A case of tuberculous peritonitis accompanied by tuberculous pleuritis

INTRODUCTION

TB peritonitis is a form of extrapulmonary tuberculosis, a peritoneal or visceral inflammation caused by Mycobacterium tuberculosis.¹ The most common sites of extrapulmonary TB in the body are the lymph nodes, bones, joints, pleura, spinal cord, brain and abdominal cavity. The disease rarely stands alone, but is usually a continuation of the tuberculosis process elsewhere, especially pulmonary tuberculosis.² The World Health Organization (WHO) estimates that globally there are 8.6 million cases of TB, 80% in 22 countries. Extra-pulmonary tuberculosis occurs in about 20% of tuberculosis, while abdominal tuberculosis accounts for about 10% of extra-pulmonary tuberculosis. The incidence and severity of abdominal TB have been reported to increase with the rising incidence of TB and HIV infection.² TB peritonitis is a rare type of abdominal TB, reported to occur in less than 5% of all TB patients. TB peritonitis cases are often found in individuals aged 25-45 years, with a female to male ratio of 1.5:1.³ TB peritonitis infection develops slowly and is characterized by nonspecific symptoms, so delayed diagnosis can increase morbidity and mortality. Patients with TB peritonitis usually present with symptoms lasting 1-12 months, and present with symptoms of abdominal pain, weight loss, loss of appetite, fever, diarrhea, constipation, rectal bleeding, edema, and ascites, which require specific investigations to diagnose.⁴

The following case report will report a patient with TB peritonitis accompanied by TB pleurisy.

CASE REPORT

A 29-year-old woman came to the emergency room of the Buleleng regional general hospital with complaints of an enlarged abdomen, and fever, the complaints had appeared since ±19 days SMRS, complaints accompanied by heartburn complaints such as nausea, vomiting were denied. Other complaints are liquid stools with a frequency of 2-3 times a day accompanied by mucus, without blood since ±19 days ago, urination within normal limits, there is a decrease in appetite. Other complaints such as coughing, tightness, weight loss are denied. Menstruation is within normal limits. The patient said he had no previous history of illness. Treatment history, the patient took Acitral 3x1, Zinc 1x1, Metronidazole 3x500 mg obtained from a general practitioner. The physical examination revealed a weak general condition, compos mentis consciousness, blood pressure 120/80, pulse 90x, respiration 20x, axilla temperature 39.5ºC, SpO2 99% on room air. Body weight 50 kg, height 160 cm with BMI 19.5 kg/m2 (normal weight). On examination of the head and neck there was no anemia, icterus, cyanosis, no oral candidiasis on the tongue, no enlarged lymph nodes and increased JVP. On thorax examination; on chest inspection, there was symmetrical movement of the chest wall, no retraction, normal fremitus, on auscultation; normal vesicular sound in the right chest, and decreased vesicular sound in the left chest, no rhonki and wheezing. Cardiac examination was within normal limits with no murmurs, gallops, and extrasystoles.

Abdominal examination; inspection found distension, on palpation; muscular defans (-) epigastric tenderness (+), undulation (+), on percussion; shifting dullness (+), checkerboard phenomenon (+), on auscultation found increased bowel noise. Examination of extremities; warm (+) on all four extremities, edema (-), CRT <2 seconds. From the results of the complete blood laboratory examination; WBC: 5.58 10³/µl, HGB: 11.2 g/dl, MCV: 81.0 fL, MCH, 26.5 pg, PLT 381 10³/µl, GDA: 90 mg/dl, Ureum: 14.0 mg/dl, Serum Creatinine: 0.56 mg/dl, SGOT; 25.3, SGPT: 21.4, Sodium: 134.2 mmol/l, Potassium: 4.06 mmol/l, Chloride: 98.9 mmol/l, Albumin: 4.25 g/dl. On complete urine examination the results were within normal limits. Complete stool; yellow color, mucus (+), blood (-) leukocytes 4-6/LPB, bacteria (+), worms (-), fungi (-), amoeba (-). On the thorax photo, there was an impression of left pleural effusion, ECG: within normal limits, BOF 3 position: there was ascites, no ileus and pneumoperitoneum. Abdominal ultrasound results: thickening of the peritoneum, ascites, suspected TB peritonitis. liver, gallbladder, pancreas, spleen, kidneys, buli-buli and uterus within normal limits. The rapid molecular test (TCM) and HIV test were negative. The patient was diagnosed with observation of ascites ec suspected TB, pleural effusion ec suspected TB and Acute Gastroenteritis. The next plan is ascites and pleural puncture and fluid analysis. Therapy given: Nacl 0.9% 20 tpm, Paracetamol 1gr IV (if fever), Ceftriaxone 1x2gr IV, Lanzoprasole 1x30 mg IV, Ondancentron 3x4 mg IV, Furosemide 40 mg PO, Spironolactone 100 mg (PO). Ascitic fluid analysis results; rivalta (+), Adenosine Deaminase (ADA): 56.51 U/l, on pleural fluid analysis; Leukocyte cell count: 1584 cells/ul, protein 5.9 g/dl, rivalta (+), Adenosine Deaminase (ADA): 50.28 U/l, Pleural LDH: 680, histopathologic examination of the fluid; there were no malignant cells. Diagnosis: TB peritonitis and TB pleurisy, followed by OAT therapy; FDC 1x3 tab. The patient was hospitalized for 5 days with an improved condition, then the Anti Tuberculosis Drug therapy program for 12 months.

