2. Outline
• Overview of Extrapulmonary Tuberculosis (EPTB)
• Clinical evaluation and treatment of EPTB
3. Extrapulmonary TB
Worldwide, between 10-25% of TB infections occur in extrapulmonary sites (outside the lung)
TB can occur in any site, including:
• Pleura
• Lymph nodes
• Bones and joints
• CNS (usually meningitis, but can occur in brain or spine)
• Larynx
• Pericardial
• Abdominal sites
• Kidneys
• Genitourinary tract
• Disseminated (miliary)
4. Extrapulmonary TB
• Especially common in children and people living with HIV, DM
• EPTB occurs ~10% in HIV(-)
• But in HIV(+),
– 33% with extrapulmonary alone
– 33% with pulmonary alone
– 33% both pulmonary and extrapulmonary
(many with negative CXRs)
5. Pathogenesis
Same for Pulmonary and Extrapulmonary TB
Droplet nuclei containing tubercle bacilli are inhaled,enter the lungs,
and travel to the alveoli.Tubercle bacilli multiply in the alveoli.
A small number of tubercle bacilli enter the bloodstream and spread
throughout the body. The tubercle bacilli may reach any part of the
body, including areas where TB disease is more likely to develop (such
as the brain, larynx, lymph node, lung, spine, bone, or kidney).
6. Pathogenesis
Within 2 to 8 weeks, special immune cells called macrophages ingest
and surround the tubercle bacilli. The cells form a barrier shell, called a
granuloma, that keeps the bacilli contained and under control (LTBI).
If the immune system cannot keep the tubercle bacilli under control,
the bacilli begin to multiply rapidly (TB disease). This process can occur
in different areas in the body, such as the lungs, kidneys, brain, or
bone.
7. Medical Evaluation of Extrapulmonary TB
• Symptoms of disease (what and how long)
• History of TB exposure, infection, or prior disease
• Past TB treatment
• Demographic risk factors for TB
• Medical conditions that increase risk for TB disease
– HIV
– Diabetes
– Other immunosuppression
– Under-nutrition
8. Extrapulmonary TB Symptoms
Can have the same symptoms as people with
Pulmonary TB:
– fever, night sweats, fatigue, loss of appetite, weight loss.
In addition, patients often develop complaints specific to the body site infected with TB.
Examples:
– Blood in the urine (TB of the kidney)
– Headache/confusion (TB meningitis)
– Back pain (TB of the spine)
– Hoarseness (TB of the larynx)
– Disseminated (milliary) TB may have no localizing signs,
may present with anemia, or low platelets
9. Diagnosis of Extrapulmonary TB
• Physical Exam
• Specimens should be obtained from the suspected sites of involvement
– AFB smear, culture
– Drug-susceptibility testing
– Nucleic acid amplification (NAA) testing
– Histopathologic examination
• Always evaluate for pulmonary TB:
symptom screen, CXR and sputum evaluation, especially in persons
with HIV
• Provider-initiated HIV testing
10. Diagnostic Challenges
• Often more difficult to diagnose extrapulmonary TB
• Because EPTB is less common, we often first think of other causes for
the patient’s symptoms
– E.g., pain in the right ankle more likely a sprained ankle than TB
of the joint
• Secondly, EPTB often occurs in body sites that are difficult to access
(e.g., the liver, which cannot be touched, or examined easily).
