This document discusses various pulmonary conditions including overinflation, emphysema, atlectasis, and α1-antitrypsin deficiency. It begins by defining emphysema and chronic bronchitis. It then covers the pathogenesis, causes, diagnosis, differential diagnosis, staging, complications, and management of emphysema. Specific types of overinflation such as bullous emphysema and subcutaneous emphysema are described. The document also discusses atlectasis including its definition, causes, and clinical manifestations. Finally, it provides details on α1-antitrypsin deficiency emphysema including its presentation, investigations, and treatments.

1. Overinflation,Emphysema
and Atlectasis
Presented by
Nancy Mohammed Alaa
Assistant lecturer of pediatrics
Assiut university

2. Objectives
• 1-What is emphysema?
• 2-Pathogenesis
• 3-Causes
• 4-Diagnosis
• 5-DD.
• 6-staging
• 7-Complications
• 8-Management
• 9- α1-Antitrypsin Deficiency

3. 1- What is emphysema?
• COPD is a long-lasting obstruction of the airways that occurs with chronic
bronchitis , emphysema.
• Chronic bronchitis is defined as a chronic cough not caused by another
condition that produces sputum (mucus) for 3 or more months during
each of the two consecutive years.
• Over-inflation is distension of airspace with or without rupture of
septa, reversible
• Emphysema is pathologically defined as distension of air spaces with
irreversible disruption of alveolar septa

5. 2-Pathogenesis
Compensatory Overi-nfltion
occurs in normally functioning pulmonary tissue when, a
sizable portion of the lung is removed or becomes partially
or completely airless
EXAMPLES: pneumonia, atelectasis, empyema, and
pneumothorax.
Obstructive Over-inflation
– results from partial obstruction of a bronchus or
bronchiole, the so-called check valve type of obstruction.
1

6. 2- Causes
1-Generalized
2-Localized
A-localized obstructive over-inflation
B-unilateral hyper-lucent lung
C congenital lobar emphysema
D-overinflation of three lobes of right lung
E-bullous emphysema
F-subcutaneous emphysema

7. 1-GENERALIZED OBSTRUCTIVE
OVERINFLATION
• Def : Acute generalized overinflation of the lung results from
widespread involvement of the bronchioles and is usually reversible.
• Causes
• 1-asthma
• 2-cystic fibrosis
• 3- acute bronchiolitis
• 4- interstitial pneumonitis,
• 5- atypical forms of acute laryngotracheobronchitis
• 6- aspiration of zinc stearate powder
• 7- miliary tuberculosis.

8. Presentation
• 1-symptoms :dyspnea ,difficult exhaling ,
chronic cough
• 2-signs:
• A-Inspection lung become overdistended
• increased respiratory rate
• Retractions at the suprasternal,supraclavicular
• Cyanosis is more common in the severe cases
• B-Percussion note is hyperresonant
• C-Auscultation:prolonged expiratory,fine crackles

9. Diagnosis
• Radiographically:
• 1- Both leaves of the diaphragm are low and flattened
• <7 ANT,10POST>
• 2- Ribs are farther apart than usual.
• 3-Lung fields are less dense.
• 4-The movement of the diaphragm during exhalation is
decreased, flattened diaphragm in severe cases
• 5-The anter-oposterior diameter of the chest is
increased<AP/TVE >0.5>
• 6- Sternum may be bowed outward<RETROSTERNAL
SPACE>2.5CM>
• 7-Tubular Heart<CT RATIO <30%>

11. 2-Localized
A-Localized Obstructive Overinflation
*Causes : foreign body , mucous plug , lymph nodes ,
endobronchial or mediastinal tumour
*Finding : when most or all lobe involved decreased breath
sound ,hyper-resonant on percussion , shifting mediastinum to
opposite side
*Treatment : remove the cause of obstruction

