Post- Primary Pulmonary Tuberculosis

Post primary tuberculosis is the term used to describe lung disease, the characteristic pathological feature of which is the tuberculous cavity formed when the caseated and liquified centre of tubercular pulmonary lesion is discharged into a bronchus.

This is the most important and the most frequent type of tuberculosis. It may arise as- -

Clinical features :

  1. Onset is usually insidious
  2. Cough is an early symptom
  3. Sputum-usually mucoid at first, but may become purulent latter on.
  4. Haemoptysis-in early stage blood stained sputum.
  5. Dyspnoea on exertion.
  6. Pleuritic chest pain.
  7. Low grade afternoon fever.
  8. Sweating especially during night.
  9. Weakness, lassitude, weight loss, loss of appetite.
  10. Symptoms of complications may be present.
  11. A few medium or course crepitations may be present over the upper lobe. The crepitations may be present only after coughing.
  12. Breath sound may be vesicular with proionged expiration.
  13. Percussion note losses its normal resonance.
  14. There may be physical sings of consolidation, cavitation, fibrosis, pleurisy with or without effusions, spontaneous pneumothorax etc.

Symptoms and signs which should always raise the suspicion of TB-

  1. Persistent cough.
  2. Hemoptysis
  3. Pleural pain not associated with acute illness
  4. Spontanious pneumothorax
  5. Lathergy
  6. Weight loss.

Investigation:

  1. X-Ray chest- Hilar lymph node enlargement, fibrotic band, patchy opacities or calcification of lesion may be seen, usually sitoated on upper lobe.
  2. Tuberculin test- Positive.
  3. Bacteriological examination- sputum for AFB is positive (at least 3 smears done) in open cases only.
  4. Biopsy of enlarged lymph nodes.
  5. Blood- High E. S. R. Lymphocytosis.

Complications:

  1. Pleurisy. 2. Pleural effusion, 3. Spontaneous Pneumo-thorax, 4. Tuberculous empyema or pyopneu-mothorax, 5. Tuberculous laryngitis, 6. Tuberculous enteritis, 7. Ischiorectal abscess & fistula-in-ano, 8. Dissemination of T. B. via blood stream to produce renal tuberculosis or tuberculous meningitis, 9. Respiratory failure and R.V.F 10. infection etc.

Treatment of Tuberculosis:

1. Bed rest- untill the acute symptoms have subsided, specially for skeletal T.B.

2. Isolation- untill the sputum positive cases are negative.

3. High calorie, high protein diet with vitamins.

4. For cough- codeine phosphate 8-15 mg orally 4-6 hourly if necessary.

5. Anti-tuberculosis chemotherapy--

a. Rifampicin- Children- 10-20mg/kg/day.

Adult, wt > 50kg- 600mg (max.)

Adult, wt < 50kg- 450mg (max.)

b. INH- Children, 10mg/kg/day.

Adult, 200-300mg/day.

Intermittent regimen, 15mg/kg

Miliary/meningitis, 10-12mg/kg.

+ Pycidoxine 10mg/day (in all cases).

c. Ethambutol - Children & adults : initial 8 weks, 25mg/kg/day.

Subsequently, 15mg/kg/day

In renal failure, according to serum level.

d. Streptomycin - Children - 30mg/kg/day.

Adults under 40 years and weighing more than 45kg. 1gm

Adults 40-60 years or weighing less than 45kg-0.75gm.

Intermittent regimens, 0.75-1gm.

Adults over 60 years or in patients with renal failure, the dose of streptomycin should be reduced according to serum levels.

N.B : Streptomycin, now a day used very rarely in patients with multiple drug resistance or hypersensitivity.

e. Pyrazinamide- Children 20-35 mg/kg/day.

Adult wt > 45kg, 1.5gm (max.)

Adult wt < 45kg, 2.0gm (max.)

N.B: Pyrazinamide, as it diffuses well into the cerebrospinal fluid, is particularly useful in the treatment of tuberculous meningitis.

6. Steroid- Corticosterlod may be used in conjunc-tion with anti-T.B drugs, such as in

a. Milliary tuberculosis.

b. Acute and severely ill tuberculous pt. at the onset of chemotherapy.

c. Corticosteroid prevent or minimise the formation of fibrous tissue and be of value in tuberculosis affecting the pleura, pericardium, intrathoracic and superficial lymphnodes, the eye and meninges or in ureteric obstruction.

Dose : Prednisolone 10-20mg daily in 2-3 divided doses for 6-12 weeks.

N.B.

  1. During impaired hepatic function, anti-TB treatment should be stopped and to be started later on when liver function tests become normal.
  2. In impaired renal function, patient can be safely treated by reducing the doses of streptomycin.
  3. During pregnancy all main drugs except strepto-mycin can be used.

