Pulmonology, illustrated text of pulmonology

Internal medicine | Pulmonology | Third edition - 2015
Ali Abdelaal | Emad M. Qasem | Asaad N. Elnakeeb
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Pulmonology
Disclaimer
This book has no relation to any lectures, handouts or
any other books written in Sohag University.
The references of this edition are:
 Pulmonology. Dr Ahmed Mowafy.
 USMLE CK book. 2012.
 Macleod's clinical examination.
 Kumar and Clark's Clinical Medicine.
 Davidson's principles of clinical practice.
The best advice we can give you is to study
Pulmonology for yourself and for your clinical
examination only.
This book is dedicated to every one of you, Try to help
anyone if you can, try to write your notes and to
reproduce this book for your colleagues.
Wherever you go, go with all your heart (Confucius).
Emad M. Qasem
Undergraduate
Reference

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Contents in brief
Pleural Effusion 4
Chylothorax 12
Hemothorax 13
Empyema 14
Pneumothorax 18
Pneumonia 23
Lung abscess 36
COPD 41
Bronchiectasis 51
Respiratory failure 57
Interstitial pulmonary fibrosis (IPF) 61
Pulmonary tuberculosis 68
Pulmonary embolism 81
Mediastinal syndrome 86
Acute respiratory distress syndrome (ARDS) 89
Bronchial asthma 92
Lung cancer 103
Pleural tumours 116

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Definition:
Collection of fluid in the pleural sac
Etiology
1. Pleural exaudate.
2. Pleural transaudate.
Pleural transaudate Pleural exaudate
Mechanism 1. Increased hydrostatic
pressure.
2. Decreased Oncotic pressure.
Abnormal permeable capillary wall
Causes 1.  hydrostatic pressure
as in:
 Congestive heart failure
 Pericardial effusion
 Constrictive pericarditis
 Constrictive
cardiomyopathy
 Massive pulmonary
embolism.
2.  Oncotic pressure as
in:
 Liver cirrhosis
 Renal failure
 Nephritic syndrome
 Malnutrition.
3. Transmission of fluid
from Peritoneum
through the
diaphragmatic defects
as in:
 Any cause of ascitis
 Meig's syndrome (
Ovarian fibroma + ascitis
Malignant pleural effusion:
1. Metastatic tumor is more
common than primary
pleural tumor.
 Lung cancer (from inside)
 Breast cancer (from outside)
 Stomach carcinoma
 Lymphoma
 Mesothelioma
2. Para malignant pleural
effusion:
No involvement of pleura by
tumor. Tumor is causing effusion
by 3 mechanisms
(a)Local Effect of tumour :
 Lymphatic obstruction
 Bronchial obstruction with
distal pneumonia
 Disruption of thoracic duct
(b) Systemic effect of tumour:
 Pulmonary embolism
 Hypoproteinemia
(c) Result of therapy:
 Radiation  lymphatic
obstruction.

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+ Rt. Pleural effusion )
 Peritoneal dialysis
4. Increased capillary
permeability:
 Small pulmonary emboli.
 Myxoedema.
5. Lymphatic obstruction.
 Drug reaction
"cyclophosphamide" 
pleurisy  effusion.
In infections:
Bacterial pneumonia  Pleural
effusion ( 30 – 40 % )
Tuberculosis: through
 As a part of primary TB:
peripheral focus or caseating
lymph node rupture into the
pleural cavity.
 Recurrent dry pleurisy.
Evidence of the disease may
disappear without treatment.
 Tuberculous caity may
rupture into pleura.
Viral and fungal infections:
Very rare.
Drug reactions:
 Direct effect  Practolol &
methysergile.
 Eosinophil reaction 
Nitrofurantoin & Beta Blockers.
 Lupus like syndrome  Isoniazid
( INH ) – phynetoin.
Oesophageal rupture:
introduction of oropharyngeal
content  mediastinum 
inflammation  rupture into pleura
 effusion.

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Clinical picture:
Symptoms:
1. No symptoms: in case of small effusions.
2. Pleuritic pain:
 Due to pleurisy.
 Sharp, localized and stitching pain.
  with 1- inspiration 2- Coughing
 As fluid accumulates and separate the
pleural layers.
3. Breathlessness: in case of large amount.
4. Recurrent Cough: Dry Cough is present.
5. Symptoms of the cause.
Signs:
1. Inspection:
 Movement: Restriction of respiratory movement on the affected side.
 Shape: Bulging of the chest on the affected side.
N.B: Retraction may be present if there is fibrosis in the lung on the same side.
2. Palpation:
 Movement: Diminished respiratory movement on the affected side.
 TVF:  TVF on the affected side.
 Trachea: Shifting of the mediastinum to the opposite side.
3. Percussion:
 Dullness or stony dullness over the affected area.
 Skodiac Sign : Hyper resonance on the upper part of the lung above
effusion due to compensatory emphysema.
4. Auscultation:
Breath sounds:
  or absent breath sound on the affected side.
The symptoms of pleural
effusion depends on:
1. The rate of formation
of effusion.
2. The amount of effusion.
3. Clinical picture of the
cause.

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 Bronchial breathing: may be heard above effusion due to compression on
lung.
  Vocal resonance.
Additional sounds:
Pleural rub: in case of dry pleurisy.
Investigations
1. Plain chest X-Ray:
Case Appears as
Small effusion Blunting of Costo-phrenic angle due to fluid.
Large effusion Homogenous opacity obliterating the costo-phrenic
angle & Raised towards axilla
Encysted effusion  Interlobar effusion:
in heart failure & disappear with diuretics.
 Paramediastinal effusion.
Sub-pulmonary
effusion
between Diaphragm & inferior surface of the lung.
Massive effusion Homogenous or massive opacification + shifting of
mediastinum to opposite side.
2. Pleural fluid aspiration " Thoracentesis ":
Indication Diagnosis of the cause.
Therapeutic : Relieving dyspnea.
Site 5th
Intercostal space, mid-axillary line.
Complications  Pneumothorax Haemothorax
 Re-expansion pulmonary edema.
 Introduction of infection.
 Injury to – Diaphragm - Lung - Spleen
Contra-indications Underlying bleeding tendency
3. Pleural fluid analysis:
Macroscopic appearance:
Syndrome of multiple negative signs of
pleural effusion:
No resp. movement. No TVF.
No resonance. No auscultatory findings.

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Transaudate Clear with slightly yellowish tint
Exaudate Straw cloloured. May be turbid  if cell count is high
Empyema Opaque and viscid
Chylous Milky white
Microscopic appearance:
Total leucocytic
count
Transaudate  < 1000 / ml3
Pyogenic " exaudate "  > 1000/ml3
Differential white
cell count
Polymorphs  pyogenic infection.
Lymphocytes  TB, Neoplasm and collagen disease.
Oesinophils (>10%)  Hodjkin lymphoma
Biochemical examination:
Protein < 3 gm/dl  Transaudate. >3 gm/dl  Exaudate
Lactate
dehydrogenase
Exaudate  Increased .
Normal is < 50 % of plasma level
Glucose Decreased  in  Bacterial infections, TB and malignancy
PH
< 7.2  Post pneumonic effusion
< 6.8  Indicates empyema
Immunological
study
Rheumatic factor  Rheumatoid arthritis.
LE cells  systemic lupus.
High level of
adenosine
deaminase
TB
Amylose
Pancreatic  pancreatitis and pancreatic tumours.
Salivary  Oropharyngeal rupture.
Bacterial examination:
 Gram staining & culture.
 Direct smear & Culture for acid fast bacilli.
Cytological examination:
For malignant cells.
4. Chest sonography:
 Confirm diagnosis.
 Detection of localized effusion.
 May detect the cause.

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5. Pleural biopsy:
Indications
If pleural fluid analysis fails to establish the etiology of
effusion
Types
 Closed needle biopsy.
 Sonographic or CT guided biopsy.
6. Thorascopy – Thoracotomy – Open biopsy
Indicated when less invasive method have failed to give biopsy.
Treatment:
Treatment of malignant effusion:
Repeated therapeutic
pleural fluid aspiration
Indicated in debilitated patients in whom short
survival is expected due to late malignancy
Chest tube drainage and
pleurodesis
Indicated when effusion is rapidly accumulated
Sclerosing agents
Include :
Bleomycin – nitrogen mastered – Radioactive gold.
It indicates sterile pleuritis  adhesion of 2 layers 
Obliterating of pleural space  Prevent formation of
effusion.
Pleurectomy and pleural
abrasion
Indication: in patients with good general condition.
Done through: Thorascopy or Thoracotomy.
Treatment of malignant cause by Radiotherapy or Chemotherapy.
Treatment of TB effusion:
 Potent anti-TB regimen with steroid  Speed reabsorption of fluid.
 Prevent pleural fibrosis.
 Dose: 20 – 40 mg/day in adults.
 Duration: 2 – 3 weeks then  gradually over 2 – 4 weeks.
Treatment of para-pneumonic effusion:
 Non specific treatment  minimal amount of effusion resolve without
specific therapy with only treatment of the cause.

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 Repeated therapeutic thoracentesis  for considerable amount of
effusion.
 Intercostal tube drainage
1. If repeated fluid aspiration failed
2. In case of encysted fluid, the tube is inserted in the suitable site of
drainage.
Questions:
1. Pleural effusion: causes, diagnosis, management (11,09,94,92,86)
2. Causes of pleural effusion? (2013)
3. Etiological diagnosis of exaudative pleural effusion (97).
Answer: write causes of exaudative effusion and how to differentiate
them by investigations.
X-Ray:
Reference:
http://radiopaedia.org/articles/pleural-
effusion
Visit it for more x-rays and U/S.
Comment
 blunting of the costophrenic angle.
 blunting of the cardiophrenic angle
 fluid within the horizontal or oblique
fissures
 eventually a meniscus (ascending angles)
will be seen, on frontal films seen laterally
and gently sloping medially (note: if
a hydropneumothorax is present, no such
meniscus will be visible)
 with large volume effusions, mediastinal
shift occurs away from the effusion (note: if
co-existent collapse dominates then
mediastinal shift may occur towards the
effusion)
 Lateral films are able to identify a smaller
amount of fluid as the costophrenic angles
are deepest posteriorly.

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Illustrations:
Ultrasonographic guided pleural fluid
aspiration


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Definition:
It is collection of chyle in the pleural cavity
Mechanism:
Formed when thoracic duct is disturbed and chyle
enter the pleural sac.
Etiology:
Malignancy
 About 50% of chylo-thorax.
 lymphoma 75 % of malignancy.
 Also associated with mediastinal metastasis
from extra-thoracic.
Trauma
 Surgical trauma  neck dissection – Cervical
sympathectomy.
 Penetrating trauma.
 Blunt trauma.
Other
causes
 Idiopathic.
 Tuberculous lymphadenopathy.
 Lt. Subclavian vein thrombosis.
 Aortic aneurism.
Diagnosis:
 Detection of dye or radioactivity un pleural fluid after ingestion of butter
containing lipophilic dye or radio-Iodine labeled triglyceride.
 This confirm diagnosis of chylothorax and exclude pseudochylous.
Pseudochylous: Chronic effusion can mimic1
the appearance of truechyle
due to appearance of fat globules derived from degenerated cells.
 Concentration of triglycerides > 110 mg/dl  indicates chylothorax.
Treatment:
1. Conservative
treatment
 Cessation of oral treatment.
 Total parentral nutrition.
 Inter-costal tube drainage.
1
Mimic = to have the same behavior or qualities as something else

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2. Active
treatment
 Surgical:  in traumatic type  detection of teared part
by injection of evan blue dye. If not able to identify the
site  duct ligated both above and below.
 Intercostal tube drainage and chemical pleurodesis.
3. Treatment of the case
Definition:
Presence of blood in the pleural sac.
Causes:
Traumatic
Cause Penetrating or non-penetrating trauma
Mechanism  Inter-costal vessels laceration.
 Pulmonary parenchymal laceration.
 Iatrogenic : Central venous catheter.
Non-
Traumatic
Causes  Pleural malignancy ( the commonest )
 Anti-coagulant therapy.
 Bleeding disorder.
 Ruptured thoracic aorta.
Treatment:
1. Immediate intercostals tube
1. Control bleeding in about 85% of cases.
2. Evacuation of blood from pleural sac  
incidence of empyema or fibro-thorax.
3. Stop bleeding from pulmonary parenchyma by
opposing the pleural surface by tempanade.
4. Provide adequate measures of continued
bleeding.
2. Immediate thoracotomy
Indications
1. Cardiac tamponade.
2. Continued bleeding.
3. Major injury  bronchial rupture.
4. Bleeding > 200 ml/hour + no evidence of
slowing over 4 – 6 hours.

