bubble_chart Overview

Acute peritonitis is an acute inflammation of the peritoneum caused by infection, chemical substances (such as gastric juice, intestinal juice, bile, pancreatic juice, etc.), or injury. Among these, bacterial infection is the most common cause.

bubble_chart Etiology

There are many causes of acute peritonitis, mainly including the following:

(1) Acute perforation and rupture of intra-abdominal organs. These mostly occur in organs that already have pathological changes. Perforation of hollow organs often occurs suddenly due to the progression of ulcers or gangrenous sexually transmitted diseases, such as acute appendicitis, peptic ulcers, acute cholecystitis, cold-damage disease ulcers, gastric or intestinal cancer, ulcerative colitis, ulcerative intestinal tuberculosis, amebic intestinal disease, diverticulitis, etc., leading to acute peritonitis. Solid organs such as the liver and spleen can also rupture due to abscesses or cancerous growths.

(2) Spread of acute infections in intra-abdominal organs. For example, acute appendicitis, cholecystitis, pancreatitis, diverticulitis, ascending infections of the female reproductive tract (such as puerperal fever, salpingitis), etc., can spread to the peritoneum and cause acute inflammation.

(3) Acute intestinal obstruction. Conditions such as intussusception, volvulus, incarcerated hernia, mesenteric vascular embolism, or thrombosis can lead to strangulated intestinal obstruction. Due to intestinal wall injury and the loss of normal barrier function, intestinal bacteria can invade the abdominal cavity through the intestinal wall, resulting in peritonitis.

(4) Abdominal surgical conditions. Sharp objects or bullets penetrating the abdominal wall can perforate hollow organs or introduce external bacteria into the abdominal cavity. Abdominal trauma can sometimes cause visceral rupture, leading to acute peritonitis. During abdominal surgery, external bacteria may be introduced into the abdominal cavity due to inadequate sterilization. Careless surgical procedures can also spread local infections or cause leakage from sutures in the stomach, intestines, bile ducts, or pancreas, leading to fistula disease. Sometimes, acute peritonitis can result from neglecting aseptic techniques during abdominal paracentesis or peritoneal dialysis.

(5) Hematogenous disseminated infections. These can cause primary acute peritonitis.

The most common bacteria in peritoneal infections are Escherichia coli, enterococci, Pseudomonas aeruginosa, Proteus, Clostridium perfringens, and other anaerobic bacteria. In most cases, the infection is mixed.

bubble_chart Pathological Changes

The pathological changes of acute peritonitis often vary significantly depending on the source and mode of infection, the virulence and quantity of the pathogens, and the patient's immune status.

Once infection enters the abdominal cavity, the peritoneum immediately exhibits an inflammatory response, manifested as congestion, edema, and exudation. The fibrin in the exudate can promote adhesion between intestinal loops, the greater omentum, and other viscera in the inflamed area of the peritoneum, limiting the spread of inflammation. However, if the infected focus is not removed, the perforated viscus is not repaired, or abdominal drainage is not performed, or if the bacterial virulence is too strong, the quantity is excessive, or the patient's immune function is compromised, the infection may spread, leading to diffuse peritonitis.

After treatment, the inflammation of peritonitis can gradually resolve, and the exuded fibrin may undergo organization, causing adhesions between the peritoneum, intestinal loops, and omentum, which may predispose to mechanical intestinal obstruction.

Once peritonitis develops, the large number of bacteria and toxins in the peritoneal exudate are absorbed through the peritoneum and enter the bloodstream via lymphatic vessels, producing a series of septicemia symptoms.

In the initial stage of peritonitis, intestinal peristalsis increases but soon weakens, progressing to intestinal paralysis. After intestinal paralysis occurs, intestinal secretion increases while absorption decreases, leading to significant accumulation of gas and fluid in the intestinal lumen. The intestinal wall, peritoneum, and mesentery become edematous, and a large amount of inflammatory exudate enters the abdominal cavity, resulting in substantial loss of water, electrolytes, and proteins, causing a sharp reduction in blood volume. It is estimated that patients with diffuse peritonitis can lose 4–6 liters of fluid within 24 hours.

