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

Un

derg

rad

uate

Refe

ren

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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.

http://radiopaedia.org/articles/pleural-effusion

http://radiopaedia.org/articles/pleural-effusion

http://radiopaedia.org/articles/hydropneumothorax



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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


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.


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

http://radiopaedia.org/articles/tension-pneumothorax



http://radiopaedia.org/articles/subcutaneous-emphysema

http://radiopaedia.org/articles/pneumomediastinum



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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)

http://www.healthline.com/health/silicosis



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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 pneumonia Bacterial 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.


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



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yellow Jaundice may occur due to haemolysis

Local:

Inspection Palpation Percussion Auscultation

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



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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



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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:



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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.

Inve

stig

atio

ns 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.


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.


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.

Differential diagnosis: 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


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.

Differential diagnosis: 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"


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).

Inspection Palpation Percussion Auscultation 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.

5 mm or more is positive in

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.

15 mm or more is positive in

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.


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: Duration: 2 months. Drugs: Isoniazid + Rifampicin +

Ethambutamol OR streptomycin. Continuous phase: Duration: 4 months. Drugs: Isoniazid + Rifampicin.

Continuous phase: Duration: 7 months. 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)?



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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.



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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.



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vi. Sudden death: may be first manifestation if occlusion involve more than 80% of the vascular bed.

vii. Findings suggesting for DVT tenderness, swelling and redness of the lower limb. Unfortunately, DVT of the leg is often clinically silent.

Investigations: 1. Chest X-Ray:

Rule out pneumonia and pneumo-thorax. Westermarck's sign Dilated pulmonary artery with pulmonary

vasculature or focal oligemia. Hampton's Hump wedge shaped peripheral opacity or pulmonary

infarction. Panna's sign enlarged right descending pulmonary artery (PA). Elevated copula of diaphragm. N.B: Hypoxia + Normal X-ray should the possibility of pulmonary

embolism.

2, ECG:

May be normal. Sinus tachycardia and atrial fibrillation. S1 Q3 T3 pattern [S wave in lead 1 – Q wave in lead 3 – an inverted T wave in

lead 3]. The most important value is to exclude myocardial infarctions as a cause of

dyspnea and chest pain.

3. Pulmonary angiography:

The gold standard for making diagnosis. Invasive .., costly and uncomfortable. Now used when interventions are planned as:

1. Suction catheter embolectomy. 2. Mechanical clot fragmentation. 3. Catheter direct thrombolysis.

4. Ventilation-perfusion (or "V-Q" scan):

Read as normal, low, intermediate or high probability of pulmonary embolism.

Doesn't diagnose or exclude pulmonary embolism in up to 75% of patients. Current indications:

1. Renal insufficiency.



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2. Anaphylaxis to I.V. contrast. 3. Pregnancy.

Area of normal ventilation and hypo perfusion.

5. Laboratory:

Arterial blood gases. Elevated LDH. D-Dimer: an end product of fibrin digestion.

It is a good negative test, if D-Dimer is not elevated, Pulmonary embolism is un likely.

Clinical prediction scores for suspected APE (1) Candian "wells" prediction score: DVT symptoms and signs 3,0. Pulmonary embolism (PE) as like as alternative diagnosis 3 Heart rate > 100 beat/minute 1,5 Immobilization or surgery in previous 4 weeks 1,5 Previous DVT or PE 1,5 Haemoptysis 1 Cancer 1 Total score: < 2 low pretest probability. 2 – 6 moderate pretest probability. > 6 high pretest probability.

(2) Dichotomized wells score: ≤ 4 PE unlikely. > 4 PE likely.

Treatment: Prophylaxis:

1. Early post operative ambulation. 2. Elastic stocking. 3. Elevation of the leg. 4. Anti-coagulants in high risk patients for about 1 week.

Low dose heparin 5000 units sub-cutaneous / 8 – 12 hours. Low molecular weight heparin (enoxaparine, Clexane) 20 – 40 mg/day.

Curative:

1. Hospitalization in CCU. 2. Anti-coagulants:

Heparin. Action: activation of anti-thrombin III.



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Dose: 5000 – 10000 units I.V. as a loading dose then 1000 units/hour infusion.

Duration: 1 week or till clinical improvement.

Questions: 1. Diagnosis of pulmonary embolism?

(13,12,11)

Radiology:



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Contents:

Superior

mediastinum Inferior Mediastinum

posterior middle Anterior

vessels Arteries: aortic arch and its 3 large branches. Veins: upper half of superior vena cava and its 2 innominate veins. Lymphatic: thoracic duct.

Arteries: descending aorta. Veins: azygos vein and hemi-azygos vein. Lymphatic: thoracic duct.

Arteries: descending aorta and pulmonary artery. Veins: lower half of superior vena cava and inferior vena cava.

Nerves Phrenic – vagus – Lt. recurrent laryngeal nerve.

Vagi and splanchinic nerves

Phrenic nerves

Tubes or other organs

Trachea. oesophagus

Oesophagus. Heart – pericardium. Tracheal bifurcation.

Thymus gland

Mediastinal cysts and tumours (1) Neural:

Nerve sheath tumour paraganglioma Nerve cell tumour Benign: neurolemanoma – neurofibroma. Malignant: neurosarcomas

Ganglio-neuromas. Ganglio-neuro-blastomas.

(2) Disorders of thymus: Thymic hyperplasia. Thymoma.

Thymic cysts. Thymolipoma.

Thymic germ cell tumour. Thymic carcinoid tumour.

(3) Germ cell tumours:

a. Benign: teratoma and dermoid cyst. b. Malignant: seminoma, teratocarcinoma and endocrinal sinus tumour.



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(4) For Gut duplication: Trachea-bronchial. bronchogenic. neuro-entric.

(5) Lymphatic cysts: Thoracic duct cyst. Cystic hygroma.

(6) Diaphragmatic hernia: Oesophageal hiatus.

bochdalek hernia. Morgagni's hernia.

Definition: Involvement of mediastinal structures in a pathological process especially as a

result of compression.

