Abdominal tuberculosis can involve the peritoneum or other abdominal organs. It is caused by Mycobacterium tuberculosis or other mycobacteria and spreads hematogenously or via ingestion. Clinical features include abdominal pain, weight loss, fever and diarrhea. Diagnosis involves ascitic fluid analysis, imaging, endoscopy and biopsy showing caseating granulomas. Treatment is with anti-tuberculosis drugs for at least 6 months. Complications include intestinal obstruction, perforation and fistula formation requiring surgery. Prevention involves screening, BCG vaccination and treating underlying conditions like HIV/AIDS.

1. ABDOMINAL TUBERCULOSIS
AND PERITONITIS
PRESENTER DR CATHERINE W TEMBA
SUPERVISOR DR RAMADHANI
27TH DECEMBER 2021

2. INTRODUCTION
• At the end of this topic one should be able to do
• Definition
• Etiology
• Pathogenesis
• Associated anatomy
• Diagnosis
• Investigation
• Management
• Prevention

3. MYCOBACTERIA TUBERCULAE

4. Definition
• Abdominal Tuberculosis is a condition in which there is tuberculous infection
of the peritoneum or other organs in the abdomen
• Causative organisms M.tuberculosis
• others
– M. bovis
– Mycobacterium avium-intracellulare complex (MAC)– atypical
mycobacterium
INTRODUCTION

5. INTRODUCTION
• These are;
• aerobic non spore
forming
• non motile bacilli
• wax coat that cause
them to retain red dye
when treated with
acid (AFB)
5

6. INTRODUCTION
• Tuberculosis (TB) is a common and major health problem,
especially in developing countries where, ignorance, poverty,
overcrowding, poor sanitation and malnutrition are prevalent
• Tb peritonitis can occur anywhere in the gastrointestinal truct
together with pancreaticobiliary system
• it can occur as primary infection or the extension from pulmonary
tuberculosis
• Gastrointenstinal tb is the 6th common site of extra pulmonary
tuberculosis

7. cont
It has been declared a global emergency by the WHO and is the most
important communicable disease worldwide.
Approximately one third of the world population is infected with tuberculosis
and about three millions die each year from this disease . Despite increased
health standards in developed countries, the incidence of tuberculosis which
was previously reported to be low in these countries, is again on the rise due to
the influx of immigrants from third world countries, increasing incidence of
human immunodeficiency virus (HIV) infection, an ageing population,
alcoholism, increased use of immunosuppressive drugs, and the emergence of
multi-resistant strains of Mycobacterium tuberculosis.

8. • The annual incidence of tuberculosis is nearly 8 million,with 2
million deaths worldwide
• In developing country-M. bovis cause TB in human and in India
M.Tuberculosis is the commonest
• Disease of poor socioeconomic status-due to poor housing and
poor nutrition
• Before the era of HIV infection >80% TB confined to lung ie
Extrapulmonary TB increases with HIV
• 40-60% TB in HIV+ patient-extra pulmonary
• Globally, proportion of co infected patient >8%
EPIDEMIOLOGY

9. • Abdominal tuberculosis is predominantly a disease of
young adults. Two-thirds of the patients are 21-40 yr old.
But can occur at any age.
• The spectrum of disease in children is different from
adults, in whom adhesive peritoneal and lymph nodal
involvement is more common than the gastrointestinal.
EPIDEMIOLOGY

10. • Mechanisms by which M. tuberculosis reach GIT:
 Hematogenous spread from primary lung usually the ‘miliary’ but
occasionally the cavitating form
 Ingestion of bacilli in sputum from active pulmonary focus
 Direct spread from adjacent organs eg. Tuberculous pyosalpinx
 Via lymph channels from infected LN
• M. bovis infx is through ingestion of unpasturized milk from cows and
primarily produce tonsilar or intestinal lesion.
• In developed world pasturization of milk has eliminated the disease
PATHOGENESIS

11. • M. avium and M. intracelluler are has no virulence in normal host,
but may cause disseminated Infection in immunocompromized
host
• Abdominal tuberculosis is usually secondary to pulmonary
tuberculosis, radiologic evaluation often shows no evidence of
lung disease
• Swallowed organisms directly penetrate the intestinal mucosa
• Mycobacterium escape killing by macrophages and cause tissue
destruction by inducing delayed type hypersensitivity with
caseous necrosis and fibrosis in attempts of healing
PATHOGENESIS

