) Another classification method, according to the different pathological changes and clinical manifestations of primary peritonitis, is divided into common type, shock type, hepatic encephalopathy type, refractory ascites type, and asymptomatic type, etc., a total of 5 types.

　　①Common type: mild congestion and edema of the peritoneum and intestinal wall, without obvious pus film, a small amount of thin, odorless yellowish pus in the abdominal cavity. Clinically, there is mild abdominal pain, body temperature of 37.5～38.5℃, mild muscle tension in the abdomen, tenderness is often localized to the lower abdomen or lower right abdomen, decreased bowel sounds, white blood cell count of 10×109～20×109/L, slow progression of the disease, no obvious signs of poisoning, equivalent to mild type.

　　② Shock type: The onset is acute, with body temperature above 39℃, severe abdominal pain, marked abdominal muscle tension, tenderness, rebound tenderness widely, disappearance of bowel sounds, and obvious toxic symptoms. Most patients develop septic shock within a few hours to 1 day after abdominal pain or fever, and it is difficult to correct, which can lead to death.

　　③ Hepatic encephalopathy type: This type is more common in patients with advanced liver cirrhosis complicated with primary peritonitis. This type has fever, not very obvious abdominal pain, but severe jaundice, severe liver function damage, high blood ammonia, and early onset of pre-coma symptoms such as confusion, gradually progressing to coma.

　　④ Refractory ascites type: This type occurs in patients with decompensated liver cirrhosis, with pre-existing chronic ascites. Diuretics can improve symptoms, but after the onset of primary peritonitis, renal function is further damaged, sodium and water retention is exacerbated, leading to the formation of refractory ascites, with poor treatment response. Patients cannot tolerate sodium and water, and there is no diuretic effect, with a very poor prognosis.

　　⑤ Asymptomatic type: accounting for about 7%, with不明显 clinical symptoms, most often diagnosed during routine abdominal puncture.

　　In addition, atypical cases of primary peritonitis account for about 35.5%, with only low fever and slight abdominal distension, without abdominal symptoms and signs.

　　Due to high incidence, mortality, and recurrence rates, prevention is particularly important. Active treatment of the underlying disease and maintaining a good liver function state is an important link in preventing SBP. Various traumatic examinations and treatments should be avoided to reduce the occurrence of sepsis. Antibiotics can be used for prophylaxis if it is necessary to perform traumatic surgery. Ascites is an important condition for infection. Low protein concentration in ascites is conducive to the occurrence and recurrence of the disease, so reducing or eliminating ascites and increasing the protein concentration in ascites is an important preventive measure.

　　High-risk patients, such as those who are insensitive to diuretics or have a high total protein content in ascites

　　1. It can effectively combat infections caused by Gram-negative bacilli from the normal intestinal flora, and no resistance is produced during the period of taking medication.

　　2. The impact on the intestinal anaerobic flora is small, and the normal flora is maintained as much as possible to prevent the implantation of pathogenic microorganisms in the intestines.

　　3. The lowest toxicity of the drug.

　　4. Economically effective. In the past, oral antibiotics that are not absorbed by the gastrointestinal tract (such as vancomycin, polymyxin B, nystatin, neomycin, etc.) and combined sulfonamide drugs have been used, but these drugs have problems with poor tolerance and resistance. Recently, it has been reported that quinolone antibacterial drugs such as FPA, due to their good tolerance and selective elimination of aerobic Gram-negative bacilli without damaging the normal anaerobic bacteria in the intestines, and their ability to significantly increase the total protein and complement C3 in ascites and the concentration of serum complement C3 in patients with liver cirrhosis and ascites, and increase the bactericidal ability of ascites, have been widely used in clinical practice. However, long-term use of FPA will also cause bacterial ecological disorder, so it is believed that patients with liver cirrhosis and ascites should not undergo long-term gastrointestinal antibacterial treatment. For high-risk SBP patients with severe disease and low resistance in chronic liver disease, oral non-absorbable antibiotics (such as FPA, ciprofloxacin, etc.) play an important role in preventing the occurrence of SBP. To prevent interference with the normal intestinal flora, intermittent administration can be adopted, such as taking for 5 to 7 days, stopping for 3 to 5 days, and repeating this process.

