Drug Sensitive Tuberculosis updates now.pptx

DRUG SENSITIVE TUBERCULOSIS
DR DEBJYOTI DEY
DNB RESIDENT
RESPIRATORY MEDICINE

Presumptive Pulmonary TB
• It refers to a person with any of the symptoms and signs suggestive of TB
• cough for 2 weeks or more
• fever for 2 weeks or more
• significant weight loss
• Haemoptysis
• any abnormality in chest radiograph.
• The following patients are also to be investigated as presumptive PTB
• Contacts of Microbiologically confirmed TB patients having cough of any duration
• Presumptive /confirmed extra-pulmonary TB having cough of any duration
• HIV positive patient having cough of any duration
• Note: Contacts of microbiologically-confirmed TB Patients, PLHIV, diabetics,
malnourished, cancer patients, patients on immune-suppressants or
steroid should be regularly screened for sign and symptoms of TB

Presumptive Extra Pulmonary TB
• It refers to the presence of organ-specific symptoms and signs like
swelling of lymph node, pain and swelling in joints, neck stiffness,
disorientation, etc., and/or constitutional symptoms like significant
weight loss, persistent fever for 2 weeks or more, night sweats.

Presumptive Paediatric TB
• It refers to children with
• Persistent fever and/ or cough for 2 weeks or more
• Loss of weight (loss of more than 5% body weight as compared to highest
weight recorded in last 3 months)/ no weight gain
• and/ or history of contact with infectious TB cases.
• Note: In a symptomatic child, contact with a person with any form of
active TB within last 2 years may be significant

Presumptive DR TB
• It refers to the patient who is eligible for Rifampicin resistant
screening at the time of diagnosis or/and during the course of
treatment for DS TB or H mono/poly resistance. This includes
following patients:
• All Notified TB patients (Public and private) - Follow-up positive on
microscopy including treatment failures on standard first line treatment and
all oral H mono/poly regimen
• Any clinical non-responder including paediatric patients

Microbiologically confirmed TB
• It refers to a presumptive TB case from whom a biological specimen is
• positive for acid fast bacilli
• positive for Mycobacterium tuberculosis on culture
• positive for tuberculosis through Rapid Diagnostic molecular test

Clinically Diagnosed TB
• It refers to a presumptive TB case
• who is not microbiologically confirmed
• has been diagnosed with active TB by a clinician on the basis of
• X-ray abnormalities
• histopathology
• clinical signs
• with a decision to treat the patient with a full course of Anti-TB treatment.
• In children, this is based on the presence of abnormalities
• consistent with TB
• on radiography
• history of exposure to an infectious case
• evidence of TB infection (positive TST)
• clinical findings suggestive of TB
• in the event of negative or unavailable microbiological results

Pulmonary tuberculosis (PTB)
• It refers to any microbiologically confirmed or clinically diagnosed TB
involving the lung parenchyma or the tracheo-bronchial tree.
• A patient with both pulmonary and extra-pulmonary TB should be
classified as a case of Pulmonary TB.
• Miliary TB is classified as PTB because there are lesions in the lungs.

Extra Pulmonary tuberculosis (EPTB)
• It refers to any microbiologically confirmed or clinically diagnosed TB
involving organs other than the lungs such as pleura, lymph nodes,
intestine, genitourinary tract, joint and bones, meninges of the brain
etc.

New TB patient
• A TB patient who has never had treatment for TB or has taken anti-TB
drugs for less than one month is considered as a new TB patient.

Previously treated TB
• A patient who has received one month or more of anti-TB drugs from any source
in the past.
• Recurrent TB patient - A TB Patient previously declared as successfully treated
(cured/treatment completed) and is subsequently found to be microbiologically
confirmed TB is a recurrent TB patient.
• Treatment after failure patients – A TB patient who have previously been treated
for TB and whose treatment failed at the end of their most recent course of
treatment.
• Treatment after lost to follow-up - A TB patient previously treated for TB for one
month or more and was declared lost to follow-up (LFU) in their most recent
course of treatment and subsequently found to be microbiologically confirmed TB
IV.
• Other previously treated patients are those who have previously been treated,
who cannot be classified into any of the above.

Transfer in A TB patient
• A TB patient who has been received for treatment in a Tuberculosis
Unit, after starting treatment in another TB unit where s/he has been
registered is considered as transferred in.

Drug Sensitive Tuberculosis updates now.pptx

Drug Sensitivity Tuberculosis Treatment
• Clinicians should follow Standards for TB care in India (STCI) guidelines for
TB treatment.
• Administer daily fixed dose combinations of first – line anti-tuberculosis
drugs in appropriate weight bands.
• Regimen for Drug-Sensitive TB (DSTB) cases: 2HRZE/4HRE
• This regimen is for H & R sensitive TB cases and cases with unknown
sensitivity pattern.
• Loose Drugs could be used as substitutions in case of adverse drug reaction
or with comorbid conditions.
• Steroids as an adjunctive therapy is useful in patients with TB pericarditis
and meningeal TB, with an initial high dose tapered downwards gradually
over 6 - 8 weeks.

Actions of Anti-TB drugs:
• Early bactericidal activity
• Sterilizing activity
• Ability to prevent emergence of drug resistance

Drugs Action Early bactericidal Sterilizing
activity
Prevention of
emergence of drug
resistance
Isoniazide (H) 1. exerting early bactericidal activity
2. prevents emergence of drug resistant mutants
to any companion drug
3. has low rates of adverse drug reactions
+ + + + + + + + + +
Rifampicin (R) 1. a potent bactericidal and sterilizing drug
2. acting on semi- dormant bacilli which multiply
intermittently and causing relapse.
+ + + + + + + + + +
Pyrazinamide
(Z)
1. a bactericidal and sterilizing drug
2. effective in eliminating the semi dormant bacilli
multiplying slowly in an acidic environment.
+ + + - + +
Ethambutol (E) 1. an effective bacteriostatic drug
2. preventing emergence of resistance to other
companion drugs.
+ + + + + +
Streptomycin
(S)
1. a bactericidal drug
2. reduce septicaemia and toxicity + - + +

Two phases of treatment:
• Intensive phase (IP) consists of 8 weeks (56 doses) of isoniazid (H),
rifampicin (R), pyrazinamide (Z) and ethambutol (E) given under direct
observation in daily dosages as per weight band categories.
• Continuation phase (CP) consists of 16 weeks (112 doses) of isoniazid,
rifampicin and ethambutol in daily dosages.
• The CP may be extended by 12-24 weeks in certain forms of TB like
CNS TB, Skeletal TB, Disseminated TB etc.
• Extension beyond 12 weeks should only be on recommendation of
specialists

Roles of Intensive Phase
• To achieve rapid killing of
actively multiplying bacillary
population
• To eliminate naturally occurring
drug resistant mutants
• To prevent the further
emergence of drug resistant
mutants
Role of continuation phase
• To elimination of persisters
which are responsible for
relapses.

Fixed Dose Combinations (FDCs)
• It refer to products containing two or more active ingredients in fixed
doses, used for a particular indication(s).
• IN NTEP, for Adults - 4-FDC (given in IP) consists of HRZE and 3-FDC
(given in CP) consists of HRE
• For paediatric patients -Dispersible 3 FDC consists of HRZ and
Dispersible 2 FDC consists of HR.