Causes: Related to superior

mediastinum Related to inferior Mediastinum

anterior middle Posterior Retrosternal

goiter. Dermoid cyst. Thymic tumour. Aortic aneurysm.

Pericardial cyst. Aortic aneurysm. Hernias through

diaphragm.

Bronchial cancer.

Bronchial cyst.

Neurogenic tumour.

Oesophageal lesions.

Para-vertebral abscess.

Hiatus hernia.

Manifestations: (1) Involvement of trachea:

Inspiratory stridor. Brassy cough.

(2) Pressure on bronchi: If incomplete and intermittent obstructive emphysema. If complete atelectasis.

(3) Involvement of oesophagus: Dysphagia. Regurgitation.



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(4) Pressure on arteries: Inequality of the pulse of upper limbs. Ischaemic manifestation pallor – pain – syncope.

(5) Obstruction of veins: Swelling of the face and neck. Arms may become edematous. Bilateral non pulsating congested neck veins.

(6) Involvement of nerves: Sympathetic Horner's syndrome. Vagus nerve cardiac arrhythmia. Phrenic nerve diaphragmatic paralysis. Recurrent laryngeal nerve Hoarseness of voice and abductor paralysis.

(7) Pleural effusion: may become chylous due to involvement of thoracic duct and Pericarditis.

(8) Several systemic and endocrine syndromes: i. Thymoma: myathenia gravis and RBCs hypoplasia.

ii. Function neural tumour: diarrhea, sweating, palpitation and headache. iii. Non-seminematous germ cells: gynecomastia and klien felter's syndrome.

Investigations: 1. Radiographic:

Chest X-ray. Convential tomography. Computerized axial tomography.

2. Contrast study: Barium swallow. Angiography.

3. Endoscopic: Mediastinoscopy. Bronchoscopy.

4. Echo-cardiography.



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Or: Non cardiogenic pulmonary edema

Definition: It is the most severe form of acute lung injury in which there is diffuse alveolar

damage characterized by capillary permeability, pulmonary edema and refractory hypoxia.

Criteria for acute lung injury and ARDS:

(1) Radiological: new, bilateral, diffuse, patchy or homogenous pulmonary infiltrate on chest radiograph.

(2) Exclusion: no clinical evidence that "heart failure – fluid overload – chronic lung disease" is responsible for infiltrate.

(3) Oxygenation: PaO2 : FiO2 ratio < 300 mmHg acute lung injury. PaO2 : FiO2 ratio < 200 mmHg ARDS.

Causes: 1. Direct pulmonary cause: 2. Indirect causes:

Infection. Pulmonary trauma. Near drawing.

Oxygen toxicity. Gastric aspiration. Toxic gas inhalation.

Sepsis. Burn. Hemorrhage.

Uremia. Drugs. Pancreatitis.

Patho-physiology: (1) Acute inflammatory phase: ARDS may be caused by lung injury diffuse alveolar damage + release of

inflammatory mediator "Cytokine-TNF" activates neutrophils to become sticky and adhere to vascular endothelium in pulmonary capillaries release the contents of their cytoplasmic granules "proteolytic enzymes" capillary permeability Protein rich fluid leak into alveolar spaces.

Alveolar collapse occurs from reduced surfactant. Hypoxemia: respiratory failure occurs from loss of functioning alveoli and V/Q

mismatch. Pulmonary hypertension.

(2) Fibro proliferative phase: Progressive pulmonary fibrosis.



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Clinical features: Inflammatory phase: Proliferative Phase:

Acute onset of progressive dyspnea & dry cough several hours or days after predisposing condition.

Tachypnea, tachycardia and cyanosis.

Multi organ failure. Bilateral crepitations.

Lung scars. Pneumo-thorax is common.

Investigations and diagnosis: (1) CT: to identify pulmonary causes of ARDS and detect complications. (2) Onset: acute. (3) PaO2/FiO2 ratio: <200 mmHg is characteristic of ARDS. (4) X-Ray: Bilateral pulmonary infiltrate due to pulmonary edema. (5) Absence of evidence of left ventricular failure. (Normal ejection fraction (EF)/

Pulmonary capillary wedge pressure (PCWP) < 18 mmHg.

Differential diagnosis: (1) Acute interstitial pneumonia pathological confirmation – bronchial lavage

(Neutrophils – esinophils). (2) Diffuse alveolar hemorrhage Hemoglobin - haemoptysis – hemosiderin In

macrophages. (3) Idiopathic acute esinophilic pneumonia cough, dyspnea, fever, esinophils,

rapid response to corticosteroids. (4) Malignancy "particularly lymphangitis carcinomatosis".

Treatment: i. General supportive treatment:

Nutrition. Fluid management. Glycemic control.

ii. Oxygenation: through: Lowest FiO2 to keep PaO2: 55-80 mmHg. Prone position. Nitric oxide.



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iii. Mechanical ventilation: with PEEP (positive end expiratory pressure) to prevent alveolar collapse.

iv. Non ventilatory adjuncts to gas exchange: Inhaled nitric oxide. Surfactant. Nebulized prostacyclin. Extra-corporeal gas exchange.

v. Pharmaceutical interventions: Corticosteroids are given in latter stages to fibrosis. Diuretics no beneficial, because ARDS is an inflammatory process. Antibiotics for infections.

Complications: Multiple organ system failure. Nosocomial pneumonia. GIT bleeding. Deep venous thrombosis.

Prognosis: Mortality rate > 50%. Age and sepsis bad prognosis. Cause of death multiple organ failure.



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Definition: It is a chronic inflammatory airway disease characterized by: Airflow limitation which usually reversible spontaneously or with treatment. Airway hyper responsiveness to wide range of stimuli. Periodicity and diurnal variability of symptoms.

Airway obstruction occurs due to a combination of:

1. Smooth muscle contraction. 2. Airway lumen secretions. 3. Edema of bronchial mucosa and accumulation of inflammatory cells.

May become irreversible over time due to:

1. Basement membrane thickening, collagen deposition, and epithelial damage. 2. Airway remodeling occurs in chronic disease with smooth muscle hypertrophy.