　　1. Ascites examination

　　The examination shows ascites to be exudative, straw-colored, and visually turbid, with a positive Levenberg reaction. However, the specific gravity is rarely over 500×10^6/L, with neutrophils >50% or >250×10^6/L, which is of diagnostic significance. The sensitivity is 100%, and the specificity is 96%. In addition, ascites is acidic, with a pH of (7.25±0.06), which is lower than that of simple liver cirrhosis ascites. The pH is negatively correlated with white blood cells and neutrophils.

　　2. Blood culture

　　The positivity rate is approximately 40% to 60%.

　　3. Other laboratory tests

　　(1) Blood leukocyte count > 10×10^9/L, with an increased neutrophil count. In patients with severe splenic hyperfunction, leukocyte counts can be normal or below normal, with platelet and red blood cell counts also below normal.

　　(2) Liver function deterioration: On the basis of low albumin levels, further decline occurs, with the albumin/globulin ratio inverted. The severity depends on the original liver function classification and the severity of abdominal infection.

　　(3) Elevated alanine aminotransferase and aspartate aminotransferase levels, along with increased lactate dehydrogenase, alkaline phosphatase, and gamma-glutamyl transferase, are more pronounced in patients with biliary obstruction or bile stasis.

　　(4) Elevated bilirubin levels are seen in patients with biliary obstruction, cholecystitis, and gallstones, with significantly increased direct bilirubin levels.

　　(5) Elevated blood urea nitrogen and creatinine levels are seen in oliguric patients, indicating renal impairment or the possibility of developing肝肾 syndrome.

　　(6) Blood ammonia levels can increase in most patients after abdominal infection, indicating the need to prevent the occurrence of hepatic encephalopathy.

　　(7) Water and electrolyte imbalance, with some patients having low sodium, low potassium, or metabolic acid-base disturbances as laboratory indicators.

　　(8) Patients with hepatic diabetes may have elevated blood sugar or abnormal glucose tolerance.

　　(9) Positive results in the agglutination test suggest severe infection, with a high possibility of Gram-negative bacterial infection.

　　(10) Alpha-fetoprotein qualitative test can be positive, and quantitative levels can also increase, but it is mostly transient and of low degree, indicating the necrosis and regeneration process of liver cells.

　　Ultrasound, CT, MRI, and other imaging examinations show the imaging characteristics of liver cirrhosis, abdominal inflammation leading to intestinal distension, and intestinal paralysis can be seen with small bowel dilation in X-ray abdominal透视. Sometimes, the colon also presents with distension.

　　1. In terms of diet, it is necessary to avoid spicy and刺激性 food, eat a light diet, and prefer a nutritious and balanced diet. Lean meat, fish, dairy products, vegetables, fruits, and other foods can be eaten appropriately, which is helpful for improving the patient's nutrition and restoring their physical condition.

　　2. It is possible to supplement with traditional Chinese medicine or physical therapy according to the doctor's diagnosis, which can improve the efficacy and relieve and improve symptoms as soon as possible.

　　First, treatment

　　The principle is to control infection, treat the primary disease, and provide symptomatic treatment.

　　1. General support and liver-protective therapy include blood transfusion, infusion of amino acids, human serum albumin, etc., to enhance the body's resistance. Supplement calories, not less than 2000 to 2500 kcal per day, to facilitate the control of inflammation. Supplement a large amount of vitamin C, B vitamins, and vitamin K. Correct imbalances in water and electrolytes in a timely manner.

　　2. The indications for the use of antibiotics are:

　　(1) Even if asymptomatic, ascites white blood cells greater than 1000×10^6/L or neutrophils greater than 500×10^6/L may be present.

　　(2) Clinical symptoms are consistent with primary peritonitis, with ascites white blood cells greater than 500×10^6/L, and neutrophils greater than 250×10^6/L, even if the bacterial culture is negative.