Advantages of FDCs
• Simplicity of treatment
• Increased patient acceptance – Fewer tablets to swallow – Prevents
'concealed' irregularity
• Increased health worker compliance – Fewer tablets to handle, hence
quicker supervision of DOT
• Easier drug management
• Reduced use of monotherapy – Lower risk of misuse of single drugs
• Lower risk of emergence of drug resistance
• Easier to adjust dosages by body weight

Drug dosages for first line anti- TB drugs
Drugs Adult (mg/kg daily) Children (mg/kg daily) Max. dose for children
(mg)
ISONIAZIDE 5 (4 - 6) 10 (7 – 15) 300
RIFAMPICIN 10 (8 - 12) 15 (10 – 20) 600
PYRAZINAMIDE 25 (20 - 30) 35 (30 – 40) 2000
ETHAMBUTOL 15 (12 - 18) 20 (15 – 25) 1500
STREPTOMYCIN 15 (15 - 20) 20 (15 – 20) 1000
Streptomycin is administered only in certain situations, like TB meningitis or if any first line drug need to be
replaced due to ADR as per weight of the patient. Ethambutol is given separately for children to monitor
ophthalmic ADR.

Daily Dose Schedule for Adults (as per weight
bands)

Treatment outcomes for drug susceptible TB
Patients
• Cured: Microbiologically confirmed TB patients at the beginning of treatment
who was smear or culture negative at the end of the complete treatment
• Treatment completed: A TB patient who has completed treatment without
evidence of failure or clinical deterioration BUT with no record to show that the
smear or culture results of biological specimen in the last month of treatment
was negative, either because test was not done or because result is unavailable.
• Failure: A TB patient whose biological specimen is positive by smear or culture at
end of treatment.
• Failure to Respond: A case of paediatric TB who fails to have microbiological
conversion to negative status or fails to respond clinically / or deteriorates after
12 weeks of compliant treatment shall be deemed to have failed response
provided alternative diagnosis/ reasons for nonresponse have been ruled out.

Treatment outcomes for drug susceptible TB
Patients
• Lost to follow up: A TB patient whose treatment was interrupted
continuously for ONE month or more.
• Not Evaluated - A TB Patient for whom no treatment outcome is assigned.
This includes former “transfer-out”.
• Treatment Regimen Changed - A TB patient who is on first line regimen and
has been diagnosed as having DRTB and switched to drug resistant TB
regimen prior to being declared as failed.
• Died: A patient who has died during the course of anti-TB treatment
• Treatment Success: TB patients either cured or treatment completed are
accounted in treatment success. It is an indicator and not an outcome.

SIDE EFFECTS OF ANTI TUBERCULAR DRUGS
AND THEIR MANAGEMENT

Side effects of first line anti-TB drugs:
Drug Main effects Rare effects
Isoniazid Peripheral neuropathy, Skin rash,
Hepatitis, Sleepiness and lethargy
Convulsions, Psychosis, Arthralgia,
Anaemia
Rifampicin Gastrointestinal: abdominal pain, nausea,
vomiting Hepatitis Generalised cutaneous
reactions Thrombocytopenic purpura
Osteomalacia, Pseudomemberanous
colitis, Pseudoadrenal crisis Acute renal
failure Haemolytic anaemia
Pyrazinamide Arthralgia, Hepatitis, Gastrointestina Cutaneous reactions, Sideroblastic
anaemia
Ethambutol Retrobulbar neuritis Generalised cutaneous reactions,
Arthralgia, Peripheral neuropathy,
Hepatitis (very rare)
Streptomycin Allergy, severe fever, Burning or tingling
sensation, Vertigo, Nausea and vomiting,
Difficult or painful urination, Blurred or double
vision,Hearing impairment – SEVERE,
Fast/irregular heart beats

Symptom-based approach to evaluation of
possible side effects of anti-TB drugs
Symptoms Cause Action to be taken
by HW
Action to be taken by MO
Vomiting or
epigastric
discomfort
Any oral
medicatio
ns
Reassure patient.
Give drugs with less
water and over a
longer period of time
(e.g. 20 minutes). Do not
give drugs on an empty
stomach
Maintain hydration
Consider treatment with anti-emetics (e.g. domperidone) and
proton pump inhibitors (e.g. Omeprazole)
Itching /
Rashes
Isoniazid
(and other
drugs also)
Reassure patient Itching without
rash or a mild
rash:
• Continue
treatment and
give
antihistamines
Itching with moderate to severe rash
• Stop all drugs till symptoms subside and give
antihistamines
• Patients with mucosal involvement, fever and hypotension
will require treatment with corticosteroids
• When the reaction subsides reintroduce drugs one by one
in this order (INH > Rifampicin > Pyrazinamide > Ethambutol)
• Re-introduce each drug in a small dose and gradually
increase over 3 days before introducing the next drug.

by HW
Tingling / burning /
numbness in the
hands and feet
Isoniazid Pyridoxine 100 mg/day orally or
parenterally until symptoms subside.
If not responding to pyridoxine > require
treatment with amitryptiline.
Joint pains Pyrazinamide Reassure
Increase intake of
liquids
NSAIDs like Paracetamol, Aspirin or
Ibuprofen and in severe cases
Indomethacin for a week to 10 days
In severe cases estimate serum uric acid
levels - If significantly raised treat with
NSAIDs and colchicine.
In severe cases with normal or slightly
elevated uric acid consider reduction of
the dose of Pyrazinamide.

by HW
Impaired vision Ethambutol Stop Ethambutol Refer to ophthalmologist for evaluation
Impaired vision may, within a few weeks, or
may not return to normal after stopping
ethambutol. Don’t restart ethambutol.
Ringing in the ears Loss of
hearing Dizziness and loss
of balance
Streptomycin Stop Streptomycin Refer to ENT specialist for
opinion
As hearing loss is usually not reversible do
not restart Streptomycin

by HW
Hepatitis:
Anorexia,
Nausea,
vomiting,
Jaundice
Isoniazid,
Rifampicin or
Pyrazinamide
STOP all anti TB
drugs, Refer patient
for evaluation
• Rule out other causes of hepatitis
• Do not restart treatment till symptoms resolve and liver
enzymes return to baseline levels
• If liver enzymes cannot be performed wait for 2 weeks
after jaundice has disappeared to restart treatment
• Restart treatment with one drug at a time starting with
Rifampicin > INH > Pyrazinamide.
• In patients with severe disease in whom treatment
cannot be stopped use a non-hepatotoxic regimen
consisting of Streptomycin and Ethambutol

Tuberculous Lymphadenitis
• Lymph node tuberculosis (LNTB) is the most common form of EPTB in
India, accounting for around 35% of EPTB cases.
• Among all tuberculous lymphadenitis, cervical adenopathy is most
common (45-75% cases), but inguinal, axillary, mesenteric and
mediastinal involvement have also been described.

Clinical features
• In addition to common constitutional symptoms
• TB of the deep lymph nodes in the chest (mediastinal TB) may
present with cough or shortness of breath.
• Abdominal LNTB patients may have abdominal pain or distension.
• The most common presentation is isolated chronic non-tender
lymphadenopathy in a young adult without systemic symptoms other
than fever, most commonly in the cervical region.