Classification: i. Extrinsic asthma:

In which an environmental inducing agent can be identified. Occurs most frequently in atopic individuals. Onset usually in childhood. Frequently associated with other atopic diseases e.g. atopic dermatitis,

allergic rhinitis. ii. Intrinsic asthma:

No causative agent can be identified. Starts usually in middle age (late onset). Not associated with other atopic diseases.

Differentiating parameters

extrinsic Intrinsic

Age of onset childhood Middle age Precipitating factor obvious Not obvious

Family history allergy Bronchial asthma

Atopic tendency Usually apparent Absent IgE level raised Not raised

Skin test Positive Negative asthma intermittent Less liable & often

severe

(7)

This part is taken from mowafy medical symphony – pulmonology.



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Allergens causing asthma: House dust mites. Animal hair and bird features. Pollens. Fungal allergens: aspergillus. Rarely foods.

Triggers of asthma attacks:

1. Allergens. 2. Air pollution: smoking, chemical oxidants released from motor vehicles exhaust. 3. Respiratory infections: especially viral. 4. Iatrogenic: aspirin or β blockers. 5. Occupational: occupational asthma occurs when agents at work place cause

asthma e.g. isocyanates, woods, formaldehyde, latex,…etc. 6. Cold air and exercise: due to histamine & leukotriene release from mast cells

caused by post thermal changes.

Pathogenesis of the bronchial asthma: 1. Immunological mechanism:

Stimulus (allergen) bronchial narrowing.

i. Exposure to specific allergen stimulation to T helper cells production of IgE (sensitization).

ii. Following initial sensitization repeated exposure to allergen leads to Antigen (allergen) and antibody (IgE) reactions on surface of mast cells leads to disruption of the cells and release of chemical mediators (histamine, bradykinin, leukotrienes, prostaglandins, esinophils) which cause bronchoconstriction (immediate phase).

iii. Other mediators as: platelet activating facto (PAF) and Major basic protein (MBP) leading to edema and cellular infiltration of bronchial wall (late phase).

2. Neural mechanism: i. Parasympathetic brochoconstriction and increase mucous secretions. ii. Sympathetic bronchodilatation.

iii. Non adrenergic non cholinergic (NANC) bronchodilitation (its neurotransmitter is called vasoactive intestinal peptide [VIP]). Deficiency of this system bronchospasm.

3. Genetic factor: i. Genetic factor plays a major role in regulation of IgE production. ii. Asthma is a polygenetic disease e.g:

Chromosome 5 contains genes controlling production of cytokines.



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Chromosome 2 contains genes controlling IgE synthesis. Chromosome 20 contains gene called (ADAM33) which strongly

associated with airway hyper responsiveness and airway remodeling.


(1) Recurrent attacks of: Wheeze. Shortness of breath and chest tightness. Cough.

(2) Symptoms occur or worsen at night (and early morning). (3) Symptoms occur or worsen after allergen exposure, exercise, cold air and upper

respiratory tract infections. (4) Family history of asthma or atopic diseases (allergic dermatitis, rhinitis).

Signs:

(1) In between the attacks: no signs are detected. (2) During the attacks: Hyperinflation of the chest, with an increased anteroposterior thoracic

diameter and a low diaphragm. Wheezing, most marking in expiration, is the most characteristic breath

sound of asthma but it is an unreliable indicator of severity. Vesicular breath sound with prolonged expiration due to bronchospasm. Tachycardia, tachypnea and working accessory respiratory muscles.



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Complications: 1. Acute severe asthma (status

asthmaticus). 2. Pneumothorax. 3. Psychological troubles. 4. Respiratory failure and cor pulmonale. 5. Complications of cough e.g: fracture of

ribs. 6. Side effects of medications: arrhythmias.

Investigations: 1. Pulmonary function test: May be normal between the attacks. Reduced FEV1 & FEV1/FVC % during the attacks. Test of reversibility (bronchodilator test): usually FEV1 improve > 15% after

inhalation of short acting β2 agonist (unlike COPD, FEV1 response < 15%).

N.B: response to bronchodilators may not be present in chronic asthma when little reversibility can be demonstrated.

Significant (>20%) diurnal peak expiratory flow rate (PEFR) variability on at least 3 days per week for a minimum of 2 weeks.

Bronchial provocation test: using histamine, methacholine or exercise to induce airway hyper responsiveness.

2. Chest X-ray: Not diagnostic for asthma. Normal chest X-ray is the most common finding. Done mainly to exclude pneumonia, Pneumothorax or shadows e.g: allergic

bronchopulmonary aspergillosis. 3. Detection of allergen: Skin prick tests: should be performed to help identify allergic cause. Specific bronchoprovocation test using inhaled antigens.

4. Blood picture: Esinophilia > 400/cm2 may be present in allergic cases. Leukocytosis due to infection.

5. Blood gases: In acute severe attacks: PaO2 with normal PaCO2. Increase in PaCO2 is a bad

prognosis and considered as indication of mechanical ventilation. 6. Sputum examination: Esinophils are detected in sputum.

yellow white long threads composed of epithelium, esinophils and mucous (casts of distal airways).

breakdown products of esinophils.



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clusters of columnar bronchial epithelium. 7. ECG: To exclude cardiac causes of dyspnea.

Classifications of degree of asthma according to severity:

Daytime asthma

symptoms

Night-time asthma

symptoms Exacerbations Spirometry

Intermittent Less than weekly Less than 2 per

month

Infrequent Brief

FEV1 at least 80% predicted FEV1 variability less than 20%

Mild persistent

More than weekly and less

than daily

More than 2 per month but not

weekly

Occasional May affect

activity or sleep

FEV1 at least 80% predicted FEV1 variability 20-30%

Moderate persistent

Daily Weekly or more

often

Occasional May affect

activity or sleep

FEV1 60-80% predicted FEV1 variability more than 30%

Severe persistent

Daily Physical

activity is restricted

Frequent Frequent

FEV1 60% predicted or less FEV1 variability more than 30%

Differential Diagnosis: 1. From other causes of wheezing: " All that wheezes is not asthma" COPD: predominantly irreversible. Cardiac asthma. Carcinoid syndrome: usually associated with stridor not wheezing. Churg-Strauss vasculitis. Upper airway obstruction due to foreign body, tumour, aryngeal edema.

