bubble_chart Overview

Peritonitis is an acute inflammatory response of the visceral and parietal peritoneum to bacterial, chemical, physical, or foreign body damage. Based on the cause, it can be classified into secondary suppurative peritonitis and primary peritonitis. According to the extent of involvement, it can be divided into diffuse peritonitis and localized peritonitis. Due to variations in patient resistance, severity of infection, and the application of treatment measures, these types can transform into one another. Timely identification of the cause, type, and severity of peritonitis, along with active implementation of appropriate treatment measures, is essential to avoid serious complications and save the patient's life.

bubble_chart Etiology

The diseases that cause secondary suppurative peritonitis include: ①Perforation of intra-abdominal organs. The most common is perforation of acute appendicitis, followed by perforation of gastroduodenal ulcers. Others include perforation of gastric cancer, colorectal cancer, gallbladder perforation, inflammatory bowel disease, and perforation of cold-damage disease ulcers, etc.; ②Inflammation of the intestines and intra-abdominal organs, such as appendicitis, diverticulitis, necrotizing enteritis, Crohn's disease, cholecystitis, pancreatitis, and suppurative inflammation of female reproductive organs, etc.; ③Blunt or penetrating abdominal injuries leading to rupture or perforation of intra-abdominal organs; ④Postoperative abdominal contamination or anastomotic leakage; ⑤Mechanical strangulated intestinal obstruction and vascular intestinal obstruction, such as intestinal volvulus, intussusception, closed-loop intestinal obstruction with intestinal necrosis, mesenteric vascular embolism or thrombosis, etc.; ⑥Iatrogenic injuries, such as colon perforation during colonoscopy, gallbladder fistula from liver biopsy or percutaneous transhepatic cholangiography, and small intestine injury after abdominal puncture, etc.

Endogenous bacteria in the gastrointestinal tract are often the pathogens of secondary peritonitis, with Escherichia coli being the most common, followed by Enterococcus, Streptococcus faecalis, Proteus, and Pseudomonas aeruginosa, etc. Studies on anaerobic bacteria show that the number of aerobic and anaerobic bacteria in the ileum is roughly equal a few days before, while the ratio in the colon exceeds 3000:1. Therefore, bacterial peritonitis is often a polymicrobial mixed infection.

Primary peritonitis refers to peritonitis caused by pathogens entering the abdominal cavity via the bloodstream, lymphatic system, intestinal wall, or female reproductive system without an obvious primary infection site in the abdominal cavity. It is much rarer than secondary peritonitis. It commonly occurs in: ①Infants and children; ②Children with nephrotic syndrome; ③Patients with cirrhotic ascites; ④Immunocompromised patients, such as those with kidney transplants or hematologic diseases treated with corticosteroids; ⑤Patients with systemic lupus erythematosus.

The main pathogens of primary peritonitis in children are pneumococci and streptococci, which may invade through the respiratory or urinary tract and spread to the peritoneal cavity via the bloodstream. In adults, it is mostly caused by endogenous bacteria from the intestines. The types of bacteria ascending through the female reproductive tract are more diverse.

bubble_chart Pathological Changes

When the peritoneal membrane is invaded by bacteria or irritated by digestive fluids (gastric juice, intestinal juice, bile, pancreatic juice), the peritoneal membrane becomes congested. Mast cells release histamine and other permeability factors, increasing vascular permeability and causing the exudation of fluid rich in neutrophils, complement, opsonins, and proteins. Bacteria bound to complement and opsonins are phagocytized locally by phagocytes or enter regional lymphatic vessels. Injured mesothelial cells can release thromboplastin, converting fibrinogen into fibrin. Fibrin deposits around the inflammatory lesion, isolating it from the free abdominal cavity and preventing the absorption of bacteria and toxins. If the infection is mild, the body's resistance is strong, and treatment is timely, peritonitis can become localized and even completely resolve. Conversely, localized peritonitis can also develop into diffuse peritonitis. Due to the death of large numbers of neutrophils, tissue necrosis, and the coagulation of bacteria and fibrin, the exudate gradually changes from clear to turbid, becoming purulent. The pus from *large intestine* bacillus infections is yellowish-green and slightly viscous; if mixed with anaerobic bacteria, the pus has a fecal odor.

