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Spectrum Of Abdominal Tuberculosis (ATB)

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WHO estimates that each year more than 8 million new cases of tuberculosis occur and approximately 3 million persons die from the disease.



Ninety-five percent of tuberculosis cases occur in developing countries.

In Pakistan, TB incidence is about 85-100/100,000 population and in Northern Pakistan it is up to 554/100,000.

Each year around 120,000 new cases are added to the existing cases.

Extrapulmonary TB:

TB can involve any organ from head to toe.

1/6 of TB cases are extra pulmonary and out of them 11- 16 % TB is confined to abdomen.

In HIV infected individuals 50% of extra pulmonary TB is abdominal.

20% of ATB patients had concomitant pulmonary TB.

Distribution:

Abdominal TB may involve:

GI tract (Enteric) 50%

Peritoneum 43%

Lymph nodes 6-8%

Solid viscera like liver spleen, kidney

and pancreas or in any combination.

Enteric TB:

Pathogenesis

Primary.

Secondary:

Swallowing of infected sputum.

Hematogenous spread from active pulmonary or miliary TB.

Ingestion of contaminated milk or food.

Contiguous spread from adjacent organs.

Enteric TB Distribution:

Esophageal TB 0.3 %

Gastric TB 0.2 %

Duodenal TB 2 %

Jejunum/Ileum 35 %

Ileocaecal 42 %

Appendix 1 %

Colon 12 %

AnoRectal 7%

High ileocecal involvement is due to relative stasis, and abundant lymphoid tissue.

Macroscopic Appearance of Enteric TB:

Ulcerative 60 %

Hypertrophic 10 %

Ulcero-hypertrophic / Stricture 30 %

Clinical Manifestations:

The S/S vague and nonspecific.

Nonspecific chronic abdominal pain 80-90 %.

Weight loss 66 %

Palpable mass 25-50 %

Fever 35 %

Altered bowel habit 20 %

Anorexia, fatigue, night sweats or bleeding P/R

Presentation can be chronic, acute, or acute-on-chronic.

Ascites common in ATB than Crohn's disease.

Laboratory Tests:

Mild anemia and increased ESR seen 50-80 %

WBC count is usually normal.

PPD positive in the > 70% of patients but has limitations

Radiology:

Barium enema and small bowel follow-through:

May show mucosal ulcerations and strictures, deformed cecum, and a gaping and incompetent ileocecal valve.

CT Scan of abdomen:

Is the most helpful imaging modality to assess intraluminal and extraluminal pathology, and disease extent.

CT finding is concentric mural thickening of the ileocecal region, with or without proximal intestinal dilatation.

Asymmetric thickening of the medial cecal wall. Lymphadenopathy with hypodense centers or ascites.

Colonoscopy:

In ileocecal TB, ulcers, strictures, nodules, pseudopolyps, fibrous bands, fistulas, and deformed ileocecal valve are seen.

In TB, ulcers tend to be circumferential and are usually surrounded by inflamed mucosa. A patulous or destroyed ileocecal valve with a fish mouth opening is more likely to be caused by TB than CD.

The endoscopic finding of aphthous ulcers with normal surrounding mucosa or the presence of cobblestoning favors the diagnosis of CD.

Diagnosis:

A presumptive diagnosis can be made if there is active pulmonary TB, with clinical/radiologic findings of intestinal TB.

Chest x-ray for active or healed TB is positive in less than 50 percent of patients.

Definitive diagnosis is based upon histology, AFB smear and C/S.

Colonoscopy with biopsy is the most useful nonoperative diagnostic test for ileocecal TB. A combination of histology and culture of biopsy material can establish the diagnosis in up to 80 percent of patients.?

Deep endoscopic biopsies should be taken from the ulcer margins and bed since TB granulomas are often submucosal.?

PCR of biopsy has higher sensitivity and specificity.

Differential Diagnosis:

D/D of Ileocecal TB includes:

Actinomycosis, amebiasis, Yersinia enterocolitica, Crohn's disease, lymphoma, and adenocarcinoma.

Biopsies are helpful.

Amebiasis is usually an acute illness, in few cases, patients may have right-sided colitis or ameboma. Biopsies obtained from these ulcers and normal areas show trophozoites of E. histolytica. Patients typically have organisms in their stool and positive IHA.?

Action When Diagnosis Is Not Clear:

Many authorities recommend initiating antituberculous therapy if there is a high index of suspicion for Enteric TB based upon clinical, radiologic, and endoscopic findings, despite nondiagnostic histological and/or bacteriological studies of biopsies.