Pathogenesis
• Various portals of entries of infection are described for acquiring
mycobacterium tuberculous lymphadenitis:
• Via respiratory tract - haematogenous and lymphatic dissemination. Hilar and
mediastinal lymph nodes are usually involved initially.
• Via tonsil - spreads via the lymphatics to the draining cervical lymph nodes.
(TB infection involving the tonsils, adenoids, and Waldeyer’s ring → Cervical
tuberculous lymphadenitis → cervical lymphadenopathy)
• Abdominal tuberculous lymphadenopathy may occur via swallowing of
sputum or milk infected with M. tuberculosis/M. bovis.

Progressions
Superficial lymph node
involvement
Multiplication of M.
tuberculosis
Delayed hypersensitivity
with marked hyperaemia,
swelling, necrosis and
caseation of the centre of
the nodes
inflammation, progressive
swelling and matting with
other nodes within a
group
Adhesion to the adjacent
skin may result in
induration and purplish
discolouration.
Softening of centre of the
enlarging gland
Caseous material may
rupture into surrounding
tissue or through the skin
with sinus formation.

Jones and Campbell classified peripheral
tuberculous lymph nodes:
• Stage 1: Reactive lymphadenitis - enlarged, firm, mobile, discrete
nodes showing non-specific reactive hyperplasia
• Stage 2: Peri adenitis -large rubbery nodes fixed to surrounding tissue
• Stage 3: Cold abscess -central softening due to abscess formation
• Stage 4: Collar-stud abscess formation
• Stage 5: Sinus tract formation

History Taking Points
• Duration of swelling: usually variable, can be acute (1-2 weeks) in
some cases to chronic (months) in some cases.
• Associated symptoms such as fever, weight loss and loss of appetite.
• Contact/past history of tuberculosis must be sought for.
• History of tobacco/alcohol/drug abuse
• Treatment history includes the history of previous ATT intake
(including drug, dose, duration and compliance).

Examination
• Size of lymph node:
• Significant if >2 cm diameter in the
inguinal region and >1 cm in other
regions.
• Consistency of lymph node:
• Hard – Malignancy/ Metastasis/ Chronic
infection
• Firm / Rubbery – Lymphoma/ Chronic
Leukemia
• Soft – Acute Leukemia
• Fixation:
• Fixed - malignancy/inflammation
• Matted - tuberculosis (conglomerated
group of lymph node)/ sarcoidosis/
lymphoma/ metastatic carcinoma
• Tenderness:
• Acute viral/ bacterial infection
• Rapid tumor expansion/ bleeding into
nodes
• Organomegaly:
• Liver/spleen
In deep-seated lymphadenopathy surveillance of all peripheral lymph node is recommended.

Investigations
• Routine investigation: CBC, LFT, KFT, ESR, RBS, HIV serology
• Radiology: Chest X-ray, Ultrasonography, CT Scan, MRI/PET- CT
• Sampling: FNA, Biopsy (Excisional biopsy > Incisional biopsy), EBUS-
TBNA/cTBNA
• Microbiological and pathological: FNAC, Molecular (NAAT), Culture
(solid/liquid), Cyto-histopathology

Treatment
• Standard first-line regimen is recommended for peripheral lymph
node TB
• Six months ATT: 2 months IP (HRZE) + 4 months CP (HRE)
• Continuation phase may be extended by 3 months

Follow Up
• Follow up of clinical response should be done at 1, 2, 4 and 6 months.
• Consider the possibility of treatment failure in patients who have worsened
or deteriorated after initial improvement.
• Imaging to be repeated if clinically indicated.
• Development of LN fluctuation – should undergo aspiration.
• Sinus tracts - Any worsening after 8 weeks of therapy – en-bloc resection of
the involved lymph node chain to avoid sinus tract formation.
• Some patients with LNTB have residual lymphadenopathy at the end of
treatment, >1 cm in size:
• Partial responders (clinical features have persisted or reappeared): Additional 3
months of HRE, followed by a biopsy sent for histology and TB culture.
• Residual fibrotic LN (clinical features have resolved): ATT need not be extended.

Pleural Tuberculosis
• Pleural TB is a leading cause of exudative pleural effusion in our
country
• pleural involvement is the second most common EPTB.

Pathophysiology
• Immunological factors: Delayed hypersensitivity type phenomenon to
nucleic acids of TB bacilli
• Due to the rupture of subpleural foci with the entry of mycobacterial
antigen into the pleural space
• Contiguous spread from lung - Haematogenous and lymphatic spread
• Reactivation of dormant TB foci

Clinical Features
• Symptoms:
• Most common clinical symptom is cough followed by chest pain.
• Fever
• Shortness of breath
• Constitutional symptoms like Night sweats, Weight loss
• On examination,
• Around 90% of tuberculous effusions are unilateral involving less than 2/3 of
the hemithorax.
• Less than half (20-50%) of the patients have associated pulmonary lesions.

Investigations
• CXR (to confirm pleural effusion)
• Sputum for AFB/NAAT
• Pleural tap/ Thoracentesis
(ultrasound-assisted) with Pleural
fluid analysis :
• Cell Types
• Cell count (total and differential)
• Protein
• Glucose
• Gram stain
• Bacterial cultures
• Stain for acid-fast bacilli
• Adenosine deaminase (ADA)
• NAAT
• Cytology evaluation
• CT chest (before pleural biopsy)
• Pleural biopsy (image-guided/
thoracoscopic) (If diagnosis is
uncertain) and Histopathology
• HIV serology
• CBC, LFT, KFTs, PT/INR

Management
• Anti Tubercular Therapy - 2HRZE + 4HRE (Total: 6 Months)
• Pleural Fluid Drainage (for symptomatic relief) via chest tube
drainage/pigtail catheter drainage

Complications
• Lack Of Response
• Drug Resistance
• Immune reconstitution inflammatory syndrome (IRIS)
• Superadded infection
• Pleural Thickening → restrictive lung pathology, fibrothorax → need
decortication
• Empyema
• Hydro-Pneumothorax

Follow Up
• Monthly visits with monitoring for adverse drug events, documentation of
vitals, fever, weight, examination findings.
• Chest radiographs should be done for monitoring at 2 months and 6
months.
• Improvement: significant/near-complete resolution of symptoms or
calcification/pleural thickening.
• In spite of treatment for 2 months if the patient is having worsening of
symptoms, lack of improvement or increasing effusion; clinical failure
should be suspected. Such patients should be:
• Evaluated for drug-resistant tuberculosis
• Evaluate for alternate diagnosis by pleural biopsy, USG , CT scan etc.

Pericardial Tuberculosis
• The most common presentation of pericardial tuberculosis is in the
form of pericardial effusion.

Pathophysiology
• Tubercle bacilli can enter the pericardium via one of the following
routes:
1. Retrograde lymphatic spread from adjacent lymph nodes
2. Hematogenous spread
3. Adjacent spread from lung, spine or pleural involvement

Clinical features
• Tuberculous pericarditis most commonly present as form of
pericardial effusion of variable duration, followed by constrictive
pericarditis, myopericarditis and rarely cardiac tamponade.
• Constrictive pericarditis may have a subacute or chronic presentation.
• Myopericarditis usually presents as pericarditis with concurrent
abnormal cardiac ejection fraction and/or elevated serum levels of
cardiac enzymes.