Regimens now used -

A. 6 month regimens -

Initial phase: (2 months)

INH + Rifampicin + Pyrazinamide + Ethambutol or Streptomycin

Continuation phase: 4 months

INH + Rifsmpicin.

B. 9 month regimens -

Initial phase (2 months)

INH + Refampicin + Streptomycin or Pyrazinamide

Continuation phase (7 month)

INH + Refampicin.

C. Other regimes -

  1. Inj. Streptomycin. 15 mg/kg/ day i.m. for 3 months (not more than 1 gm/day).
  2. Tab. INH, 300 mg/day for 18 months.
  3. Tab. PAS, 300/kg/day for 18 months

Or,

  1. Inj. Streptomycin (dose as above).
  2. Tab. INH (dose as above).
  3. Tab. Thiacetazone, 3mg/kg/day for 18-months.

Or,

  1. Inj. Streptomycin (dose as above).
  2. Tab. Ethambutol, 25 mg/kg. day for 8 weeks, then 15mg/kg/day.
  3. Tab INH (dose as above).

If the patient is hypersensitive to Streptomycin, then give -

  1. Cap. Rifampicin 450-600mg/day for 9 months in empty stomach.
  2. Tab. INH (dose as above).
  3. Tab. Thiacetazone (dose as above).

For poor patient (Cheapest regimen)

Isoniazid (300 mg) plus Thiacetazone (150 mg.) given in a single daily dose by mouth for 12 months is above 80-95% effective.

Or,

  1. Inj. Streptomycin. 1gm. twice weekly for 12 months.
  2. Tab. Isoniazid. 15 mg/kg/day twice weekly for 12 months.
  3. Tab. Pyridoxine. 10 mg. twice weekly for 12 months.

Pyridoxine should always be added in addition to Isoniazid to prevent the peripheral neuropaihy 1tab. (10 mg.) t.d.s for same period.

Chemoprophylaxis of TB:

INH 5mg/kg by mouth daily for 1 year should be considered in -

- non vaccinated tuberculin positive children under 3 years.

- unvaccinated contacts who have recently become tuberculin positive.

- immunocompromised patient.

- adolescents with high degree of tuberculin sensitivity.

INH 5mg/kg by mouth daily for 6 wks should be considered in- -

- infants of highly infectious patients.

Pleural Effusion

It is a condition of exudative or transudative fluid inside the pleural sac.

Causes:

Common causes -

  1. Tuberculosis of the lung and pleura.
  2. Lobar pneumonia.
  3. Malignant diseases.
  4. Infarction of the lung.
  5. Subdiaphragmatic disoder e.g subphrenic abscess, pancreatitis etc.
  6. Cardiac failure

Others-

  1. Trauma.
  2. Viral infection.
  3. Nephrotic syndrome
  4. Advanced cirrhosis of liver
  5. Malnutrition
  6. Connective tissue diseases
  7. Lymphoma
  8. Amoebic liver abscess.
  9. Post M.I syndrome
  10. Rheumatoid disease
  11. Acute Rheumatic fever
  12. Myxoedema
  13. Uraemia
  14. Wigs syndrome

Clinical features:

Symptoms-

1. Symptoms of pleurisy may present as -

a. Sharp, stabbing and unilateral pleural pain.

b. Pain may radiate to tip of the shoulder or anterior abdomen.

c. Pain aggrevates by cough and Relieved by breath holding.

2. Pain may be absent.

3. Pyrexia occurs in most cases and continuous type.

4. Dyspnoea is the principal Symptom.

5. Heaviness, or discomfort feeling due to accumu-lation of fluid in the pleural sac.

6. Symptoms due to underlying causes i.e. P.T.

Signs -

General examination -

Appearance - ill looking.

Temparature - Raised.

Decubitus - lies on the affected by

Cyanosis - Present.

Respiration - Rate increased.

Systemic examinations (Respiratory System).

Inspection - Fullness of the chest.

Chest Movement - Restricted on the affected side.

Palpation -

1. Trachea and apex beat:

- shifted to the opposite side

2. Vocal fremitus -

- diminished in the affected part

- increased in the upper part (Apex) due to compensatory emphysema.

Percussion-

Percussion note stony dull on the affected part.

Auscultation :

  1. Breath sound - Absent or markedly diminished.
  2. Volcal resonance -Absent or diminished. above the effusion breath sound increased (Vesicular) and vocal resonance increased.

Investigations :

  1. E S.R is high when the aetiology of the underlying disease is tuberculosis or malignancy.
  2. Pleural aspiration is an absolute proof that an effusion is present. Aspirated fluid should be send for bacteriological and cytological examination and Biochemical test.
  3. Pleural biopsy may be done when exact aetiology cannot be settled.
  4. X-ray chest (PA view)- will show a dense homogeneous opacity obliterating the cardiophrenic and costophrenic angles on the affected side. Trachea and heart may be shifted to the opposite side.
  5. Others- sputum for AFB and cytology; tuberculin test.