• Resource-limited settings may not have diagnostic capability to obtain
clinical specimen for testing EPTB
11. TB Lymphadenitis
Epidemiology
• TB lymphadenitis represents 30% of EPTB;
• Represents reactivation at site seeded hematogenously during primary TB
– Peak age from children, to 30-40 years old
– Female to male ratio: 1.4 to 1
– HIV-infected
Known historically as “scrofula” or the “King’sEvil”, this refers to TB of the
superficial lymphatics usually of the neck
12. TB Lymphadenitis
Typical Presentation
Most often presents as isolated chronic,
non tender unilateral mass in ant or post
cervical triangles
– Firm discrete mass or matted
nodes fixed to surrounding structures
– Multiple nodes may be involved
– Overlying skin may be indurated
– Uncommon: fluctuance, draining
sinus; bilateral involvement
Differential diagnosis
Non-tuberculous mycobacteria,
other infections, sarcoid, neoplasm
13. TB Lymphadenitis
Primary Diagnostic Tests
• Fine needle aspirate is safer but less sensitive than biopsy
– Combining both cytology and microbiology can increase
sensitivity to 91%
• Nucleic acid amplification tests (NAAT) are underutilized
– Automated NAAT (Xpert) active study
14. Pleural Tuberculosis
• Second most common site of extrapulmonary TB
• Up to 20% in countries where HIV common
• Rupture of sub-pleural focus into the pleural space with inflammatory
response
• Symptoms: pleuritic chest pain, SOB, fever
• HIV-infected more likely to have +smear/culture and +pleural biopsy
15. Pleural Tuberculosis
• Pleural effusion:
Unilateral
Exudative, lymphocytic
pH 7.3-7.4
Smear positive <5%
Culture positive <50%
• Pleural biopsy
Pathology and microbiology
combined sensitivity 65-95%
• Adenosine deaminase (ADA) level
– Overall several meta- analyses show
sensitivity of ADA around 91% and
specificity 89%
– Similar performance in HIV infected
16. Miliary TB
Milliary TB occurs when tubercle bacilli
enter the bloodstream and are carried to
all parts of the body
Wide range of presentations
May include on one extreme ARDS and
on the other extreme failure to thrive
without fever
Symptoms may be dominated by
whatever organ system is primarily
involved
Typical patient has a febrile wasting
syndrome of 2-4 months duration
17. Miliary TB: Diagnosis
The typical patient has an under lying disease that has lead to
immunosuppression to some degree.
Non-specific symptoms are the rule
Rigors are present rarely
All organs can be involved
Many findings such as organomegaly are more common in children
18. CXR Findings in Miliary TB
CXR shows miliary pattern in
more than half of cases
In those with an initial normal
CXR, a miliary pattern will become
apparent in days to weeks
later
The size of nodules is generally
1-3 mm
19. Miliary TB: Diagnosis
Sputum smear is positive in about 25% of cases in both HIV and non-
HIV patients
In sputum smear neg milliary TB, bronch led to an immediate
diagnosis in 65% and this increased to 79% with culture
Nucleic acid amplification (NAAT) of Bronchial wash fluid can help.
20. Miliary TB: Prognosis
Prognosis is related to co-morbidity and those factors that lead to a
delay in diagnosis.
HIV patients respond to treatment in a similar fashion to non-HIV
patients
20% mortality is found and this has been stable for 30 years.
Delay in diagnosis is the key factor in mortality of miliary TB
21. Skeletal TB
Bone and joint disease due to TB affects all ages but the greatest risk appears
to be in those >age of 65y
Spinal TB or Pott’s is the most common followed by hip and then knee
Diagnosis is ideally made with isolation of the organism from the affected area
The diagnosis is supported by
– Mono articular disease
– Cold abscesses
– Positive PPD
– Epidemiological risks
– Chest x-ray with findings consistent with TB
22. Skeletal TB
• Skeletal TB is a haematogenous infection & affects almost all bones
• TB commonly affects spine & hip joint
• Constitutional symptoms generally occur before symptoms related to spine
manifest
• Lower Thoracic & Lumbar vertebrae are most common sites of involvement
followed by middle thoracic & cervical vertebrae
23. Spinal TB
• Infection generally begins with inflammation of the
anterior aspect of the intervertebral joints;
typically,it spreads behind the anterior ligament to
involve the adjacent vertebral body.
• Once two adjacent vertebrae are involved,
infection enters the adjoining intervertebral disc
space. This tends to occur later in Pott's disease
than in bacterial vertebral osteomyelitis and may
have the radiographic appearance of relative disc
sparing. Eventually, the avascular disc tissue dies;
there is vertebral narrowing and subsequent
vertebral collapse.
• Gibbus deformity, a form of structural kyphosis,
distorts spinal canal anatomy
• Formation of a "cold abscess"(soft tissue mass) at
the site is common.