Clinical features
• Clinical features attributable to pericardial disease:
• Chest discomfort, shortness of breath, orthopnoea
• Features of congestive heart failure, ascites out of proportion to minimal or
absent pedal oedema
• Tamponade – hypotension, muffled heart sound, raised JVP, tachycardia,
pulsus paradoxus (>10 mm of Hg drop in SBP with inspiration)
• Constitutional symptoms: fever with night sweats, significant weight
loss, loss of appetite
• Pericardial calcification, cardiomegaly

Investigations
• CBC, LFT, RFT
• HIV Serology
• Chest X-Ray
• CECT Thorax
• ECG
• Echocardiogram
• Cardiac MRI
• Pericardiocentesis and Pericardial fluid
analysis for
• Cell types
• Cell counts and Differential counts
• LDH
• Malignant cytology
• Cultures
• GeneXpert
• ADA

Treatment
• 2HRZE + 4HRE (for a total duration of at least 6 months).
• Use of Corticosteroid: an initial adjuvant corticosteroid therapy may be
used (Conditional recommendation, very low certainty in the evidence).
• In HIV negative pt – corticosteroids may reduce deaths from all causes and the need
for repeat pericardiocentesis.
• Prednisone in a dose of 1mg/kg for 4 weeks followed by 0.5mg/kg for 4 weeks and
tapers gradually over next two to four weeks.
• Surgical Intervention:
• Pericardiocentesis – indicated as an urgent intervention in cardiac tamponade
• Pericardiectomy – on treatment option in constrictive pericardial disease as a late
complication

Central Nervous System Tuberculosis
• TB of Central Nervous System (CNS) is the most severe form of TB and
is almost always fatal if left untreated.
• The leptomeningeal form is the most common and most severe form
of CNS TB.
• Tuberculomas and brain abscesses are less common than Tuberculous
meningitis (TBM) and have lower mortality and morbidity.

Pathogenesis
Primary Infection
Encountered by
macrophages
Infected macrophages
reach regional lymph
nodes
Disseminated via the
bloodstream to various
organs including the CNS
Macrophages contain the
bacilli in granuloma,
establishing a focus of
latency with dormant
bacilli within.
Due to certain unknown
mechanisms, dormant
bacilli gets reactivated
leading to rupture of focus manifesting in the form
of TB meningitis or latent foci may enlarge at their
original site, leading to the formation of
tuberculoma

Spectrum Of CNS TB
• Meningeal Involvement: most common form of CNS TB. Meningeal involvement
may be further divided into:-
• Leptomeningeal involvement: It implies the involvement of pia-arachnoid layers and it is the
most severe form of CNS TB.
• Patchy-meningeal involvement: It implies the involvement of dura mater.
• Parenchymal involvement – it includes
• Cerebritis & TB abscess
• Tuberculomas
• Miliary TB
• TB encephalopathy
• Spinal TB
• TB radiculomyelitis
• Myelitic tuberculomas
• Extrinsic (epidural abscess)

Clinical Features
• TB Meningitis:
• Vomiting
• Altered sensorium
• Anorexia
• Seizures
• Vision impairment
• Meningeal signs
• Papilledema
• 1 or more cranial nerve palsy
• Optic atrophy
• Constitutional symptoms
• History of recent (within the past year)
close contact with an individual with PTB
or positive TST or IGRA ( only in children
• Tuberculomas And
Abscess
• Mass lesion causing focal
neurological deficits
depending on anatomical
location and/or seizure
• found in concurrence
with TBM

A. Contrast-enhanced CT
scan demonstrates an
intense enhancement of the
basal meninges. Note the
widening of the temporal
horns, due to
communicating
hydrocephalus.
B. Axial gadolinium-
enhanced T1-weighted MR
image demonstrates marked
enhancement in the basal
subarachnoidal cisterns
BASAL EXUDATES

Tuberculoma
Gadolinium enhanced MRI showed a ring-enhancing mass in the right parietal lobe
Magnetic resonance imaging (MRI) of
the brain with gadolinium contrast
showing multiple ring enhancing lesions

Tuberculous arachnoiditis
Tuberculous arachnoiditis, on
sagittal T1-weighted (A)
T2-weighted (B)
short tau inversion recovery (C)
images

Investiagtions
• CBC, CRP, LFT, RFT,
Electrolytes
• HIV Serology
• Chest X Ray- PA view
• USG whole abdomen
• Mantoux (optional)
• NCCT/CECT head-
Preferred as initial
investigation
• MRI brain (and spine if
indicated) in selective
cases
Lumber puncture with CSF analysis
(Perform CT head prior to procedure)
• Cell count & type
• Protein
• Sugar
• Gene Xpert /
TrueNat
• Grams stain
• Bacterial culture
• AFB stain
• AFB
culture/sensitivity
• India Ink
• Cryptococcal antigen
• Fungal smear & culture
• Cytopathology
• Wet mount
• VDRL
• Toxoplasma PCR
• Viral PCR

TBM diagnostic criteria
A. Clinical
1. Fever and headache lasting for more than 14 days
(mandatory).
2. Vomiting, alteration of sensorium or focal deficit (optional).
B. Cerebrospinal fluid
1. Pleocytosis with more than 20 cells, predominantly (greater
than 60%) lymphocytes, protein greater than 100mg%, sugars
less than 60% of corresponding blood sugars.
2. Negative India ink studies and cytology for malignant cells
(in relevant situations).
C. Radiological
CT head showing 2 or more:
1. Exudates in basal cisterns or in Sylvian fissures
2. Hydrocephalus
3. Infarcts
4. Gyral enhancement
D. Extra neural tuberculosis
1. Active TB of lungs, G.I.T, G.U.T, lymph nodes, skeletal system
or skin - by radiological or
2. Microbiological tests or by presence of caseation necrosis on
histopathological examination.
Based on presence of these features in
combination of one or more, TBM can be
clinically categorised as:
1. Definite tuberculous meningitis
(i) Clinical criteria (A)
(ii) Bacterial isolation from CSF or diagnosis at autopsy
2. Highly probable tuberculous meningitis
(ii) All 3 of (B), (C) and (D)
3. Probable tuberculous meningitis
(ii) Any 2 of (B), (C) and (D)
4. Possible tuberculous meningitis
(ii) Any one of (B), (C) and (D).

British MRC Grading (Severity)
• Grade 1 TBM: MILD - Glasgow coma score (GCS) of 15 with no focal
neurological deficit; those without altered consciousness or focal neurological
signs
• Grade 2 TBM: MODERATE - GCS of 15 with a focal neurological deficit, or a
GCS of 11–14; those with altered consciousness who are not comatose and
those with moderate neurological signs, e.g. single cranial nerve palsies,
paraparesis, and hemiparesis
• Grade 3 TBM: SEVERE - GCS of ≤10; for comatose patients and those with
multiple cranial nerve palsies, hemiplegia or paraplegia, or both.
• Severity assessment helps to stratify patients and is useful to predict
prognosis

Management
• Primary therapy: Antitubercular drugs
• Intensive phase - 4 drugs HRZ + E/S x 2 months
• Continuation phase - 3 drugs HRE x at least 8-10 months
• ATT should be continued for a minimum duration of 12 months, which may
be further extended in case of partial or no response in confirmed cases.
• Experts recommend therapy for a duration of at least 12-18 months in case
of tuberculomas or abscesses.
• Lesions may persist after therapy; therefore, extended therapy beyond 18
months may not be required in most of the cases.

