Acute suppurative peritonitis affecting the entire abdominal cavity is referred to as acute diffuse peritonitis, which can be classified into primary peritonitis and secondary peritonitis.
Etiology
Secondary Peritonitis
Secondary peritonitis is the most common type and is primarily caused by perforation of hollow organs, trauma leading to abdominal wall or visceral rupture, or retroperitoneal organ injuries. Common causes include acute perforation of gastric or duodenal ulcers, which allows gastric contents to enter the abdominal cavity, causing chemical irritation and triggering chemical peritonitis, which later progresses to suppurative peritonitis. Acute cholecystitis with necrosis and perforation of the gallbladder results in bile peritonitis. Traumatic rupture of the intestines or bladder, contamination of the peritoneal cavity, or bacterial entry through wounds can also rapidly lead to peritonitis. The spread of inflammation from intra-abdominal organs, such as acute appendicitis or purulent infections of the female reproductive organs, is another frequent cause. Bacterial-laden exudates disseminate within the abdominal cavity, causing peritonitis. Other causes include intraoperative contamination of the abdominal cavity, anastomotic leakage from the gastrointestinal tract, bile duct, or pancreas, as well as severe infections of the anterior or posterior abdominal wall. The most common causative organisms are Escherichia coli and Klebsiella pneumoniae, followed by Bacteroides and streptococcal species. In most cases, these represent mixed infections with high toxicity.
Primary Peritonitis
Primary peritonitis, also known as spontaneous peritonitis, occurs without an identifiable intra-abdominal source. The primary pathogens include hemolytic streptococci, pneumococci, or Escherichia coli. Bacteria can invade the peritoneal cavity through the following pathways:
- Hematogenous spread: Pathogens from respiratory or urinary tract infections disseminate to the peritoneum via the bloodstream, commonly seen in infants and young children.
- Ascending infection: Bacteria from the female genital tract, such as in gonococcal peritonitis, directly spread to the peritoneal cavity through the fallopian tubes.
- Direct spread: Urinary tract infections can allow bacteria to directly spread through the peritoneal layers to the peritoneal cavity.
- Transmural infection: Under normal circumstances, bacteria within the gut lumen cannot cross the intestinal wall. However, in conditions such as cirrhosis with ascites, nephrotic syndrome, scarlet fever, or malnutrition, where host defenses are compromised, intestinal bacteria may translocate across the gut barrier into the peritoneal cavity, leading to peritonitis.
The extent of infection in primary peritonitis depends on the properties of the purulent material and the types of bacteria involved.
Pathophysiology
When gastrointestinal contents and bacteria enter the peritoneal cavity, an immediate host response occurs, with peritoneal congestion, edema, and loss of luster. Large amounts of serous exudates are produced to dilute toxins within the abdominal cavity. This progression involves recruitment of macrophages and neutrophils, along with necrotic tissue, bacteria, and consolidated fibrin, causing the exudate to become turbid and transform into pus. Pus dominated by Escherichia coli is typically yellow-green, often thickened by mixed infections involving other pathogens, and emits a foul, fecal odor.
The outcome of peritonitis depends on two factors: the systemic and localized peritoneal defense mechanisms of the patient, and the nature, quantity, and duration of bacterial contamination. Bacterial endotoxins stimulate the host’s cellular defense mechanisms, activating inflammatory mediators. Cytokines, produced by macrophages, can enter the peritoneal cavity directly through compromised intestinal barriers or originate from injured peritoneal tissues. In the later stages of the disease, intraperitoneal cytokines can cause organ damage. Nitric oxide (NO), an end-stage mediator, disrupts the tricarboxylic acid cycle, leading to cellular hypoxia, organ failure, and death.
Furthermore, the abdominal organs become immersed in purulent fluid, with severe peritoneal congestion, edema, and excessive exudation causing dehydration and electrolyte imbalance. Hypoproteinemia, anemia, fever, vomiting, intestinal paralysis, and significant fluid accumulation in the intestinal lumen result in reduced blood volume, leading to hypovolemic shock. Bacterial toxins entering the bloodstream can also induce septic shock. Paralysis and distension of the intestines may elevate the diaphragm, impairing cardiopulmonary function and exacerbating circulatory and respiratory insufficiency, culminating in death.
In young and healthy individuals with strong immune responses, the pathogenicity of bacteria is counteracted. Mild cases of peritonitis may result in adherence between affected organs, adjacent intestines, and the omentum, encapsulating the focus of infection and confining it to a specific area within the abdominal cavity, evolving into localized peritonitis. The exudates may gradually be absorbed, resolving the inflammation, and leading to self-repair. In cases of localized pus formation, abscesses may develop in areas such as the subphrenic space, iliac fossa, between intestinal loops, or the pelvic cavity.