12. • The mucosa becomes hyperemic, edematous, and, in
some cases, ulcerated.
• The serosal surface is normally covered with multiple
tubercles, and mesenteric lymph nodes are frequently
enlarged and thickened.
• Histologically, the granuloma, with caseating granulomas
found most commonly in the lymph nodes
PATHOGENESIS

13. • The gross lesion appearance can be
– ulcerative
– hypertrophic
– ulcerohypertrophic
• These pathological changes are responsible for
complications followed TB infx. I.e perforations,
obstructions, bleeding etc
PATHOGENESIS

14. ABDOMINAL TUBERCULOSIS CLASSIFICATION
• Gastrointestinal tuberculosis
• Tuberculosis pf the mesentery
• Peritonial tuberculosis
• Tuberculosis of the solid viscera
• Miscellaneous

15. 1.Ileocaecal -ulcerative
-hyperplastic-mass
2.TB Peritonitis -acute
-chronic
3.Ileal- stricture type
4.Anorecto-sigmoidal -fistula
-fissure
-abscess
-mass
SITES COMMONLY INVOLVED WITH ABDOMINAL
TB
5.TB mesenteric lymphadenitis
6.TB intra abdominal organs as
part miliary TB –liver;
spleen and other organs
7.Tuberculous omentum
NB: TB is not uncommon in
stomach, duodenum and
jejunum

16. • Spread from LN
• Intestinal lesions
• Tubercular salpingitis
Abdominal LN and peritoneal TB may occur
without GIT involvement in ~1/3 of the cases.
.
Peritoneal involvement occurs from:

17. 1. Ascitic- peritoneal fluid, pale, straw-coloured fluid Patient comes with the
complaint of distension of the abdomen. – increased abdominal pressure 
respiratory compromise, umbilical hernia, inguinal hernia.
2. Encysted (loculated) type – localized swelling- Inflammation confined to
one part of the abdominal cavity.
3. Fibrotic type – masses composed of mesenteric & omental thickening, with
matted bowel loops. Wide spread adhesions  adhesive obstruction.
4. Purulent form . Rare – usually secondary to tuberculous salpingitis –
pockets of adherent intestines and omentum containing tuberculous pus. –
cold abscesses.
Forms of peritoneal TB

18. • The clinical presentation of abdominal tuberculosis can be
– Acute
– chronic
– acute on chronic..
• Complication are:
– Int. obstructions
– Perforation
– Fistula formation
– Obstructive jaundice
• Most patients have constitutional symptoms
Clinical presentation.

19. • Anorexia and malaise(70%)
• Loss of wt (40-90%)
 Pain (80-90%)
 Diarrhoea (11-20%)
 Fever (40-70%)
 Mass in RIF - hard nodular ,non-mobile, non tender with
impaired resonance, mimic carcinoma caecum .
 Constipation, alternating constipation
 Malabsorptionmalnutrition features
 But generally different part involved may present differently in
some aspects and more than one site may be involved
Symptoms and signs

20. • Oesophageal tuberculosis is a rare entity, constituting
only 0.2 per cent of cases of GI tuberculosis.
• Oesophageal involvement occurs mainly by extension of
disease from adjacent lymph nodes.
• The patient usually presents with low grade fever,
dysphagia,odynophagia and an ulcer,
• Most commonly midoesophageal
OESOPHAGEAL TUBERCULOSIS

21. • Stomach & duodenum ~1% of total cases
• Mimics PUD but with shorter hx & not responsive to
conversional PUD rx
• Can mimic Gastric ca
• Duodenal obstruction-extrinsic compression by TB LN->GOO
• Also pt can present with hematemesis, perforation, fistulae,
obstructive jaundice
• CXR usually normal
• Endoscopy – non specific
GASTRODUODENAL TB

22. • This is the commonest part involved due to ;
– Abundant lymphoid tissue at this site- Payer Patches
– Increased physiological stasis
– Increased rate of fluid & electrolyte absorption
– Minimal digestive activity
• 85% to 90% of patients demonstrating disease at this site
• Ileo caecal tuberculosis usually presents with a
mass in the right iliac fossa.
• May present with features of int. obstruction
ILEOCAECAL TB

23. ILEOCAECAL TB
Ileo caecal TB
Stenosing lesion in the Ileocaecal region with circumferential
thickening, with history of constipation, loss of weight in a
veterinarian. Biopsy revealed features favouring Ileocaecal TB
Ileo caecal TB
Proliferative lesion involving the Ileo caecal Junction with multiple
Ulcerations. Biopsy revealed Ileo caecal TB.