Management
• Steroids: Use of steroids was found to be associated with a reduced risk of
death. Such benefits were not statistically significant in HIV positive patients.
• The following recommendations have
been made regarding the use of
steroids in TBM
1. HIV negative patients –
recommended for at least 4 weeks
2. HIV positive patients – may be
used after ruling out opportunistic
infections e.g., cryptococcal
meningitis and cerebral
toxoplasmosis
• Steroids are indicated in TBM at a dose of 0.4mg/Kg
(dexamethasone), to be tapered over 6-8 weeks.
• Most accepted regimen - IV
DEXAMETHASONE
0.4mg /Kg x 2 weeks followed by
0.3mg/kg x 1 week followed by
0.2mg/Kg x 1 week followed by
4mg/day x 1 week followed by
1mg/day x 1 week and stop.

Management
• Surgery - indicated in special situations -
• Presence of associated obstructive hydrocephalus
• Features of raised ICP
• Large space-occupying tuberculomas with raised ICT
• In addition – if features of associated compartmental shifts
• Complications – physician need to assess and manage the metabolic
or pathological complications such as
a) Metabolic - electrolyte disturbances, Pituitary dysfunction
b) Medical – vasculitis related stroke, drugs toxicity & interactions, seizures, co-
infections
c) Surgical – hydrocephalus, raised intracranial pressure.

Follow Up
• For further follow-up, repeat imaging may not be required unless clinically
indicated (new-onset seizures, neurological signs or symptoms).
• Assessment for response to therapy is based on clinical assessment.
• If clinically no response within 6 - 8 weeks of effective therapy, further
evaluation should be done to rule out the following:
• Drug-resistant TB
• Other infectious causes
• Neurocysticercosis
• Toxoplasmosis
• Cryptococcomas
• Malignancy – primary or metastatic
• IRIS – usually within 3-6 months of therapy

Abdominal Tuberculosis
• Intestinal TB is the most commonly encountered sub-type, followed
by peritoneal and lymph node TB.
• Presumptive Abdominal TB: A patient with abdominal pain,
distension, fever, unexplained weight loss, chronic diarrhoea or an
abdominal mass.

Classifications
PERITONEAL INTESTINAL ESOPHAGEAL GASTRO-
DUODENAL
PERIANAL PANCREATIC HEPATO-
BILIARY
• Abdominal
distension
• Pain abdomen
• Fever
• Recurrent
intestinal
colic
• Partial/
incomplete
intestinal
obstruction
• Chronic
diarrhoea
• Weight loss
• Palpable mass
abdomen
• Lower
gastrointestinal
bleeding
• Dysphagia
Odynophagia
• Hematemesis
• Constitutional
symptoms
• Gastric outlet
obstruction
• Gastrointestinal
bleed
• Simple/
Complex
peri-anal fistula
• Persistent
discharge
• Fistulae which
recur after
multiple
surgeries
• Abdominal pain
• Obstructive
jaundice
• Dilated
pancreatic or
bile duct with
(peri )-pancreatic
mass or cyst
• Constitutional
symptoms
• FUO
• Hepatomegaly
. Jaundice
• Elevated ALP
• SOL
• Hepatic abscess

Management Of Peritoneal Tuberculosis
• Medical management (the cornerstone of treatment):
• Intestinal and peritoneal: 6 months of first-line ATT (2 HRZE+ 4 HRE), with the
decision to extend treatment made on a case to case basis.
• Pancreatic and hepato-biliary TB: 6 months with the decision to extend
treatment made on a case to case basis.
• Referral: Presumptive intestinal and presumptive peritoneal TB
where the diagnosis is uncertain require referral to a
gastroenterologist or radiologist for further evaluation and tissue
sampling for testing.
• Follow-up: Patients are assessed at 2 months (end of IP) and at 6
months after starting treatment

Management Of Intestinal Tuberculosis
• Recommended standard treatment for adult and children with ITB:
2RHZE/4RHE.
• Duration of the treatment may be extended depending on the clinical
response as per clinician discretion.
• Management of complications:
• Strictures can be managed with endoscopic dilatation, but some cases require
resection of the stricture or hemicolectomy.
• Oesophageal and gastroduodenal TB patients rarely require surgery; ATT
alone is usually adequate.
• Duodenal strictures may be treated with balloon dilatation. Bypass surgery
may be required if this is not successful.

Management Of Intestinal Tuberculosis
• It is also important to understand that successful treatment of ITB need not
necessarily result in resolution of strictures.
• Endoscopic evaluation when feasible may show mucosal healing which can be taken as an
end point for ATT.
• Diffusion weighted MRI is an alternative.
• Endoscopic or surgical interventions may be needed.
• Monitoring Response
• Routinely, patients should be monitored for drug induced liver injury(DILI) at 2, 3 and 6
months.
• There are no standard guidelines regarding the frequency and modality of assessing response
and is left to the discretion of the treating physician.
• In a confirmed case response should be monitored clinically at 3 and 6 months, if required
imaging may be done in selected patients.
• Worsening or no clinical response after initial treatment may indicate treatment failure.
• However, in the first 3 months deterioration may be due to paradoxical reaction.

Management Of Pancreatic and Hepatobiliary
Tuberculosis
• ATT is the mainstay of
treatment
• The duration of treatment is
controversial with
differences of opinion
amongst various guideline
bodies.
• Index TB guidelines endorse
a standard 6 months
therapy, which can be
extended up to 1 year as per
clinician discretion.
• Role of surgery
• Tuberculous abscesses may need surgical
drainage
• TB causing biliary obstruction frequently
requires initial decompression with
endoscopic retrograde cholangio-
pancreatography (ERCP) or percutaneous
transhepatic cholangiography (PTC)
• Biliary strictures may necessitate the
placement of stents
• Biliary diversion surgery is an alternative
treatment for extensive strictures

The treatment regimen has to be modified according to the degree of liver dysfunction, as follows:
Child Turcotte Pugh
score
Liver disease Treatment recommended
Child’s grade A
cirrhosis
CTP </=7
Stable
MELD score <18
Regimens containing 2 hepatotoxic drugs (rather
than the three in the standard regimen): Avoid
Pyrazinamide
• 9 months of isoniazid and rifampicin,
plus ethambutol (until or unless isoniazid
susceptibility is documented)
• 2 months of isoniazid, rifampicin, streptomycin,
and ethambutol, followed by 6 months of
isoniazid, rifampicin, and ethambutol
Child’s grade B
cirrhosis or
CTP 8-10
Advanced
MELD score
18–25
Regimens containing only 1 potentially hepatotoxic
drug: Rifampicin preferred over isoniazid, Pyrazinamide not to be used
Child’s grade C
cirrhosis or
CTP >/=11
Very advanced, MELD
score >25
Regimens containing no potentially hepatotoxic drugs:
18-24 months therapy using a combination of
Streptomycin/Amikacin/Kanamycin, Ethambutol, and
levofloxacin, or other second-line oral drugs

Skeletal Tuberculosis
• Skeletal tuberculosis is the 3rd most common form of Extrapulmonary
Tuberculosis and it is the most disabling form of TB.