2. From other causes of paroxysmal dyspnea: Tetany. Myasthenia crises. Recurrent pulmonary emboli. Hysterical dyspnea.

3. Drug induced cough e.g: ACELs 4. Vocal cord dysfunction (factitious asthma).



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Treatment: Components of asthma treatment:

1. Patient and family education. 2. Assessment and monitoring of asthma severity. 3. Environmental control and avoidance of risk factors (triggers). 4. Establish individual medication plan for long term management. 5. Establish individual plans for managing exacerbations. 6. Provide regular follow up care.

Goals of treatment:

1- Aim for no symptoms / near normal lung function on minimal treatment. 2- Prevent asthma exacerbations. 3- Avoid adverse effects from asthma medications. 4- Prevent development of irreversible limitation.

i. Pharmacotherapy: A stepwise approach to the management of asthma:

Step 1: Mild intermittent

Short acting β2 agonist e.g: salbutamol inhaler (ventolin).

No daily medication needed

Step 2: Mild persistent

As step 1 Low dose inhaled corticosteroid (≤ 500 µg) e.g: beclomethazone dipropionate.

Long acting inhaled β2 agonist e.g: salmeterol (metrovent).

Cromones e.g: Disodium cromoglycate (Intal) inhaler.

Anti-leukotrienes (singulair) Sustained release Theophyline.

Step 3: Moderate persistent

As step 1 + Anti-cholinergic drug e.g: Ipratropium bromide inhaler (Atrovent).

Medium dose inhaled corticosteroid (500-1000 µg) beclomethazone diproprionate.

Long acting inhaled β2 agonist e.g: salmeterol (metrovent).


Anti-leukotrienes (singulair) Theophyline.

Step 4: Severe

As step 3 High dose inhaled corticosteroid (> 1000 µg) beclomethazone.



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persistent Long acting inhaled β2 agonist e.g: salmeterol (metrovent).


Anti-leukotrienes (singulair) Theophyline.

ii. Immunotherapy: (Desensitization) Allergen immunotherapy indicated when: There is a clear evidence of relationship between symptoms and exposure to

allergen. Poor response with pharmacological therapy.

Pharmacology of drugs used in treatment of bronchial asthma: Medications used for asthma is classified as either reliever or controller (preventer).

a. Reliever Drugs: (short acting bronchodilators) Drugs which aim to relieve patient symptoms during the attacks.

(1) Short acting β2 agonist: Drugs Salbutamol (ventolin) 100 µg inhaler. 2 puff as needed.

Terbutaline (Bricanyl) 250 µg inhaler. 2 puff as needed. Mechanism: stimulation of β2 receptors result in bronchial smooth

muscle relaxation. Advantages: aerosol delivery of these drugs provides more rapid onset

of action and less side effects than oral delivery. Side effects: Tachycardia, Tremors (important), Glaucoma,

Hypertension. (2) Anti-cholinergic drugs: Ipratropium bromide (atrovent) inhaler.

They are non selective anti-muscarinic agents. May be addictive to β2 agonists especially to relieve asthma

exacerbation (Combivent). The major disadvantages of the anti-cholinergics are that they are slow

to act (60 to 90 minutes may be required before peak bronchodilatation is achieved) and they are of only modest potency.

(3) Methylxanthines e.g: Theophyline: Theophyline has a bronchodilator effect given orally, suppository or

slow I.V. infusion in severe cases. Some authorities now place these compounds in the "controller" class. It is used as a long acting drug to guard against nocturnal asthma and

IV route in a case of acute severe asthma. Side effects: Gastritis, nervousness, headache, arrhythmias and convulsions. Wide range of drug interactions: e.g. erythromycin, cimetidine and

propranolol decrease its clearance. Smoking and phenytoin increase its clearance. MCQ.



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b. Controller (preventer) drugs: drugs used in between attacks. Drugs are taken on long term aiming to get control of the disease. They include anti-inflammatory agents and long acting bronchodilators. Inhaled corticosteroids are at present the most effective controllers.

MCQ. (1) Inhaled corticosteroids:

The anti-inflammatory effect of corticosteroids decreases airway inflammation, hypersensitivity and exacerbation. Beclomethasone dipropionate. Budesonide (pulmicort). Fluticasone Propionate (flixotide).

Side effects: Dysphonia. Oropharyngeal candidiasis: avoided by mouth washing after use.

(2) Systemic steroids: Oral steroids: prednisone, prednisilone. Injected steroids hydrocortisone, Dexamethasone. The dose should be kept as low as possible to minimize side effects. Systemic side effects of corticosteroids: See endocrinology.

(3) Cromones: Disodium cromoglycate (Intal). Nedocromil sodium. Administration: only by inhalation. Mechanism of action: their major therapeutic effect is to inhibit the

degranulation of mast cells, preventing the release of the chemical mediators, So, these drugs used to be called mast cell stabilizers, but this term is now obsolete since the drugs may have suppressive effect on esinophils and macrophages.

Role of therapy: They are most effective in atopic patients and in exercise induced asthma.

(4) Anti-leukotrienes: montelukast (singulair tab). (5) Long acting β2 agonists:

Salmeterol (metrovent). Formeterol (Oxis)

Mode of transmission: inhaled. Used in combination with inhaled corticosteroids.

(6) Anti-IgE: Omalizumab: is a humanized anti-IgE antibody. Mode of administration: Sub cutaneous every 2 – 4 weeks.



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Acute severe asthma

Definition: The term (status asthmaticus) was defined as asthma that had failed to resolve

with therapy in 24 hours. This term has now been discarded and replaced by (acute severe asthma) i.e. severe asthma that has not been controlled by the patient's use of medication.

Clinical picture: Symptoms: A,B,C,D

1. Anxiety. 2. Breathlessness at rest. 3. Sweating. 4. Difficult speech: patient unable to complete sentences in one breath.