After recovery from peritonitis, varying degrees of intra-abdominal adhesions may remain, which are often without adverse consequences. However, some adhesions may result in intestinal twisting or angulation, causing obstruction and leading to mechanical intestinal obstruction, referred to as adhesive intestinal obstruction.
Clinical Presentation
The symptoms of peritonitis vary depending on the underlying cause and can either have a sudden onset or develop gradually. Peritonitis caused by rupture or perforation of hollow organs often presents abruptly, whereas conditions like appendicitis or cholecystitis generally begin with symptoms of the primary illness and later progress to manifestations of peritonitis.
Abdominal Pain
Abdominal pain is the most significant clinical symptom. The severity of pain depends on factors such as the underlying cause, the extent of inflammation, age, and the patient's overall health. The pain is often severe, intolerable, and constant. It worsens with deep breathing, coughing, or movement, leading patients to adopt a forced posture. The pain typically originates from the site of the primary lesion and spreads throughout the abdomen as inflammation progresses.
Nausea and Vomiting
Stimulation of the peritoneum may provoke reflex nausea and vomiting, with the vomitus often containing gastric contents. In cases of paralytic intestinal obstruction, the vomitus may consist of yellow-green bile or even brown, fecal-like material.
Fever and Pulse
Changes in body temperature and pulse rate are correlated with the severity of inflammation. Initially, both may remain normal, but fever and tachycardia gradually develop as the condition progresses. If the primary lesion involves an inflammatory process, fever is usually present before the onset of peritonitis and becomes more pronounced afterward. In elderly or debilitated patients, fever may be absent. Tachycardia is common, and a rapid pulse accompanied by a drop in temperature is often a sign of worsening condition.
Infection
Patients may exhibit high fever, rapid pulse, shallow and rapid breathing, profuse sweating, and dry mouth. As the condition deteriorates, signs such as pallor, weakness, dry skin, cold extremities, rapid breathing, cyanosis of the lips, thready weak pulse, sudden fluctuations in body temperature, hypotension, and altered consciousness may develop. These indicate severe dehydration, metabolic acidosis, and shock.
Abdominal Signs
The typical signs of peritoneal irritation include abdominal tenderness, rebound tenderness, and abdominal muscle rigidity. The severity of muscle rigidity depends on the etiology and the patient’s general condition. For example, perforation of the stomach, intestines, or gallbladder can result in marked abdominal rigidity, sometimes described as "board-like stiffness." In infants, elderly individuals, or severely debilitated patients, muscle rigidity may be subtle and easily overlooked. Other important signs include abdominal distension and reduced or absent abdominal breathing. Worsening abdominal distension is a sign of disease progression. Percussion of the abdomen may reveal tympany due to gastrointestinal distension, and in cases of gastric or duodenal perforation, the hepatic dullness may become diminished or absent. Extensive intraperitoneal fluid may produce shifting dullness on percussion. Auscultation often reveals reduced or absent bowel sounds.
Rectal Examination: Fullness and tenderness in the anterior rectal area suggest pelvic infection or the formation of a pelvic abscess.
Auxiliary Examinations
White Blood Cell Count
An elevated white blood cell count and neutrophil percentage are typical findings. However, in critically ill patients or those with weakened immune responses, the white blood cell count may remain normal.
Upright Abdominal X-ray
Features such as diffuse small bowel distension and multiple air-fluid levels are indicative of paralytic ileus. Free air beneath the diaphragm is often observed in cases of gastrointestinal perforation.
Ultrasound Examination
Ultrasound can detect varying amounts of fluid in the peritoneal cavity but cannot differentiate the nature of the fluid. Ultrasound-guided diagnostic peritoneal aspiration or lavage can aid in diagnosis. Aspiration is typically performed in the lower abdomen below the anterior superior iliac spine, assisted by percussion or ultrasound localization. The nature of the aspirated fluid provides clues to the underlying cause. For example, tuberculous peritonitis yields grass-green transparent ascites; acute gastric or duodenal perforation may produce yellow, turbid, bile-stained fluid without an odor, or include food particles if perforation occurs after a recent meal; acute severe pancreatitis may produce bloody fluid with elevated amylase levels; acute perforation of an inflamed appendix yields thin purulent fluid with a foul odor; and strangulated intestinal obstruction produces bloody, malodorous fluid. Non-clotting blood suggests intraperitoneal hemorrhage, whereas aspirated whole blood that clots upon standing may indicate accidental vascular puncture. The aspirate can also be examined microscopically and cultured to identify bacteria. When intraperitoneal fluid is less than 100 mL, fluid aspiration may be unsuccessful, in which case saline infusion followed by re-aspiration can be performed.