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Definition:
Collection of pus within the pleural cavity
Causes:
Traumatic
Iatrogenic
Lung resection – oesophageal tears –
paracentesis – liver biopsy
Non-
iatrogenic
Stabbing – gunshot wounds
Non-traumatic
Thoracic
sepsis
Pulmonary diseases :
 TB  Pneumonia.  Mediastinitis.
 Osteomyelitis of ribs, sternum and vertebra
Extra-
thoracic
sepsis
Sub-phrenic and hepatic abscesses
Clinical picture:
Symptoms:
1. General: (FAHM) Fever – Anorexia – Headache – Malaise.
2. Chest pain: take form of dull chest wall discomfort.
3. Dyspnea: due to compression of underlying lung by emphysema.
4. Cough: in case of broncho-pleural fistula it is associated with purulent
diacharge.
Signs:
1. As in pleural effusion.
2. Finger clubbing in case of chronic empyema.
3. Empyema necessitantis: describe lesion that rupture chest wall, sub-
cutaneous tissue leading to (discharging sinus).
Diagnosis:
1. Blood picture:

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 Leucocytosis.
 Mild normocytic normochromic anaemia.
2. Plain chest X-ray:
 Early stage  as pleural effusion.
 Late stage (Complicated fluid collection)  more extensive imaging + air
fluid level … indicating association with pneumo-thorax or broncho-pleural
fistula.
3. Chest CT scan:
 Confirm diagnosis.
 Determine extent of parenchymal pleural disease.
4. Thoracentesis:
 Required to assess the bio-chemical and bacteriological properties of
pleural fluid.
 N.B: The fluid should be examined for:
Macroscopic Colour, turbidity and odour
Bio-chemical PH, LOH, glucose, total protein and amylase
Bacteriological Gram stain and culture
Microscopical Total leucocyte count and differential white
cell count.
Complications:
3E
1. Empyema necessitans.
2. Chronic Empyema.
3. Extension (both to chest wall and to mediastinum).
2F
4. Fistula (broncho-pleural fistula).
5. Fibrosis (Fibro-thorax).
H 6. Hypoproteinemia.
Treatment:
1. Anti-microbial therapy:
 The choice of antibiotic is determined by culture and sensitivity test.
 Anaerobe  Benzyl penicillin + metroniadazole.

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 Pneumococci  High dose of benzyl penicillin
 Gram (-ve) aerobes  3rd
generation cephalosporins + Aminoglycosides.
 Tuberculosis  Anti-tuberculous drugs.
2. Drainage:
1. Closed drainage  Intermittent: with repeated aspiration.
 Continuous inter-costal tube under water seal.
2. Fibrinolytic and allegation therapy
Instillation of anti-septic antibiotics + fibrinolytics as " streptokinase " 
sterilize pleural space and lyses of adhesions.
3. Open drainage:
Resection of lowest rib above and below it. Pus can be aspired with
insertion of tube with water seal.
4. Video assisted thoracoscopic surgery.
5. Thoracotomy and decortication
6. Thoracoplasty.
Chronic empyema: If the empyema remains for more than 2 months
 It is described as chronic. After this period the lung doesn't
expand any more.
Questions:
1. Causes, management and complications of empyema (2010).
2. Treatment of empyema thoracis (2014).
Illustrations:
Accumulation of pus
in the pleural space

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Empyema necessitantis case
Coronal reformat CT thorax with contrast
Causative organisms
Of empyema necessitantis
 Mycobacterium
tuberculosis: thought to be
most common cause and may
account for ~70% of cases 3
 Actinomyces spp: considered
second most common cause
 Blastomycosis spp.
 Aspergillus spp.
 Mucormycosis spp.
N.B:
Most common organisms to cause empyema are
 childhood
o Pneumococcus
 adults
o penicillin-resistant staphylococcus
o gram-negative bacteria
o anaerobic bacteria: usually polymicrobial

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Definition:
It is Presence of air in the pleural cavity.
Causes:
Spontaneous. Traumatic.
Primary:
1. In apparently health patient.
2. No history of pre-existing lung
disease.
3. Due to rupture of pulmonary bleb
intra-pleural.
Non-iatrogenic:
Open and closed chest injuries 
barotraumas " diving trauma"
Secondary:
Occurs as a result of disease:
1. Chronic bronchitis.
2. TB.
3. Empyema.
4. Cystic fibrosis.
5. Necrotizing pneumonia (staph. And
klebseilla infections).
Iatrogenic:
1. Accidental:
 Complication of pleural fluid
aspiration.
 Complication of pleural
biopsy.
 Complication of trans-
bronchial biopsy.
 Baro-trauma "mechanical
ventilation"
2. Artificial:
 Diagnostic: during
thoracoscopy  to enable the
doctor to visualize the surface
of the lung.
 Therapeutic: old method of
treatment of TB cavity.
Clinical picture:
Symptoms:
1. Chest pain:  Sudden Unilateral.   by deep respiration and cough.

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2. Dyspnea: depends on the amount of pneumo-thorax and presence of lung
disease.
3. Cough: Dry and irritative.
4. Symptoms of the cause.
Signs:
1. General:
 Simple pneumo-thorax: tachycardia and tachypnea.
 Tension pneumo-thorax: anxious, restlessness, cyanosis, tachycardia and
hypotension.
2. Local:
Inspection Palpation Percussion Auscultation
Shape:
Unilateral bulge.
Movement:
Diminished.
Mediastinum:
shifted to
opposite side.
Movement and TVF:
Diminished.
Hypo-resonant
on the affected
side.
Diminished
breath sound.
Amphoric
breathing in
tension pneumo-
thorax.
3. Signs of the cause.
Types:
1. Open pneumo-thorax: pleura is connected with the atmosphere.
2. Closed pneumo-thorax: defect in the visceral layer or parietal pleura is closed.
3. Tension pneumo-thorax: The defect is valve like  permits air passing into
pleural cavity on inspiration but preventing escape of air during expiration 
leads to  acute mediastinal shift  kinking(2)
of great vessels.
Investigations:
1. Chest x-ray:
 Distinct visceral pleural line  absence of lung markings "Jet black".
 Lung: partially or completely collapsed.  In severe cases : lung appears as
globular mass at the hilum.
 Diaphragm: depressed copula.
(2)
a bend in something long and thin

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 Mediastinum: Shifted to the opposite side.
 The costo-phrenic angle: abnormally deepened when pleural air collects
laterally producing the deep sulcus sign.
2. Blood gases analysis:
 severe cases  type 1 respiratory failure.
 In association with (COPD)  Type 2 respiratory failure.
3. Pleural manometer:
In closed type: pressure  but remains (-ve) less than atmospheric pressure.
In Opened type: pressure oscillates around zero, Equals atmospheric pressure.
In tension type: pressure is progressively rising, more than atmospheric pressure.
X-ray Comment:
 visible visceral pleural edge see as a very thin, sharp white line
 no lung markings are seen peripheral to this line
 the peripheral space is radiolucent compared to adjacent lung
 the lung may completely collapse
 the mediastinum should not shift away from the pneumothorax unless a tension
pneumothorax is present (discussed separately).
 subcutaneous emphysema and pneumomediastinum may also be present

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Treatment:
Depends on  The volume of pneumo-thorax
 presence of underlying lung disease.
1. Conservative management:
In Small volume of pneumo-thorax (< 20%).
 absorption of gas is fasted by breathing high oxygen concentration.
N.B:
 high concentration of (O2) should be avoided in COPD and respiratory failure 
due to its inhibitory effect on the respiratory center.
 Chest X-ray: should be repeated at week interval until full expansion occurs.
 Rest: avoid heavy exercise.
2. Active treatment:
In Large and moderate volume of pneumo-thorax (>20%)
 Inter-costal tube drainage  under water seal drainage.
indications
 Tension pneumo-thorax.
 Large pneumo-thorax (>20%).
 Presence of pleural fluid.
 Severe manifestations of dyspnea.
 Bilateral Pneumo-thorax.
 Failed manual aspiration.
Site
Common
2nd
inter-costal space, mid
clavicular line.
alternative
4th
& 5th
inter-costal space, mid
axillary line.
N.B: Alternative site preferred in:
1. Women for cosmetic appearance.
2. If pleura contains fluid.
3. Traumatic pneumo-thorax.

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 Other methods for active treatment:
1. Aspiration.
2. Flutter valves.
3. Inter-costal tube drainage & chemical pleurodesis for recurrent
spontaneous pneumo-thorax.  By (Concentrated glucose 50% +
tetracycline + Silver nitrates solution + talc powder).
4. Parietal pleurectomy  If pleural abrasion at thoracotomy or thoracic
procedures occurs.
Risk factors for Pneumothorax
Risk factors differ between traumatic and non-traumatic types of pneumothorax.
Risk factors for TP include:
1. playing hard contact sports (e.g. football)
2. performing stunts that may cause damage to the chest
3. history of violent fighting
People at highest risk for PSP are those who are:
1. young and thin
2. male
3. between the ages of 10 and 30
4. affected by congenital disorders like Marfan’s syndrome
5. smokers
6. exposed to environmental or occupational factors, such as silicosis
7. changes in atmospheric pressure and severe weather changes(JThorac Dis)
The primary risk factor for SSP is having previously diagnosed lung disease. It is most common in
individuals over 40.
Complications of pneumothorax
1. Failure of lung re-expansion due to persistent air leak.
2. Respiratory Failure (type 1 ).
3. Heart Failure.
4. Recurrence (same side or opposite side).
5. Pyo-pneumothorax...following penetrating trauma, suppurative
pneumonia , rupture lung abscess or during intercostal tube insertion.
6. Haemopneumothorax
7. Re-expansion pulmonary oedema .. may follow the rapid re-expansion of
completely collapsed lung.
Questions:
1. Pneumothorax: causes, c/p, management and treatment? (13,12,10,09,06,85)
2. Complications of pneumothorax? (2014) TTT of spontaneous pneumoth. (11)

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Definition:
Acute inflammation of the lung parenchyma "Distal lung, alveoli and respiratory
bronchioles".
Or it is a syndrome caused by acute infection characterized by clinical and
radiological signs of consolidation of part or parts in one lung or both lungs.
Classification:
Anatomical classification:
1. Lobar pneumonia: involve one or two lobes.
2. Segmental pneumonia: Confined to lung segment or segments.
3. Sub-segmental pneumonia: it is more confined.
4. Broncho-pneumonia: patchy, poorly localized, bilateral, It is usually follow
bronchitis in contrast to lobar pneumonia which occurs in previously healthy
lung.
Causal classification:
Infectious pneumonia Non-infectious
pneumoniaBacterial Non-Bacterial
Gram (+ve) 
 pneumococci (
streptococcus pneumonia)
 staph. Aureus.
Gram (-ve) 
 H.Influenza.  E.coli.
Viral:
Measles, CMV, EPV.
Fungal:
candida.
Parasitic:
Toxoplasma.
Chemical  Lipoid.
Physical  after
radiotherapy on chest.
classification
anatomical etiological
"causal"
Emperical
"clinical"

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 Pseudomonas.
 Klebseilla.
Atypical " organism devoid cell
wall" 
 Mycoplasma.  Coxiella.
 Legionella.  Chlamydia.
Anaerobes 
 Peptococcus.  Bacteroids.
TB.
Collagen disease 
Lupus pneumonia.
Emperical or clinical classification:
1. Community acquired pneumonia (CAP): pneumonia occurring in the community.
2. Hospital acquired pneumonia (HAP): nosocomial pneumonia.
3. Aspiration pneumonia.
4. Immuno-compromised pneumonia.
HAP:
Pneumonia occurring after 2 days of hospital admission.
Depends on:
Time of occurrence:  Early onset  staph or strept.  Late: pseudomonas.
Type of hospitalization:  ICU or not.  Ventilated or not.
Organism:
 Staph.aureus. Gram (-ve): pseudomonas, H.influenza and klebsiella.
 Atypical organisms: legionella (air conditioners).
N.B: Over 90% of ICU acquired pneumonia occurring during mechanical
ventilation.
Predisposing factors:
 Splenectomy.
 Old age & extreme
young.
 Chronic lung disease.
 Chronic liver disease.
 Chronic renal disease.
 Chronic heart disease.
 Immuno-deficiency.
 Diabetes mellitus.
 Smoking and alcohol.
Pathology:
The entire cycle is relatively short running in course (7-10 days).