Signs:

1. Respiratory rate: > 25 cycles / minute. {35 cycles in department's book!}. 2. Tachycardia: > 110 beats / minute. {120 beat in department's book!}. 3. Pulsus paradoxicus in some patients (inspiratory fall of systolic blood pressure >

10 mmHg). 4. Chest auscultation: Inspiratory and expiratory wheeze. (Biphasic wheeze). 5. PEFR: 33-50% of predicted.

Criteria of diagnosis Any one of: Peak expiratory flow rate: 33-50%

Respiratory rate ≥ 25 cycles / minute. Heart rate ≥ 110 beats/minute.

Unable to complete sentences in one breath.

Life threatening asthma

Any one of the following in a person with severe asthma

Silent chest PEFR(8) < 33% exhaustion Oxygen saturation < 92%

arrhythmia PaO2 < 60 mmHg despite treatment with O2.

Low blood pressure. (Normal) PaCO2

(8)

PEFR = Peak Expiratory Flow Rate.



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Cyanosis

Altered level of consciousness.

Poor respiratory effort.

Near fatal asthma High PaCO2 Fatality in asthma is due to cardiac arrest secondary to hypoxia and acidosis.

Treatment of acute severe asthma: is given to maintain the oxygen saturation above

92%.

β : The first line therapy. Salbutamol is given either parentrally or by inhalation. The inhaled forms are superior to the parentral route and have fewer side

effects. Parentral route is reserved for patients who are so dyspneic that they

can't take deep enough breaths.

100 mg/6 hours for the first 24 hours I.V. then prednisone 60 mg orally should be given daily for 2 weeks then gradual tapering.

It should be given as soon as possible because peak onset of action can take 4-6 hours.

Infusion very slowly (Over 20 minutes). Careful monitoring is required. I.V. aminophylline in the treatment of acute severe asthma in one word is

a bad medicine, as several studies have failed to show any benefit plus undesired side effects e.g. arrhythmia .

Plenty of oral and I.V. fluids. Potassium supplements may be necessary because repeated doses of salbutamol can lower serum potassium.

Indications: Deteriorating PEFR. Persistent hypoxemia or hypercapnea. Exhaustion, confusion or drowsiness. Coma or respiratory arrest. Previous history of mechanical ventilation. Tidal volume < 4ml/kg. Vital capacity < 15 ml/kg. Apnea or respiratory rate > 40 cycles / minute.

Types:



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Bronchodilatation. Rest of respiratory muscles. Mobilization of secretions. Improve cardiac

performance.

Used when there is: Fatigue or exhaustion. Deterioration of

consciousness. Arrhythmia and

hypotension.

Questions: 1. Bronchial asthma: diagnosis, management and emergency treatment? 2. Treatment of acute attacks of bronchial asthma? 3. Acute severe asthma (2011)? 4. Management of chronic bronchial asthma? 5. Bronchodilators and steroids in asthma? 6. Extrinsic allergic alveolitis, agents producing it, C/P and treatment (94)? 7. D.D of bronchial asthma? A: causes of wheezy chest. 8. Status asthmaticus?



Page 103

The most common malignant neoplasm in men. It constitutes:

16% of all malignant tumors 28% of all cancer deaths 6% of all deaths

Etiological factors:

The most common cause of lung cancer It depends on:

o Duration of smoking. o Number of cigarettes smoked. o Type of cigarette. o Age of initiation of smoking.

It's also seen in non smokers especially in females "passive smoker" It contains large no. of potentially carcinogenic substances as: Benzopyrene Arsenic

Nickel radioactive isotopes as "polonium"

Sources: diesel engines & commercial space heating. Carcinogens: benzopyrene, aromatic hydrocarbons.

Proved occupational carcinogens include: asbestos – arsenic – mustard gas

Low vitamin A in diet risk in smokers. Also it's related to quantity of B-carotene.

It may occur in localized area of pulmonary scarring and in patient with more diffuse lung fibrosis.

The risk in patient with COPD.

One of inherited condition in xenobiotic metabolism is the aryl hydrocarbon hydroxylase (AHH) system.

This enzyme converts polycyclic hydrocarbons of cigarettes → epoxide that is highly carcinogenic.

The of (AHH) appears to be controlled by single gene, so pt. that has high level of AHH activity may be susceptible to lung cancer.



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Classification:

a. squamous cell carcinoma: Accounts 40%. Arises from bronchial epithelium. Tends to be centrally & spreads intraluminal. Histologically characterized by st. layer of malignant cells.

b. adenocarcinoma: Accounts 20%. Tends to be as peripheral nodules. Histologically glandular or acinar structure of mucin.

c. large cell carcinoma: Accounts 10-15%. Characterized by absence of pathological features as gland formation or

keratin. Tends to be peripherally.

d. adeno-squamous carcinoma e. broncho-alveolar carcinoma f. mixed carcinoma

Arise from major bronchi. Characterized by: small cell size – abundant mitotic figures – paucity

cytoplasm.


any new cough that persists longer than 2 weeks in pt > 40 years should be suspected as lung cancer.

may be due to a. Pleural effusion – atelectasis – tumor – micro-embolism. b. Co-morbid disease: COPD – disseminated diffuse broncho-alveolar cell

carcinoma.

Due to direct invasion or metastatic involvement of pain sensitive intrathoracic structure.

Peripheral tumor invades parietal pleura sharp intermittent.



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Central tumor perivascular / per bronchial nerve poorly localized deep vague persistent discomfort.

Pleural effusion dull aching chest pain in 25%.

May be the only symptom. Consists of blood streaked sputum. Massive Hemoptysis: uncommon & associated with central squamous cell

carcinoma.

indicates direct mediastinal extension or denopathy involvement of lt. recurrent laryngeal nerve.

Wheezes obstruction of trachea or main stem bronchus by intraluminal tumor or extrinsic compression.

Dysphagea esophageal compression by mediastinal lymph node. Fever – chills & purulent sputum.

Bone pain due to skeletal involvement. Headache, nausea & vomiting: due to ICT. Back pain: due to involvement of vertebral bodies. Abdominal pain.

8. patient of lung cancer may be completely asymptomatic.