Pathophysiology
• It is paucibacillary
• Predominantly hematogenous spread, followed by the lymphatic or
contiguous spread.
• The primary site of disease lies almost always in the lungs and rarely
at other sites like genito-urinary sources.
Granuloma
formation
Caseous
necrosis
Hyperaemia
induced
osteopenia
Pathological
fracture

Clinical Features
SPINE TUBERCULOSIS
• Persistent localized pain in spine region
>6 weeks, night pains (most common
symptom)
• Local tenderness / cold abscess
• Recent onset deformity in the back
• Recent neurological deficit (lower limb
motor or sensory loss/ bowel and bladder
incontinence and possibly respiratory
paralysis)
• Persistent heaviness around the waist /
Girdle pain
• Fever, cough, weight loss & night pains
• History of close contact with TB
OTHER JOINTS/BONES
• Persistent localized pain & swelling >6
weeks
• Mono-articular joint involvement
• Discharging sinus (+/-)
• Fluctuant swelling with or without
inflammation
• Painful restriction of involved joint
movements
• Wasting around the area
• Fever, cough, weight loss & night pains
• History of close contact with TB

Classification of Spinal Tuberculosis
• Spinal TB is classified into four types based on location within the
vertebrae:
• Paradiscal: most common variety, due arterial spread (disc and adjacent
para-discal body is supplied by the same artery)
• Central: due to venous spread
• Anterior: subperiosteal spread
• Appendiceal or posterior: least common, structural instability of the spine

Investigations
• CBC, LFT, KFT, FBS, PPBS, HbA1C,
ESR, CRP
• HIV serology
• Imaging is a cornerstone for
diagnosis for spinal TB.
• Gadolinium contrast enhanced MRI
(CE-MRI): It is the investigation of
choice
• Non contrast MRI
• CT scan
• X-rays
• PET-CT scan
• CT guided or C-arm guided
biopsy is the preferred procedure
to access tissue for
microbiological /
histopathological diagnosis.
• Bacterial culture
• AFB staining
• NAAT
• Mycobacterial culture
• Histopathological examination
• LPA

Management of Spinal TB
• Drug Therapy:
• Drugs: 2HRZE (Intensive phase) plus 10 HRE (Continuation phase)
• Duration: 12 months (extendable to 18 months on case-by-case
basis)

Surgical management and its indications
In patients with neurological deficit
1. Neural complications developing
or getting worse or remaining
stationary during the course of non-
operative treatment (3-4 weeks)
2. Paraplegia of rapid onset
3. Severe neurological deficits
i. flaccid paraplegia
ii. Complete sensory/motor loss
iii. Bowel or bladder incontinence
4. Painful paraplegia in elderly
patients
In absence of neurological deficit
a. When diagnosis is uncertain and open
biopsy is indicated
b. Mechanical instability of spine
c. Suspected drug resistance
d. Spinal deformity – severe kyphotic
deformity at presentation (example >60
degrees) or progressive kyphotic
deformity
e. Mass effect - dysphagia/stridor
f. Cold abscess - not responsive to
repeated aspiration with ATT

Complications and sequelae:
• Early onset paraplegia: Secondary to acute inflammation, good prognosis with
treatment.
• Late onset paraplegia: Reappearance of neural deficit after a disease-free period
of at least 2 years in patients who completed ATT and achieved healed status.
Occurs due to progression of deformity in healed patients, or a result of relapse
of infection.
• Deformity: Kyphosis is the most common deformity occurring due to collapse of
vertebrae. Predominantly the anterior spine is involved. Deformities interfere
with lung function. Surgical correction is required in most cases.
• Cold abscess can be formed on either side of the spine, anteriorly or posteriorly.
It can extend to involve loco-regional structures according to the level of spinal
lesion. cold abscess may lead to pseudo-flexion deformity at the hip joint. In
addition to ATT, it requires drainage (USG or CT guided). Extended drainage using
a pigtail is better than a single time aspiration.

Follow Up:
• The protocolized follow up of spinal TB patients is as follows: (Regular follow up
of spinal TB patients is essential in order to take a timely call on surgical
intervention)
1. Patients with neurological deficits require staging and grading of their deficit on each visit.
2. Patients without neurological deficit should be assessed weekly for neurological signs.
3. Repeat X-rays of the spine every 3 months.
4. Repeat CE-MRI
a. After 6 months, if there is suspicion of poor treatment response (but is not required in most)
b. At treatment completion (12 months) it would be prudent to assess healing before discontinuation
of therapy.
c. Findings of quiescent burnt out infection which do not warrant continuation of ATT such as
bony/fibrous ankylosis or thin walled cysts without enhancement must be identified.
5. After completion of treatment, follow up every 6 months for at least 2 years.

Follow Up:
• Drug resistance is to be suspected in patients with spinal tuberculosis
on ATT for 5 months or more showing:
1. Poor clinical and radiological response.
2. Appearance of a fresh lesion of osteoarticular tuberculosis
3. Deterioration of spinal deformity
4. Appearance of discharging sinus
5. Wound dehiscence of previously operated scar

Treatment Of TB Of Other Joints And Bones:
• Non surgical treatment:
• 12 months of ATT: 2HRZE/10HRE
• analgesia
• rest to the joint
• above-knee skin traction or skeletal traction for around 4 weeks
• Surgical treatment:
• In cases with synovitis and early arthritis, surgery is rarely required
• Synovectomy and joint debridement are indicated if the response to nonoperative
treatment is inadequate at 6 to 8 weeks.
• In advanced arthritis, arthrolysis with joint debridement is applicable
• In subluxation/dislocation, excision arthroplasty (e.g., Girdlestone), arthrodesis or
total hip replacement are indicated.

Cutaneous Tuberculosis
• Cutaneous tuberculosis is rare and thereby a high index of suspicion
should be kept.
• ETIOLOGY
• M.tuberculosis
• M.bovis
• BCG (rarely)

Classification of Cutaneous Tuberculosis

Clinical features
• Presence of ulcer or discharging sinus over lymph node, bone & joints
• Persistent asymptomatic reddish/ reddish brown lesion of >6 months
duration which may show scarring
• Persistent warty or verrucous lesion of > 6 months duration
• Note:
• Fever and other constitutional symptoms are generally absent in isolated
cutaneous TB
• To ask for past history of tuberculosis
• To elicit the exposure to known or suspected tuberculosis cases and to look
for other sites of dissemination

Investigations
• Routine investigations: Complete blood counts, liver/kidney function
tests, ESR, Mantoux Test
• Chest radiograph
• Skin Biopsy
• taken from active edge
• Histopathological examination (if compatible with TB, mainstay of diagnosis)
• Microbiological tests GeneXpert
• AFB stain and culture (poor sensitivity)

Treatment
• 6 months of ATT; 2HRZE followed by 4HRE
• No role of topical or oral steroids
• First Follow up at 4-6 weeks - majority improves
• To look for ADRs
• Subsequently every 6-8 weeks to look for resolution, if no response
after 8 weeks - alternate diagnosis/DR-TB; refer to higher centre

Otorhinolaryngeal Tuberculosis
• The common forms of extra-nodal ENT TB include laryngeal,
sinonasal, oropharyngeal, para/retropharyngeal TB, salivary gland TB,
thyroid gland TB, TB otitis media and TB mastoiditis.
• Laryngeal TB is highly infectious and needs appropriate precautions.