Treatment:

Treatment should approach both the effusion and its cause.

Symptomatic-

  1. Rest in bed. and O2 inhalation in proped up position in severe cases.
  2. Salicylates or Aspirin in usual dose may be given.
  3. Aspiration of plearal fluid may be necessary to relieve breathlessness. To avoid repeated effusion treatment by pleuredesis can be given in malignancy.

Specific treatment -

Treatment of underlying cause e.g.-

  1. Antituberculous chemotherapy for about a year or more in tuberculosis cases.
  2. In post pneumonic cases removal of fluid in addition to antimicrobial agent for lung lesion may be given.
  3. In malignant effusion cytotoxic agents may be given intrapleurally. Irradiation of the hemithorax may also be helpful.

Spontaneous Pneumothorax

Accumulation of air in the pleural space is known as pneumothorax. It is classified as spontaneous (primary of secondary) or traumatic. Primary pneumothorax occurs in the absence of an underlying cause, where as secondary pneumothorax is a complication of pre-existing pulmonary disease.

Types:

  1. Close type- in this communication between pleura and lung seals off as the lung deflates and does not reopen.
  2. Open type- in this communication is generally with a bronchus (bronchopleural fistula) and does not seal off when the lung collapses.

    The term 'open' is also applied to a pneumothorax resulting from a penetrating wound of the chest wall.

  3. Tension (valvular) pneumothorax- in this com-mication between pleura and lung pesists but is small and acts as a one way valve which allows air to enter the pleural space during inspiration and coughing but prevents it from escaping.

Causes:

  1. Rupture of subpleural emphysematous bulla or pleural bleb.
  2. Rupture of subpleural tuberculous focus into the pleural space.
  3. Rarely- lung abscess, pulmonary infarction, carcinoma lung.

Clinical features :

  1. The onset is usually sudden with pain & feeling of tightness on the affected side- that may be aggravated by deep breathing.
  2. Breathlessness
  3. Cyanosis in some case
  4. In close type- breathlessness is seldom severe & gradually improve.
  5. In open type- breathlessness dose not improve.
  6. In tension type- breathlessness is progressive & accompanied by central cyanosis.
  7. Features of underlying disease

On examination :

Inspection-

- movement of chest is restricted to the affected side : res. rate-

- cyanosis

Palpation-

- trachea & mediastinum (apexbeat) shifted to opposite side.

- vocal fremitus- ¯

Purcussion-

- hyperresonant

- obliteration of liver & cardiac dullness.

Auscuitations-

- breath sound- I or absent

- vocal resonance- diminished on affected side.

Investigation:

  1. Chest x-ray- sharply defined edge of deflated lung & there is complete translucency between this & chest wall with no lung marking.

Management:

  1. Oxygen inhalation
  2. Water seal drainage
  3. Antibiotic therapy
  4. Treatment of underlying cause.

Pulmonary Aspiration Syndrome

Classification :

  1. Aspiration of toxic materials- such as, acid, alcohol, volatile hydrocarbons, oils, animal fats etc. These produce a chemical pneumonitis.
  2. Aspiration of non-toxic materials- liquid with a pH more than 7.3 or particulate materials. Here the damage relates to the composition and/or volume of the aspirated material.
  3. Bacterial aspiration- onset of a bacterial pneu-monia 24 hour or s6 after the inhalation of an inoculum of bacteria.

Causes:

  1. Loss of air way protective reflexes as in anaesthetised, comatose, heavily sedated or neuroloflcally compromised patients.
  2. Oesophageal disorder or decrease gastric emptying time.
  3. Iatrogenic factors- presence of nasogastic tube or tube feeding.
  4. In infant & children- faulty feeding practice.

Clinical features :

Chemical damage to the lungs produces broncho--spasm and a massive exudation of fluid into the lungs. This causes dyspnoea, wheezing, cough with produc-tion of frothy pink sputum. Hypoxia, hypotension, tachycardia & ARDS may develop. Signs of infection may be present.

Investigation:

  1. Chest X-ray show patchy alveolar infiltrates.
  2. Arterial blood gas analysis-PaCO2 (low or normal). PaO2 (low).
  3. Sputum for C/S

Management:

  1. Suction of secretions to clear the oropharynx.
  2. intubation to be done if air way protective reflexes are thought to be compromised.
  3. O2 therapy with a mask to deliver 50% inspired O2 concentration. Mechanical ventilation- if PaO2 below 65mm Hg (8.6 kpa).
  4. Bronchodilators to control wheeze.
  5. Antibiotics - a course of appropriate antibiotic should be given.
  6. Fluids - hypovolaemia due in part to extravasation of fluids into the lungs, to be corrected.

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