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Tuberculosis in Children I

Tuberculosis in Children I


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paediatrics lecture notes on tuberculosis from college of medicine, university of ibadan, Nigeria
paediatrics lecture notes on tuberculosis from college of medicine, university of ibadan, Nigeria

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Published by: ibnbasheer on Jun 06, 2009
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Tuberculosis in Children

By Professor K. Osinusi


An important infectious disease globally About 30% of the world’s population are the organism that causes tuberculosis

infected by   8 to 10 million people develop the disease About 3 million of them are in sub-Saharan

annually Africa


Worsening economic situations Multidrug resistance HIV pandemic Decline of national tuberculosis control programmes Large number of displaced persons living in poor conditions as a result of conflicts and wars

Aetiological agent mycobacterium tuberculosis and mycobacterium bovis mycobacterium africanus Characteristics of mycobacteria It multiples slowly It is resistant to many anti- microbial drugs It remains viable in macrophages by subverting macrophageskilling Its waxy coat together with its many components substances depress immune responses against it.

Sources of Infections: Most important source is sputum of persons with open tuberculosis Mode of Spread: Inhalation Ingestion Penetration of skin and mucous membrane Predisposing Factors: Age Sex Malnutrition Intercurrent infection Overcrowding & poor living conditions

Tuberculosis is a chronic inflammatory disease i.e inflammation of prolonged duration in which active inflammation, tissue destruction and attempt at repair proceed simultaneously The tubercle bacilli being of low toxicity evokes an immune response called delayed hypersensitivity reaction. Granulomatous inflammation is a specific type of chronic inflammation which occurs in TB A focal area of granulomatous inflammation is known as granuloma In tuberculosis the granuloma is referred to as a tubercle which is classically characterized by the presence of

Primary focus ) + ) Primary Complex regional lymph nodes ) Primary Focus - Size – varies from a few millimeter to 2 centimeter in diameter - Site – usually situated in the sub-pleural region - Symptoms & signs  May be symptomless  May be associated with minor symptoms like malaise and anorexia  May be associated with muco-cutaneous manifestations ie erythema nodosum and phlycternular conjunctivitis Primary complex can heal or progress into active disease Risk of primary infection developing into an active disease is about 15% in the first ten years after infection

Ways in which primary infection can progress to active disease
• • • • • • Primary focus can spread to contiguous part of the lungs giving rise to tuberculous pneumonia. Primary focus and the regional lymph nodes may merge and give rise to an area of consolidation. Extensive caseation and liquefaction can develop giving rise to cavity formation. The inflamed nodes may compress the neighbouring bronchi giving rise to atelectasis or emphysema. Node may erode through endobronchial tuberculosis. the bronchial wall causing

There may be discharge of the tubercle bacilli into the lumen leading to bronchogenic dissemination to other areas of the lungs. Nodes may erode into the blood vessels giving rise to haematogenous spread to other tissue. The affected nodes may develop fibrosis and encapsulation

• •

Period between primary and the appearance of clinical evidence of various forms of TB
Pulmonary tuberculosis – within a few months of primary infection. Miliary and meningeal tuberculosis – 2-6 months. TB adenitis - 3-9 months. Bones and joints – several years. Renal and genital tuberculosis – may take over a decade. Pulmonary lesions occurring as a result of reactivation of a dormant tuberculosis focus previously established in the body takes a number of years after primary

Commonest form of tuberculosis – occurring alone or in combination with other forms in 70% of cases. Pulmonary tuberculosis in children consists mainly of primary complex and direct progression of its component. Pathological findings include: * Hilar enlargement which may lead to bronchial compression with resulting hyperinflation or atelectasis. * Consolidation – patchy or lobar with or without pneumothorax and pleural effusion. * Cavitation.

Clinical Features
Early symptoms are usually vague Chronic cough Fever Anorexia Weight loss Failure to gain weight Haemoptysis Signs: - Dyspnoea - Tachypnoea - Localized wheezing - Decreased breath sounds - Crepitations - Bronchial breath sounds - Chest examination may reveal no abnormality - Clinical features of reactivation tb in older children are similar to those of the primary infection but cough is usually productive and there may be chest pain.

History  Detailed history of current illness  Past medical history  Family and social history  History of contact INVESTIGATIONS  Tuberculin skin test  Chest radiograph  Hilar adenopathy  Parenchymal lesions - Patchy infiltrates - Consolidations - Atelectasis - Pleural effusion - Cavities 17. Bacteriological investigations - Sputum ) staining - Gastric washings ) and culture 4. ESR 5. FBC

Differential Diagnosis

 Pneumonia Bacterial Viral Mycoplasma     Lung abscess Bronchiectasis Pulmonary fungal infections Pulmonary neoplasm

TB pleural effusion occurs when: - Sub pleural primary focus ruptures into the pleural cavity. - A caseous node ruptures into the pleural cavity. - During haematogenous spread. - As a result of allergic response to tuberculo-protein. Clinical Features: Symptoms: Fever Weight loss Chest pain on deep inspiration Signs: Dullness to percussion Diminished or absent breath sounds.

- Sero-Fibrinous, sometimes blood-stained - Protein 2-4 g/dL - High white cell count with predominance of lymphocytes - Culture yields tubercle bacilli in less than 20%.

Most severe form of disseminated TB. Clinical Manifestations: - Variable, depending on the load of organism, organs affected and immune status of the child. - Onset of symptoms may be explosive or insiduous. Symptoms: Fever Anorexia Weight loss Cough Wheezing Signs: Generalised lymphadenopathy. Hepato-splenomegaly. Respiratory distress signs of meningitis or peritonitis present in 2040% of cases. Choroidal tubercles.

Tuberculin skin test CXR CSF tap Histological examination of Lymph node Liver biopsy Marrow biopsy

Diff. Diagnosis of miliary picture on CXR
Sarcoidosis Eosinophilic pneumonia Pulmonary fungal infection Chicken-pox pneumonia Childhood histiocytosis syndrome

Comprises: - Tuberculous meningitis - Tuberculoma Tuberculous meningitis Occurs about 2-6 months after the primary infection Most common in children aged 6 months to 4 years Arises as a result of haematogenous spread of tubercule bacilli to the cerebral cortex and meninges.

Clinical Manifestation
Can be divided into 3 stages Stage I: Non-specific symptoms like: Fever Headache weight loss Irritability Drowsiness

Stage II
Lethargy Nuchal rigidity Seizures Positive Kernig’s sign Vomiting Stigns of brainstem involvement Cranial nerve palsies + other focal neurological signs

Stage III
Hemiplegia or paraplegia Coma Decrebrate rigidity Opisthotonus Fundoscopy may show papilloedema and choroidal tubercles.

• • • Tuberculin skin test CXR Examination of CSF

CSF Picture: May be straw-coloured or may be clear and colourless WBC 10-500cells/cmm with predominance of lymphocytes Protein may be over 1GM/dl Glucose – Low, less than 40mg/dl Staining with ZN stain may yield Afb Culture may be positive

Depends on the stage of disease at commencement of therapy. Stage I Prognosis good Stage III - Mortality is high and a high percentage of those who survive have complications like: - blindness deafness paraplegia mental retardation speech disturbance cranial nerve palsies Hydrocephalus

Presents as an intracranial space-occupying lesion Usually infratentorial May be single or multiple

CLINICAL MANIFESTATION Headache Fever Convulsion Lateralizing signs Investigations Tuberculin skin test Skull X-ray CXR CT Scan of the brain shows discrete masses with surrounding oedema Diagnosis is often made at surgical exploration for intracranial tumour.

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