ABDOMINAL TUBERCULOSIS

Introduction

TB can involve any part of GIT from mouth to anus, peritoneum & pancreatobiliary system.

Very varied presentation possible

TB of GIT- 6th most frequent extrapulmonary site.

HIV & TB

Before era of HIV infection > 80% TB confined to lung

Extrapulmonary TB increases with HIV 40 –60% TB in HIV+ pt - extrapulmonary Globally, propotion of coinfected pt > 8 % ~ 0.4 million people in India coinfected. 16.6% abdominal TB pt in Bombay HIV

+.

Incidence severity of

abdominal TB will increase with

the HIV epidemic

Pathogenesis

Mechanisms by which M. tuberculosis reach the GIT:

Hematogenous spread from primary lung focus

Ingestion of bacilli in sputum from active pulmonary focus.

Direct spread from adjacent organs.

Via lymph channels from infected LN

Most common site - ileocaecal region Increased physiological stasis Increased rate of fluid and electrolyte absorption Minimal digestive activity Abundance of lymphoid tissue at this site.

Distribution of tuberculous lesions

Ileum > caecum > ascending colon > jejunum

>appendix > sigmoid > rectum > duodenum

> stomach > oesophagus

More than one site may be involved

Peritoneal involvement occurs from : Spread from LN

Intestinal lesions or

Tubercular salpingitis

Abdominal LN and peritoneal TB may occur without GIT involvement in ~ 1/3 cases.

Peritoneal tuberculosis occurs in 3 forms.

• Wet type - ascitis.

• Encysted (loculated) type - localized swelling.

• Fibrotic type - masses composed of mesenteric &

omental thickening, with matted bowel loops.

Clinical Features

Mainly disease of young adults

~ 2/3 of pt. are 21-40 yr old

Sex incidence equal.

Clinical presentation Acute / Chronic / Acute on Chronic.

Constitutional symptoms Fever (40%-70%) Weight loss (40%-90%) Anorexia Malaise

Pain (80%-95%) Colicky (luminal stenosis) Continous ( LN involvement)

Diarrhoea (11%-20%) Constipation Alternating constipation and diarrhoea

Tuberculosis of esophagus

Rare ~ 0.2% of total cases

By extension from adjacent LN

Low grade fever / Dysphagia / Odynophagia / Midesophageal ulcer

Mimics esophageal Ca

Gastroduodenal TB

Stomach and duodenum each ~ 1% of total cases

Mimics PUD - shorter history, non response to t/t

Mimics gastric Ca.

Duodenal obstruction - extrinsic compression by tuberculous LN

Hematemesis / Perforation / Fistulae / Obstructive jaundice

Cx-Ray usually normal

Endoscopic picture - non specific

Ileocaecal tuberculosis

Colicky abdominal pain

‘Ball of wind’ rolling in abdomen

Borborygmi

Right iliac fossa lump - ileocaecal region, mesenteric fat and LN

Obstruction Most common complication

Pathogenesis Hyperplastic caecal TB

Strictures of the small intestine--- commonly multiple

Adhesions

Adjacent LN involvement traction, narrowing and fixation of bowel loops.

Perforation

2nd commonest cause after typhoid

Usually single and proximal to a stricture

Clue - TB Chest x-ray, h/o SAIO

Pneumoperitoneum in ~ 50% cases

Malabsorption

Pathogenesis bacterial overgrowth in stagnant loop

bile salt deconjugation

diminished absorptive surface due to ulceration

involvement of lymphatics and LN

Segmental / Isolated colonic tuberculosis

Involvement of the colon without involvement of the ileocaecal region

9.2% of all cases

Multifocal involvement in ~ 1/3 (28% to 44%)

Median symptom duration <1 year

Colonic tuberculosis

Pain --- predominant symptom ( 78%-90% )

Hematochezia in < 1/3 - usually minor

Overall, TB accounts for ~ 4% of LGI bleeding

Other features--- fever / anorexia / weight loss / change in bowel habits

Rectal and Anal Tuberculosis

Hematochezia - most common symp. Due to mucosal trauma by stool

Constitutional symptoms

Constipation

Rectal stricture

Anal fistula – usually multiple

Diagnosis and Investigations

Non specific findings---

Raised ESR

Positive Mantoux test

Anemia

Hypoalbuminaemia

Immunological Tests

ELISA

Response to mycobacteria variable & reproducibility poor

Value of immunological tests remain undefined

Ascitic fluid examination

Straw coloured

Protein >3g/dL

TLC of 150-4000/µl, Lymphocytes >70%

SAAG < 1.1 g/dL

ZN stain + in < 3% cases

+ culture in < 20% cases

Adenosine Deaminase (ADA)

Aminohydrolase that converts adenosine inosine

ADA increased due to stimulation of T-cells by mycobacterial Ag

Serum ADA > 54 U/L

Ascitic fluid ADA > 36 U/L

Ascitic fluid to serum ADA ratio > 0.985

Coinfection with HIV normal or low ADA

Colonoscopy

Colonoscopy - mucosal nodules & ulcers Nodules

Variable sizes (2 to 6mm) Non friable Most common in caecum especially near IC valve.

Tubercular ulcers Large (10 to 20mm) or small (3 to 5mm) Located between the nodules Single or multiple Transversely oriented / circumferential contrast to Crohns Healing of these ‘girdle ulcers’ strictures

Deformed and edematous ileocaecal valve

Colonoscopic Diagnosis

8 –10 Bx from ulcer edge

Low yield on histopath as mainly submucosal disease

Granulomas in 8%-48%

Caseation in ~ 1/3 (33%-38%) of + cases

AFB stains - variable

Culture positivity in 40%

Combination of histology & culture diagnosis in 60%

Laparoscopic Findings

Thickened peritoneum with tubercles-

Multiple, yellowish white, uniform (~ 4-5mm) tubercles

Peritoneum is thickened & hyperemic

Omentum, liver, spleen also studded with tubercles.

Thickened peritoneum without tubercles

Fibro adhesive peritonitis

Markedly thickened peritoneum and multiple thick adhesions

Caseating granulomas + in 85%-90% of Bx

Management

ATT for at least 6 months including 2 months of Rif, INH, Pzide and Etham

However in practice t/t often given for 12 to 18 months

2 recent reports obstructing lesions may relieve with ATT alone

However most will need surgery