• Noncontiguous spinal disease (eg, disease at more
than one level) is uncommon
24. Pott’s paraplegia
• Most serious complication of spinal TB
• Occurrence is reported to be as high as 30 % in patients with spinal TB
• Early onset paraplegia develops during active phase of infection
• Paraplegia of late onset can appear many years after disease has become
quiescent even without any evidence of reactivation, occurs due to osteophytes
and other chronic degenerative changes at a site of prior infection.
• Most commonly, paraplegia develops due to mechanical pressure on cord, but in
a small number of patients cord dysfunction may occur due to non-mechanical
cause
25. Bone & Joint TB
• Other sites
• Knee joint, foot bones, elbow joint and hand
bones
• Rarely, it also affects the shoulder joint
• Two basic types of disease patterns have been
observed: granular and exudative (caseous)
• Though both patterns have been observed, one
form may predominate
• The caseous exudative type is characterized
by bone destruction,local swelling, abscess
formation, sinus formation, and constitutional
symptoms; it occurs most often inchildren.
• The granular type is more insidious and less
destructive than the caseous exudative type,
andabscess formation is less common; it
occurs most often in adults.
26. Central nervous system Tuberculosis
• Central nervous system (CNS) tuberculosis (TB) includes
Three clinical categories:
• Tuberculous meningitis,
• Intracranial tuberculoma, and
• Spinal tuberculous arachnoiditis.
27. Neurological TB - TB Meningitis
• Accounts for 70-80 % of cases of neurological
TB
• In bacteraemic phase of primary lung
infection, metastatic foci can become
established in any organ, which can become
active after a variable period of clinical
latency
• Rupture of a subependymally located tubercle
(Rich focus) results in release of infectious
material into subarachnoid space
28. Neurological TB - TB Meningitis
• Salient pathological features of TBM include
• Inflammatory meningeal exudate Ependymitis
• Vasculitis Encephalitis
• Disturbance of cerebrospinal fluid (CSF) circulation & absorption
• Focal neurological deficits & features of raised intracranial tension may precede signs of meningeal
irritation
• Focal or generalised seizures are encountered in 20-30 %
• Cranial nerve palsies can occur in 20-30%
• 6th nerve involvement being most common
• Complete or partial loss of vision is a major complication of TBM
29. Clinical manifestations - TB Meningitis
The prodromal phase
lasting two to three weeks, characterized by the insidious onset of malaise,
lassitude, headache, lowgrade fever, and personality change.
The meningitic phase
with more pronounced neurologic features
eg, meningismus, protracted headache, vomiting, lethargy, confusion, and
varying degrees of cranial nerve and long tract signs.
The paralytic phase
in which the pace of illness accelerates rapidly; confusion gives way to stupor
and coma, seizures, and often hemiparesis
30. Categorization - TB Meningitis
Based upon mental status and focal neurologic signs as follows:
• Stage I patients are lucid with no focal neurologic signs or evidence of
hydrocephalus.
• Stage II patients exhibit lethargy, confusion; they may have mild focal
signs, such as cranial nerve palsy or hemiparesis.
• Stage III represents advanced illness with delirium, stupor, coma,
seizures, multiple cranial nerve palsies, and/or dense hemiplegia.
31. Neurological TB - TB Meningitis
• In untreated cases, progressive deterioration in level of consciousness,
pupillary abnormalities & pyramidal signs may develop due to increasing
hydrocephalus & tentorial herniation
• Terminal illness is characterised by deep coma & decerebrate or
decorticate posturing
• Without treatment, death usually occurs in 5-8 weeks
• Atypical presentations include acute meningitic syndrome simulating
pyogenic meningitis, progressive dementia, status epilepticus, psychosis,
stroke syndrome, locked- in-state, trigeminal neuralgia, infantile spasm &
movement disorders
32. Tuberculoma
Tuberculomas are conglomerate
granulomatous foci within the
brain parenchyma; that develop
from deepseated tubercles
acquired during a recent or
remote hematogenous bacillemia.
Observed on histopathology or
radiographic imaging
Contrast enhanced MRI of brain
(sagittal view, T1 weighted image)
showing solitary enhancing ring
lesion
33. Spinal Tuberculous Arachnoiditis
A focal inflammatory disease at single or multiple levels producing
gradual encasement of the spinal cord by a gelatinous or fibrous exudate.