Clinical features
SUSPECTED TB OTITIS MEDIA SUSPECTED LARYGEAL TB SUSPECTED
SINONASAL/OROPHARYNGEAL
/DEEP NECK TB ABSCESS
Chronic painless otorrhea
Early hearing loss
Facial nerve palsy
Mastoid bone necrosis
Multiple tympanic membrane
perforations
Pale exuberant granulation tissue
Chronic hoarseness
Productive cough
Dysphagia/odynophagia
Stridor
Vocal cords
Ulcerative lesions
Nodular lesions
Polypoidal lesions
Edema
Erythema
Moth-eaten appearance with
distorted architecture
Nasal discharge/obstruction
Epistaxis
Dysphagia/odynophagia
Drooling of saliva
Polypoidal granulation tissue
Edema of uvula/palate/epiglottis
Deep neck abscess
Past history of tuberculosis or any exposure to known or suspected tuberculosis cases

Investigations
• Routine investigations: Complete blood counts, liver/kidney function tests,
ESR, CRP, HIV, Mantoux Test, chest radiograph
• Complete ENT review:
• Rhinoscopy + otoscopy + laryngoscopy followed by tissue sampling(preferably
PUNCH BIOPSY)
• Pure tone audiometry (if indicated)
• CT PNS/temporal bone/head/
• Cervical spine with contrast (as indicated)
• Processing of tissue sample:
• NAAT/AFB staining/MGIT culture
• Histopathology
• other relevant cultures (fungal/bacterial)

Management
• Unlike other EPTB, laryngeal TB is highly infectious and needs appropriate
precautions.
• Anti-tubercular therapy: 2HRZE + 4-10 HRE.
• Total duration: 6-12months.
• Longer duration preferred in bony involvement as in TB Otitis Media,
osteomyelitis of nasal bones/petrous apex/anterior skull base/cervical
spine etc.
• Treatment may be stopped after completion of entire duration of
treatment and resolution of all signs and symptoms.
• No role of steroids.
• Aspiration of large abscesses in case of impending complications,
preferably ultrasound guided to avoid procedure related complication.

Follow Up
• If no adequate response by 2 months, suspect and investigate for
drug-resistant TB.
• Drug related complications
• Primarily vestibulotoxic – Streptomycin
• Primarily ototoxic – Kanamycin, Amikacin
• Pure tone audiometry is investigation of choice
• In resource limited setting, screen with Rinne/Weber tests
• In case of lack of a suitable alternative drug, the risk of further hearing loss
versus risk and benefit of adding drugs from DR-TB regimen should be
weighed.

Ocular Tuberculosis
• Ocular Tuberculosis can cause moderate-severe visual impairment.
• Posterior uveitis is the most common presentation

Pathogenesis
• Primary ocular TB is rare.
• Most cases of ocular TB are secondary due to hematogenous spread
from tuberculosis elsewhere in the body.
• Posterior uveitis is the most common presentation of intraocular TB.
• Ocular TB is usually paucibacillary.

Clinical Features
• The common presentations of ocular TB are choroid tubercle,
choroidal tuberculoma and granulomatous uveitis.
• Less common presentations include subretinal abscess, recurrent non
granulomatous uveitis, scleritis, eyelid granuloma, etc.
• Ocular TB may present with
• red eye
• blurred vision
• Photophobia
• eye pain
• Floaters
• flashing lights (photopsia).

Investigations
• Principle of investigations:
• To identify the ocular pathology
• To identify/rule out coexisting tuberculosis of other organs of the body
• Chest X-ray, Contrast-enhanced CT (CECT) : To identify coexisting pulmonary tuberculosis
• USG or CECT of the abdomen: To identify peritoneal or intra-abdominal lymph node
tuberculosis.
• If any neck lymph nodes are present, an FNAC or biopsy should be done
• An HIV test should be done in all cases of ocular TB
• Ocular diagnostic modalities: Help in characterising the type of involvement in ocular TB
• Slit-lamp microscopy
• Optical Coherence Tomography (OCT)
• Fundus Fluorescein Angiography (FFA).

Treatment
• ATT: 2 months of RHEZ + 4 months of RH
• The total duration of treatment is a minimum of 6 months which can be
extended up to 9 months
• Add pyridoxine 10 mg/day
• Corticosteroids : Topical steroids eye drops for severe/anterior chamber
inflammation and Systemic corticosteroids for severe inflammation.
• Paramacular and optic nerve head TB requires treatment with ATT together
with systemic corticosteroids (oral prednisolone 1 mg/kg/day) followed by
tapering doses depending on the clinical response.

Treatment
• Among the ATT drugs, ethambutol and linezolid can produce optic
neuritis as adverse effects.
• Development of neovascularization warrants photocoagulation of the
retina.
• Indications for surgery:
• complications of retinal vasculitis: vitreous haemorrhage, tractional or
combined retinal detachment, epiretinal membrane, etc.
• complications of uveitis: cataract and glaucoma

Follow Up
• Frequency of follow up: 1-2 weeks in 1st month followed by monthly
for 3 months & then 3 monthly
• Eye: Clinical grading of inflammation using fundus photographs & OCT
scans (if available)
• Steroids:
• Topical: Monitor IOP, cataract and any signs of bacterial/ fungal infection
• Systemic steroids: Monitor body weight, blood sugar & blood pressure

Urogenital Tuberculosis
• It is classified into three broad categories
• Urinary tuberculosis: Involvement of the kidneys, ureters, bladder and/ or
urethra.
• Female genital tuberculosis: Involvement uterus, fallopian tubes, ovaries,
vulva and/ or vagina.
• Male genital tuberculosis: Involvement of the epididymis, prostate, testes
and/or penis.

Urinary Tuberculosis Pathophysiology
Urinary tuberculosis occurs
as a result of hematogenous
spread from a pulmonary
focus.
Tubercle bacilli are seeded in
the renal cortex to form
cortical granulomas.
May remain dormant for
years.
Foci get activated during
diminished host immunity
Spread to renal medulla to
cause papillitis.
Papillary necrosis in the
renal medulla causes
cavitary changes.
May progress to
pyelonephritis or
pyonephrosis.
Tuberculous involvement of
the renal pelvis leads to the
subsequent involvement of
the ureters and the lower
urinary tract.
Strictures and dilatations of
the ureters are common in
end-stage urinary
tuberculosis.
Lower urinary tract disease
manifests with granulomas
and fibrosis of the urinary
bladder.

Clinical Features Of Urinary Tuberculosis
• Urinary tuberculosis is mostly asymptomatic(till the ureter and/or bladder
is involved)
• Urinary tuberculosis is suspected when patients present with the following
symptoms for 2 weeks or more with no response with antibiotics for 3-7
days:
• Lower urinary tract symptoms like dysuria, increased frequency, nocturia etc.
• Hematuria
• Flank pain
• Systemic systems like fever, weight loss, night sweat may also present.
• On clinical examination
• Suprapubic pain
• Renal angle tenderness - present in case of pyelonephritis.

