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IN THE NAME OF GOD

IN THE NAME OF GOD. TUBERCULOSIS OF THE GASTROINTESTINAL TRACT. Dr. N. Aletaha MD. Definition . Abdominal tuberculosis: A condition in which there is tuberculous infection of the peritoneum or other organs in the abdomen

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IN THE NAME OF GOD

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  1. IN THE NAME OF GOD

  2. TUBERCULOSIS OF THE GASTROINTESTINAL TRACT Dr. N. Aletaha MD

  3. Definition • Abdominal tuberculosis: • A condition in which there is tuberculous infection of the peritoneum or other organs in the abdomen • Any region of the gastrointestinal tract can be involved with tuberculosis

  4. Gastrointestinal TB is uncommon, making up 3.5% of extrapulmonary cases in the United States.

  5. Abdominal tuberculosis • Is prevalent in developing countries • In recent years there has been an upsurge of gastrointestinal tuberculosis in the United States due to the influx of immigrants from high-risk areas and the AIDS epidemic.

  6. PATHOGENESIS • Robert Koch, a German Scientist who found out the causative organism for TB in1882.

  7. PATHOGENESIS • Mycobacterium tuberculosisis the pathogen responsible for most cases of intestinal tuberculosis. • In some parts of the world, Mycobacterium bovis, an organism found in dairy products (uncommon human pathogen in Western countries).

  8. Gram negative bacillus – Mycobacterium tuberculosis

  9. Tuberculous enteritis

  10. Pathogenesis of TB enteritis • Swallowing of infected sputum • Hematogenous spread from active pulmonary or miliary TB • Ingestion of contaminated milk or food • Contiguous spread from adjacent organs

  11. Pathogenesis • DISTRIBUTION OF DISEASE • Any portion of the gastrointestinal tract may be affected. • The most common site of intestinal involvement is the ileocecal region. The affinity of M. tuberculosis for this site may be due to its relative stasis and abundant lymphoid tissue.

  12. Pathogenesis • The organism penetrates the mucosa and localizes in the submucosal lymphoid tissue, where it initiates an inflammatory reaction with subsequent lymphangitis, endarteritis, granuloma formation, caseation necrosis, mucosal ulceration, and scarring.

  13. macroscopic appearance of the intestinal lesions • Ulcerative (60 percent): multiple superficial ulcers. This pattern has been associated with a virulent clinical course. • Hypertrophic (10 percent): scarring, fibrosis, and pseudotumor lesions. • Ulcerohypertrophic (30 percent): an inflammatory mass centering around the ileocecal valve with thickened and ulcerated intestinal walls. The ulcerohypertrophic form is more commonly seen in ileocecal TB

  14. CLINICAL MANIFESTATIONS • The symptoms and signs are vague and nonspecific. • The presentation can be acute, chronic, or acute-on-chronic.

  15. CLINICAL MANIFESTATIONS • Symptoms • Nonspecific chronic abdominal pain is the most common complaint (in 80 to 90 percent of patients) • Anorexia, fatigue, fever, night sweats, weight loss, diarrhea, constipation, or blood in the stool

  16. CLINICAL MANIFESTATIONS • A palpable right lower quadrant abdominal mass (in 25 to 50 percent of patients). • Small bowel obstruction • colonic perforation • The presence of ascites may help to distinguish ileocecal TB from Crohn's disease.

  17. CLINICAL MANIFESTATIONS • Fistulaand intestinal stricture may occur. • Bowel obstruction is the most common complication and may be due to progressive stricture or adhesions

  18. Laboratory tests • mild anemia • increased sedimentation rate in 50 to 80 percent of patients • The white blood count is usually normal. • positive tuberculin skin test (PPD skin test can be negative in older or immunosuppressed patients).

  19. Radiologic findings • Barium enema and small bowel follow-through mucosal ulcerations and strictures, a deformed cecum, and a gaping and incompetent ileocecal valve.

  20. Radiologic findings • CT scan concentric mural thickening of the ileocecal region, with or without proximal intestinal dilatation. Asymmetric thickening of the medial cecal wall is occasionally seen. Characteristic lymphadenopathy with hypodense centers, representing caseous liquefaction, may be present in the adjacent mesentery.

  21. Colonoscopic findings • Ulcers • Strictures • Nodules • Pseudopolyps • Fibrous bands • Fistulas • Deformed ileocecal valves

  22. Differential diagnosis • Crohn's disease • Lymphoma • Cecal carcinoma. • Actinomycosis • Amebiasis • Yersinia enterocolitica • Typhlitis • Mucoceles • Drug-induced lesions (lesions due to nonsteroidal anti-inflammatory drugs)

  23. Differential diagnosis • Biopsies are helpful in identifying lymphomatous or carcinomatous cells. • Amebiasis is usually an acute illness (in a minority of cases: chronic right-sided colitis or a right colon ameboma). Biopsies from these ulcers show trophozoites of E. histolytica. Patients typically have organisms in their stool and a positive ameba serology. • Y. enterocoliticacan produce mesenteric adenopathy, ulcerations, and thickening of the bowel mucosa. Usually, this infection has a shorter history and resolves spontaneously.

  24. Differential diagnosis • maindifferential diagnosis at endoscopy is Crohn's disease (CD) • This distinction is important since the use of steroids for a misdiagnosis of CD may have harmful consequences in patients with TB enteritis (eg, causing miliary TB)

  25. Differential diagnosis • Aphthous ulcers with normal surrounding mucosa or the presence of cobblestoning favors the diagnosis of CD because these lesions are rarely seen with TB. • TB ulcers tend to be circumferential and are usually surrounded by inflamed mucosa.