Signs:

(a) Thoracic (b) Extra-thoracic (c) General Evidence of co-existing COPD. Stridor. Localized persistent wheezes. Dullness with absence of breath

sound ipsilateral tracheal shift atelectasis contra lateral massive pleural effusion

Hyper resonance due to pneumo-thorax.

Classical signs of consolidation due to post obstructive pneumonia.

Clubbing of fingers. Supra clavicular &

scalene lymphadenopathy.

Bone tenderness. Hepatomegaly &

jaundice due to liver metastasis.

Signs of ICT.

Weight loss. Anxiety &

depression. Dyspnea &

jaundice. Pallor.



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(d) Clinical feature of superior sulcus tumour: Sulcus refers to anterior groove made by subclavian artery on anterior superior surface of lung & its pleura.

1. Pancoast syndrome: Consists of: pain, hypothesia on lower part of the shoulder & inner aspect of the

arm, wasting & weakness of small ms of hands. Causes: due to involvement of lower part of brachial plexus by tumour. Radiologically: apical mass shadow & local bone destruction usually

1st & 2nd rib. Vertebral body and transverse process.

2. Paraneoplastic syndrome: Metabolic: as hypercalcemia, SIADH, ectopic ACTH. Non metastatic: neuromuscular syndrome, peripheral neuropathy,

autonomic neuropathy, cerebellar ataxia, polymyositis & dermatomyositis syndrome.

Investigations:

(1) plain radiology (2) CT scan (3) MRI

shows various radiological patterns as: Solitary lung nodules. Parenchymal lung

mass. Unilateral hilar mass. Lobar collapse &

pleural effusion.

very useful in detecting: Presence of small

nodules not seen in x-ray status of pleural space.

Detect invasion of chest wall & Mediastinum by tumour.

(4) Others: as Ultrasound. Position emission

tomography (PET scan).

Principle: non invasive mean of diagnosis. Examination of 3 serials – fresh early morning specimen provides diagnosis.

N.B: central bronchogenic lesion are more likely to have (+ve) specimen than peripheral.

The most useful investigation. may show :- normal appearance, evidence of distortion, extrinsic

compression.

N.B: bronchoscopy done with fluoroscopic or CT scan guidance permits biopsy of more peripheral lesion not directly visualized by trans-bronchial lung biopsy.

inoperability of bronchoscopy due to: a. Paralysis of vocal cord.



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b. Definite tracheal involvement. c. Definite cranial involvement. d. Tumour involvement to level of right tracheo-bronchial junction.

Patient with pleural effusion requires analysis & define stages by detecting malignant cells.

Diagnose malignant effusion or pleural tumour.

For metastasis using bone – brain – liver scans.

Early detection of lung cancer (1) Genetic predisposition: People differ in their ability to activate potential carcinogens. Extent of biologic effects of carcinogens may vary from person to person. possible markers of genetic susceptibility to lung cancer:

1. metabolic phenotypes aryl hydrocarbon hydroxylase (AHH) glutathione-S-transferase.

2. another types: DNA repair activity

(2) Molecular markers: Changes in gene, gene products & chromosomal abnormalities are

considered as biomarker of premalignancy or early cancer. E.g:

1. dominant oncogenes: K-ras mutation → are associated with less aggressive course of NSCLC. H-ras mutation → are associated with more aggressive course.

2. tumour suppressor gene: Mutation or inactivation of retinoblastoma gene & p53 gene are found

in both SCLC & NSCLC. 3. abnormal chromosomes: as 3, 11, 13, 17.

(3) Sputum immunostaining: Monoclonal antibodies that recognize SCLC & NSCLC determinants were

used to immuno stain specimens.



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(4) Other biomarkers: as growth markers. (5) Lung imaging fluorescence endoscopy (LIFE): laser induced fluorescence fluorescence spectroscopy

(6) MMR. (7) Sputum cytology. (8) Tumour markers: as carcin embryonic antigen "CEA".

Treatment

Surgical: remain the most effective form of treatment. criteria for selection Histopathology. Anatomical extent of tumour. Physiological status of the patient.

N.B: ⅔ of the patients are inoperable at the time of presentation due to: advanced age poor resp function other significant medical conditions

types of operations:

1. Pneumonectomy. 2. Lobectomy. 3. Bronchoplastic procedures. 4. Wedge resection.

complications 1. LRTI in residual lung tissue 2. post-operative pneumonia 3. injury of recurrent laryngeal nerve. 4. persistent air leak

Radiotherapy:

1. radial radiotherapy: treatment field includes: Primary tumour mass. ipsilateral & contra lateral hilar Lymph Nodes The Mediastinum. ipsilateral supraclavicular Lymph Nodes

dose



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50-60 Gy (5000-6000 rad) over period of 4 to 6 weeks.

2. Palliative treatment: indications hemoptysis dyspnea dt large bronchus obstruction pain dt bony, chest wall or nerve affection mediastinal compression

3. Chemotherapy: NSCLC are relatively resistant to currently available agents.

4. Combined modalities of treatment: surgery + radiotherapy surgery + chemotherapy

5. Endo bronchial treatment: photodynamic surgery laser therapy endoscopic brachy therapy cryotherapy

1. Chemotherapy: Unlike NSCLC, it is more sensitive to chemotherapy. Available agents include:

Cyclophosphamide + doxorubicin + umcristine. Doxorubicin + cyclophosphamide + etoposide. Cisplatine + etoposide.

Complications: Myelo-suppresion.

Alopecia. Nausea and vomiting.

2. Radiotherapy: It is more sensitive to radiotherapy than NSCLC.

3. Surgery: It is contraindicated in all patients. As it is systemic disease.



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Metastatic tumors of the lung (9)

Cancers that may spread to this area are those of the: 1. large bowel (colon and rectum) 2. breast 3. bladder 4. testicle 5. stomach 6. oesophagus 7. kidney (renal) 8. malignant melanoma.

N.B: Sarcomas can also spread to the lungs.

Clinical Picture: The symptoms can include:

1. a cough that doesn't clear up 2. Breathlessness coughing up bloodstained sputum. 3. Persistent pain or discomfort in the chest.

