Complication of tuberculosis and management

1. Tuberculous
Meningitis

2.  Tuberculous meningitis is now rare in
developed countries in previously healthy
individuals, but remains common in developing
countries and is seen more frequently as a
secondary infection in patients with AIDS.

3. Pathophysiology:
 Tuberculous meningitis most commonly occurs
shortly after a primary infection in childhood or as
part of miliary tuberculosis. The usual local source of
infection is a caseous focus in the meninges or brain
substance adjacent to the CSF pathway. The brain is
covered by a greenish, gelatinous exudate,
especially around the base, and numerous scattered
tubercles are found on the meninges.

4. Clinical features:
 Onset is much slower than in other bacterial
meningitis –over 2-8 weeks. Untreated tuberculous
meningitis is fatal in a few weeks but complete
recovery is usual if treatment is started at stage 1.
When treatment is started at a later stage, the rate of
death or serious neurological deficit may be high as
30%.

5. Symptoms:
• Headache
• Vomiting
• Low-grade fever
• Lassitude
• Depression
• Confusion
• Behaviour changes

6. Signs:
• Meningism (may be absent)
• Oculomotor palsies
• Papilloedema
• Depression of conscious level
• Focal hemisphere signs

7. Staging of severity:
 Stage I (early): Non specific symptoms & signs
without alteration of consciousness.
 Stage II (intermediate): alteration of consciousness
without coma or delirium + minor focal neurological
signs.
 Stage III (advanced): stupor or coma, severe
neurological deficit, seizures or abnormal movement.

8. Investigations

9. Lumbar puncture:
 The CSF is under increased pressure.
 It is usually clear but, when allowed to stand, a fine
clot ('spider web') may form.
 The fluid contains up to 500 × 106 cells/L,
predominantly lymphocytes.
 There is a rise in protein and a marked fall in
glucose.
 The tubercle bacillus may be detected in a smear of
the centrifuged deposit from the CSF but a negative
result does not exclude the diagnosis.

10.  The CSF should be cultured but, as this result will
not be known for up to 6 weeks, treatment must be
started without waiting for confirmation.
 Brain imaging may show hydrocephalus, brisk
meningeal enhancement on enhanced CT or MRI,
and/or an intracranial tuberculoma.

11. Management:
 Symptomatic:
Fluid and Nutrition
If fever- Paracetamol
If convulsion- anticonvulsive.
 As soon as the diagnosis is made or strongly
suspected, chemotherapy should be started using
one of the regimens:

12. TREATMENT REGIMEN
1)Unsupervised regimen : 6 months regimen,Daily dosing
First 2 months:Isoniazide
Rifampicin
Pyrazinamide
Last 4 months:
Isoniazide
Rifampicin
2)Nine months:
Isoniazide
Rifampicin
12

13. TREATMENTREGIMEN
3)Supervised (Directly observed):6 months,thrice daily
First 2 months:
Isoniazide
Rifampicin
PZA
Last 4 months:
Isoniazide
Rifampicin
4)A less costly:Supervised daily
First 2 months:
INH
Rifampicin
PZA
Ethanbutol
Streptomycin
Last 6 months:
INH
Thiacetazone
13

14. Pyridoxine should
be used to prevent
INH induced
peripheral
neuropathy.

15. 15
The use of corticosteroids in
addition to antituberculous
therapy has been controversial.
• Recent evidence suggests that it
improves mortality but not focal
neurological damage,

16. • Surgical ventricular drainage may be needed if
obstructive hydrocephalus develops.
• Skilled nursing is essential during the acute phase of
the illness, and measures should be put in place to
maintain adequate hydration and nutrition.

17. Miliary
Tuberculosis

18. Miliary Tuberculosis
Definition : The clinical disease that results from the
uncontrolled hematogenous dissemination of
Mycobacterium tuberculosis.

19. Spread:
Spread usually occurs
to the most vascular
organ i.e Liver, Spleen,
Bone marrow and Brain

20. Etiology :
 Erosion of infection into pulmonary vein.
 Bacteria reach the left side of the heart ---enter the
systemic circulation, & seed organs such as the liver
and spleen.
 The bacteria enter the lymph nodes, drain into a
systemic vein and reach the right side of the heart,
there bacteria may seed—or re-seed--- the
lungs,causing the “Miliary” appearance.

21. Pathogenesis:can arise as a
result of :
1. Progressive primary infection.
2. Lymphatic & hematogenous dissemination within 6
months of primary infection.
3. Typically in patients with impaired immunity.
4. Reactivation of a latent focus with subsequent
spread.
5. Iatrogenic spread is rare.( catheterization,solid
organ transplantation)

22. Risk factor:
 Direct contact.
 Living in unsanitary condition.
 Having an unhealthy diet.
 Homeless.
 HIV/AIDS

23. S/S:
 Miliary TB may present acutely but more frequently
is characterised by 2-3 wks of fever,night
sweats,anorexia, wt loss,dry cough.
 Enlarged lymphnode.
 Hepatomegaly(40%).
 Spleenomegaly(15%).
 Pancreatitis(<5%).
 Adrenal insufficiency.
 Stool may be diarrheal.

24. Diagnosis:
 Previous TB history.
 Examination of all accessible fluids for AFB ( sputum
smear,smear from bronchoscopy wash,gastric
aspirate smear,urine smear,pleural fluid, and
peritoneal fluid.
 CSF may be less commonly positive—only examine
when neurological s/s present.
 Auscultation of chest : Frequently normal, but in
more advanced disease, widespread crackle are
evident.

25. Diagnostic Tests:
 Chest x-ray:The classical
appearances of fine 1-2
mm lessions ( Millet seed
) distributed throughout
the lung field.
 Fundoscopy: show
choroidal tubercle.
 Bronchoscopy.
 TB skin test.
 Open lung biopsy.
 Blood cultures.

26.  Faster: AFB sputum smear, rapid nucleic acid
assays(NNA) and PCR.
 Slow: metabolic assay; test production of CO2 or
consumption of CO2 by bacteria.
 Slowest: detection of mycobacterial growth in
culture media ( 4-8 wks)

27. Common lab Findings:
 Anaemia.
 Leukopenia
 Leukocytosis
 Thrombocytopenia
 Thrombocytosis
 Hyponatremia
 Elevated alkaline phosphatase
 Hyperbillirubinemia
 Elevated ESR >50

28. Common lab Findings (Cont…)
 Hypoxemia (PO2 <60)
 Sterile pyuria.

29. Treatment:
 About 25% 0f patients with miliary TB also have
tuberculous meningitis.
 The standard treatment recommended by WHO is
with INH and Rifampicin for 6 months , as well as
ethambutol anm pyrazinamide for last 2 months.
 If there is evidence of meningitis then treatment is
extended to 12 months.

30. THANK YOU
Dr. Asif Nawas
TMC-5th