CT Scan
CT imaging is highly effective in diagnosing solid organ involvement in the abdomen and is one of the most efficient auxiliary tools for identifying the causes of secondary peritonitis. It also provides information on the amount of intraperitoneal fluid, with diagnostic accuracy reaching up to 95%.
If a pelvic abscess is suspected, transrectal aspiration can assist in diagnosis. For women, a transvaginal ultrasound or posterior fornix aspiration procedure may provide additional diagnostic insights.
Diagnosis
The diagnosis of peritonitis is generally straightforward when considering the history, clinical signs, white blood cell count, and imaging findings from X-ray, ultrasound, or CT. However, pinpointing the primary source of infection can sometimes be challenging. In such cases, exploratory laparoscopy may help identify the primary lesion. In children, sudden abdominal pain, vomiting, and apparent abdominal signs during a respiratory tract infection require careful evaluation to discern whether the condition is primary peritonitis or a result of pulmonary inflammation irritating the intercostal nerves.
Treatment
Treatment includes non-surgical and surgical approaches.
Non-Surgical Treatment
Non-surgical treatment may be appropriate for patients with mild conditions, those with symptoms persisting for over 24 hours but showing gradual improvement in abdominal signs, or patients with significant heart, lung, or other organ comorbidities who are unable to tolerate surgery. Non-surgical measures are also implemented as preparation for surgery when necessary.
Positioning
Half-sitting positions help direct peritoneal exudates towards the pelvic cavity, reducing absorption and alleviating toxic symptoms while promoting localization and drainage of inflammation. This position also facilitates downward movement of abdominal organs, relaxation of abdominal muscles, and mitigation of respiratory and circulatory disturbances caused by abdominal distension. Patients with shock may benefit from a flat supine position or elevation of the head, torso, and lower limbs by approximately 20 degrees.
Fasting and Gastrointestinal Decompression
Patients with gastrointestinal perforation are subjected to fasting and the placement of a nasogastric tube for continuous gastrointestinal decompression, which evacuates the contents and air from the gastrointestinal tract. This reduces further leakage into the abdominal cavity, eases intestinal distension, improves blood circulation in the stomach wall, facilitates localization and absorption of inflammation, and supports the recovery of gastrointestinal motility.
Correction of Fluid and Electrolyte Imbalances
Fasting, gastrointestinal decompression, and significant peritoneal exudation can lead to disturbances in fluid and electrolyte balance. The total volume of fluids to be replenished (including crystalloid and colloid solutions) is calculated based on patient input and output as well as physiological requirements to address dehydration and acid-base imbalances. Severe cases may require plasma or albumin transfusions to correct hypoproteinemia caused by extensive peritoneal exudation, as well as blood transfusions for anemia. Continuous monitoring of pulse, blood pressure, urine output, central venous pressure, blood counts, and arterial blood gas analyses helps guide adjustments to infusion content and rate to maintain urine output at 30–50 mL per hour. Patients with severe toxic symptoms or shock related to acute peritonitis can receive specific doses of corticosteroids to alleviate symptoms and stabilize their condition if fluid and blood transfusions prove insufficient. Vasoconstrictors or vasodilators, such as dopamine, may be applied based on pulse, blood pressure, or central venous pressure measurements, offering a relatively safe and effective option.
Antibiotic Therapy
Secondary peritonitis often involves mixed infections caused primarily by Escherichia coli, enterococci, and anaerobic bacteria. Antibiotic selection considers the types of causative organisms. While high-dose combination therapy was historically favored, recent opinions suggest that a single broad-spectrum antibiotic might be more effective. Adjustments to antibiotics are made based on bacterial culture and drug sensitivity test results. It should be noted that antibiotic therapy cannot replace surgery, as surgical intervention is essential for curing certain cases.
Caloric and Nutritional Support
Patients with acute peritonitis have a metabolic rate approximately 140% higher than normal, necessitating daily caloric intake of 12,550–16,740 kJ (3,000–4,000 kcal). Inadequate caloric supplementation leads to the depletion of significant amounts of protein, reducing resistance and impairing healing ability. Alongside glucose infusions for caloric supply, albumin and amino acids need to be supplemented. Intravenous infusions of lipid emulsions provide additional high-calorie content. Patients unable to eat for prolonged durations require early parenteral nutrition. Those with jejunostomy created during surgery may receive enteral nutrition after gastrointestinal function recovers.