DISCUSSION

TB peritonitis has nonspecific clinical symptoms. The most common complaints are abdominal pain (73%) and ascites (93%) followed by loss of appetite and weight, nausea, vomiting, cough, fever (58%), diarrhea, constipation and night sweats, ascites can be caused by peritoneal tuberculosis or can originate from liver disease, malignancy, heart, kidney and other infectious diseases.⁵ Peritoneal TB with ascites may present with less tenderness than pyogenic peritonitis with perforation.⁵ Peritoneal TB has been classified as the more common "wet type", which is characterized by ascites, and the rarer "plastic or fibroadhesive type", which manifests as an abdominal mass consisting of adherent bowel loops.⁶ TB can reach the peritoneum hematogenously, via the lymphatic system, from ingestion of contaminated sputum from pulmonary TB, contaminated food (especially unpasteurized milk in the case of Mycobacterium bovis), or through direct contact from adjacent foci of infection.⁷ In tuberculous peritonitis, clinical symptoms are non-specific or variable. Complaints and symptoms occur slowly over months, so patients are often unaware of their condition. Complaints range from 2 weeks to 2 years with an average of more than 16 weeks.⁷

On physical examination of patients with tuberculous peritonitis, the most common symptoms are fever, ascites, abdominal swelling, abdominal pain, pallor and fatigue, pleural effusion, hepatomegaly, splenomegaly, intra-abdominal tumor, checkerboard phenomenon, lymphadenopathy, and lung & pleural involvement (based on chest photograph).⁷ Infection of the adjacent pleura may reach the peritoneum, resulting in peritoneal tuberculosis. Pleural effusion is observed in 22 to 32% of patients with peritoneal tuberculosis and pulmonary source in 15 to 20% of cases.⁸ No single test can effectively rule out the diagnosis of peritoneal TB. TB, and a combination of socio-epidemiologic history (e.g., travel, homelessness, incarceration, sick contacts, drug use) and immunologic risk assessment is essential. Classic symptoms such as fever, weight loss, and night sweats may be absent.⁸

The patient was directed to the diagnosis of tuberculous peritonitis and pleural tuberculosis based on several symptoms such as an enlarged abdomen, fever, gastrointestinal complaints such as diarrhea, and typical signs of tuberculous peritonitis, namely the checkerboard phenomenon and unilateral pleural effusion (often, pleural effusion is unilateral, mild to moderate in volume, which is 25 to 75% of patients).⁸ Furthermore, evaluation with other supporting examinations should be done to confirm the diagnosis since most of the patients' complaints are not typical symptoms.⁹

Patients were evaluated for etiology according to standard protocols. Complete blood count, liver function tests, renal function tests, chest X-ray, abdominal ultrasonography, and ascitic fluid analysis, including cell count, albumin, protein, adenosine deaminase activity (ADA).⁹ Changes in hematological indices including white blood cell count, erythrocyte sedimentation rate are nonspecific. Mild to moderate normochromic, normocytikanemia and thrombocytosis are frequent findings. The white blood cell (WBC) count is usually normal but, lymphomonocytosis is not uncommon.¹⁰ The erythrocyte sedimentation rate is almost always elevated but in at least 50% of cases Usually in TB peritonitis, the ascitic fluid is straw-colored with protein >30g/l, and a total cell count of 500-1500/ìl, the cells being predominantly lymphocytes (>70%). A low serum-ascites albumin gradient (<11 g/l) is seen in 100% of patients with TB peritonitis, but the specificity remains low. Due to its low accuracy, ascites LDH measurement is not routinely used.¹⁰ In TB pleurisy, biochemical features include elevated protein levels of more than 4.5 g/dl and slightly elevated DHL.¹⁰ The diagnosis of TB pleurisy is usually made through a combination of clinical history, pleural fluid analysis (predominantly lymphocytic cell count, protein concentration >3.0 g/dl, elevated lactate dehydrogenase often >500 IU/l, and glucose level <60 mg/dl), positive culture in sputum or pleural fluid, and positive ADA level >40 U/l.¹⁰