• Symptoms develop and progress slowly over weeks to months and may
culminate with a meningitis syndrome.
• Patients present with the subacute onset of nerve root and cord
compression signs: spinal or radicular pain, hyperesthesia or paresthesias;
lower motor neuron paralysis; and bladder or rectal sphincterdysfunction
35. Abdominal TB
• Tuberculous enteritis is a form of extrapulmonary TB that can involve
any aspect of the gastrointestinal tract.
36. Pathogenesis
• Swallowing infected sputum
• Hematogenous spread from active pulmonary or miliary tuberculosis
(TB)
• Ingestion of contaminated milk or food
• Contiguous spread from adjacent organs
37. Abdominal TB - Gastrointestinal TB
• With widespread pasteurisation of milk, abdominal TB caused by M. bovis is now
seldom
• Gastrointestinal TB can be ulcerative, hypertrophic, ulcerohypertrophic, diffuse
colitis & sclerotic forms
• Gastrointestinal TB is a chronic illness with abdominal pain as most common
symptom.
• Diarrhoea, anorexia, weight loss and fever are also common
• Other symptoms include a moving lump in abdomen, nausea, vomiting, malaena, &
constipation
• Doughy feel of abdomen, mass in right iliac fossa due to hyperplastic caecal TB, lymph node
enlargement & rolled up omentum
• Abdominal distension with increased peristaltic activity is generally associated with intestinal
obstruction
• When intestinal perforation develops, signs of peritonitis is apparent
38. Abdominal TB - Peritoneal TB
• TB peritonitis have an acute onset & subjected to emergency surgery
• Ascitic
• Often insidious onset
• Abdominal distension, dilated veins and transverse solid mass in the abdomen
• Encysted or loculated form present with localised abdominal swelling
• Fibrous
• Widespread adhesions cause coils of intestine to be matted together & distended which may act
as “blind-loop”
• Result in steatorrhoea, malabsorption syndrome & abdominal pain
• Adherent loops of intestine & thickened mesentery may felt as lump(s) in abdomen
• Purulent
• Rarely develops secondary to TB salpingitis
• Cold abscess, entero-cutaneous & entero-enteric fistulae can develop
39. Abdominal TB - Imaging
• Oral and intravenous contrast enhanced computed tomography
• CT finding is concentric mural thickening of the ileocecal region, with
or without proximal intestinal dilatation
• Characteristic lymphadenopathy with hypodense centers,
representing caseous liquefaction
Colonoscopy — Colonoscopic findings of ileocecal TB may include
ulcers, strictures, nodules, pseudopolyps,fibrous bands, fistulas, and/or
deformed ileocecal valves
40. Abdominal TB - Gastrointestinal TB
CT Abdomen - shows ascites,
marked omental thickening in
both flanks, and stranding in the
mesentery
Diffuse calcified mesenteric lymphadenopathy
41. Histopathology
• Granulomas associated with TB tend to be large and confluent, often
with caseation necrosis. Ulcers are lined by aggregate epithelioid
histiocytes, and disproportionate submucosal inflammation is seen.
• In contrast, granulomas associated with CD are infrequent, small,
nonconfluent, and noncaseating.
• CD is also characterized by focally enhanced colitis and a high
prevalence of chronic inflammation in endoscopically normal
appearing areas
42. Other Gastrointestinal Sites
• Hepatobiliary & pancreatic TB are rare
• Associated with disseminated/miliary TB (DTB/MTB) & more often in immune compromised
• Clinical manifestations are non-specific & depend on site & extent of disease
• Anorexia, malaise, low grade fever, weight loss, night sweats malena, pancreatic mass or
abscess & obstructive jaundice
• Pancreatic TB may present as acute or chronic pancreatitis, or mimic malignancy
• Splenic TB presents as hypersplenism or splenic abscess, or as a solitary splenic
lesion
• Multiple TB abscesses described in patients with HIV infection
• Pre-operative diagnosis is difficult & diagnosis is often confirmed on histopathological
examination of excised specimen
43. Pericardial TB
• TB pericardial involvement present as
• Acute pericarditis
• Chronic pericardial effusion
• Cardiac tamponade
• Pericardial constriction
• Pericardial involvement most commonly
results from direct extension of infection from
adjacent mediastinal lymph nodes, or through
lympho-haematogenous route from a focus
elsewhere
44. Genitourinary TB
• Genitourinary TB (GUTB) complicate up to 3-
4% with pulmonary TB
• Presents with dysuria, haematuria which may
be painless, flank pain, renal mass, sterile
pyuria, & recurrent urinary tract infection
• Rarely acute presentation mimicking
pyelonephritis also described
• Other uncommon manifestations include
nonhealing wounds, sinuses or fistulae &
haemospermia
Testicular tuberculosis. Computed
tomographic scan of the pelvis showing a
large, irregular, mixed solid and cystic left
testicular mass (arrow).