  26. Differential diagnosis • A patulous valve with surrounding heaped up folds or a destroyed valve with a fish mouth opening is more likely to be caused by TB than CD. • Tissue samples for PCR and culture in making the distinction between ileocolonicCrohn's disease and intestinal tuberculosis.

  27. Differential diagnosis • Granulomas associated with TB is large and confluent often with caseation necrosis, ulcers are lined by aggregate epithelioidhistiocytes, and disproportionate submucosal inflammation is seen.

  28. Differential diagnosis • Granulomas associated with CD are infrequent, small, nonconfluent, or noncaseating. Microgranulomas, focally enhanced colitis, and high prevalence of chronic inflammation in endoscopically normal appearing areas also characterize CD

  29. DIAGNOSIS • known active pulmonary TB and/or revealing chest x-ray, with clinical/radiologic findings in the bowel suggestive of intestinal TB. (a chest x-ray is positive less than 50 percent) • Definitive diagnosis is based primarily upon histology • Ziehl-Neelsen staining for acid-fast bacilli & Culture (colonoscopy with biopsy)

  30. DIAGNOSIS • Deep endoscopic biopsies should be taken from the ulcer margins and bed since TB granulomas are often submucosal in comparison to the mucosal location of CD granulomas.

  31. DIAGNOSIS • PCR of biopsy specimens (higher sensitivity and specificity than routine culture, results can be obtained in 48 hours instead of weeks). • laparotomy

  32. TREATMENT • Medical treatment of tuberculous enteritis is similar to treatment of pulmonary TB, with conventional antituberculous chemotherapy (RIPE: rifampicin, isoniazid, pyrazinamide, and ethambutol) for two months, followed by rifampicin plus isoniazid (RI) for an additional four to seven months. • Isoniazid (300 mg/day), pyrazinamide (15 to 30 mg/kg/day), and rifampin (600 mg/day),ethambutol (15 mg/kg)

  33. TREATMENT • Surgery is usually reserved for patients who have developed complications, including free perforation, confined perforation with abscess or fistula, massive bleeding, complete obstruction, or obstruction not responding to medical management

  34. Tuberculous peritonitis

  35. Peritoneal tuberculosis • Peritoneal tuberculosis • is an uncommon site of extrapulmonary infection caused by Mycobacterium tuberculosis (TB). • The risk is increased • in patients with cirrhosis, HIV infection, diabetes mellitus, underlying malignancy, following treatment with anti-tumor necrosis factor (TNF) agents, and in patients undergoing continuous ambulatory peritoneal dialysis.

  36. Pathogenesis • Hematogenous spread from active pulmonary or miliary TB • Reactivation of latent tuberculous foci in the peritoneum that were established from hematogenous spread from a primary lung focus • Transmurallyfrom an infected small intestine or contiguously from tuberculoussalpingitis (Much less frequently)

  37. CLINICAL MANIFESTATIONS • Ascites develops secondary to "exudation" of proteinaceous fluid from the tubercles, similar to the mechanism leading to ascites in patients with peritoneal carcinomatosis. • More than 90 percent of patients with TB peritonitis have ascites(Wet form) at the time of presentation • Remainder present with a more advanced "dry" phase, representing a fibroadhesive form of the disease

  38. CLINICAL MANIFESTATIONS  • Ascites (93 percent): most common features • Abdominal pain (73 percent) • Fever (58 percent). • Classic doughy abdomen is associated with the fibroadhesive form of tuberculous peritonitis and is rarely seen.

  39. CLINICAL MANIFESTATIONS • Tuberculosis of female reproductive tract (fallopian tube, endometrium, ovaries) by extension from an intraabdominal focus, hematogenous seeding, or ascending from lower genital tract (cervix, vagina, vulva) infection. • clinical manifestations have been reported including a pelvic mass, infertility, abnormal uterine bleeding, and pelvic pain

  40. CLINICAL MANIFESTATIONS • physical examination were nonspecific in most reports. • Many patients had a diffusely distended tender abdomen. • The classic doughy abdomen is associated with the fibroadhesive form of tuberculous peritonitis and is rarely seen.

  41. CLINICAL MANIFESTATIONS • The salient clinical findings reported in decreasing order of frequency were abdominal tenderness, hepatomegaly, and ascites

  42. Laboratory studies • mild to moderate normochromicnormocytic anemia in most patients • old tuberculosis was visible on chest x-ray in only 33 percent. • There are several reports describing increasedserum CA-125 concentrations in patients with tuberculous peritonitis. In a series of 10 patients, for example, the mean CA-125 level was 475 U/mL, decreasing to normal levels (<35 U/mL) with treatment.

  43. DIAGNOSIS  • paracentesis reveals an exudative fluid with a high protein content and leukocytosis that is usually lymphocytic (although neutrophils occasionally predominate). • Tuberculous peritonitis should be considered in all patients presenting with unexplained lymphocytic ascites with a serum-ascites albumin gradient of <1.1 g/dL

  44. DIAGNOSIS  • The gold-standard for diagnosis is culture growth of Mycobacterium on ascitic fluid or a peritoneal biopsy. • The diagnosis usually requires a peritoneal biopsy performed under direct visualization via laparoscopy or mini laparotomy • serum CA-125 can be increased in ascitesdue to any cause and is therefore more likely to cause confusion than to assist in diagnosis

  45. DIAGNOSIS  • Visual diagnosis during laparoscopy or mini-laparotomy can be diagnostic in up to 95 percent of cases. Typically, the visceral and parietal peritoneum is studded with multiple whitish nodules or tubercles.

  46. tubercles

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