Sedation, Analgesia, and Oxygen Therapy
Sedation and oxygen therapy help alleviate patient discomfort and feelings of fear. Pain management using opioid analgesics such as pethidine is recommended for confirmed diagnoses, post-treatment plans, and postoperative cases. For undiagnosed patients or those requiring further observation, analgesics are withheld to prevent masking of clinical signs.
Surgical Treatment
The majority of cases of secondary peritonitis require timely surgical intervention.
Indications
Indications for surgery include:
- Peritonitis symptoms and signs not improved or worsened after 6–8 hours of the aforementioned non-surgical treatments (typically no more than 12 hours).
- Significant primary intra-abdominal conditions, such as gastrointestinal perforation, gallbladder gangrene, strangulated intestinal obstruction, ruptured intra-abdominal organ injury, or peritonitis caused by anastomotic leakage shortly after gastrointestinal surgery.
- Severe intra-abdominal inflammation accompanied by a large amount of fluid accumulation, severe intestinal paralysis, or toxic symptoms, particularly when signs of shock are present.
- Unclear causes of peritonitis showing no trend toward localization.
Anesthesia Methods
General anesthesia or epidural anesthesia is commonly employed. Local anesthesia may be considered for critically ill patients experiencing shock.
Management of the Primary Cause
The surgical incision should align with the location of the affected organ. If the primary lesion cannot be determined, a right paramedian incision is recommended, which can be extended upward or downward as needed. For patients with a history of abdominal surgery, the original incision or part of it can be reused whenever possible. Special care should be taken with the intestines during laparotomy, and adhesions should be dissected carefully to avoid intestinal damage. Exploration must be meticulous and gentle, and the treatment plan is determined after identifying the cause of the peritonitis. For instance, perforated gastric or duodenal ulcers may require repair or partial gastrectomy, although perforation of longer duration, extensive intra-abdominal contamination, or poor patient condition may only allow for repair of the perforation. Appendices or gallbladders with suppurative gangrene should be removed promptly. In cases of severe gallbladder inflammation with unclear anatomical layers or patients who are not suitable for surgery, cholecystostomy with abdominal drainage can be performed, often under local anesthesia with ultrasound guidance. Necrotic bowel segments should be resected promptly. Necrotic colon segments that cannot be resected and anastomosed in one stage can be managed with externalization of the necrotic segment or a colostomy.
Thorough Cleaning of the Abdominal Cavity
Immediately after laparotomy, pus and exudative fluid in the abdominal cavity should be aspirated using suction equipment, along with food residues, feces, and foreign materials. Pus commonly accumulates near the primary lesion, subphrenic space, paracolic gutters, and pelvic cavity. The abdominal cavity can be irrigated thoroughly with metronidazole and saline until it is clean. Any purulent material, pseudomembranes, or fibrinous partitions present in the abdominal cavity should be cleared to facilitate drainage. Antibiotics are generally avoided within the abdominal cavity to prevent severe adhesions.
Adequate Drainage
The goal is to remove residual fluids and any continued exudate from the abdominal cavity through drainage tubes, reducing infection within the peritoneal cavity and preventing postoperative intra-abdominal abscesses. Commonly used drainage tubes include silicone, latex, or double-lumen tubes, which are placed in the lowest position near the lesion to ensure unobstructed drainage. Severe infections may require placement of more than two drainage tubes, and postoperative intraperitoneal irrigation can be performed. Indications for placement of drainage tubes in the abdominal cavity include:
- Inability to completely remove necrotic tissue or the presence of large amounts of necrotic material that cannot be cleared.
- Prevention of leakage following procedures such as gastrointestinal perforation repair.
- Significant fluid or blood accumulation at the surgical site.
- Pre-existing localized abscesses.
Postoperative Management
Postoperative care involves continued fasting, gastrointestinal decompression, fluid replenishment, administration of antibiotics, and nutritional support while ensuring proper functioning of the drainage tubes. Antibiotic selection should be adjusted based on results from bacterial cultures and antibiotic sensitivity tests of the purulent fluid obtained during surgery. Therapy with antibiotics can be discontinued once the patient's condition improves, and clinical signs of infection subside. The abdominal drainage tube can be removed once the drainage fluid becomes clear, its daily volume falls below 10 mL, and the patient experiences no fever, abdominal distension, or other symptoms, indicating resolution of peritonitis. Attention should also be given to the function of vital organs, such as the heart, lungs, liver, kidneys, and brain, as well as the potential development of disseminated intravascular coagulation (DIC).
In recent years, with the continued advancement of laparoscopic surgical techniques, their application in the diagnosis and treatment of diffuse peritonitis has become more widespread, offering particular advantages for cases of peritonitis with unclear etiology.