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Stage of
congestion
Stage of red
hepatization
Stage of grey
hepatization.
Stage of
resolution.
Affected
lobe
Enlarged Enlarged Enlarged  in size
Colour Heavy dark red red grey Yellow
Consistency Wet spongy consolidated consolidated Soft
Capillaries Dilated
Dilated and
congested
Less marked
Exaudate is
phagocytosed
by
macrophages
Alveolar
space
contents
Contains
serous
exaudate and
polymorphs
Excess fibrin in
form of network
containing RBCs
and PMNL.
Alveolar wall thick
 RBCs  hemolysis
  PMNL and
macrophages.
Clinical picture:
Symptoms:
1. Acute onset of Fever, anorexia, headache and malaise (FAHM).
2. Cough:
 Dry at first.
 With brownish rusty sputum  during stage of red hepatization.
 With watery sputum  during resolution.
3. Dyspnea: that may be severe.
4. Chest pain: due to overlying pleurisy, pleuritis stitching pain or stabling.  with
cough and sneezing.
Signs:
General:
1. Fever with or without rigor.
2. Tachycardia and tachypnea: RR to HR may be 1 : 2 (normal 1 : 4).
3. Herpes labialis: herpes simplex affection of the lips especially with
pneumococcal infection.
Plus 3 colours as following:
White Pale toxic face
Blue Cyanosis in severe cases

Page 26
yellow Jaundice may occur due to haemolysis
Local:
Shape:
usually normal.
movement:
 on affected
side.
Trachea:
central.
TVF:  over the
affected side.
Impaired note
over the
affected lobe.
Bronchial breathing.
 vocal resonance.
Crepitation: First  fine
late inspiratory.
Then  coarse
inspiratory.
Give your attention to systemic and other systems affection as indicated in diagram

Page 27
Indices of severe pneumonia:
1. Tachypnea: > 30 cycle/minute.
2. Tachycardia: > 125 beat/minute.
3. PaCO2: > 50 mmhg.
4. Mental disturbances.
5. Evidence of renal insufficiency.
6. Hypotension.
Complications:
1. General:
 Septicemia.
 Septic shock.
 Peritonitis.
 Meningitis.
 Pericarditis.
 DIC (disseminated
intravascular coagulations).
2. Pleura:
 Pleurisy  Empyema.  Pleural effusion.
3. Lung:
 Delayed resolution  unresolved pneumonia.
 Failure of resolution  organization of exaudate  lung fibrosis "cornification".
 Lung abscess.
 Respiratory failure.
Investigations:
1. Chest X-Ray:
1. Detect pathology  show homogenous hazy
shadowing occupying anatomical distribution of the
lobe.
2. Radiological sign of complication  as lung abscess or pleural effusion.
2. Microbiological tests:
 Gram staining of sputum.
 Culture sensitivity test of sputum.
 Blood culture is positive in about 30% of cases.
Dyspnea, high fever and abnormal X-Ray film are
the main ways to distinguish pneumonia from
bronchitis.
Specific sputum colors are useless in determining
etiology.
First Chest X-Ray can
be falsely negative in
20% of cases

Page 28
 Microscopic analysis  to determine if the infection originate from upper
airway or lower airway.
The squamous epithelial cells:
In pneumonia  the count is < 10 sq. ep. Cells / low power field.
Macrophages:
The home of macrophages is distal lung. So, the presence of
macrophages regardless number  indicates lower respiratory infection.
Neutrophils:
> 25 cells / LPF can be used as evidence of infection.
3. Blood examination:
 WBCs  leucocytosis.
 Liver function test.
 ESR  .
 Renal function test.
4. Blood gases:
 May show hypoxemia and hypocapnea with respiratory alkalosis due to
shunting of blood through consolidated lung.
 Hypercapnea may occur if there is co-existing chronic bronchitis and
emphysema.
Differential diagnosis:
 Collapse.  Pleural effusion.
 Fibrosis.  Pulmonary infection.
Treatment:
1. Specific
Benzyle penicillin " penicillin G" :
 Drug of choice for bacteriologically confirmed pneumococcal pneumonia.
 Dose: 1 – 2 g. IV / 6 hours. Or: IM  for first 2 days.
 Followed by: phenoxymethyle penicillin, %500 mg/ 6 hours  for 7 – 10
days.
Ampicillin:

Page 29
 500 mg to 1 gm/6 hours. IV.  Followed by 250 – 500 mg/6 hours orally.
Amoxicillin:
 500 mg – 1 gm/8 hours. IV.  Followed by 250 – 500 mg/8 hours orally.
 If patient is allergic to penicillin, use macrolids.
Erythromycine:
 500 mg – 1 gm/6 hours for 2 days.
 Followed by: 250 – 500 mg/6 hours orally for 7 days.
Cefaroxime:
 Used as alternating to parentral erythromycin.
 1.5 gm/ 8 hours. IV.
2. Supportive measures:
1. Pleuritic chest pain  analgesic.
2. Hypoxemia  O2 therapy.
3. Fluid and electrolyte replacement  in severe pneumonia, patient may
become dehydrated.
4. Total parentral nutrition (TPN)  when mechanical ventilation is prolonged.
5. Inotropics as (Dopamine and dobutamine)  if complicated by
hypertension.
6. Intensive care unit (ICU)  severe pneumonia.
3. Prevention:
Vaccination: Pneumovax "pneumococcal vaccine"
Questions:
1. Causes, C/P, Complications and
management of pneumonia
(04,99,95,92,87,86) Classification (09,12)
It is the severity of the disease
not the etiology that drives the
initial therapy.
Health care workers don't need
pneumococcal vaccine.

Page 30
Definition:
Slowly resolved, recurrent, or if it doesn't improve in 15 days.
Causes:
1. Inadequate treatment, concerning type and dose of antibiotic.
2. Bronchial obstruction especially neoplasm or TB.
3. Inappropriate chemotherapy especially for TB, mycoses or klebseilla (specific
etiology).
4. Repeated aspiration as in: achalasia or pharyngeal pouch.
5. Underlying lung pathology as: abscess or bronchiectasis.
6. Immuno-deficiency as: D.M., AIDs and alcoholism.
Indices of Hospitalization of a case of pneumonia
CURB56
1. Confusion.
2. Uremia (Elevated BUN above 30 mg/dl, Na+ less than 130 mmol/l, glucose above
250 mg/dl.
3. Respiratory distress (RR > 30 cycles/min, PO2 < 60 mmHg, PH < 7.35)
4. BP low
5. Age > 65 years

Page 31
Staphylococcal
pneumonia
Pneumonia due to
Gram (-ve) infection
etiology  Account for 5% of causes of
community acquired pneumonia
(CAP) but may produce
nosocomial pneumonia.
 Route: aspiration of oral secretion
or haematogenous route.
 N.B: CAP caused by
haematogenous spread is
associated with endocarditis or
infected vascular site.
Organism:
1. Klebseilla
2. p. aerogenosa
3. E.coli.
Commonly associated with
nosocomial pneumonia.
 9-20 % of CAP due to
Gram (-ve) bacteria.
Clinical
picture
Symptoms:
In case of aspiration  fever,
dyspnea, cough, purulent sputum
are prominent Resp. tract symptoms
 may be mild or absent.
Signs:
 Evidence of lobar consolidation
may be not present.
 In case of endocarditis 
Murmer, arthritis, splenomegaly,
haematuria and heart failure.
Symptoms:
 Sudden onset of productive
cough.
 The sputum may be blood
tinged.
 May be associated by
production of classic
current jelly sputum.
Investigations
1. Gram stain & culture sensitivity.
2. Blood picture  leucocytosis with
neutrophilia.
3. Chest X-Ray  Segmental or
central consolidation.
1. Chest X-Ray  typical
consolidation.
2. Classic bulging fissure sign 
due to intense inflammatory
reaction to organism
"Klebseilla" occurs in middle
lobe.
Treatment  Penicillinase resistant penicillin
(nafcillin or oxacillin) 1-2 gm/day.
I.V.
 Duration: uncomplicated type 
10 – 14 days.
 Complicated type  4-8 weeks.
 Penicillin allergic patients or
resistant to methicillin or oxacillin
 use vancomycin.
Hospitalization is necessary.
 Anti-pseudomonal penicillin
"Piperacillin".
 Anti-pseudomonal 3rd
generation cephalosporins.
 Duration: 2 weeks or until
patient has been febril for 5-
7 days & neutrophils <
500/mm3
.

Page 32
Organisms:
 influenza virus (A&B).
 Para influenza virus.
 Adenovirus.
 varicella zoster virus.
 CMV.
Clinical picture:
1. Mainly immune-competent patient.
2. Can't be differentiated from bacterial pneumonia.
Diagnosis:
1. Viral culture.
2. Serology  ELISA.
3. PCR.
Treatment:
Symptomatic:
General supportive measures: bed rest and anti-pyretics.
Chemo-prophylaxis:
1. Amantadine  100 – 200 mg/day for 3-5 days.
2. Remantadine  100 mg twice daily for 3-5 days.
3. I.V. Acyclovir  5 mg/Kg/every 8 hours for 7 – 10 days.
D.D of apical Lung disease:
1. TB.
2. Pancost tumor.
3. Onchylosis.
4. Bronchiectasis sicca hemorrhagica.
5. Klebseilla pneumonia.

Page 33
Mycoplasma pneumonia
Etiology:
 Free living non-motile bacteria that lack cell wall.
 It is mostly recognized as a cause of Atypical "CAP" in general population.
 Transmission: Via aerolised respiratory droplets produced by infected
individuals.
Clinical picture:
Symptoms:
1. It is manifested as minor respiratory infection "pharyngitis or trachea-
bronchitis".
2. Onset: gradual.
3. General: Fever, chills, headache and malaise.
4. Cough:  Initially  dry.  Then  productive of mucoid or
mucopurulent sputum.
5. Pleuritic chest pain.
6. Sinusitis may occur.
Signs:
1. Minimal or disproportionate to patient complaint.
2. Chest examination: normal despite of radiographic abnormalities &
evidence of consolidation.
Extra-Pulmonary signs:
1. Meningitis.
2. Myocarditis.
3. Skin  Erythema Nodosum.
4. Blood  Cold type autoimmune hemolytic anemia.