Intestinal loops soaked in pus may develop paralytic ileus. The presence of large amounts of air and fluid in the intestinal lumen causes intestinal distension. The accumulation of fluid in the intestinal lumen, massive inflammatory exudate in the abdominal cavity, and edema of the peritoneal membrane, intestinal wall, and mesentery lead to the loss of water, electrolytes, and proteins into the third space, sharply reducing extracellular fluid volume. Combined with the absorption of bacteria and toxins into the bloodstream, this results in hypovolemia and septic shock, triggering a series of changes in endocrine, renal, pulmonary, cardiac, and cerebral metabolism. The most common complications are metabolic acidosis, acute renal failure, and adult respiratory distress syndrome, ultimately leading to irreversible shock and patient death.

bubble_chart Clinical Manifestations

Secondary suppurative peritonitis:

The mode of onset varies depending on the primary disease. For example, gastric perforation manifests as sudden, persistent knife-like pain in the mid-upper abdomen that rapidly spreads to the entire abdomen. Acute appendicitis presents with migratory right lower abdominal pain accompanied by nausea, vomiting, and fever. Postoperative intra-abdominal infection or anastomotic leakage, on the other hand, manifests as fever, abdominal pain, abdominal distension and fullness, and intestinal paralysis. When the inflammation involves the parietal membrane, peritoneal irritation signs appear: abdominal pain, abdominal tenderness, rebound tenderness, and abdominal muscle tension. These are most pronounced at the primary lesion site and spread outward. Their severity is related to the disease cause, extent of the lesion, the patient's age, and constitution. For instance, in cases of gastric perforation, due to the strong irritation from gastric acid and bile, the abdominal muscles become board-like rigid. Abdominal respiratory movements weaken or even disappear. If accompanied by a large amount of free gas in the abdominal cavity, the liver dullness may shrink or disappear. Borborygmi weaken or disappear. In elderly and debilitated patients, even with peritonitis, signs may not be obvious, leading to delayed diagnosis.

Stimulation of the visceral peritoneum can cause nausea and vomiting. As intestinal paralysis develops, abdominal distension and fullness and repeated vomiting may occur.

Bacterial infection and toxin absorption lead to elevated body temperature, increased pulse rate, and often an elevated white blood cell count, averaging between 12,000 and 18,000, with neutrophils accounting for 85–95%. Toxic granules are commonly seen on smears. Urine often becomes concentrated with increased specific gravity, sometimes showing positive ketones, and may exhibit protein and tubular casts.

In the advanced stage of acute diffuse peritonitis, patients become extremely weak, with sunken eyes, flaring nostrils, and pale lips, often succumbing to peripheral circulatory failure, renal failure, or pulmonary failure.

Primary peritonitis:

Pediatric patients may have a history of upper respiratory infection before onset, followed by symptoms such as abdominal pain, nausea, vomiting, abdominal distension and fullness, and intestinal paralysis, often accompanied by fever and systemic toxic symptoms. Physical examination reveals abdominal tenderness, rebound tenderness, and abdominal muscle tension, though in young children, due to underdeveloped abdominal muscles, tension may not be obvious. Rectal examination often shows tenderness, with white blood cell counts typically exceeding 10,000 and neutrophils accounting for over 90%. Gram staining of peritoneal puncture fluid smears may reveal positive cocci.

In patients with liver or kidney diseases who develop peritonitis, due to the presence of ascites, abdominal pain, tenderness, rebound tenderness, and muscle tension are less pronounced than in secondary peritonitis. If turbid ascites is obtained via peritoneal puncture, with a white blood cell count >500/μl, the diagnosis is essentially confirmed.

If ascending infection from the female genital tract is suspected, abdominal pain and signs are most prominent in the lower abdomen. Gynecological examination and posterior vaginal fornix puncture for pus may be performed if necessary.

bubble_chart Diagnosis

Based on medical history and the presence of peritoneal irritation signs, the diagnosis of secondary peritonitis is usually not difficult. However, in some patients, determining the disease cause and deciding whether immediate surgery is required can be challenging. This necessitates close observation of the disease progression and conducting necessary examinations.

