Abdominal tuberculosis

Tuberculosis continues to pose a global health problem with 7-9 million cases diagnosed yearly.
With immigration and the appearance of the HIV pandemic the incidence has gone up
considerably in advanced countries.

The incidence in developing countries is unknown but is very high. For example in Nigeria 10% of
post mortems patients over 10 years and 24% of adults presenting with ascitis showed evidence of
tuberculosis.

Aetiology

The causative organisms of abdominal tuberculosis are;

1. Mycobacterium tuberculosis which can be contracted by
a. Ingestion of contaminated material including materials including milk.
b. Swallowing infected sputum coughed out by the patient if he/she has open
pulmonary tuberculosis
c. Part of military tuberculosis
2. Mycobacterium bovis contracted by drinking non pasteurised milk

Pathology and pathophysiology

The portal of entry of the organism is the Peyer’s patches of the terminal ileum following which
through lymphatic spread the mesenteric lymph nodes where. Usually the infection is arrested and
may only be seen later by the presence of calcified lymph nodes.
On the other hand the disease may progress by causing a chronic granulomatous lesion which
contains a collection of epitheloid and langhans’s giant cells with caseation in the lymph nodes

Two common entities are encountered in abdominal tuberculosis

1. Gastrointestinal tuberculosis
a. Acute
b. Chronic
2. Tuberculous peritonitis
a. Acute
b. Chronic
3. co-existence of both conditions.

Others may include reticulo-endothelial tuberculosis.

Peritonitis is usually part of military tuberculosis but may also be secondary to gastrointestinal or
genitor-urinary tuberculosis.

Gastrointestinal tuberculosis
Tuberculosis may affect any part of the gastrointestinal tract from the oesophagus to the anus. The
commonest site of affection is however, the small intestine and even here the terminal ileum is the
commonest affected.
 Intestinal tuberculosis
There are three types
1. the ulceroconstrictive
2. hypertrophic or hyperplastic
3. a combination of ulceroconstrictive and hyperplastic

Ulceroconstrictive intestinal tuberculosis

This type of intestinal tuberculosis affects the small bowel especially the terminal ileum and starts
with multiple thin ulcers in the Peyer’s patches. These ulcers are circumferential in disposition
since they follow the lymphatics. They cause dense fibrosis which results in strictures of the small
bowel and intestinal obstruction.

Hypertrophic or hyperplastic intestinal tuberculosis

It affects the ileo-caecal area. The terminal ileum and the caecum have thickened walls and narrow
lumina. There is an increase of subserosal fat or the appearance of invasion of the serosa of the
terminal ileum by mesenteric fat. The mucosa is fibrotic and narrowed. There is caseation of the
lymph nodes of the mesentery. There is the formation of a mass in the right iliac fossa.

Tuberculous appendicitis
Not common. Appendix looks normal at operation.

Oesophageal tuberculosis
Rare and causes dysphagia. The ulcer mimics carcinoma and viral and fungal oesophagitis.

Gastric tuberculosis is rare

Anorectal
Ulcer
Wart-like growths
Lupoid (nodular)
Military
Fistula-in-ano

Tuberculous peritonitis

Two types of tuberculous peritonitis are discernible i.e. acute and chronic tuberculous peritonitis.

1. Acute tuberculous peritonitis

a. Ascitis
b. Scattered tubercles with acute inflammatory reaction. Tubercles may simulate fat
necrosis of pancreatitis or nodules of carcinomatosis peritonei.
c. Thickened omentum forming a transverse band across the abdomen.
d. Profuse, clear and straw coloured effusion which may sometimes bloody or
chylous.
2. Chronic tuberculous peritonitis
There are four types of this condition
a. Ascitic – straw coloured fluid similar to what is seen in the acute form. The
peritoneum is studded with tubercles
b. Fibrous or caseous: intestine and viscera are matted together. There is minimal
ascitic fluid. It can lead to intestinal obstruction or fistulation.
 c. Encysted form. There is local encystment of peritoneal fluid in the right iliac fossa
and the pelvis.
d. Purulent : rare and is due to cold abscess formation from caseating lymph nodes.

Reticulo-endothelial tuberculosis

Liver
Mainly part of miliary tuberculosis seen in 50% of patients who die from tuberculosis. There may
be diffuse involvement of the liver, macronodular forms and tuberculous cold abscess form.
Spleen
Splenomegaly, and tuberculous splenic abscess.