Page 34
Investigations:
1. Chest radiography: variable infiltrates. May be broncho-pneumonia or
interstitial pneumonia with Kirlys lines.
2. C.B.C: normal in most patients, but mild to moderate leucocytosis  in 25% of
patients.
3. Cold agglutinins: Titre  > 1/32 in up to 70 % of patients.
4. Coomb's test: may be positive in some patients.
5. Culture: may be detected in the sputum or throat washing using special media.
6. DNA probe test: now available and detect M.pneumoniae very rapid.
Treatment:
Drugs:
Erythromycin , tetra-cycline (500 mg- 3 times)
Doxy-cycline, clathromycin, azithromycin.
Duration:
2 weeks of treatment are effective.
Legionella pneumonia
Legionellosis
Legionnaires' disease - Legion Fever.
 Auto-immune haemolysis: secondary to cold agglutinins develop in some patients.
 Extra-pulmonary as:
 CNS  meningitis, encephalitis and peripheral neuritis.
 CVS  myocarditis and pericarditis.
 Skin  erythema nodosum.
Organism:

Page 35
 Gram (-ve) cocco-bacilli (pleomorphic) usually related to contaminated water
cooling systems ahd shower.
 Usually affects patients with underlying lung disease.
Clinical picture
1. Clinical picture of pneumonia.
2. Severe general manifestations.
3. GIT manifestations.
4. Acute renal failure may develop.
Investigations:
1. C.B.C  lymphopenia and pancytopenia.
Hyponatremia (cause of it written as SIADH  which means Syndrome
of inappropriate anti diuretic hormone secretion).
2. Chest X-Ray: patchy bilateral shadow.
Treatment:
Clathromycin or Ciprofloxacin up to (21) days.
Clinical Hint Just to know 
Why legionellosis causes Hyponatremia unique from other infections
?!!!!
L. pneumophila can destroy the JG apparatus and thus the patient will
not secrete renin
Questions:
1. Lobar pneumonia: C/P & diagnosis (13,85).
2. Staphylococcal pneumonia (10).
3. Loffler's pneumonia (98).
4. Atypical pneumonia (09).
5. Viral pneumonia (10).

Page 36
Lung abscess
Definition:
 It is localized area of necrosis and suppuration within the lung parenchyma.
 It may be single or multiple and frequently contain air fluid level.
Classification:
Based on duration and the cause
1. According to duration:
 Acute abscess: 4-6 weeks.
 Chronic abscess: > 6 weeks.
2. According to cause:
 Primary abscess: due to infection as aspiration or pneumonia in normal chest.
 Secondary abscess: due to pre-existing condition as obstruction and spread.
Putrid abscesses: it is abscess with bad (foul) odours associated with
anaerobic organisms.
Etiology:
Predisposing factors of lung abscesses:
1. Aspiration of oro-pharyngeal flora:
 Dental or peri dental sepsis.
 Para nasal sinus infections.
 Depressed conscious level as in anaesthia, epilepsy and diabetic coma.
 Impaired laryngeal closure as tracheostomy tube or cuffed endo-tracheal
tube.
 Disturbances of swallowing as pharyngeal pouches and achalasia.
 Delayed gastric emptying as gastro oesophageal reflux disease (GERD) and
vomiting.

Page 37
2. Necrotizing pneumonia:
 Staph. Aureus.
 Klebseilla.
 Strept. Milleri/ intermedius.
 Pseudomonas aeroginosa.
3. Haematogenous spread:
 UTI (urinary tract infection).
 Infective endocarditis.
 Abdominal sepsis.
 Infected canula.
 I.V. drug abuse.
 Septic thrombo-phlebitis.
4. Pre-existing lung disease
 Bronchiectasis.  Cystic fibrosis.  Bronchial obstruction as F.B.
5. Infected pulmonary infarction.
6. Trauma.
Organisms:
Lung abscess may be caused by wide variety of different organisms and it is
common to obtain mixed bacterial growth from single abscess.
Anaerobic
organisms
Aerobic organisms Less common
Bacteroid fragilis.
Micro aerophilic
streptococci.
Peptostreptococci spp.
Gram (+ve) as:
 Staph. Aureus.
 Strept. Pyogens.
 Strept. Pneumonia.
Gram (-ve) as:
 Klebseilla.
 Pneumonia.
 P. aeroginosa.
 E. coli.
T.B.
Fungi.
Entameba
histolytica.
Clinical picture:
Symptoms:
1. General: Fever, anorexia, headache and malaise. (FAHM).
2. Suppurative syndrome: cough and expectoration of excessive sputum
(>100 ml/day) purulent and paroxysmal.
3. Haemoptysis: is common and may be life threatening.
4. Dyspnea.

Page 38
5. Chest pain: may be dull aching or pleuritic pain due to pleurisy.
6. In chronic abscess: Retension syndrome period of no or mild expectoration
with severe general manifestations.
Signs:
1. General: Fever, tachypnea and tachycardia.
2. Local: signs of cavity
 No signs of deep or small abscess.
 The same as pneumonia.
 Post tussive suction: in case of acute abscess.
3. In case of chronic abscess:
Sign of cavity + fibrosis (Unilateral chest retraction and trachea may be
shifted to the same side).
4. Clubbing of fingers: may develop within a few weeks if treatment is
inadequate (chronic).
Investigations:
1. Radiography:
1. Chest X-Ray:
 A dense shadow is initial finding before rupture.
 Cavity with fluid level: wall is thin  acute | wall is thick  chronic.
2. Thoracic CT:
 Very helpful in finding the extent of both lung abscess and emphysemas.
 Fluroscopy with ultrasound:
 May be helpful in guiding peri-cutaneous diagnostic thin needle
aspiration of abscess.
2. Blood picture:
 Leucocytosis  may be > 20,000 / mm3
.
 Normocytic normochromic anaemia.
3. Microbiological sampling:
 Blood culture  (+ve) in cases of caused by haematological spread.
 Sputum  Gram staining.
 Culture sensitivity.
 Acid fast smear and mycobacterial cultures.

Page 39
 Cytological examination  If cavity carcinoma is suspected.
4. Bronchoscopy:
Diagnostic Therapeutic
 To obtain material for culture.
 To exclude possibility of airway
obstruction by F.B.
 Removal of F.B.
 Instillation of antibiotics.
 Endo-bronchial drainage of
abscess.
1. From other causes of cavity or suppurative syndrome as:
 Infective cystic lung disease.
 Empyema with broncho-pleural fistula.
 Bronchiectasis.
2. Hiatus hernia.
3. Hydatid cyst.
4. Pulmonary haematoma.
5. Cavitating pneumo-coniotic lung lesions.
6. Cavitating lung cancer.
Complications:
1. Local:
 Chronicity.
 Bronchiectasis.
 Pneumonitis.
 Fibrosis.
2. Extension to pleura:
 Empyema.
 Pleural effusion.
 Pleural adhesion.
 Pyo-pneumothorax.
3. Haematogenous spread:
Pyema  brain abscess.
4. Amyloidosis.
Treatment:
1. Antibiotics:
 Drugs: Benzyle penicillin – Clindamycine – Metroniadazole.
 Dose: Benzyle penicillin  6-12 g. I.V.
Metroniadazole  500 mg. I.V. / 8 hours by infusion.
Clindamycin  600 mg. I.V. / 6-8 hours, then switching to oral therapy
at dose of 300 mg/ 6-8 hours.

Page 40
 N.B:
1. Once the patient is febrile and abscess is stabilized radiologically. It is
possible to  dose of penicillin and shifting to oral form as:
 Phenoxy-methyl penicillin (penicillin V) 0,5-1 gm/6 hours +
 Metroniadazole: 400 mg/ 8 hours.
2. Other antibiotics as: amoxicillin – clavulinic acid and cefotaxim.
Duration: usually: 4-6 weeks but may need to be extended for 3 months.
2. Postural drainage:
Helping patient to clear purulent material.
3. Bronchoscopy:
Aspiration + instillation of antibiotics.
4. Surgery:
 Inter costal tube drainage under water seal.
 Open drainage by pneumostomy.
 Thoracotomy and lung resection in :
1. Massive and life threatening haemoptysis.
2. Suspicious that it is cavitating tumour.
3. Failure of medical treatment.
X-Ray:
Questions:
1. Diagnosis of lung abscess (87) Complications & D.D (13).
 a cavity containing an air-fluid
level.
 In general abscesses are
round in shape, and appear
similar in both frontal and
lateral projections.
 Additionally all margins are
equally well seen

Page 41
Definition:
 It is a disease characterized by the presence of air way obstruction and
Emphysema.
 The air flow limitation is usually progressive and not fully reversible.
Chronic bronchitis:
It is chronic disease of bronchial tree characterized by cough and expectoration
daily for 3 successive months for at least 2 successive years & not attributed to
other pulmonary or cardiac causes or (6 months in 1 year or 2 months in 3
successive years).
Emphysema:
It is permanent dilatation and destruction of lung distal to terminal bronchioles
without obvious fibrosis.
Etiology:
1. Cigarette smoking:
1. Active smoking  chronic hyper secretion of mucous  reversible after
cessation
 progressive persistant air flow obstruction  not reversible.
2. Passive smoking  exposure during childhood   FEV during adulthood.
3. Maternal smoking during pregnancy  Low Birth weight (LBW).
2. Air pollution:
increase  mortality and prevalence of COPD.
3. α1- anti-trypsin deficiency:
 α1- anti trypsin: it is a polymorphic glycoprotein responsible for majority of
anti-protease activity of the serum.

Page 42
 There is association between α1- anti trypsin deficiency and development of
early COPD before 40 years old.
4. Occupation: as exposure to dust.
5. Chronic broncho-pulmonary infection: chronic infection lead to airway
damage and progressive airway obstruction.
Pathology:
Chronic bronchitis Emphysema
 Simple: hypertrophy of mucous
glands  cough with whitish
mucoid expectoration.
 Chronic obstructive: there is
organic narrowing and
progressive decline in air flow
due to:
1. Mucous gland hypertrophy.
2. Infiltration of wall by
inflammatory cells (neutrophils
+ CD8 + T-lymphocyte).
Classified according to site of damage:
 Centri-acinar emphysema:
concentrated around respiratory
bronchioles with smoking.
 Pan-acinar emphysema: affect the
whole acinus with α1- anti trypsin
deficiency.
 Peri-acinar or irregular: enlarged air
space along of acinar units or affect
lung parenchyma in patchy distribution
without respect of acinar structure.
Pathogenesis:
Cigarette smoking α1- anti trypsin deficiency
Only 15-20% of smokers develop COPD.
It leads to:
  protease amount in neutrophils.
  anti-protease activity due to direct
oxidative effect of smoking.
  elastin synthesis due to smoking  
Lysyle oxidase  tissue elastin.
This lead to degradation of lung
connective tissue in alveolar wall
by protease  emphysema.
Pathophysiology:
1. Lung mechanics:
 FEV1.
 residual volume.
 total lung capacity.
2. Muscle wasting:
 Pulmonary over inflation +
malnutrition.
 Loss of weight due to 
metabolic requirement of
3. Pulmonary
Hypertenstion:
Hypoxia  pulmonary
hypertension  Rt.
Ventricular

Page 43
respiratory muscles  due to 
work of breathing.
hypertrophy 
dilatation  edema.
4. Pulmonary gas exchange:
Usually patient with COPD show combination of emphysema and chronic
bronchitis with predominance of certain feature over the other.
Type A (pink puffer). Type B (Blue Bloater).
 This patient has dominant
emphysema.
 There is normal or low level of CO2
+ Hypoxemia.
 Hypoxemia  Respiratory
activation fighting for O2.
 So, there is :
 Severe dyspnea (puffer).
 No cyanosis (pink).
 Patient has dominant chronic
bronchitis.
 There is hypoxemia +
hypercapnea.
 This patient is non fighter for O2.
 So, there is:
 No dyspnea.
 Cyanosis (blue).
 Cor-pulmonale (edema –
Bloater).
Type A (pink puffer) Type B (blue bloater)
Severe dyspnea with pursed lip
breathing
Mild dyspnea
Small sputum volume Large sputum volume
Usually thin patient Usually obese
No cyanosis Cyanosis
No edema Edema
Investigations
Near normal blood gases Abnormal blood gases
Radiological evidence of emphysema
No radiological evidence of
emphysema
Impaired transfer factor No reduction in transfer factor
Clinical picture:
Symptoms:
1. History of heavy smoking for many years at least 20 packs – years.
2. Cough: often present on waking up at first. Then, through out the day.
3. Productive cough:

Page 44
 Initially  mucoid. Then  purulent sputum with exacerbation of disease.
 Often worse in winter months and after chest infections.
 Daily sputum production for 3 or more months in 2 successive years defines
chronic bronchitis.
4. Dyspnea:
 Slowly progressive over years.
 Commonly the reason why patient seeks medical attention.
5. Wheezes: that are usually persistant and continuous but not specific to COPD due
to turbulence of air flow in large airways.
6. Chest tightness.
7. Haemoptysis: may be due to infection but bronchial carcinoma should be
considered.
Signs:
1. General signs:
 No signs in mild cases.
 Tachycardia and pulsus
parodoxicus.
 Prominent accessory respiratory
muscles in neck.
 elevated shoulder with professional
attitude.
 edema of lower limb.
 Tachypnea.
 Puffy eyelids.
 Congested neck veins.
 Enlarged congested liver.
 Flapping tremor due to
hypercapnea.
 an inspiratory tracheal tug  due to contraction of low flat diaphragm.
N.B:
 The breathing pattern is characteristic:
 Prolonged expiratory phase.
 Some patients adopt to pursed lip breathing during expiration  expiratory
airway collapse and improve oxygenation.
 Clubbing is not a feature of COPD and suggest malignancy or bronchiectasis.
2. Local:
Inspection & palpation Percussion Auscultation
 Barrel shaped chest +
kyphosis.
 Horizontal rib and prominent
sterna angle wide sub costal
angle.
Hyper resonance with
loss of normal cardiac
and liver dullness.
 Prolonged
expiration.
 Rhonci  through
out the chest and
biphasic.

Page 45
 Hoover's sign: the horizontal
position of diaphragm acts to
pull in the lower rib during
expiration.
 May be basal
crepitations.
3. Other examination:
 Sign of pulmonary artery hypertension.
 Liver: may be enlarged, tender, pulsating and palpable below costal margin.
 Peripheral vasodilatation  due to hypercapnea  warm peripheries with
high volume pulse.
 Pitting peripheral edema.
Complications:
1. Lung:
 Recurrent chest infections.
 Bronchiectasis.
 Pneumo-thorax.
 Respiratory failure.
2. Heart:
 Right sided heart failure.
 Myocardial hypoxia   risk
of ischaemic Heart Disease
(IHD).
3. Renal:
 Renal hypoxia 
salt and water
retension.
 Proteinuria.
4. Stomach:
 Peptic ulcer.
5. Complication of
chronic cough:
 Rupture bullae.
 Hernia.
 Insomnia.

Page 46
Investigations:
Radiological investigations:
1. Plain chest X-Ray:
 Bronchial wall thickening  parallel line opacities.
 Over
inflation of
the lung
Diaphragm
Low
In mid clavicular line  below ant. End of 6th
& 7th
rib.
Flat
Perpendicular height from line drawn
between the costo-phrenic and cardio-
phrenic angles and the lower border of
diaphragm less than 1.5 cm.
Obtuse costo-phrenic angle.
 Vascular changes: due to loss of alveolar wall:
 Size and number of pulmonary vessels at periphery of lung.
 Area of translucence is surrounded by hair line walls "Bullae".
 Hyper translucence of lungs with transverse rib and wide inter costal spaces.
2. Chest CT:
High resolution and thin cut (1-5 cm) section.
3. Fluoroscopy:
 range of diaphragmatic movement only (1 cm) in severe COPD | normally > 3
cm.
Physiological assessment:
1. Spirometry:
  FEV1  < 80%.
  FEV1/FVC ratio  < 70%.
  Peak expiratory flow rate (PEFR).
2. Lung volumes:
  Residual volume (RV).
  total lung capacity (TLC).
3. Reversibility to bronchodilators:

Page 47
 By: measuring changes in FEV1 after the use of bronchodilator as B2 agonists as
"Salbutamol" inhaler (2 buffs)  improvement in FEV1 < 15% over basal line.
 N.B: unlike bronchial asthma FEV1 response > 15%.
 Importance:
 To help distinguish those with marked reversibility who have underlying
asthma.
 To aid further management.
4. Arterial blood gases:
To confirm the degree of
 Hypoxemia.  Hypercapnea.  H+
concentration.
5. Reversibility to corticosteroids:
By: measuring (FEV1) before and after administration of (30 mg) predinsolone
for 2 weeks.
Non-physiological assessment:
1. Polycythemia  should be suspected when hematocrit value (HV) is > 47 % In ♀
| > 52% in ♂.
2. α1- anti trypsin level  should be measured in all patients < 40 years of age and
in case of (+ve) family history.
3. ECG  P. pulmonale, RVE in cor-pulmonale.
4. ECHO  to assess cardiac functions.
Bronchial asthma Congestive heart failure Bronchiectasis
 Reversible air flow
limitation.
 Onset: early in life.
 (+ve) family history.
 Symptoms at night and
early morning.
 Allergy, rhinitis or
eczema
 Bronchodilator test:
FEV1 > 15%.
 Fine basal crepitation
on auscultation.
 Chest X-Ray: dilated
heart and pulmonary
edema.
 Pulmonary function
test:
 Volume restriction.
 No air flow limitation.
 Large volume of
purulent sputum.
 Clubbing of fingers.
 Coarse crepitation.
 Chest X-Ray:
bronchial
dilatations.

Page 48
Treatment:
Prevention:
1. Smoking cessation  is vital even in late stage of the disease.
2. Influenza and pneumococcal vaccination.
3. Avoid of atmospheric pollution.
Management:
 Long term
management.
 Pulmonary
rehabilitation.
 Of acute
exacerbation.
Long term management:
 Bronchodilator  Corticosteroids.  Oxygen therapy.
Action:
  symptoms & 
tolerance to exercise.
 Relaxation of air way
smooth muscles.
  ciliary beat frequency.
Types:
1. B2-agonists:
Rapid onset – for
symptomatic relief.
2. Anti-cholinergic:
 Affect both central and
peripheral airway.
  Functional residual
capacity.
3. Theophylline:
 Improve exercise
tolerance.
 Anti-inflammatory
action.
  diaphragmatic
contraction.
N.B: has narrow
therapeutic index.
Action: anti-inflammatory.
Includes:
1. Oral:
Significant
improvement in FEV1 >
15% occur in 10-20% of
patients after oral
corticosteroids.
2. Inhaled:
In dose of 100 µg
bectomethasone
should be given to
those who show a
response to either oral
or inhaled.
Importance:
 Improve survival.
 Improve exercise
tolerance.
 Improve
polycythemia.
  arterial pressure
of pulmonary
artery.
Types:
1. Long term  for 15
hours in patient with
chronic respiratory
failure.
2. Short term  for
temporary relief.
3. Portable oxygen
therapy  for
exercise related
hypoxemia.

Page 49
Pulmonary rehabilitation:
To prevent the condition that occur with lack of exercise and immobility due
to dyspnea.
Acute exacerbation:
 Antibiotics:
Organisms: H.influenza, strept.
Pneumonia, moraxella catarrhalis
virus.
Drugs:
Amoxicillin 250 mg/ 3 times daily.
Tetracycline 250 mg/ 4 times daily.
 Bronchodilators:
24-48 hours  nebulized
bronchodilator (B2 agonists or anti-
cholinergic).
Then  metard dose inhaler.
If no response  I.V. aminophylline
(0.5 mg/kg/hour)
 Diuretics:
In patient show fluid retention due to
respiratory failure and cor-
pulmonale.
 Anti-coagulant:
 Prophylactic sub cutaneous
heparin is often given to patient
with exacerbation of COPD due
to pulmonary emboli.
 α1- anti trypsin replacement: monthly infusions is indicated in patient
with serum level < 310 mg/L and abnormal lung function.
Comparison between COPD and bronchial asthma:
Clinical data COPD Bronchial asthma
Smoking history +ve Usually –ve
Course of disease progressive Intermittent
Cough Early morning Night/early morning
Sputum purulent Not purulent
Dyspnea All the time Only in attacks
Central cyanosis May be present
Absent (may be present in
acute severe asthma).
Generalized wheezing Common In attacks
Peripheral edema May be present Not a feature
Spirometry:  FEV1 always In attacks
Bronchodilator test FEV1 improve < 15% FEV1 improve > 15%
Response to cortisone Poor good

Page 50
Questions:
1. Management of COPD (09,03,95)
diagnosis (9-09)
2. Treatment of COPD (12).
3. Pathology of chronic bronchitis.
4. Diagnosis , complications and
treatment of emphysema (04,92,87).
5. Risk factors and complications of
COPD (2014)
Answer: risk factors are as the
etiology mentioned above.
Test yourself(3)
:
Answer : (b)
(3)
Source: USMLE CK book. Pulmonology.
Clinical Notes
(a) If the case describes a patient who is
young and a non smoker, you should
answer alpha-1 antitrypsin
deficiency as the most likely cause.
(b) Full reversibility in response to
bronchodilators is defined as greater
than 12% increase and 200 ml
increase in FEV1.
(c) Inhaled anti-cholinergic agents are
the most effective in COPD.
(d) If medical therapy is not sufficient,
refer to transplant.
A 65 years old woman is admitted to hospital with CAP. Sputum Gram stain shows Gram
positive diplococci but the sputum cultures doesn't grow a specific organism.
Chest X-Ray shows a lobar infiltrate and a large effusion. She is placed on cefotriaxone and
azithromycin. Thoracentesis reveals a marked elevated LDH and protein level with 17.000
WBCs/µl.
Blood cultures grow streptococcus pneumonia with a minimal inhibitory concentration
(MIC) to penicillin less than 0.1 µg/mL. Her oxygen saturation is 96% on room air. Blood
pressure is 110/70 mmHg. Temperature is 38.9°C, and pulse is 112 b/min.
What is the most appropriate next step in management of this patient?
a. Repeated thoracentesis.
b. Placement of chest tube for suction.
c. Add ampicillin to treatment.
d. Place patient in intensive care unit.
e. Consult pulmonary.

Page 51
Definition:
Chronic abnormal dilatation and obstruction of bronchi caused by destruction of
elastic or muscular component of bronchial wall.
Or, Persistent dilatation of bronchi accompanied by chronic suppurative
inflammation of bronchial wall.
Etiology:
1. Broncho-pulmonary infection:
T.B – bronchitis – Measles - Pneumonia
2. Obstruction:
Intra-luminal:
 Aspirated F.B.
 Mucoid impaction.
 Slow growing neoplasm.
Extra-luminal:
 Hilar lymphadenopathy.
3. Congenital anatomical defects:
Trachea-bronchial:
 Bronchomalacia.
 Bronchial cyst.
Vascular:
 Pulmonary sequestration – pulmonary artery aneurism.
Pulmonary agenesis.
Lymphatic: yellow nail syndrome.