Under the combined effects of reduced blood volume and toxemia, the adrenal cortex secretes large amounts of catecholamines, leading to increased heart rate and vasoconstriction. Increased secretion of antidiuretic hormone and aldosterone results in water and sodium retention, with water retention exceeding sodium retention, leading to hyponatremia. The reduction in extracellular fluid and acidosis decrease cardiac output and impair myocardial contractility. Meanwhile, abdominal distension and fullness, along with elevated diaphragm, reduce the patient's ventilation volume, causing rapid breathing and tissue hypoxia. Under the combined effects of hypovolemia, low cardiac output, and increased antidiuretic hormone and aldosterone, the glomerular filtration rate decreases, leading to reduced urine output. Due to increased metabolic rate and inadequate tissue perfusion, anaerobic metabolism occurs, resulting in lactic acidosis. All these factors can lead to disturbances in fluid, electrolyte, and acid-base balance, as well as damage to the functions of vital organs such as the heart, lungs, and kidneys, which, without effective treatment, can result in patient death.

bubble_chart Clinical Manifestations

The main clinical manifestations of acute peritonitis include abdominal pain, abdominal tenderness, and abdominal muscle rigidity, often accompanied by nausea, vomiting, abdominal distension and fullness, fever, hypotension, rapid pulse, shortness of breath, leukocytosis, and other signs of toxicity. Since this condition is mostly a complication of a disease within the abdominal cavity, symptoms of the primary disease often appear before and after its onset.

(1) Symptoms

1. Acute abdominal pain Abdominal pain is the most prominent and common symptom, usually occurring suddenly, persisting, and spreading rapidly. Its nature depends on the type of peritonitis (chemical or bacterial), the extent of inflammation, and the patient's response. When organs such as the stomach, duodenum, or gallbladder perforate, causing diffuse peritonitis, digestive fluids irritate the peritoneum, leading to sudden, severe pain throughout the abdomen, sometimes even triggering so-called peritoneal shock. In some cases, before secondary bacterial infection occurs, the peritoneum may exude large amounts of fluid, diluting the irritants, resulting in temporary relief of abdominal pain and peritoneal irritation—a false improvement. However, once secondary bacterial infection sets in, the abdominal pain intensifies again. Peritonitis caused by bacterial infection usually begins with localized pain at the primary site (e.g., appendicitis, cholecystitis). When perforation occurs, the abdominal pain develops more gradually, presenting as distending pain or dull pain, unlike the severe pain caused by acute perforation of the stomach or gallbladder. The pain gradually worsens and spreads from the primary site to the entire abdomen. The intensity of abdominal pain varies among individuals: some patients report extremely severe, persistent pain, while others describe only dull pain or discomfort. Weak or elderly patients, such as those with severe cold-damage disease, may not feel pain during acute perforation.

2. Nausea and vomiting These are common early symptoms. Initially, due to peritoneal irritation, nausea and vomiting are reflexive, intermittent, and involve gastric contents, sometimes mixed with bile. Later, due to paralytic ileus, vomiting becomes persistent without nausea, with the vomitus consisting of brownish-yellow intestinal contents, possibly foul-smelling.

3. Other symptoms In cases of acute perforation of hollow organs leading to peritonitis, collapse due to peritoneal shock or toxemia is common, often accompanied by subnormal or normal body temperature. As the collapse improves but peritonitis progresses, the temperature gradually rises. If the primary disease is an acute infection (e.g., acute appendicitis or acute cholecystitis), the temperature is usually higher than before when peritonitis develops. In acute diffuse peritonitis, due to massive peritoneal exudation, severe congestion and edema of the peritoneum and intestinal wall, accumulation of fluid in the paralyzed intestinal lumen, and dehydration from vomiting, the effective circulating blood volume and total blood potassium levels decrease significantly. Additionally, reduced renal blood flow, worsening toxemia, and impaired cardiac, renal, and peripheral vascular function often lead to hypotension and shock. The pulse may be thready and rapid or even imperceptible. Other symptoms include thirst, oliguria or anuria, abdominal distension and fullness, and absence of anal flatus. Frequent hiccups may occur, possibly due to inflammation spreading to the diaphragm.