24. Circumferential ulceration is characteristic of intestinal
tuberculosis presenting with stricture.
24

25. 1. Obstruction is the most common due to:
 Hyperplastic ileocaecal TB
 Stricture of the small intestines- commonly
multiple
 Adhesions
 Adjacent LN involvement
All may cause traction, narrowing & fixation of
bowel loops
COMPLICATIONS ILEOCAECAL TB:

26. 2. Perforation
 2nd most common cause of SI perforation after
typhoid
 Usually single or proximal to a stricture
 Pneumoperitoneum in CXR
COMPLICATIONS ILEOCAECAL TB:

27. 3. Malabsorption
 Common
 Pathogenesis:
 Bacterial overgrowth in stagnant loop
 Bile salt deconjugation
 Diminished absorptive surface due to
ulceration
 Involvement of lymphatics & LN
COMPLICATIONS ILEOCAECAL TB:

28. • May involve the colon without the involvement
of ileocaecal region
• 9.2% of all cases.
• sigmoid, ascending and transverse colon.
• Multifocal involvement in ~1/3 (28-44%)
• Median symptom duration <1year
COLONIC TB

29. • Pain is predominant symptom (78-90%)
• Hematochezia in <1/3-usually minor
• Overall, TB accounts for ~4% of LGIB
• Other features: fever/anorexia/weight
loss/change in bowel habit
COLONIC TB

30. COLONIC TB
A Case of Colonic Tuberculosis
Mimicking Crohn's Disease.
Nodular ulcers with thickened mucosa
covered with
fibrin.

31. • Hematochezia- most common symptom due to
mucosal trauma by stool
• Constipation
• Rectal stricture, fistulas
• Anal fistula-usually multiple
RECTAL & ANAL TB

32. • NON SPECIFIC TESTS:
Raised ESR
Positive Mantoux test
Anemia
Hypoalbuminemia
CXR
Diagnostic workout

33. • Pale Straw colored
• Protein >3g/dl
• TLC 150-4000/μl, lymphocytes >70%
• ZN Stain +ve in <3% cases
• +ve culture in <20% cases
ASCITIC FLUID EXAMINATION

34. Aminohydrolase that converts adenosine → inosine
• ADA increased due to stimulation of T-cell by mycobacterial Ag
 Serum ADA >54 U/L
 Ascitic fluid ADA >36 U/L
• In co infection with HIV → Normal or low ADA
ADENOSINE DEAMINASE (ADA)

35. • NODULES
 Variable sizes (2-6mm)
 Non friable
 Most common in caecum especially near IC valve
• TUBERCULAR ULCERS
 Large (10-20cm) or small (3-5mm)
 Located between the nodules
 Single or multiple
 Transversely oriented/circumferential contrast to Crohns
 Healing of these “girdle ulcers” → strictures
• Deformed and edematous ileocecal valve
COLONOSCOPY /BIOPSY

36. • 8-10 Bx from the ulcer edge
• Low yield on histopathology as mainly mucosal
disease
• Granuloma in 8-48%
• Caseation in ~1/3 (33-38%) of the positive cases
• AFB stains is variable
• Culture positive in 40%
• Combination of histology & culture give dx in
60%
COLONOSCOPIC DIAGNOSIS

37. • 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 & multiple thick adhesions.
LAPAROSCOPY /Bx

38. • Anti-TB Rx for atleast 6months including 2months of
Rifampicin, Isoniazide, Ethambutol & Pyrizinamide.
• The therapy for MAC infection is evolving; drugs that have been
successfully used in vivo and in vitro include amikacin,
ciprofloxacin, cycloserine, and ethionamide. Clarithromycin has
also been successfully used in combination with other agents
• TB of the abdomen will need surgery for their complications
MANAGEMENT

39. • Ascites – therapeutic tapping
• Intestinal oabstruction
• Adhesions
• Intestinal perforation
• Intestinal fistula
• Purulent peritonitis
COMPLICATIONS

40. • Intestinal obstruction- resection & end to end
anastomosis (entero-enterostomy), or ileotransverse
colonostomy
• Adhesions-relieve the adhesions
• Intestinal perforation- resection & end to end
anastomosis as in intestinal obstruction
• Intestinal fistula- resect & end to end anastomosis
• Purulent peritonitis-laparatomy, abdominal lavage and
drainage
SURGICAL MANAGEMENT

41. • Early Diagnosis & treatment
• Screening of close contacts of known
TB patients
• BCG vaccination
• Healthy living-Housing, proper milk
prep, close follow up of HIV infected
patient
PREVENTION OF TB INFECTION AND ITS
COMPLICATIONS

42. REFERRENCE

43. Referrence

44. REFFERENCE