disease | Tuberculous Peritonitis |
Subcutaneous nodular peritonitis is primarily caused by direct spread from intestinal tuberculosis, mesenteric lymph node subcutaneous nodules, and fallopian tube subcutaneous nodules, with a few cases resulting from hematogenous disseminated subcutaneous nodules. It can occur at any age, most commonly between 20 and 30 years old, and is more prevalent in women than in men.
bubble_chart Pathological Changes
Due to factors such as differences in the body's reactivity and immune status; the quantity, virulence, type, and mode of invasion of the subcutaneous node bacteria; and variations in treatment measures, the pathological changes of the peritoneum can manifest as three types: exudative, adhesive, and caseous. The adhesive type is the most common, followed by the exudative type, while the caseous type is the least common. Clinically, these three types often coexist and are referred to as the mixed type.
1. Exudative type: The peritoneum is congested and edematous, covered with fibrin exudate, and exhibits numerous small yellow-white or gray-white subcutaneous nodules, which may coalesce. The abdominal cavity contains serofibrinous exudate, and the ascitic fluid is yellow, sometimes slightly bloody.
2. Adhesive type: The peritoneum is markedly thickened with significant fibrous tissue proliferation. The intestinal loops may adhere tightly to each other or to other organs, and the bowel may be compressed by fibrous bands, leading to obstruction. The mesentery becomes thickened and shortened, and the greater omentum also thickens and hardens, forming a lumpy mass. In severe cases, the abdominal cavity may become completely obliterated.
3. Caseous type: The primary pathological feature is caseous necrosis. The intestinal loops, greater omentum, mesentery, or intra-abdominal organs adhere to each other and form multiple small compartments filled with turbid or purulent fluid. Additionally, caseous necrotic mesenteric lymph nodes contribute to the formation of subcutaneous nodular abscesses. Sometimes, these compartments may rupture into the bowel, vagina, or abdominal wall, forming fistulas.bubble_chart Clinical Manifestations
It can be divided into acute and chronic types, with the latter being the most common.
Acute subcutaneous nodular peritonitis is mostly caused by hematogenous dissemination of miliary subcutaneous nodules, or it may result from the sudden rupture of intra-abdominal subcutaneous nodular lesions and mesenteric lymph node nodules. Patients often experience acute abdominal pain, which spreads throughout the abdomen, accompanied by low-grade fever, abdominal distension and fullness, and other symptoms. Physical examination reveals widespread grade I tenderness, rebound tenderness, and abdominal muscle rigidity. Systemic toxic symptoms are less severe than those of bacterial peritonitis. The white blood cell count is not elevated.
Chronic subcutaneous nodular peritonitis usually develops slowly. It manifests as chronic subcutaneous toxic symptoms, such as emaciation, lack of strength, poor appetite, anemia, night sweats, and irregular low-grade fever. Based on the main clinical manifestations, it can be divided into three types: ascitic, adhesive, and caseous ulcerative.
The ascitic type has a slow onset, with the abdomen gradually enlarging until a large amount of ascites appears, accompanied by abdominal dull pain, abdominal distension and fullness, and diarrhea. Physical examination reveals grade I abdominal tenderness and shifting dullness on percussion. Abdominal paracentesis yields a straw-yellow exudate, which may occasionally be bloody or appear turbid with a coffee-bean color, containing yellow flaky microcrystals (cholesterol). Exudative subcutaneous nodular peritonitis can exist alone or as part of multiple serositis, combined with subcutaneous nodular pleuritis, pericarditis, or meningitis.
The adhesive type is characterized by recurrent incomplete small intestinal obstruction. It often presents with paroxysmal abdominal pain, abdominal distension and fullness, accompanied by nausea and vomiting. Physical examination often reveals a doughy sensation in the abdominal wall. Sometimes, varying sizes of intestinal patterns and peristaltic waves can be palpated, with abdominal distension, flatulence, and hyperactive borborygmi. Diarrhea may occur after the obstruction is relieved. Patients often exhibit a chronic sexually transmitted disease-like appearance due to malnutrition and emaciation.The clinical symptoms of the caseous ulcerative type are severe. Due to caseous necrosis and liquefaction of subcutaneous nodular lesions, sometimes accompanied by secondary purulent bacterial infection, patients may experience remittent fever, progressive emaciation, anemia, lack of strength, and even cachexia. Abdominal pain, diarrhea, or symptoms of intestinal obstruction such as abdominal distension and fullness, and absence of bowel movements and gas are common. Masses of varying sizes can be palpated in the abdomen, with tenderness. The abdominal wall may feel doughy or board-like. When caseous liquefactive lesions rupture into the abdominal cavity, localized purulent peritonitis occurs. If the lesions penetrate the abdominal wall, there may be redness and swelling, or even rupture leading to abdominal wall fistulas or umbilical fistulas.
bubble_chart Auxiliary Examination
A strongly positive tuberculin reaction in subcutaneous nodules, an increased erythrocyte sedimentation rate, straw-yellow exudate from abdominal puncture fluid, positive bacterial culture from animal inoculation of subcutaneous nodules, multiple calcifications found on abdominal X-ray, and signs of intestinal tuberculosis on barium meal examination all aid in diagnosis. If necessary, laparoscopy and peritoneal membrane biopsy can be performed.
bubble_chart Diagnosisbubble_chart Treatment Measures
Patients with tuberculous peritonitis should enhance nutrition and take appropriate rest. A combination of multiple anti-tuberculosis drugs should be used, such as streptomycin and isoniazid. After 2-3 months, switch to isoniazid and sodium aminosalicylate, with a treatment course of no less than one and a half years. If drug resistance or adverse reactions occur, alternative medications such as rifampin, ethambutol, thioacetazone, or prothionamide may be considered.
For ascitic-type tuberculous peritonitis, after active anti-tuberculosis treatment, ascites drainage may be performed if necessary, followed by intraperitoneal injection of streptomycin, isoniazid, and hydrocortisone to promote ascites absorption.
Surgical intervention is required for adhesive-type abdominal tuberculosis complicated by acute complete intestinal obstruction, caseous-type complicated by intestinal perforation, or localized peritonitis leading to encapsulated abscess formation, or when abdominal wall fistula or vaginal fistula occurs. For loose and localized adhesions, adhesiolysis may be performed. For dense and localized adhesions, forced separation should be avoided, and resection of the affected intestinal segment or side-to-side anastomosis of the proximal and distal bowel may be considered. Primary abdominal tuberculosis lesions, such as tuberculous salpingitis or intestinal tuberculosis, should be resected whenever possible. For unresectable caseous lesions, incision and curettage may be performed, followed by placement of anti-tuberculosis drugs. For chronic incomplete intestinal obstruction, non-surgical therapies such as fasting, fluid replacement, gastrointestinal decompression, and administration of Chinese and Western medications should be prioritized, as they are often effective.