Page 52
4. Immuno-deficiency syndrome:
 Congenital: congenital gamma globinemia.
 Acquired: HIV
5. Hereditary abnormalities:
 Ciliary defects - α1- anti trypsin deficiency – cystic fibrosis.
6. Hyper immune response:
 Allergic broncho-pulmonary aspirgillosis.
7. Miscellaneous:
 Aspiration injury.
 Toxic gases.
 Auto-immune: Systemic lupus erythromatosis.
Pathogenesis:
 Pulmonary infections  destroy the bronchial wall then dilatation.
 Bronchial obstruction  collapse and secondary infection  bronchial dilatation.
Pathology:
Site: Bilateral, basal and patchy.
Shape:
Cylindrical. Tubular varicose fusiform Secular "cystic"
Clinical picture:
Symptoms:
1. Suppurative syndrome (5) ch.ch:
 Excessive sputum.
 Purulent.
 Foeted.
 Paroxysmal.
 Positional:  on leaning forward.
2. Haemoptysis:

Page 53
 Due to mucosal ulceration.
 (Bronchiectasis sicca haemorrhagica)  haemoptysis not associated with
suppuration (dry form) when involved area is limited to upper lobes. E.G: Post
T.B. and Friedlander pneumonia.
3. General: Fever, anorexia, Headache and malaise (FAHM).
4. Dyspnea: regarded as late symptoms and usually indicate wide spread lung
disease.
5. Chest pain: due to pleurisy
6. Sinusitis may be present.
Signs:
General:
 Fever.
 Tachypnea.
 Tachycardia.
 Puffy eyelids.
 Clubbing of fingers.
 Edema of lower limb.
Local: ( bilateral, basal and patchy).
Shape:
 Bulge: in case
of pleural
effusion.
 Retraction:
in case of
collapse.
Movement:
Diminished on
the affected
side.
Trachea:
 Shifted to same
side as in
fibrosis.
 To other side as
in pleural
effusion.
TVF:
  on basal
parts.
  on upper
lung zone due
to emphysema.
 Dullness on the
affected side 
basal bilateral.
 Hyper
resonance in
upper lung zone
due to
compensatory
emphysema.
Breath sound:
 Bronchial.
Persistence early &
mid inspiratory &
expiratory crackles:
 Crepitations.
 Localized to one or
more areas.
 Descriped as coarse
crakles.
 Not shifted by
coughing.
Complications:
1. General:
 Septicaemia.
 DIC.
 Meningitis.
 Amyloidosis.
 Multiple organ failure.
 Clubbing.

Page 54
2. Pleural:
 pleurisy  Pleural effusion.  Empyaema.
3. Lung:
 Pneumonia & lung abscess.  Fibrosis.  ARDs ( acute resp. distress)
 Respiratory failure & cor-pulmonale  in late stage of disease.
4. Operative complications:
 Hemorrhage.
 Empyema.
 Atelectesis.
 Pneumothorax.
 Pneumonia.
 Broncho-pleural fistula.
Investigations:
1. Plain chest Radiography:
Specific findings:
1. Honey comb appearance "Ring shadows"
2. Cystic shadows "Soup bubble appearance" (0,5 – 2 cm in diameter)
3. Parallel line or "Train line appearance" inflamed dilated but evacuated bronchi.
4. Radiological sign of complication: pneumonia – lung abscess.
5. Appearance of pulmonary hypertension in extensive disease.
6. Kartagner syndrome: dextrocardia – sinusitis.
2. Computed Tomography:
 High resolution CT (HRCT) has become the
investigation of choice in bronchiectasis.
 It provides useful non invasive means of
establishing disease.
3. Bronchography:
Was the investigation of choice when it is necessary to confirm diagnosis of
bronchiectasis with certainty and was considered a mandatory if surgical
treatment was contemplated.
4. Bronchoscopy:
Assessing the cause and site of haemoptysis.
It is impossible to
diagnose
Bronchiectasis
without an imaging
study of the lungs
such as a CT scan.

Page 55
5. Sputum examination:
 Culture and sensitivity test.
 Gram's staining.
 Culture for acid fast bacilli.
6. Other laboratory investigations:
 Blood picture:
Leucocytosis.
Anaemia.
 ECG:
Show evidence of cor-pulmonale
in advanced cases
 Urea
and
creatinine.
Treatment:
Medical treatment:
1. Antibiotics:
Indicated to treat acute exacerbation.
Drugs: ampicillin, amoxicillin, (amoxicillin clavunate), (trimethoprem
sulfamethoxazol) and flouroquinilones.
Duration: 10-14 days.
2. Postural drainage:
It is very important in management especially in patient with sputum volumes >
30-50 ml/day.
3. Hydration:
To avoid inspissations of secretions
4. Corticosteroids:
 Used in patient with significant air flow limitation not respond to
bronchodilator if patient is a stable case.
 Also in allergic broncho-pulmonary aspergillosis and autoimmune diseases as
inflammatory bowel disease.
 Predinsolone  30-40 mg/day for 10 days.
5. Bronchodilators.
6. Mucolytics.

Page 56
7. Human immune-globulins: in cases with immuno-deficiency syndromes.
Surgical treatment:
Indications:
 Repeated remission & exacerbation.
 Localized lesion.
 Life threatening haemoptysis.
 Saccular haemoptysis.
 Specific organisms
Type of lung resection:
 Segmentectomy.
 Wedge resection: remove small peripheral triangular piece.
 Lobectomy.
 Pneumectomy.
 Pleura-pneumectomy.
Contra-indications:
 Bilateral brochiectasis.
 Evidence of ciliary dysfunction.
 Complicating asthma.
 Co-existing COPD.
Questions:
1. Aetiology, pathogenesis and
C/P of Bronchiectasis? (2009)
2. Investigations and treatment
of Bronchiectasis? (94,87)
3. Complications of
Bronchiectasis? (2013)
CT picture of bronchiectasis

Page 57
Definition:
The lungs can't fulfill their primary
function of maintaining adequate gas
exchange at rest or during exercise.
This results in an inability to maintain
normal blood gases. So that PO2 is low
with or without rise in PCO2.
Types:
1. Type 1: hypoxemia without CO2
retention.
2. Type 2: hypoxemia with hypercapnea.
Causes:
Type 1 Type 2
 Chronic
bronchitis
 Pneumonia.
 Asthma.
 Pneumothorax.
 Pulmonary
embolism.
 Pneumoconiosis.
 Bronchiectasis.
 Congenital heart
disease.
 Chronic
bronchitis.
 Drug
overdose.
 Poisoning.
 Myathenia
gravis.
 Polyneuropathy.
 Poliomyelitis.
 Primary muscle
disease.
 Acute respiratory
distress. Tetanus
Clinical picture:
Clinical picture of hypoxemia Clinical picture of hypercapnea
1. Central cyanosis.
2. CNS: Irritability – convulsions –
coma.
3. CVS: tachycardia -  COP –
Cor-pulmonale.
4. Chest: Tachypnea – Dyspnea.
5. Secondary polycythemia.
1. CNS: Irritability – confusion – coma.
2. CVS: Cerebral vascular disease - 
intracranial tension – warm flushed
skin – bounding pulse.
3. Sympathetic: tachycardia – sweating.
4. GIT: gastric dilatation – paralytic ileus.

Page 58
Diagnosis:
1. Clinical picture.
2. Arterial blood gases analysis :
 PaO2  < 60 mmHg.
 PaCO2  > 49 mmHg.
Treatment:
Aim:
1. Maintain air way patent.
2. Ensure adequate alveolar ventilation and oxygenation.
3. Treat primary cause:
 Treatment of the cause: e.g: antibiotics for infection.
 Type 1  O2 therapy in high concentration up to 50%.
 Type 2  mechanical ventilation + we can use respiratory stimulant as
doxaprom.
Important Notes
Blood gases analysis:
Normal values of arterial
Acute Resp.
failure
Chronic Resp.
failure
Acute on top
of chronic
PH  7,35 – 7,45  Normal 
PaO2  80 – 100 mmHg.   
PaCO2  35 – 45 mmHg.   
HCO3  22 – 27 mEq. normal  
Saturation O2  95 – 99 %
N.B: Respiratory failure
may be:
 Acute  Opiate
overdose.
 Chronic  COPD.

Page 59
Types of respiratory failure:
Type 1 respiratory failure Type 2 respiratory failure
Hypoxemia  PaO2
 60 mmHg.
Hypoxemia  PaO2
Hypercapnea  PaCO2   50 mmHg.
Use ordinary respiratory mask Use venturi mask.
Respiratory and metabolic acidosis:
Respiratory acidosis Metabolic acidosis
PH  
PaCO2  
HCO3 normal 
Treatment of respiratory failure:
Type 1:
 O2 therapy 50% (high concentration).
 By ordinary mask.
 Follow up by (ABGs) arterial blood gases.
 May need mechanical ventilation.
Type 2:
 O2 in low controlled therapy (24-28%).
 By venturi mask.
N.B: If high O2 concentration  apnea as no stimulus to respiratory center.
Acute on top of chronic:
 Respiratory stimulant.
 Ventillation.
Indications of mechanical ventilation:
 Rapid  in hypercapnea.
 Tachypnea > 35 breath/minute.
 Mental confusion.
 Exhaustion.
N.B: indications of
mechanical ventilation:
 Any  in CO2 level.
 O2 still < 60 mmHg.
 Failure to control
secretions.

Page 60
Questions:
1. Give an account on respiratory failure. (13)
2. O2 therapy: indications, methods and hazards (10,02,00)
Complete4
:
1. Pulmonary embolism can cause type ……… respiratory failure.
Case study5
:
65 year-old women who recently underwent hip replacement comes to the
emergency department with acute onset of shortness of breath and tachycardia.
The chest X-ray is normal, with hypoxia on ABG, An increase A-a gradient, and an
ECG with sinus tachycardia.
What is the most appropriate next step in management?
a. Intravenous unfractionated heparin.
b. Thrombolytics.
c. Inferior vena cava filter.
d. Embolectomy.
e. Spiral CT scan.
f. Ventilation/Perfusion "V-Q" scan.
g. Lower extremity Doppler study.
h. D-Dimer.
4
Source: Dr. Azza mahmoud Oral examination.
5
Source: USMLE CK book. Step 2. Pulmonology part.
Answers:
Complete: Type 1
Case study: A. Intravenous unfractionated heparin

Page 61
Definition:
Inflammatory fibrotic infiltration of the
interstitium affects the capillary
endothelium and alveolar epithelial lining
cells. It produces a disease with similar
clinical, radiographic and physiological
features.
The inflammatory process is limited specifically to the area between the alveolar
epithelial & capillary endothelial basement membrane.
This group of disorders involves:
1. Alveolar epithelium.
2. Alveolar space.
3. Pulmonary microvasculature.
4. Respiratory bronchioles
Classification:
Clinical classification
1. CT Diseases :
 Scleroderma
 SLE
 RA
 Ankylosing spondylitis
 Behcet’s Disease.
 Polymyositis
 Dermatomyositis
 mixed CT disease
 sjögren syndrome.
2. Occupational:
 inorganic dusts
 Silica
 coal dust
 Asbestos
 beryllium
 Aluminum
 mixed dusts
 Hard metal (titanium oxide, tungsten and cadmium)
IPF:
81 in 100,000 prevalence in males
67 in 10,000 in women
200 in 10,000 incidence in age more than 75
30-40% of all ILD (IPF)

Page 62
 organic
 farmer lung
 air candy
 aspergillosis
 detergents
 Bagassosis
 Bird breeder’s lung
 saun-taker's disease
 coffee worker's disease
 humifier lung
 chicken handler’s disease
 wood dust worker's disease
 chemicals e.g synthetic fiber lung
 Gases, fumes and vapors:
 gases e.g oxygen , sulfur dioxide, chlorine gas
 fumes e.g oxides of zinc, copper, magnesium , cadmium, iron, nickel
 vapors e.g mercury
3. Idiopathic Disorders :
 Acute interstial pulmonitis
 unusual interstitial pulmonitis
 desqumative interstitial pneumonitis
 cryptogenic organizing pneumonia
 non-specific interstitial pneumonia
 lymphocytic interstitial pneumonia
4. Drug induced:
 Chemo therapeutic agents: busulfan, bleomycin , cyclophosphamide.
 Antibiotics: nitrofurantion , sulphonamide, penicillin
 Others: diphenythydantion, procaimamide, gold
 Poisons: paraquant
 Radiation: external, inhaled
 Infectious agents: residue of active infection of any type
5. unclassified :
 sarcoidosis
 histocytosis
 Good pasture’s syndrome
 idiopathic pulmonary haemosidrosis
 wegner’s granulomatosis
 churg- strauss $