Urinary Tuberculosis Investigations
• Urine Analysis:
• Urine R/M, C/S: concurrent
bacterial infection with coliforms
• Urine for NAAT
• Urine AFB: ZN staining
• Urine C/S for TB: Liquid MGIT
• CBC with ESR, Liver Function
Tests, Renal Function Tests
• Chest X-ray: for evidence of
pulmonary focus
• HIV (ICTC): higher association
with EPTB
• Imaging:
• Ultrasonography of the urinary
tract: Initial imaging of choice - to
identify any lesions in the urinary
tract/kidney
• Intravenous urography and/or
cystography
• CECT with CT urography
• Cystourethroscopy with or without
biopsy (may be considered)
• MR Urography (only in special cases
e.g., patients with deranged KFT)

Urinary Tuberculosis Management
• The aim of the management:
• to achieve cure
• to prevent long term sequelae
• to restore functionality of the kidneys and the urogenital tract, wherever
possible.
• Anti-tubercular therapy (ATT) daily regimen to be given for 6 months
in the following regimen:
• HRZE: 2 months (Intensive phase) + HRE: 4 months (Continuation Phase)
• Urology consultation : In case of urinary tract abnormalities.
• Reconstruction surgeries are indicated for ureteric strictures and
reduced bladder capacity

Urinary Tuberculosis Algorithm

Urinary Tuberculosis Complications
• Progression to end-stage renal disease.(Major complication)
• hypertension
• secondary amyloidosis

Urinary Tuberculosis Follow Up
• All patients with urinary tuberculosis will be followed up after 4 weeks
after treatment initiation.
• The following parameters will be monitored during the follow-up visits:
• Improvement in urinary symptoms
• Resolution of systemic symptoms
• Improvement in renal function
• Repeat urine mycobacterial C/S (if positive at the time of diagnosis)
• A repeat ultrasonography KUB to be performed after 4-6 weeks of ATT.
• To refer to urology, if the USG comes abnormal.
• Repeat urine mycobacterial C/S should be done at 2 months and 6 months

Male Genital Tuberculosis
• Male Genital Tuberculosis (MGTB) is defined as a patient with scrotal
pain or swelling for 2 weeks or more not responding to a 7-to-14-day
course of antibiotics.

Pathophysiology of MGTB
• The most common route of spread is hematogenous
• From a primary pulmonary focus to the epididymis (highly vascular)
and the prostate followed by contiguous, canalicular or urinary
spread to testes, seminal vesicles, urethra and penis.
• Isolated testicular involvement is uncommon due to the presence of
blood testis barrier
• Malignancy should be ruled out if testes is involved in isolation.

Clinical Features of MGTB
• Men present with the symptoms
(non responsive to antibiotics)
• Scrotal swelling(most common)
• Scrotal pain
• Discharging scrotal sinuses
• Pelvic pain
• Increased urinary frequency
• Nocturia
• Dysuria
• Hematuria
• Hematospermia
• Infertility
• Systemic symptoms may/may not
be present.
• On Examination:
• Enlarged, hard epididymis +/-
Tenderness
• Thickened, beaded vas
deferens
• Prostatic indurations or
nodules on Digital Rectal Exam.
• Non tender testicular mass
• Perineal or scrotal fistula
• Hydrocele
• Inguinal
lymphadenopathy(rare)

Diagnostic Algorithm for Male Genital TB

Male Genital TB treatment
• Anti-Tubercular Therapy (ATT): Weight based Daily Regimen:
• (H/R/Z/E) for 2 months during the intensive phase
• H/R/E for 4 months, during the continuation Phase
• Aspiration of abscesses: Done against gravity - to prevent fistula
formation.
• Surgical intervention:
• Strictures
• Fistulae

Complications And Follow Up of MGTB
• Patients on treatment are followed up after 8 weeks to assess
response.
• There can be improvement in constitutional symptoms if present
initially.
• Resolution of infertility may not be seen
• Long term complications:
• Infertility
• Sexual dysfunction
• Scrotal and perineal fistulas and strictures

Female Genital Tuberculosis
• Occurs more commonly in pre-menopausal women.
• It is generally secondary to pulmonary involvement with
hematogenous spread. It may also spread by lymphatic route or by
direct spread from abdominal TB.
• FGTB may even develop after sexual intercourse with a man with
tuberculosis of the penis or epididymis(rare).
• Fallopian tubes are most commonly involved followed by uterine
endometrium.

Clinical Features of FGTB
• May be asymptomatic
• Constitutional symptoms
• Fever
• Malaise
• Anorexia
• weight loss.
• The most common form of presentation:
Infertility (either primary or secondary)
• long standing menstrual disturbances
• Chronic abdominal/pelvic pain
• Palpable abdominal mass
• Vaginal discharge of varying duration and
quality
• Urinary disturbances such as incontinence.
• On Examination:
• General examination
• Fever
• Lymphadenopathy
• Abdominal examination
• Mass abdomen (vague or definite)
• Ascites
• Doughy feel of abdomen
• Vaginal examination
• Uterine enlargement (Pyometra)
• Adnexal masses and induration
• Tubo-ovarian mass
• Fullness and tenderness in pouch of
Douglas

Investigations of FGTB
• CXR: To look for coexisting Pulmonary TB.
• HIV Testing
• USG pelvis: To look for anatomic changes.
• Urine Pregnancy Test: to rule out pregnancy
• Endometrial aspirate:
• It is to be taken preferably during the luteal phase of Menstrual Cycle.
• Endometrial biopsy/curettage
• The following samples are to be subjected to saline for:
• WHO approved NAAT – [Sensitivity - 35-46%; Specificity - 100%]
• Microscopy (Fluorescent/ZN staining)
• Culture (MGIT/LJ) and drug sensitivity
• Note: A positive Xpert is confirmatory but a negative test does not always rule out TB

Diagnostic Criteria of FGTB
• Based on any one of:
• Laparoscopic appearance typical for FGTB (tubercles, caseation or
beaded tubes).
• Any gynaecological specimen positive for AFB on microscopy,
GeneXpert or positive for M. tuberculosis on culture.
• Any gynaecological specimen with findings consistent with FGTB on
histopathological examination.

Treatment of FGTB
• ATT: HRZE (2 months) + HRE (4 months).
• Gynecological assessment for diagnosis and treat complications.
• Surgical Management:
• Large, persistent tubo-ovarian abscesses(despite medical treatment): For
drainage.
• Removal of the uterus, both tubes and ovaries – in case of
• Persistent disease
• Tubercles
• Pyosalpinx
• Tubo-ovarian mass
• Non-healing ulcers.

Follow Up of FGTB
• Assess response to treatment at
completion of 6 months of ATT by
USG pelvis.
• If persistent tubo-ovarian masses:
Rule out drug resistance by FNAC
• Infertility:
• Permanent consequence of FGTB
• Does not indicate treatment failure or
re-infection
• Does not warrant repeated courses of
ATT.
• Indications of laparoscopy: Assessing
the prognosis and fertility outcome:
• If tubes, ovaries and uterus are
normal: Spontaneous conception or
ovulation induction
• If fallopian tubes are still not patent:
In-Vitro Fertilization and Embryo
Transfer.
• If ovaries are normal but tubes and
uterus are damaged: Surrogacy.
• If both ovaries are destroyed by the
disease process, or endometrium is
involved: Adoption.

Reference
• National TB elimination Programme, Central TB division, Training
modules for programme managers and medical officers
(https://tbcindia.gov.in)

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