45. Genitourinary Tuberculosis
• Often involves the fallopian
tubes, also the endometrium
• Likely important cause of
infertility worldwide (1-17%)
• Other symptoms include:
chronic pelvic pain, menstrual
irregularities, abdominal masses
46. Cutaneous TB
• Accounts for 0.1-2.5% of all with skin diseases
• Several clinical types of cutaneous TB
• In those not previously exposed to M.TB, TB of skin &
TB chancre
• Previously sensitised hosts develop lupus vulgaris,
scrofuloderma & TB verrucosa cutis
• Other lesions seen are tuberculids which includes
lichen scrofulosorum, papulonecrotic tuberculid,
erythema induratum & erythema nodosum
• Lupus vulgaris is most common variety seen in
India, followed by TB verrucosa cutis &
scrofuloderma
• Other types are distinctly rare
• Localised & generalised skin complications due to
Bacille Calmette Guerin (BCG) vaccination
Reddish brown plaques
PAPULONECROTIC
TUBERCULIDS
VERRUCOSUS CUTIS
47. TB in Otorhinolaryngology
• Focus shifted on to otorhinolaryngological
TB with advent of HIV infection & AIDS
• Patients with laryngeal TB present with
hoarseness of voice
• Pain is also important feature which radiate
to one or both ears & lead to odynophagia
• Occasionally, presentation can be similar to
that encountered in acute viral laryngitis
• Laryngeal TB may co-exist with carcinoma
48. Ocular TB
• Choroid is most commonly affected
• Choroidal tubercles when present can provide
valuable diagnostic clues to diagnosis of
DTB/MTB
• Tuberculids & phlyctenulosis occur in post-
primary TB
• Phlyctenulosis can involve conjunctiva,
cornea or lid margin
Choroidal tuberculomas
49. More recently
• More recently, evidence has accumulated on the accuracy of CBNAAT
MTB/RIF for various forms of EPTB.
• CBNAAT MTB/RIF should now be considered a central test in the
work-up of EPTB, and may be used along with conventional tools,
such as microscopy, liquid cultures (that are the most sensitive
technologies for MTB detection), and histopathology (biopsy) to
arrive at the final diagnosis.
50. M. Pai and R. Nathavitharana , Extrapulmonary Tuberculosis: New Diagnostics and New Policies , Indian J Chest Dis Allied Sci 2014;56:71-73]
51. Major Goals of EPTB Treatment
1.Cure patient, minimize risk of death/disability, prevent transmission
to others
2. Provide safest, most effective therapy in shortest time
3. Prescribe multiple drugs to which the organisms are susceptible
4. Never treat with a single drug or add single drug to failing regimen
5. Ensure adherence and completion of therapy
52. Treatment of Extrapulmonary TB
• In most cases, treat with same 4 drug regimens used for pulmonary
TB
• Culture-negative TB/ (culture not done)
– Failure to isolate M. TB from person with clinical evidence does
not exclude TB
– If high likelihood of TB, initiate therapy with INH, RIF, PZA,and
EMB
53. Treatment of Extrapulmonary TB
• Special considerations for therapy
– Disseminated TB or TB meningitis in children: treat for 9–12
months
– For bone and joint TB, 9 months favoured
– Treat HIV+ patients with EPTB same as with pulmonary only TB,
6-9 months based on clinical factors (disseminated disease,
cavitary pulmonary disease with slow response to therapy, etc.)