Others
Pancreas, adrenal etc.

Clinical features of abdominal tuberculosis

A complex illness with presentation that reflect the site of involvement and may mimic many other
diseases.
Generally there may be
1. Abdominal pain of insidious onset
2. weight loss anorexia
3. fever and night sweats
4. diarrhoea
5. vomiting
6. abdominal distension
7. abdominal mass

The presentation can be divided into

1. Acute presentation
2. Chronic presentation

Clinical presentation acute abdominal tuberculosis

This presentation is seen in 30% of patients and include

1. Acute appendicitis
2. Acute or subacute intestinal obstruction
3. Acute tuberculous peritonitis
a. Straight forward peritonitis from military tuberculosis
b. Perforation of tuberculous ulcer with attendant peritonitis
c. There is abdominal pain, distension, vomiting, abdominal tenderness, guarding and
the presence of free peritoneal fluid

Clinical presentation of chronic abdominal tuberculosis

This may be the presentation of over 70% of patients with abdominal tuberculosis
1. A mass due to hyperplastic or hypertrophied ileo-caecum or omentum is present in 50% of
these patients.
2. abdominal pain
3. abdominal distension
4. Ascitis
5. Doughy abdomen due to glued bowel and omentum
6. pyrexia of unkown origin
7. intestinal obstruction
8. malnutrition

Investigations

1. General
a. Full blood count (FBC) which will show a low haemoglobin, and lymphocytosis
b. Raised ESR in 70% of patients
c. Liver function tests may show hypoalbuminaemia
2. Tuberculin tests
a. Mantoux test which may be positive in 15-100% of patients
b. Heaf test
c. Tine test
3. Chest x-ray
a. Healed or active tuberculous foci
b. Mediastinal lymph node enlargement
c. Pleural effusions
4. Abdominal X-ray
a. Ascitis
b. Loculated fluid collection
c. Calcified lymph nodes and other masses
d. Dilated loops of bowel
5. Peritoneal tap
a. Forms web-like clot when left standing
b. Microscopy
i. Positive for Acid Fast Bacilli (AFB) in 83% of patients.
ii. About a litre of peritoneal fluid is however needed for this diagnosis
iii. There is lymphocytosis. White cell count in peritoneal fluid is greater than
500/ml.
c. Biochemistry
i. Protein is greater than 30g/dl
ii. Glucose
iii. Determination of Adenosine Deaminase activity.
d. Culture on Lowenstein –Jensen (L-J) medium.
6. Barium studies
a. Barium meal and follow through
b. Small bowel enemas
c. Five radiological types
i. Hyperplastic disease
ii. Ulcerative disease
iii. Mixed hyperplastic and ulcerative
iv. Carcinoma-like lesions
v. Stricture formation short and annular. Fistula formation and diverticular.
d. Barium enema only indicated in colonic disease
7. Abdominal ultrasonography for abdominal masses including enlarged liver and spleen and
will detect the presence of cold abscesses in these organs
8. Colonoscopy and biopsy
9. Laparoscopy method of choice if available
10. Percutaneous liver biopsy under ultrasound control
11. Therapeutic trial with antituberculous drugs
12. Laparotomy
 Treatment of abdominal tuberculosis

Treatment of abdominal tuberculosis is mainly medical and involves the use of a combination of
drugs to prevent the development of resistance.
Treatment takes anything up to 18 months and hence compliance is a big problem and patients
may give up taking their drugs when they start feeling better after a couple of months treatment.
The WHO is therefore championing the treatment of tuberculosis by the direct observation
treatment (DOTS) where patients are supervised to take their drugs under direct observation by
health care workers.

Medical treatment
1. Classical usually covers 18 months and uses three drugs streptomycin, isoniazid and
thiacetazone or ethambutol.
2. Shorter courses that use a combination of four or three drugs that includes Rifampicin
which is either added to the classical or given as a substitute for streptomycin. This has
allowed the treatment to be reduced to 6-12 months depending on the combination used.
3. Improvement of nutrition

Surgical treatment
1. Acute peritonitis from perforated small bowel or purulent peritonitis
2. Appendicectomy
3. Intestinal obstruction
a. Resection and anastomosis of strictures
b. Sticturoplasty
In all these patients operation should be followed by an intensive medical treatment to get a cure
finally.

In the long term the course of the cured patient may be complicated by recurrent episodes of small
bowel obstruction secondary to adhesions.