Secondary lung cancer should be suspected if patient has already been diagnosed with a cancer and has some of these symptoms, particularly if they don't respond to other treatment such as antibiotics. Sometimes, secondaries or metastases are found before a primary cancer has been diagnosed. Occasionally, it may not be possible to find the original cancer - this is

called an .

Investigations: A number of tests may be done to diagnose a secondary lung cancer, including:

This may be taken to show the size and position of the cancer.

(

9) References of this part:

Cherry NI, et al. Oxford Textbook of Palliative Medicine. 4th

edition. Oxford University Press. 2009.

Souhami, et al. Oxford Textbook of Oncology. 2nd

edition. Oxford University Press. 2001.

Tobias, Hochauser. Cancer and its management. 6th

edition. Wiley Blackwell. 2010.



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This uses low-dose radioactive sugar to measure the activity of cells in different parts of the body. A very small amount of a mildly radioactive substance is injected into a vein, usually in your arm. A scan is taken a couple of hours later. Areas of cancer are usually more active than surrounding tissue and show up on the scan.

Most commonly during a CT scan. A local anesthetic is used to numb the area, and then a needle is inserted to remove a small piece of tissue.

Secondary lung cancer may also cause fluid to collect in the space between the two membranes (the pleura) that surround the lungs. This is known as a pleural effusion. If this happens, it may be possible to remove some of the fluid and examine it for cancer cells.

It’s a secondary lung cancer because the cells look like the cells from the original cancer. For example, if a stomach cancer has spread to the lungs, the cells will look like stomach cancer cells rather than lung cancer cells.

Treatment The treatment for a secondary lung cancer depends on the individual situation, including general health and the type of primary cancer. Sometimes a combination of treatments is used.

Chemotherapy is commonly given to reduce and control secondary cancers in the lung. The type of chemotherapy you have will depend on whether you've had chemotherapy before and how long ago.

Hormonal therapy is also commonly used to treat secondary cancers in the lung when they have developed from certain cancers, such as breast or prostate cancer, that are responsive to hormonal treatments. The type of hormonal therapy you have will depend on which hormonal treatments you've already been given.

This may only be an option if the primary cancer has been controlled and there is no evidence of the cancer having spread anywhere else in the body.

It also requires the cancer to be affecting just one small part of the lungs, which is easy to get to, and not attached to important blood vessels or nerves.

A short course of radiotherapy to relieve some symptoms of secondary lung cancer, such as breathlessness or coughing up blood (haemoptysis).

If the cancer is causing a blockage in the bronchus or one of the large airways, laser therapy may be used to burn the tumour out of the airway. This may relieve some of the symptoms, though it does not destroy the cancer completely.



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If the cancer is causing pressure on structures close to the bronchus, a small tube called a stent may be inserted to hold the bronchus open. The stent can remain in the lung permanently and does not generally cause any problems.

A special form of internal radiotherapy (brachytherapy) called endobronchial radiotherapy may be given when the tumour is blocking one of the airways.

Using a flexible tube called a bronchoscope, a thin tube (catheter) containing radioactive material is placed close to the tumour. The radioactive material gives a dose of radiation to the tumour. It’s left in place for a few minutes to give the treatment and is then removed together with the catheter. Usually only one session of treatment is needed.



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Carcinoid tumours

of the lung

Etiology In the past, pulmonary carcinoid tumors were believed to be derived from

neural crest cells; however, they currently are understood to be of

arising from stem cells of the bronchial epithelium

known as Although these neoplasms are capable of producing a variety of substances,

including biologically active peptides and hormones, most are inactive. Unlike carcinoma of the lung, no external environmental toxin or other stimulus

has been identified as a causative agent for the development of pulmonary carcinoid tumors.

Pathophysiology

Asymptomatic (Between 25% and 39% of patients).

Symptoms directly involving the bronchopulmonary tree. As bronchial obstruction. All of the sequelae resulting from bronchial obstruction can follow, including:

1. Persistent atelectasis. 2. Recurrent pneumonia. 3. Pulmonary abscess. 4. bronchiectasis.

Carcinoids characteristically are vascular tumors and can bleed secondary to bronchial irritation.

Although most tumors are broad-based intrabronchial lesions, a few present on a mobile stalk and have a polypoid appearance. If large enough, this latter form can create a ball-valve mechanism within the bronchus, producing hyperinflation in the pulmonary parenchyma distal to the tumor.

Peripheral pulmonary carcinoid tumors most often are asymptomatic and usually are discovered incidentally. They are one of the differential diagnoses considered in evaluation of a solitary pulmonary nodule.



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Atypical carcinoid tumors can present in the same locations as typical carcinoids, but they occur more commonly as peripheral lesions. At least 50% of pulmonary atypical carcinoid tumors present in the periphery of the lung. They have a more aggressive nature and a greater tendency to metastasize.

As neuroendocrine tumors, carcinoids are capable of producing a variety of biologically active peptides and hormones, including:

1. Serotonin. 2. adrenocorticotropic hormone (ACTH). 3. antidiuretic hormone (ADH). 4. melanocyte-stimulating hormone (MSH).

has been implicated in the development of carcinoid syndrome. This syndrome is characterized by a constellation of symptoms, including

1. Tachycardia. 2. Flushing. 3. Bronchoconstriction. 4. Hemodynamic instability. 5. Diarrhea. 6. Acidosis.

Reported in 2-12% of patients with bronchial carcinoid tumors. This syndrome characteristically occurs in the presence of metastatic disease to the liver; however, bronchial carcinoid tumors, especially large ones, are capable of producing the syndrome in the absence of metastatic disease.

have been reported in association with typical and atypical carcinoid tumors. Although fewer than 1% of pulmonary carcinoid tumors produce Cushing syndrome, it is the second most common neuroendocrine syndrome produced by these tumors.

In addition, these tumors are responsible for the development of about 1% of cases of Cushing syndrome. When a patient is found to have an ectopic source of ACTH production, the lesion is generally a pulmonary neoplasm of some type.