Page 63
Pathogenesis:
1. Epithelial cell apoptosis with loss of BM integrity.
2. Production of growth factors in response to alveolar epithelial injury with
hyperplastic type II cells and myofibroblast recruitment
Evaluation of ILD
1. Extensive History
 Age, sex, underlying co morbidities, drugs, smoking, occupational history.
 duration of symptoms
2. physical Examination:
3. Lab. Investigations
 imaging, spirometry, lung volumes and DLCO(6)
 LFTS ,CBC,ANA, RF, hypersensitivity panels, ANCA, anti GRM , CRP, ESR
 pulmonary function e.g spirometry, lung volumes, diffuse capacity
 imaging e.g PA/LAT CXR
 HRCT
History:
Nature of the first symptoms
I- Dyspnea and cough with little sputum production
II- co morbid diseases e.g. CT diseases, rashes, Reynaud's phenomenon ,
dysphagia
III- immune deficiency diseases
IV- drugs
V- environmental /occupational exposures with dates and durations as
asbestosis, silica
VI- smoking status
VII- previous malignancies and treatment
VIII- family history of lung diseases
6
Means: diffusing capacity or transfer factor of the lung for carbon monoxide (CO)

Page 64
Examination:
1. Breathlessness
2. Cyanosis
3. Clubbing
4. Skin rashes & ulcers
5. Joint swelling
6. Leg oedema
7. Auscultation:
 Lung crackle send inspiratory fine dry or Velcro type
Clinical Picture:
1. Dyspnea: the first symptom on exertion then at rest.
2. Wheezing: not common complaint and may only accompany periods of cough.
3. Cough is common.
4. Weight loss and fatigue are sufficiently frequent symptoms
5. Digital clubbing is common
 Occur in 50% of patients but rarely associated with hypertrophic
arthropathy.
6. Cyanosis on exertion and later at rest is one of cardinal features
7. Auscultation:
 Intensity of breath sound is normal
 scattered late inspiratory ronchi may be heard
 Crepitations common… fine (Velcro rale) and sometimes are localized
 Heart is vertical , P2 might be accentuated and progression to right ventricular
8. Hypertrophy and failure is usual
Investigations:
1. Laboratory:
 CBC with differential WBCs count
 ESR
 KFTS & LFTS
 Serological tests: For CT diseases.

Page 65
2. Radiology:
 Usually abnormal
1. Chest X Ray.
2. HRCT scan.
 Radiological pattern of disease
 Reticulo-nodular alveolar shadows
 Honey comb appearance.
 pleural involvement
 Inter lobar septal thicking
 Hilar adenopathy
 Patchy abnormalities predominant in the periphery of lung and lower lobes
3. Pulmonary Function tests
1. Spirometry.
2. Lung volumes.
3. Diffuse capacity.
 It's important for assessing severity of lung involvement determining
obstructive and restrictive patterns.
 Most IPF has restrictive pattern.
4. Reduction on Thin Layer Chromatography (TLC), Functional residual capacity
(FRC) and (RV).
5. Decreased FEV1 & FVC but the changes is in proportion as FEV1/FVC normal
or increased
6. Reduction in lung volumes called lung stiffness and worsen with progression
of disease
4. Arterial Blood Gas (ABG):
 May be normal or reveal hypoxemia and respiratory alkalosis.
 CO2 retention is rare and usually a manifestation of End stage disease
5. Fiber optic bronchoscope.
6. Isotope scan.
7. Bronchoscopy.
Reticular and honey comb
changes often associated with
ground glass opacification and
traction bronchiolitis

Page 66
 Initial procedure of choice
 Endo bronchial lesions: sarcoidosis, wegner’s granulomatosis, inflammatory
and stricture of the major airways.
8. Lung biopsy & histopathological Examination
 Trans bronchial biopsy: diagnostic
 Broncho-alveolar lavage (BAL): normal count:
 CD4:CD8 = 1.5
 macrophages 85%
 lymphocyte 5-10%
 neutrophils less than 2%
 eosinophils less than 1%
 cytogenic analysis:
 PAS stain
 Monoclonal antibodies (OKT6) in histocytosis.
 Asbestos exposure: one asbestos body/ ml
 The utility of BAL in the clinical assessment of disease progression or
response to therapy still be established
 CD4:CD8 : more than 2 is seen in sarcoidosis , TB , fungal infections
 CD4:CD8 : less than 2 is seen in hypersensitivity pneumonitis
9. Surgical biopsy
Indications:
 Assess disease activity.
 Exclude neoplasm or infection.
 Identify a more treatable condition.
 Establish a definitive diagnosis before starting a treatment with serious side
effect.
 Provide specific diagnosis in patient with atypical or progressive pattern and
normal or atypical Chest X-Ray finding.
Contraindications:
 Serious CVD.

Page 67
 Radiographic evidence of diffuse end stage disease (honey comb).
 Sever pulmonary dysfunction.
Treatment:
1. corticosteroid:
 Main treatment.
 dose: large dose to maximum effect
 1-5 mg/kg / day prednisolone
2. potentially alternative treatment:
 cyclophosphamide
 pencillamine
 cyclosporine
 interferon alpha and beta
 High dose N- acetyl cystayine
3. Lung Transplantation.
Complications:
 Progressive RF.
 Bronchial carcinoma.
 Pulmonary embolism.
 Drug toxicity.
 Pneumonia.
 Cor pulmonale.
 Pneumothorax.
Bad prognostic signs:
 Old age.
 Male.
 Smoking.
 Honey combing.
 6-MWT-spo2 less than 88 %.
 Lower DLCO.
 Less than 40 %.
 Higher rate of acute exacerbation.
 Pulmonary HTN.

Page 68
 Primary
pulmonary TB.
 Secondary
pulmonary TB.
 Miliary TB.
 Extra-
pulmonary.
Definition:
 It is first infection with tubercle bacilli.
 Usually include involvement of draining lymph
node in addition to initial lesion.
 Also called child hood type, as it is frequent in young children.
 Infection occurs by inhalation of tubercle bacilli.
Pathology:
 Primary pulmonary complex = Triad of Gohan's focus: composed of:
1. Gohan's focus: it is the initial lesion at the periphery of the lung underneath
pleura.
2. Tuberculous lymphadenitis.
3. Tuberculous lymphangitis.
Fate:
1. Healing: with mild infection with good immunity.
2. Spread:
 Direct  to lung tissue.
 To pleura  pleurisy.
 Haematogenous:
 Small number  destroyed.
 Moderate number  isolated organ tuberculosis.
 Large number  military TB.
 Bronchial spread.
Childhood type

Page 69
3. Encapsulation and reactivation.
Clinical picture:
 The majority of primary TB has
fewer symptoms or discovered
accidentally.
 The child may have General
symptoms  unwell, loss of
appetite and failure to gain
weight.
 Cough may occur  sputum
production is very rare in
children.
 Auscultation:
 Crepitations: heard over an
extensive primary focus.
 Wheezes: due to pressure of glands on bronchi.
Diagnosis:
1. Chest X-Ray:
 Lymphadenopathy and parenchymal lesion.
 Hilar lymph nodes were most commonly involved.
 Para tracheal lymph node may also involve.
 Evidence of segmental or lobar consolidation or obstructive emphysema.
2. Tuberculin test: Postitve.
3. PCR.
Complications:
 Collapse.
 Consolidation.
 Bronchiectasis.
 Obstructive emphysema.
 Erythema nodosum.
 Pleural effusion.

Page 70
The most important type of TB due to  frequent and positive smear is the main
source of infection.
Pathogenesis:
Arise in 3 ways
1. Direct progression of primary lesion.
2. Reactivation of a quiescent primary lesion.
3. Exogenous infection.
N.B: reactivation of primary lesion occurs when the immunity of patient declines as in:
 Malnutrition.
 Poor housing
condition.
 Pulmonary silicosis.
 Alcoholism.
 HIV infection.
 Cigarette smoking.
Clinical features:
1. Age:
 In developed countries  middle age or elderly.
 In developing countries  variable with predominance of young & middle ages.
2. Symptoms:
 General symptoms: Tightness, malaise, loss of appetite, night fever and night
sweat (helps in diagnosis).
 Symptoms related to respiratory system:
1) Cough  persistent, with or without sputum.
 Sputum: mucoid, purulent and blood tinged.
2) Haemoptysis  classic symptoms vary from blood staining of sputum to
massive. It is due to erosion of bronchial artery which bleeds at systemic
pressure.
3) Chest pain  varies from dull ache to tightness to pleuritic pain.

Page 71
4) Wheeze  localized due to end bronchial tuberculosis.
3. Signs:
1. Tachypnea: with advanced disease.
2. Fever: variable.
3. Clubbing of fingers: unusual.
4. Pallor, hectic flush and cachexia: in advanced cases.
5. Post tussive crepitations: in upper zone.
6. Sign of consolidation with pneumonia.
7. Sign of pulmonary fibrosis as shifting of trachea in chronic cases.
Investigations:
1. Chest radiography:
 Normal chest film not completely excludes Pulmonary TB.
 Characteristic appearance:
1. Soft confluent shadows alone  exaudative process.
2. Linear shadows  Fibrosis.
3. Calcification  healed disease.
4. Tuberculoma  It is a cavity may be blocked, filled with purulent or
caseating material.
5. Enlargement of hilar or para tracheal lymph nodes.
 Radiological classification:
Minimal Moderately advanced Far advanced
 Only infiltration.
 Lesion: non cavitary.
 Not extended more
than ant. End of 2nd
Rib.
 Cavity lesion.
 Diameter > 4 cm.
 Not extended more
than 4th
Rib.
 Diameter of cavity &
extension more than
of moderate cases.
2. Sputum examination:
It is of great value in diagnosis of pulmonary TB.
1. Direct smear  using ziehl-nelsen stain or fluorescence stain.
2. Culture  On Lowenstein Jonson media  grows after 3-8 weeks.

Page 72
3. Rapid diagnosis  now is possible within 2-6 days using radiometric culture
system (Bactec system).
If sputum is not available:
1. Gastric lavage. 2. Laryngeal swabs.
3. Fine needle aspiration. 4. Mediastinoscopy.
5. fiberoptic bronchoscopic specimens (bronchial wash – bronchial brushing).
3. Newer diagnostic
techniques:
 Serological diagnosis: by
ELISA.
 Polymerase chain
reaction (PCR) capable
of detecting of single
organism in sputum.
4. Tuberculin testing:
 Most patients with past
primary TB have
positive tuberculin test.
5. Liver function
tests.
6. Blood picture:
 Normocytic
normochromic
anaemia is common
with pulmonary TB.
 Normal WBCs.
10 mm or more is positive in
 Recent arrivals (less than five years) from high-prevalence countries
 Injection drug users
 Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless
shelters, etc.)
 Mycobacteriology lab personnel
 Persons with clinical conditions that place them at high risk (e.g., diabetes, prolonged corticosteroid therapy,
Tuberculin test
A standard dose is 5 tuberculin units (TU - 0.1 ml) is injected
intradermally (between the layers of dermis) and read 48 to 72
hours later. This intradermal injection is termed the Mantoux
technique. A person who has been exposed to the bacteria is
expected to mount an immune response in the skin containing the
bacterial proteins.
The reaction is read by measuring the diameter of induration
(palpable raised, hardened area) across the forearm in millimeters.
If there is no induration, the result should be recorded as "0 mm".
Erythema (redness) should not be measured.
If a person has had a history of a positive tuberculin skin test,
or had a recent tuberculin skin test (within one year), another skin
test should be used.
1. An HIV-positive person
2. Persons with recent contacts with a TB patient
3. Persons with nodular or fibrotic changes on chest X-ray consistent
with old healed TB
4. Patients with organ transplants, and other immunosuppressed
patients

Page 73
leukemia).
 Children less than four years of age.
 Persons with no known risk factors for TB
False negative result
1. Infectious mononucleosis
2. Live virus vaccine - The test should not be carried out within 3 weeks of live virus vaccination.
3. Sarcoidosis
4. Hodgkin's disease
5. Corticosteroid therapy/Steroid use
6. Malnutrition
7. Immunological compromise.
Clinical Hint
Extensive pulmonary shadow in Chest X-Ray + normal WBCs  favors diagnosis of TB.
Differential Diagnosis:
1. Pneumonia: segmental pneumonia + soft upper zones opacities  mimic
pulmonary TB.
2. Carcinoma of the bronchus  in the middle aged & elderly age group.
3. Lung abscess.
4. Pulmonary infarction.
Complications:
1. Pleura: Pleurisy and Empyema.
2. Larynx: tuberculous laryngitis  in patient with (+ve) sputum.
3. Cor-pulmonale.
4. COPD.
5. Carcinoma of the bronchus.