(2) Signs

Patients with peritonitis often exhibit a pained expression. Coughing, breathing, or turning the body can worsen abdominal pain. They are forced to lie supine with legs flexed, breathing shallowly and rapidly. In the late stage of toxemia (third stage), due to high fever, lack of food intake, dehydration, and acidosis, the central nervous system and vital organs enter a state of depression. At this point, patients appear mentally depressed, with cold extremities, pale and gray complexion, dry skin, sunken eyes and cheeks, a pinched nose, and cold sweat on the forehead.

Abdominal examination may reveal the classic triad of peritonitis—abdominal tenderness, muscular rigidity of the abdominal wall, and rebound tenderness. In localized peritonitis, these signs are confined to one area of the abdomen, whereas in diffuse peritonitis, they are present throughout the abdomen, accompanied by shallow abdominal respiration, loss of abdominal wall reflexes, and decreased or absent borborygmi. Tenderness and rebound tenderness are almost always present, but the degree of muscular rigidity varies depending on the patient's overall condition. In cases of acute perforation of a peptic ulcer, the abdominal wall muscles may exhibit board-like rigidity, whereas in severely debilitated patients—such as those with perforation due to intestinal typhoid fever or advanced-stage toxemia—muscular spasm or rigidity may be minimal or even absent. When there is a significant amount of peritoneal effusion, shifting dullness may be detected. In cases of gastrointestinal perforation leading to free air in the peritoneal cavity, liver dullness is diminished or absent in approximately 55–60% of cases. If inflammation becomes localized, forming an abscess or inflammatory mass near the abdominal wall, a poorly defined mass may be palpable. Masses or abscesses in the pelvic region may sometimes be detected through rectal examination.

Acute peritonitis can be classified from the following various perspectives:

1. According to the extent of inflammation, it can be divided into diffuse peritonitis and localized peritonitis.

2. Based on the origin of the disease, it can be categorized as secondary peritonitis or primary peritonitis. The vast majority of peritonitis cases are secondary peritonitis, which either arises from pre-existing diseases or injuries of intra-abdominal organs or results from trauma and external contamination. Primary peritonitis is rare, where there is no pre-existing intra-abdominal pathology, and pathogens infect the peritoneum through hematogenous or lymphatic spread from extra-abdominal foci. This is commonly seen in immunocompromised individuals, such as those with cirrhosis, nephrotic syndrome, or in infants and young children.

3. Based on the initial nature of the disease, it can be classified as sterile peritonitis or infectious peritonitis. Sterile peritonitis often occurs due to gastric, duodenal acute perforation, acute pancreatitis, etc., where gastric juice, intestinal fluid, pancreatic juice, or other fistula diseases enter the abdominal cavity and irritate the peritoneum. However, if the condition persists untreated, bacterial infection usually develops within 2–3 days, making it indistinguishable from infectious peritonitis.

bubble_chart Auxiliary Examination

The white blood cell count and the proportion of neutrophils are generally significantly increased, with common left shift and toxic granules. In patients with severe diffuse peritonitis, due to the massive infiltration of white blood cells into the abdominal cavity, the peripheral white blood cell count may not be high, but the proportion of neutrophils remains elevated. The same applies to the elderly or those with compromised immune function.

Urine becomes concentrated due to dehydration, and protein and casts may appear, with urine vinegar ketones possibly testing positive.

Blood generation and transformation tests may reveal acidosis and electrolyte disturbances.

Culture of peritoneal effusion often yields pathogenic bacteria.

X-ray examination may reveal gas under the diaphragm.

bubble_chart Treatment Measures

The basic principles for treating acute peritonitis are to control and eliminate existing infections, prevent their spread and expansion, and correct the pathophysiological disturbances caused by peritonitis.

Generally, once the diagnosis of acute peritonitis is confirmed and the primary lesion is identified or suspected, surgery should be performed as early as possible if the patient's condition permits. This includes procedures such as suturing gastrointestinal perforations, removing lesions like the appendix or gallbladder, and draining or cleaning purulent exudates in the abdominal cavity.

For cases diagnosed as primary peritonitis, or diffuse peritonitis lasting more than 1–2 days with signs of localization, or for elderly, frail patients with severe toxic symptoms, initial medical supportive treatment may be administered while closely monitoring the progression of the condition.

Medical supportive treatment can also be considered as preoperative preparation, as surgical intervention may still be necessary if required. Medical supportive treatment includes:

1. Bed rest, preferably in a semi-recumbent position tilted 30°–45° forward to facilitate the flow of inflammatory exudates toward the pelvis for easier drainage. In cases of severe shock, a supine position should be adopted.