– In tuberculous meningitis, ethambutol should be replaced
by streptomycin / Fluroquinolones.
54. Treatment & outcome
• While 6 month treatment is sufficient for vast majority of patients, each patient should
be individually assessed & , where appropriate, treatment duration may be extended
for a given patient
• Patients receiving anti TB treatment should be carefully monitored for adverse drug
reactions, especially drug induced hepatotoxicity
• Usefulness of corticosteroids in treatment of EPTB is controversial & not well
established
• When diagnosis of TB is established with certainty, additional oral corticosteroid
treatment may be helpful in selected patients with life-threatening forms of EPTB –
TB meningitis and pericarditis
55. Treatment of Extra pulmonary TB
• Although sometimes required for diagnosis, surgery plays little role in
the treatment of extrapulmonary TB.
• It is reserved for management of late complications of disease such
as:
– Hydrocephalus
– Obstructive uropathy
– Constrictive pericarditis
– Neuro- logical involvement from Pott’s disease (spinal TB).
• For large, fluctuant lymph nodes that appear to be about to drain
spontaneously, aspiration or incision and drainage appear beneficial
56. Use of other drugs in EPTB
• To address problem of drug interaction between Rifampicin & some of anti-
retroviral (ARV) drugs, such as Nevirapine, antiretroviral treatment can be
initiated after DOTS treatment is completed
• In HIV co-infected TB patients in later stages of immunosuppression, concomitant
anti-retroviral & anti TB treatment may required & in such cases ARV regimen
needs to be suitably modified, e.g. Nevirapine replaced with Efavirenz
• High index of clinical suspicion, timely & judicious use of invasive diagnostic
methods & confirmation of diagnosis, early institution of DOTS & close clinical
monitoring for adverse drug reactions, are key to successful management of EPTB
57. Conclusion
• TB remains a major cause of death worldwide
• New molecular diagnostics have made earlier
and improved diagnosis of active disease
possible
• Newer antiTB drugs offer the promise of
shortened treatment regimens for drug-
sensitive disease and more effective treatment
for drug-resistant disease and latent infection
• New vaccines against TB in advanced clinical
trials offer hope for future TB control
• Although these scientific developments are
promising, the global economic crises continue
to hinder TB-control programs
• Rise and spread of drug resistance and
synergistic interaction with the HIV epidemic
are posing difficult challenges and threatening
global efforts at TB control
• Strong political and financial commitments will
be required to achieve global control of TB and
avert millions of unnecessary deaths
61. Lymphatic TB Treatment
Treatment
A six-month regimen including HRZE (two months HRZE, four
months HR) is recommended
Although the disease is pauci-bacillary, the development of nodes
during therapy or at the end of therapy is common
Usually there is no evidence of bacteriological relapse
No role for steroids except perhaps in unusual circumstances of IRIS
with HIV co-infection
62. Treatment of Bone and Joint Disease
Same therapy as for other forms of TB (RIPE)
Nine months is favoured
Myelopathy with or without functional impairment responds
medically
A randomized trial of the Medical Research Council comparing
surgical debridement with multi-drug regimens found no benefit
to surgery
There are instances where surgery should be considered
63. Genitourinary TB – Treatment
• Treat with a standard regimen- INH, rifampin, PZA, ethambutol
– Concerns for adverse effects of PZA on the fetus have not been
supported by experience
– PZA is recommended by the WHO and other international
organizations
• 6 months usually sufficient
• Surgery usually only needed if large tubo-ovarian abscess
64. Extra-pulmonary TB and HIV
In PLHIV, their immune systems cannot respond as strongly to a TB
infection so they are not able to contain the TB bacilli outside of
the blood stream
Primary TB infection is still the lungs, but TB bacilli then access the
blood stream and spread through the body, finding other sites to
multiply and cause disease
Usually TB bacilli remain in the site where they first infected the body
and do not gain access to the blood stream, however people
living with HIV who are also infected with TB often have TB bacilli
in their blood
65. Transmission of Extrapulmonary TB
• Outside the lungs (extrapulmonary) usually not infectious, unless
person has:
• Concomitant pulmonary disease,
• Extrapulmonary disease in the oral cavity or larynx, or
• Extrapulmonary disease with open site, especially with aerosolized
fluid.