Abdominal upright and supine X-ray plain films can reveal the presence of free gas under the diaphragm due to gastrointestinal perforation, as well as X-ray manifestations of strangulated intestinal obstruction, such as small-span coiled intestinal loops in various configurations and the displacement of the jejunum and ileum in cases of intestinal volvulus. In cases of incarcerated internal hernia, isolated, prominently distended intestinal loops may be seen, which do not change position over time, or there may be pseudotumor-like shadows. Blurring or disappearance of the extraperitoneal fat line directly indicates peritoneal inflammation.

Diagnostic peritoneal puncture plays an extremely important role. If purulent fluid is aspirated, or even a small amount of fluid is found to contain numerous white blood cells or pus cells under high-power microscopy, the diagnosis can be confirmed. If necessary, fine-needle puncture without anesthesia can be performed at different sites in the abdominal cavity, and the aspirated fluid can better reflect the intra-abdominal condition.

If abdominal pain is primarily localized to the middle and lower abdomen, a rectal examination should be performed. If the glove is stained with bloody material, it suggests intussusception, intestinal volvulus, inflammatory bowel disease, or neoplastic sexually transmitted disease changes. Tenderness or a sense of fullness in the rectouterine or rectovesical pouch indicates inflammation or pus accumulation. In married women, pus can also be aspirated via posterior vaginal fornix puncture.

If necessary, B-mode ultrasound and computed tomography can be used to assess whether there are inflammatory changes in the corresponding intra-abdominal organs.

bubble_chart Treatment Measures

Since secondary peritonitis is mostly a polymicrobial mixed infection, antibiotics effective against both aerobic and anaerobic bacteria should be combined. A common approach is the combination of aminoglycoside antibiotics or ampicillin with metronidazole. Alternatively, third-generation cephalosporins that are effective against both types of bacteria, such as cefotaxime and ceftazidime, can be used.

Secondary peritonitis in the vast majority of cases requires surgical treatment to remove the lesion, repair perforations, aspirate pus, and, if necessary, drain the abdominal cavity. The abdominal incision and anesthesia method depend on the location of the primary lesion. If the disease cause is unclear, an exploratory laparotomy incision, such as a right midline rectus incision, can be made. The incision can be extended upward or downward if necessary.

Regarding peritoneal lavage, localized peritonitis should not undergo peritoneal lavage in principle to avoid the spread of infection. For diffuse peritonitis with severe peritoneal contamination or the presence of foreign bodies like gastrointestinal contents, and if the patient's condition permits, a large amount of normal saline can be used to lavage the abdominal cavity. After aspirating the lavage fluid, 500ml of a 1% neomycin solution can be used for peritoneal lavage if necessary, but attention should be paid to whether the patient's respiration is suppressed. Alternatively, 1% povidone-iodine can be diluted 10-fold with normal saline, and 1000ml of the diluted povidone-iodine can be used for peritoneal lavage, but it is contraindicated in patients with hyperthyroidism, renal insufficiency, or iodine allergy. Sometimes continuous peritoneal irrigation can also be applied.

Regarding abdominal drainage, it should be determined based on the nature of the lesion and the surgical approach. For diffuse peritonitis where the lesion has been completely removed and the abdominal cavity has been thoroughly cleaned, drainage is generally not placed in principle. If there is infected necrotic tissue at the lesion site, or if gastrointestinal fistula cannot be guaranteed despite treatment, drainage such as a Penrose drain, silicone tube, or double-lumen tube should be placed.

Most surgical incisions for peritonitis patients undergo initial (first-stage) suturing. If the incision is heavily contaminated, absorbable catgut can be used to suture the peritoneum, with several nylon tension sutures placed through the full thickness of the incision. The incision can then be packed with saline-soaked gauze and covered with sterile dressings. The gauze should be changed daily. After 4–5 days, when secretions decrease and healthy granulation tissue forms, delayed primary closure can be performed, often avoiding severe infection of the incision.

Postoperatively, the patient should be placed in a semi-sitting position to allow pus to flow into the pelvic cavity. Since the absorption capacity of the pelvic peritoneum is weaker than that of the upper abdomen, this reduces toxin absorption. Even if an abscess forms, it can be drained through the rectum or the posterior vaginal fornix.

Primary peritonitis can often be controlled with antibiotic therapy and generally does not require surgical treatment. If it is difficult to distinguish from secondary peritonitis, exploratory laparotomy is still advisable. If it is primary peritonitis, the pus can be aspirated, and the abdominal cavity does not require drainage. The appendix can also be removed simultaneously.