2. Fasting and gastrointestinal decompression.

3. Correcting fluid, electrolyte, and acid-base imbalances. Adequate fluid infusion should be administered to ensure a daily urine output of around 1,500 ml. If possible, fluid intake should be adjusted based on central venous pressure measurements. Additionally, the amount of potassium chloride or sodium salts to be infused should be calculated based on blood electrolyte test results, and sodium bicarbonate therapy should be considered based on blood CO₂ combining power or pH levels.

4. If conditions permit, intravenous hyperalimentation therapy or small transfusions of plasma or whole blood should be administered to improve the patient’s overall condition and enhance immunity.

5. Antibiotic therapy is the most critical medical treatment for acute peritonitis. Secondary peritonitis is often a mixed infection of aerobic and anaerobic bacteria, so broad-spectrum antibiotics or a combination of several antibiotics should be used. If the causative pathogens can be identified, antibiotics should be selected based on sensitivity test results.

6. For severe pain or dysphoria, if the diagnosis is clear, medications such as pethidine or phenobarbital may be administered as appropriate. If shock is present, active anti-shock treatment should be implemented.

bubble_chart Prognosis

With advances in diagnosis and treatment, the prognosis of acute peritonitis has improved compared to the past. However, the mortality rate remains around 5-10%. Primary peritonitis occurring in patients with cirrhosis and ascites can be as high as 40%. Delayed diagnosis and late treatment, as well as cases involving children, the elderly, and those with heart, lung, kidney diseases, or diabetes, have a poorer prognosis.

bubble_chart Prevention

Early and appropriate treatment of intra-abdominal inflammatory diseases that may cause peritonitis is the fundamental measure to prevent peritonitis. Strict aseptic techniques should be followed for any abdominal surgery, including procedures like abdominal paracentesis. Administering oral antibiotics before intestinal surgery can reduce the occurrence of peritonitis.

bubble_chart Differentiation

Based on symptoms and signs, the diagnosis of acute peritonitis is generally not difficult.

Peritoneal puncture and examination of peritoneal effusion are extremely important for the diagnosis of peritonitis.

For secondary peritonitis, the location of the primary lesion should be identified to consider further treatment. However, when the signs of peritonitis are obvious, this can sometimes be challenging. Generally, X-ray examination revealing free gas under the diaphragm suggests gastrointestinal perforation. If symptoms show no improvement after gastrointestinal decompression and initial treatment, the possibility of gallbladder rupture should be considered. For female patients, salpingitis and oophoritis should be considered more often, while elderly patients should be evaluated for the possibility of colorectal cancer or diverticular perforation.

Pleuritis, pneumonia, and other conditions can cause fever and upper abdominal pain. Acute myocardial infarction may present with severe upper abdominal pain. Acute pancreatitis, perinephric abscess, and even herpes zoster can also manifest with fever and abdominal pain. However, based on medical history, signs, and corresponding examinations, differentiation is not difficult.

The symptoms and signs of primary peritonitis are similar to those of secondary peritonitis, and laboratory results are often identical. However, primary peritonitis can only be treated non-surgically, which is distinctly different from secondary peritonitis. Therefore, careful differentiation is necessary. The key points for distinguishing primary peritonitis from secondary peritonitis are as follows:

1. Primary peritonitis mainly occurs in patients with compromised immune function, such as those with cirrhotic ascites or nephrotic syndrome, as well as in infants and young children, especially girls under 10 years old. Secondary peritonitis, on the other hand, is generally not limited to such populations.

2. Primary peritonitis in patients with cirrhotic ascites has a more gradual onset, and the "triad of peritonitis" among abdominal signs is often less pronounced. In infants and young children, primary peritonitis has a more acute onset, and the "triad of peritonitis" is also less evident compared to secondary peritonitis.

3. The absence of a primary intra-abdominal infection site is the key distinction between primary and secondary peritonitis. X-ray findings of free gas under the diaphragm are evidence of secondary peritonitis.

4. Peritoneal puncture to obtain ascites or peritoneal effusion for bacterial smear and culture. Primary peritonitis is typically caused by a single bacterial infection, whereas secondary peritonitis is almost always a mixed bacterial infection.