　　(3) Clinical symptoms are typical, even though the ascites cell count has not reached the above standards. The selection of antibiotics can be determined based on the positive bacteria in ascites culture and drug sensitivity. In cases where the bacterial culture has not yet been reported or the culture is negative, medication can be based on clinical symptoms. Considering patients with liver cirrhosis complicated with primary peritonitis, Gram-negative bacteria are more common in infections, so antibiotics against Gram-negative bacteria and those with minimal liver toxicity, such as ampicillin (ampicillin), cefamandole, and others, or more broad-spectrum antibiotics can be used. The duration of medication is determined by the condition, generally requiring about 2 weeks to gradually alleviate the symptoms, followed by a reduction in dosage and maintenance for 2 to 4 weeks based on the condition.

　　3. The use of diuretics includes antisterone 40 to 100 mg, three times a day. For those with unsatisfactory effects, hydrochlorothiazide (dihydrochlorothiazide) 25 mg, three times a day, or rapid-acting furosemide injection can be cautiously added. Close observation is required during the use of diuretics to prevent excessive diuresis leading to electrolyte imbalance and triggering the occurrence of hepatic encephalopathy.

　　4. Local drainage or peritoneal lavage can alleviate inflammatory stimulation and absorption of toxins. Abdominal fluid drainage of 1000 to 2000 ml per day or every other day, followed by the injection of antibiotics, should be stopped after the inflammation improves. This method allows antibiotics to be directly applied to the peritoneum, which may be helpful in controlling infection. It is not advisable to drain too much fluid at a time to avoid triggering hepatic encephalopathy. Alternatively, two tubes can be used: one tube for infusing Ringer's compound sodium chloride solution and 5% glucose 2000 to 3000 ml, and the other tube for draining 3000 to 4000 ml, once per day or every other day. However, peritoneal puncture may lead to secondary infection, so it should be used with caution. Abdominal fluid reinfusion is not recommended for patients with primary peritonitis. For patients with refractory ascites, it is advisable to infuse lost albumin while draining ascites to increase serum albumin levels and improve the albumin-to-globulin ratio.

　　5. Treatment for shock: Patients with primary peritonitis who develop shock indicate a high possibility of Gram-negative bacterial infection. For this infectious shock, the treatment should increase the dose of antibiotics, at least in a dual combination. To enhance the body's resistance, improve liver microcirculation, and use vasoconstrictive pressors with caution, and closely observe the damage to the liver caused by drugs to prevent liver necrosis.

　　6. Treatment for patients with hepatic encephalopathy: Patients with low liver function may further damage their liver function after developing primary peritonitis, leading to hepatic coma. It is important to control the amount of albumin infusion in the early stage of hepatic encephalopathy and can add liver amino acid infusion (branched-chain amino acids), liver amino acid infusion (Gan Nao Qing) and so on. Glutamine sodium, glutamine potassium, arginine, and levodopa can also be used according to the condition.

　　After the diagnosis of primary peritonitis is established, routine use of H2 receptor antagonists or proton pump inhibitors should be considered, such as omeprazole (Losec), lansoprazole (Dakopride), famotidine (Gao Shuda), cimetidine (Taiwamy), etc., taken orally or by intravenous infusion, to prevent stress ulcers or acute gastric mucosal bleeding on the basis of portal hypertension. If upper gastrointestinal bleeding has occurred, these drugs should be administered promptly for rescue treatment.

　　As for the prevention and treatment of hepatorenal syndrome, 24-hour urine volume should be measured and renal function monitored, and treated according to acute renal failure. If abdominal inflammation can be controlled in time, renal function may recover.

　　7. Treatment of the cause should be given and controlled in a timely manner for patients with liver cirrhosis complicated by enteritis, dysbacteriosis, acute cholecystitis, and upper respiratory tract infection. For patients with primary peritonitis and non-cirrhotic liver disease, timely and effective treatment of the primary disease is beneficial for the treatment of primary peritonitis.

　　II. Prognosis

　　The mortality rate of this disease is high, with literature reports ranging from 48% to 95%, with half of the deaths occurring within 5 days after infection, and the majority within the first 3 days. Early diagnosis and treatment lead to better prognosis. The mortality rate of intestinal bacterial infection is higher than that of non-intestinal infection. Poor prognosis is associated with peripheral blood and ascitic fluid neutrophils >80%, total serum bilirubin >130μmol/L, and serum albumin 25×109/L.