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or

can be produced by pulmonary carcinoid tumors, although it more commonly is associated with small cell lung carcinoma. The production of excess circulating AVP creates hyponatremia

secondary to water retention. Patients present with weight gain, weakness, lethargy, and mental confusion and, in severe cases, can develop convulsions and coma.

Treatment: All pulmonary carcinoid tumors should be treated as malignancies. Because surgical resection is the only treatment known to achieve cure, all

pulmonary carcinoid tumors without evidence of distant metastatic disease should be resected completely as long as no contraindication to surgery exists.

1. Lymph node dissection should accompany resection. 2. The most commonly used procedures are formal lobectomy,

segmentectomy, or pneumonectomy. 3. Patients with marginal pulmonary reserve may be good candidates for

complete resection and cure if a bronchoplastic or parenchymal-sparing procedure can be performed.

4. Thoracoscopic or open wedge resection of a peripheral carcinoid tumor should be reserved for patients with limited pulmonary reserve who cannot tolerate anatomic resection.

Contraindications Formal resection of carcinoid tumors of the lung only is contraindicated in patients who would not otherwise tolerate the operative procedure or who are found to have widespread metastatic disease.



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The most common tumours of the pleura are metastatic neoplasm, predominantly of lung, breast or colonic origin.

Tumour arising primarily from the pleura are rare, but still continue a variety of benign and malignant lesion from several different cells of origin.

Malignant mesothelioma The most common primary malignant tumour arising from pleura. It also arising from peritoneal cavity, tunica vaginalis and pericardium. 80% of all cases of mesothelioma are pleural in origin.

Etiology:

The major cause of mesothelioma is asbestos inhalation. Approximately 70% of cases are associated with asbestos exposure. The carcinogenicity of asbestos is due to physical properties of fiber not

chemical composition.

The long period between asbestos exposure to the development of mesothelioma is 30-40 years suggesting the necessity of multiple genetic alterations for eventual malignant transformation of mesothelium.

It is found that lacking of glutathione-S-transferase M1 (GsTM1) gene associated with risk of incidence of mesothelioma among asbestos exposed patients.

GsTM1 is important in detoxification of several carcinogens including poly-cyclic aromatic hydrocarbons.

Therapeutic irradiation. Inhalation of other fibrous silicate as erionate.

Clinical picture: (1) Age: mostly presented in the 5th – 7th decades of life. Patient has mesothelioma early in life has history of childhood exposure

to asbestos. (2) First symptoms in patient with pleural effusion dyspnea, cough and chest

pain.



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(3) As disease progress dyspnea become more severe with loss of weight. (4) Local spread of the disease cardiac tamponade superior caval

obstruction. oesophageal obstruction. spinal cord and intercostal nerves involvement. N.B: Tumour very frequent grows through thoracotomy scars and through needle

tracks. Some patients are asymptomatic at diagnosis with unilateral pleural effusion

found accidentally on routine chest radiograph. Mesothelioma is typically a unilateral disease only 10% of patients have

bilateral involvement in more advanced stages of the disease. (5) Examination: Inspection: scoliosis towards the side of malignancy. Palpation: palpable chest mass. Percussion: unilateral dullness. Generally: finger clubbing and hypertrophic pulmonary osteoarthropathy.

Investigations:

(1) Chest X-ray: Large unilateral pleural effusion with contralateral shifting of

mediastinum. Pleural mass with diffuse pleural thickening. In later stage of disease ipsilateral mediastinal shift secondary to

encompassment of lung by tumour and significant unilateral loss of lung volume.

In advanced mesothelioma Mediastinal widening due to direct tumour invasion or lymph

nodes involvement. Enlargement of cardiac margins secondary to pericardial invasion.

(2) CT: Important in detecting invasion of chest wall, ribs and mediastinal

structures. (3) MRI: Useful in detecting extension of mesothelioma through the diaphragm

into pleural cavity.

There are no special serum biomarkers for malignant mesothelioma. Pleural fluid analysis:

Level of protein, LDH and lymphocytes.

Helpful for detecting presence of malignant cells. But, difficult



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PH . Glucose .

in distinguishing epitheloid from endocarcinoma.

Demonstrate restrictive patterns due to pleural effusion, tumour encasement of lung or chest wall involvement.

Often establish the diagnosis of pleural malignancy but may not provide enough diagnostic material to confirm the presence of mesothelioma.

By video assisted thoracoscopic biopsy or open thoracotomy. Concurrent bronchoscopy may be important in distinguishing between

mesothelioma and metastatic adenocarcinoma of lung.

Treatment approach: All therapies for malignant mesothelioma are primary palliative as malignant

mesothelioma response to multiple forms of therapy is poor and cure is rare. Surgery, radiotherapy and chemotherapy are single modality therapies that have

received attention in mesothelioma.

Multiple agents. Single and combination are used. Single doxorubicin has the highest single agent response rate. Combination methotrexate + cisplatine OR mitomycin + Cisplatine.

It is more responsive to radiation. N.B: curative radiotherapy involving therapy to the entire involved pleural

surface is technically difficult and associated with high risk of radiation pneumonia, myelitis, hepatitis and myocarditis.

a. Pleurodesis: It is a reasonable approach to palliation of patient with dyspnea. N.B: chemical pleurodesis is often unsuccessful because the bulky

tumour covering pleural cavity prevents opposition of pleural surface. b. Parietal pleurectomy:

Surgical stripping of the pleura and pericardium from apex of lung to the diaphragm is more successful than pleurodesis in recurrence of pleural effusion.

c. Pleuro-peritoneal shunting: An alternative approach to relieve rapid accumulation of pleural fluid.

d. Extra-pleural pneumonectomy (EPP):



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Involving complete removal of ipsilateral lung along with parietal and visceral pleura, pericardium with portion of phrenic nerve and majority of hemi-diaphragm.

Under investigation

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Ali Abdelaal Emad M. Qasem

House officer 6th grade Sohag university hospitals Sohag faculty of medicine

Asaad N. ElNakeeb 6th grade

Sohag faculty of medicine

Health & Medicine

Pulmonology, illustrated text of pulmonology