Ultrasound is an important tool for the diagnosis of peritoneal tuberculosis due to its accessibility, low cost, and ease of performance. Ultrasound is diagnosis-oriented and should be the first diagnostic investigation if peritoneal tuberculosis is suspected, especially in high-risk populations.^11,12 In TB peritonitis, the most common ultrasound result is ascites (84.2%), ascites is easy to recognize and appears echoed if it is free fluid without debris. The presence of internal echoes is characteristic of exudative ascites. Peritoneal thickening (89.4%), omental thickening (73.6%), sonography is more sensitive than CT in detecting diffuse peritoneal thickening, especially in the presence of ascites, which is usually found in chronic inflammation. Mesentery involvement is common and can be found in the early stages and is characterized by wall thickening, associated with increased echogenicity and the presence of multiple lymph nodes in it. Other abdominal lesions are as follows: Splenic nodules, ileocaecal involvement, hepatic nodules, in advanced stages of the disease, lymph nodes can be visualized sonographically as hypoechoic areas with irregular borders due to ossified conglomerates of necrosis.¹² ADA has been studied in body fluids, including ascitic fluid to diagnose TB peritonitis and shown to have high sensitivity and specificity.¹² Tuberculous peritonitis shows an increase in ascitic fluid adenosine deaminase levels to more than 36 U/l. While serum ADA levels also increased to more than 54 U/l, the ratio of ascitic fluid ADA to serum ADA was above 0.98. The presence of all these findings indicates the presence of tuberculosis. ADA acts as a catalytic enzyme in the deamination of adenosine nucleosidase into inosine nucleosidase. ADA is found in lymphocytes and stimulation of lymphocytes increases ADA activity in body fluids. This lymphocyte stimulation is caused by the tuberculosis bacteria which activates the cellular immune response and in turn increases ADA levels. In studies using metaanalysis and systematic review, the results of data calculated from 20 studies including studies that had a total of 2,291 patients showed a pooled sensitivity of 0.90 (95% CI: 0.85 -0.94), a pooled specificity of 0.94 (95% CI: 0.92-0.95), and a DOR of 149 (95% CI: 86-255). The results of the pooled analysis suggested a clinically important diagnostic value of ascitic fluid ADA for tuberculous peritonitis.^12,13 In patients also with pleural tuberculosis where ADA testing can also establish the diagnosis, ADA quantification is an enzyme produced by macrophages and activated T lymphocytes. This quantification is usually elevated, i.e. levels higher than 40 U/l, making it necessary to consider differential diagnosis with other pathologies such as rheumatoid arthritis, systemic lupus erythematosus, lymphoma, some adenocarcinomas, and empyema. The sensitivity of this method varies from 90 to 100% and the specificity of this method varies from 89 to 100%. This method of diagnosis is more sensitive for pleural tuberculosis than pleural histopathologic examination and bacteriologic tests.^12,13

Many doctors prefer a combination of clinical examination with other methods such as laparoscopic biopsy and histopathological examination of peritoneal tissue (which can show caseation necrosis), acid-fast bacilli (AFB) staining, as well as radio-imaging techniques such as abdominal computed tomography (CT) scanning for diagnosis. But all these methods are time-consuming, expensive, insensitive, invasive, or non-specific, making them ineffective for use in daily practice. While CT scans show non-specific findings, both cultures and smears mostly fail to give positive results. No more than 3% of cases show positive AFB smears, while only 20% show positive cultures.¹³ Complications of laparoscopy include bowel perforation, bleeding, infection, and death, but these are rare, seen in <3% of cases. Complications may be more common in fibroadhesive types.¹³ Treatment of tuberculous peritonitis is the same as for pulmonary tuberculosis, i.e. patients should receive at least 6 months of therapy. Patients who have not received treatment and are not resistant to oral antituberculosis drugs are treated with a first-line regimen consisting of an initial phase including Isoniazid 5 mg/kgBW, 15 mg/kgBW Etambutol, Rifampicin 10 mg/kgBW, and Pyrazinamide 25 mg/kgBW given daily for 2 months, then an advanced phase including a combination of Isoniazid (10 mg/kgBW) and Rifampicin (30mg/kgBW) 3x a week for 4 months. This therapy guideline gives good results after 2 months. Treatment of tuberculous peritonitis can be given for 9-12 months (2HRZE/710RH). The treatment guideline can use a Fixed Drug Combination (FDC), which consists of a combination of 2 or 4 types of drugs in one tablet with a dose according to the patient's weight packaged in a package for one patient consisting of an intensive phase every day for 56 days RHZE (150/75/400/275), and an advanced stage of 7 to 10 months RH (150/150) 3x a week. This guidance may improve patient compliance.¹³

CONCLUSION

Early diagnosis, immediate treatment, and follow-up of TB peritonitis are very important to reduce mortality from the disease. From this case it can be concluded that clinical and supporting examinations (radiology) are needed to make the correct diagnosis and body fluid analysis examination can help confirm the diagnosis, with the advantages of being non-invasive, easy to perform, cost-effective, and mostly available in health facilities.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

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