66. Use of other drugs in EPTB
• In EPTB patients known to have co-existent HIV infection, Category I regimen is to be used under
DOTS strategy / FDC
• All HIV co-infected TB patients should receive a Rifampicin-containing regimen
67. Tuberculosis of the Spine
• Infection begins in cancellous area of vertebral body, commonly in
epiphyseal location & less commonly in central or anterior area of
vertebral body
• Infection spreads & destroys epiphyseal cortex, intervertebral disc & adjacent
vertebrae
69. MRI scan
A B
B - MRI dorsolumbar spine of another patient
(sagittal view, T2 weighted image) showing
destruction of D10 & D11 vertebrae reduction in
intervening disc with anterior granulation tissue
& cord compression (arrow)
A - MRI scan of dorsolumbar spine,
(coronal view, T1 weighted image)
showing central hypointense lesion
(arrow) with reduced vertical height
of vertebra & paraspinal cold abscess
70. Ocular TB
Sclerokeratitis
TB uveitis can present as pan uveitis
or as chronic granulomatous
iridocyclitis
Anterior chamber granuloma with
granulomatous keratic precipitates
and hypopyon
(A) Recurrent sclerokeratitis resulting in corneal thinning
and melt with adjacent active scleritis.
(B) Chest (CT) revealed enlarged lymph nodes with
necrosis involving pretracheal, paratracheal, and
subcarinal groups
71. Use of Steroids in Extrapulmonary TB
• Unless drug resistance is suspected, adjuvant corticosteroid
treatment is recommended for TB meningitis and pericarditis
72. Congenital TB
• Rare manifestation
– Difficult to distinguish from infection acquired after birth
• Transmission in utero can occur 2 ways-
– Hematogenous spread through the umbilical vein to the fetal
liver
– Ingestion/aspiration of infected amniotic fluid
• Mothers are often asymptomatic
73. Congenital TB
• Cantwell criteria:
– Primary hepatic complex/caseating granuloma on biopsy
– TB infection of the placenta
– Maternal genital tract TB and lesions in the infant in the first
week of life
Symptoms in infant can be nonspecific
• High mortality rate
• Treat infants with four drugs
74. Testing for TB in Pregnant Women
When Should Testing for TB Occur in Pregnant Women?
As soon as possible if symptoms are present
For LTBI screening, should be done early in second trimester
What Test Should be Used?
TST is valid and safe in pregnancy
IGRAs can be used but limited data on their accuracy in pregnant
women
75. Chest X-Rays and Pregnancy
All TST/IGRA positive patients should have a CXR with abdominal
shielding
Should not be delayed; identification of TB disease
has implications for treatment and infection control
Radiation exposure for 2 view CXR = 0.1mGy
– 10x lower than 9 month exposure to environmental background
– This level of exposure considered negligible risk to fetus
76. TB and Pregnancy
Untreated TB is more of a risk to the mother and fetus than treating TB
Pregnant women should be assessed for their TB risk
TSTs and CXRs are safe during pregnancy
Treatment for LTBI can prevent development of TB disease and
transmission of TB to the fetus or infant
77. Monitoring and Follow-up
• Assess patient’s response to treatment:
– Clinical evaluation, bacteriological examination if possible,chest
radiograph (if pulmonary as well)
– As in pulmonary smear- negative disease, the weight of the patient
is a useful indicator
• Conduct clinical evaluations at least monthly; after 2 months of therapy, if
symptoms do not resolve, reevaluate for
– Potential drug-resistant disease
– Non-adherence to drug regimen
– Other cause of clinical presentation if M. tuberculosis not confirmed
78. Extrapulmonary TB: Take home points
Not uncommon, especially in HIV-infected persons
Difficult to diagnose because can mimic many diseases, limited
diagnostics in some countries
Respiratory isolation key until PTB ruled out
Always get HIV test in patients w/ EPTB.
Treat it like you would pulmonary TB, except:
– Steroids in meningeal and pericardial disease