Others suggest prompt diagnostic exploratory laparotomy in the absence of a definitive nonoperative diagnosis, since diseases such as CD, lymphoma, or malignancy can mimic TB in every way

Management:

Standard ATT as per pulmonary TB.

Surgery is usually reserved for patients who have developed complications.

Obstruction may be exacerbated during antituberculous therapy due to healing by cicatrisation.

The surgical resection should be conservative.

Peritoneal TB:

Peritoneum is uncommon site of TB.

The risk is increased in patients with cirrhosis, HIV , diabetes mellitus, malignancy, and in patients with peritoneal dialysis (CAPD).

Infection usually is primary but It can also occur via hematogenous spread,transmurally and contiguously from tuberculous salpingitis

As the disease progresses, the visceral and parietal peritoneum become studded with tubercles.

Ascites develops secondary to "exudation" of proteinaceous fluid from the tubercles.

More than 90 percent of patients with TB peritonitis have ascites at the time of presentation, while the remainder present with a more advanced "dry" phase, representing a fibroadhesive form of the disease

Clinical Manifestations:

More than 70 % patients have symptoms for more than four months because of insidious nature of disease and frequently it is unsuspected.

Common symptoms are abdominal pain, fever, and weight loss.?

On examination many patients had a diffusely distended tender abdomen.

The classic doughy abdomen is associated with the fibroadhesive form and is rarely seen.

Diagnosis:

Peritoneal biopsy is gold standard.

Blind peritoneal biopsies is associated with complications including death

In US, peritoneal biopsy via laparoscopy or mini laparotomy has surpassed blind percutaneous peritoneal biopsy.

Laparoscopy appears to be relatively safe complication rate was 2.7 percent in four series comprising 110 patients.

Peritoneal biopsy via mini-laparotomy should be considered if laparoscopy is non-diagnostic.

Laboratory Tests:

CA-125 level. In a series of 10 patients with tuberculous peritonitis, the mean CA-125 level was 475 U/mL, decreasing to normal levels (<35 U/mL) with treatment

Imaging:

Common radiologic features such as peritoneal thickening, omental caking, and the presence of ascites with fine mobile septations on ultrasound and CT imaging may suggest the diagnosis .

Peritoneal Fluid Analysis:

Ascitic fluid with protein content >3.0 mg/dL is seen in in more than 95 percent of patients .

The serum-ascites albumin gradient (SAAG) is <1.1 g/dL.

Leukocyte count of 150 to 4000 mm3, with a relative lymphocytic pleocytosis

AFB smear of ascitic fluid has low yield.

Direct smear for Ziehl-Neelson stain has a reported sensitivity of 0 to 6 percent.

In most series, the frequency of a positive ascites culture is less than 20 percent

The yield of culture may be increased to 83 percent if 1 liter of ascitic fluid, concentrated by centrifugation, is cultured

Polymerase Chain Reaction (PCR):

Polymerase chain reaction (PCR) assays show promise of rapid detection of mycobacteria. However, the utility of ascitic fluid PCR assays in detecting TB peritonitis has not been well established

Adenosine Deaminase Assay (ADA):

ADA is a purine-degrading enzyme that is necessary for the maturation and differentiation of lymphoid cells.

(ADA) of ascitic fluid has been proposed as a useful non-culture method of detecting tuberculous peritonitis.

Sensitivity and specificity of ADA levels in tuberculous ascites have been reported as high as 100 and 97 percent respectively, if a cut off value of >33U/L is used.

Treatment:

Standard ATT as for pulmonary TB

The addition of corticosteroids for the first two to three months of treatment may reduce the incidence of late complications.However, its efficacy has not been established, and potential risk of tuberculous dissemination in the setting of multi-drug resistance

Response to Treatment:

Fever usually resolves within one week of commencing anti-tuberculous treatment.

More than 90 percent of patients have improvement in abdominal ascites within weeks of initiating treatment

Prognosis:

Mortality ranged from 8 to 50 percent in various series.

Advanced age, delay in initiating therapy, and underlying cirrhosis have been associated with higher mortality rates

Summary:

Abdominal TB has complex symptomatology and high index of suspicion is needed for diagnosis.

Diagnosis of abdominal tuberculosis is based upon combination of radiological evidence, histo-pathology finding and the demonstration of current or recent past history of pulmonary tuberculosis.

Yield of mycobacterium for the diagnosis of abdominal tuberculosis is very poor.

Anti TB therapy is the mainstay of treatment and surgery is reserved for complications.

Colonoscopy and biopsy may help in early decision and excluding other diseases.

Minimal laparatomy or laparoscopic biopsy may provide early information in peritoneal TB.

Trial of ATT may be justified in endemic area after reasonable efforts to exclude the serious illnesses like malignancy.
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