Page 74
The most common forms of extra
pulmonary TB are
1. Lymph node TB
 This is the most common form of
extra pulmonary TB.
 Lymph nodes in the neck and
above the clavicles are
commonest sites.
 Any lymph node in the body can
become infected, and often the
enlarged, swollen lymph nodes
cause other problems because of
their size.
Diagnosis:
 A sample of the infected node is
tested for TB bacilli.
2. Pleural TB
 There is a small space in between the layers of pleura (parietal and visceral), in
which the TB bacilli can sit and multiply.
 As a result, the area becomes inflamed and the person infected has fever and
experiences pain when breathing.
 This inflammation leads the pleura to secrete liquid, and a mass of liquid
assembles in between the two layers of the pleura. This is called a pleural
effusion.
Diagnosis:
 A sample of the pleural effusion fluid should be taken to be examined for TB
bacilli. This is done by inserting a needle through the chest wall into the space
between the pleura layers, and taking out some of the fluid.

Page 75
3. TB of the bone and the joint:
 TB bacilli sit in the bone or the joint. This causes pain and swelling of the
affected area.
Diagnosis
 To diagnose TB of the bone or joint, an X-ray must be taken, and often more
sophisticated ways of X-rays like CT Scans (computer tomographic scans) or an
MRI (magnetic resonance imaging).
 As with the other forms of extra pulmonary TB, TB bacilli must then be
extracted from the bone or joint by accessing it with a needle and taking out a
small sample.
4. TB of the central nervous system
 TB bacilli can infect both brain and spinal cord, and most often they cause TB
meningitis – an infection of the thin layer that covers the brain.
 The symptoms depend on where in the brain the TB bacilli sit – usually people
with TB meningitis
 Become very sleepy.
 Don't react normally.
 Cannot move their hands or feet or walk anymore.
 They cannot speak or focus their eyes.
 TB meningitis is dangerous and difficult to treat.
Diagnosis
 To diagnose it, health practitioners must perfom a lumbar puncture – insert a
needle into the back of the patient to access the fluid around the spinal cord
(which is connected to the brain), and examine if there are TB bacilli in the fluid.
The fluid is called central spinal fluid, or CSF.
5. TB of other places
 TB can infect any part of the body, and other places where TB can infect are the
abdominal cavity (the belly region that contains important organs such as the
liver, the spleen and the bowels; this is then called abdominal TB), and the
region of the kidneys, the bladder and the urinary tract, that is the pathway
that urine follows when it leaves the body. This kind of TB is called genitourinary
TB (from genital and urinary after the sites where it manifests).

Page 76
Definition:
 It is produced by acute dissemination of tuberculosis bacilli via blood stream.
 This term is derived from radiographic picture of diffuse discrete nodular
shadows about size of amillet seed (2 mm) that is characteristic for the disease.
Clinical picture:
Symptoms:
 In children: may be associated with an acute or sub acute febrile illness.
 In adults:
 Onset: is insidious.
 Gradual development of vague, ill health, fatigue and anorexia.
 Cough, breathless, haemoptysis and night sweat  are less common.
Signs:
1. Fever.
2. May be no physiological signs.
3. Auscultation: the chest frequently normal although crepitation may develop
later.
4. Splenomegally, hepatomegally and generalized lymphadenopathy.
5. Choroidal tubercle: over 90% of children with military TB.
Diagnosis:
 Chest radiography:
 Abnormal shadows distributed, vary from faint shadows (1-2 mm) in
diameter to large dense shadows up to (5-10 mm)
 Bilateral pleural effusion.
 Tuberculin skin test:
 Usually (+ve) except in advanced disease it is (-ve).
 Direct smear of sputum and gastric lavage.

Page 77
Treatment of tuberculosis:
Drugs:
1. First line Drugs:
Drug Dose Preparation Side effects
INH (Isoniazid) 
300 mg/day.

300 mg/day.
 Tablets  50 –
100 – 300 mg.
 Syrup: 50
mg/5ml.
 Aqueous
solution.
Idiosyncrasy.
Neurotoxicity.
Hepatotoxicity.
Rifambicin 
<50 kg  450 mg.
>50 kg  600 mg.

600 mg/day.
 Capsule (150-300
mg).
 Vial suspension.
 Aqueous solution
(IV – IM).
Gastrointestinal
reaction.
Hepatotoxicity.
Orange discoloration
of body fluids.
Pyrazinamide 
<50 kg  1.5 gm.
50 - 75 kg 2 gm.
> 75 kg  2.5 gm.

2 gm/day.
 Tablets (500 mg). Hepatotoxicity.
Acute gouty arthritis.
GIT symptoms.
Ethambutole 
1.6 gm / day

1 gm / day.
 Not in children < 5
years old.
 Tablets (100 –
400 mg) for oral
administration.
Retro bulbar neuritis.
Peripheral neuritis.
Cutaneous reaction.
Streptomycin 
15 mg/kg/day.

20-40 mg/kg/day.
 Aqueous solution
in vial (1 gm).
Ototoxicity.
Nephrotoxicity.
Rifabutin 
300 mg
 Capsule (150
mg).
Hepatotoxicity.
Rifapentine 
600 once / week.
 Tablet (150 mg). Hepatotoxicity.

Page 78
2. Second line drugs:
Drug Dose Preparation Side effects
Cycloserine 15 mg/kg/day Capsule (250 mg)  CNS effect: headache
and restlessness.
Ethionamide 15-20 mg/kg/day Tablets (250 mg)  GIT.
 Hepatotoxicity.
 Neurotoxicity.
Amikacine 15 mg/kg/day Aqueous solution
(IV – IM).
 Ototoxicity.
 Nephrotoxicity.
 Teratogenicity.
Capreomycin 15 mg/kg/day 
single dose.
Vials (IV – IM).  Nephrotoxicity.
 Ototoxicity.
PAS (Para-
Aminosalicylate
Sodium)
 Adults:
8-12 gm/kg/day.
 Children.
200 – 300
mg/kg/day.
Tablets (500
mg).
Granules (4 gm)
packets.
 GIT
 Hepatotoxicity.
 Hypothyroidism
Coagulopathy.
Fluoroquinilones  Adults:
500-1000 mg/day
 Children:
No due to
affection of bone
and cartilage
growth.
Tablets (250 –
500 – 750 mg).
Aqueous
solution IV.
 GIT
 Neurological.
 Cutaneous reaction.
Principles of anti tuberculous
chemotherapy combination:
(1) Kill tuberculous bacilli rapidly.
(2) Prevent emergency of drug resistance.
(3) Eliminate persistent bacilli from host tissue to prevent relapse.

Page 79
Regimens for pulmonary tuberculosis
chemotherapy
Standard 6 months short course. Standard 9 months chemotherapy
Initial Phase:
 Duration: 2 months.
 Drugs: Isoniazid + Rifampicin +
Pyrazinamide + Ethambutamol.
Initial phase:
 Drugs: Isoniazid + Rifampicin +
Ethambutamol OR streptomycin.
Continuous phase:
 Drugs: Isoniazid + Rifampicin.
Continuous phase:
 Drugs: Isoniazid + Rifampicin.
Corticosteroid therapy in tuberculosis:
Indications:
 Very seriously ill patients.
 Controlling drug hypersensitivity.
 Pericarditis – Peritonitis – Pleural
effusion.
 TB meningitis  Prevent mortality.
 Genito-urinary TB  prevent ureteric
stricture.
Dose:
Predinsolone: 40 mg/day  for 6 weeks, then   gradually over 4 weeks.
Control and prevention:
BCG vaccination:
 It doesn't prevent infection but limits multiplication and dissemination of
mycobacteria.
 It is given obligatory in Egypt in first 3 months of life.
Chemoprophylaxis:
 Types:

Page 80
Primary chemoprophylaxis Secondary chemoprophylaxis
 Giving chemotherapy to individuals
who have not so far been infected (-
ve) tuberculin test.
 E.g: suckling child can't be
separated from TB mother for fear
of malnutrition.
 To individuals (+ve) tuberculin test with
normal chest film and have been
infected   development of disease.
 (+ve) tuberculin test in patients with
silicosis.
 House holds contacts of newly diagnosed
patient.
 Children < 5 years with strongly (+ve)
tuberculin test.
Drugs:
Isoniazid  adults  300 mg/day.
 Children  5 mg/kg  300 mg/day.
With total duration of one year.
Questions:
1. Diagnostic steps for TB cases (07,00)?
2. Diagnosis of pulmonary TB (94) treatment (11)?
3. Diagnosis of TB effusion (06)?
4. Treatment of broncho-pulmonary TB (97,92,87,85)?
5. Anti-tuberculous treatment: Drugs, course and hazards (03,00,94,92)?
6. Management of positive case of pulmonary TB (13,09,06)?
7. Tuberculin skin test (12,09)? 9. Military TB? (7,10)?
8. Pott's disease (13)?

Page 81
Etiology:
1. Deep venous thrombosis (DVT): commonest cause
 Predisposing factors:
 Slow circulation.
 Injury of endothelium.
 Hyper coagulability.
 Risk factors of DVT:
 Operative  especially pelvic and bone surgery.
 Oncology  cancer stomach, leukemia and lymphoma.
 Old age.
 Obesity.
 Oral contraceptives.
 Others: Congestive heart failure and coagulation disorders as Protein C & S
deficiency.
 Sites of DVT:
 Deep veins of legs partially the iliac, femoral and popliteal veins.

Page 82
2. Detached thrombi from right side of the heart:
 Infective endocarditis.
 Atrial fibrillation.
 Myocardial infarction.
3. Paradoxical embolism:
 From the left side of the heart if there is left to right shunt: Ventricular septal
defect (VSD).
4. Rare:
 Fat embolism.
 Air embolism.
 Amniotic fluid embolism.
Clinical picture:
 Unfortunately, there is no clinical or laboratory finding that will confirm
or exclude the diagnosis of pulmonary embolism.
 The clinical picture of pulmonary embolism is not specific. So, successful
management of pulmonary embolism requires a combination of clinical
suspicion and appropriate use of diagnostic tools.
 The clinical presentations are ranging from asymptomatic to sudden
death depend on the size of embolus.
(1) Small sized emboli:
 Recurrent small pulmonary emboli  occlusion of large number of pulmonary
arterioles.
 Usually asymptomatic, but non specific symptoms of tachypnea, dyspnea, and
tachycardia or pleuritic chest pain may occur.
 May result in development of pulmonary hypertension & sub acute cor-
pulmonale may occur.
(2) Medium sized emboli:
 Pleuritic chest pain.
 Cough and haemoptysis.
 Dyspnea.
(3) Acute massive pulmonary embolism (APE):
i. Acute dyspnea.
ii. Acute chest pain  similar to angina pain due to  Distension of
pulmonary artery  Reflex coronary spasm.
iii. Sudden appearance of pulmonary hypertension.
iv. Acute right sided heart failure.
v. Shock  It is obstructive shock which there is marked  of blood flow to
the lung   blood to left atrium   COP (cardiac output)  shock.

Pulmonology, illustrated text of pulmonology

Pulmonology, illustrated text of pulmonology

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Pulmonology, illustrated text of pulmonology