12. B- Unilateral Hyperlucent Lung
(Swyer james macleod syndrome)
Causes:1-one or more episodes of pneumonia
• 2-after bronchiolitis obliterans
• 3-idiopathic
Clinical picture
• 1-may present with pneumonia
• 2-discovered accidently on CXR
• 3-may be haemoptysis
Investigations
• 1-CXR unilateral hyperlucent, apparently small lung,
• 2-chest CT :may reveal bronchiectasis
Treatment
• No specific treatment ,less symptomatic with time

13. C-Congenital Lobar Emphysema (CLE)
Pathogenesis:
Congenital deficiency of bronchial cartilage,redundant bronchial mucosal
flaps , bronchial stenosis , external compression by aberrant vessels lead to
bronchial obstruction
CP:
• 1-onset :during neonatal period,may be delayed at 5-6th mon
• 2-Signs range from mild tachypnea,wheezes to severe dyspnea,cyanosis
• 3-associated anomalies:PDA,VSD,renal,rib cage
Investigations :
• 1-CXR;radiolucent lobe mostly left upper ,mediastinal shift,atlectasis of
normal lung may occur
• 2-CT CHEST : aberrant anatomy of lesion

14. 3-MRI/MRA:show any vascular lesion that can cause
extraluminal compression
4- nuclear imaging: perfusion defect in affected lesion
Treatment
1-surgical :immediate excision of lobe in case of cyanosis,severe
respiratory distress
2-medical :some pt respond to selective intubation of the the
unaffected lung

16. D- Overinflation of all three lobes of right
lung
• Causes :
1-anomalous location of left pulmonary artery that compress
right main bronchus
2-absent pulmonary valve type of tetratology of Fallot
3-2nd aneurysmal dilatation of pulmonary artery
• Treatment :
1-intubatation of unaffected bronchus
2-high frequency ventilation

18. E-Bullous Emphysema
• Definition :
Bullous emphysematous blebs or cysts {pneumatoceles}result from
overdistension,rupture of alveoli forming single or multiloculated cavity
• Causes:
1-congenital rupture of alveoli during birth
2-aquired: after pneumonia or tuberculous lesion
• Pathology: cyst may become large,contain fluid :air fluid level
• Treatment :aspiration or surgery only in case of severe respiratory
,cardiac compromise as usually resolve spontaneously

20. F- Subcutaneous Emphysema
• Defenition :free air finds its way into subcutaneous
tissue
• Causes :
• 1- in neck and thorax :
Pneumothorax,pneumomediastinumare the most
common causes ,may occur after tracheotomy,deep
ulcers in pharyngeal region,esophygeal
wounds,perforating lesion of larynx
• 2-in face :fracture orbit
• 3-complication of thoracocentesis,asthma,abd surgery
4-infection by gas forming organisms

21. • Clinical picture:
1-tenderness at site of emphysema
2-crepitant on palpation of skin
• Treatment:
1- surgical intervention only if dangerous compression
of trachea by surronding air in soft tissue
2-minimze activity that increase airway
pressure{cough}
3-resolution occur by resorption of air after elimination
of source

23. 1-CXR
2-CT SCAN
3-ABG: Low oxygen (hypoxia) and high carbon
dioxide (hypercapnia) levels often indicate chronic
bronchitis,
4-Lung function test<spirometry>
increased: total lung capacity,residual vol,
decreased: FEV1 ,diffusion capacity
4-diagnosis of emphysema

24. 5-Differential Diagnosis
• 1-CLINICAL
• Bronchiectasis :chronic production of copious
purulent sputum, coarse crackles and clubbing
upon physical examination, and abnormal
findings on chest radiographs and CT scans.
• Chronic asthma: distinction is a significant
bronchodilator response,family history of
allergy,associated atopy,eosinophilia

25. 2-Radiological :
• A-hypertranslucent hemithorax
• A-pneumothorax

26. B-cystic lung disease
• 1-bronchogenic cyst
• 2-congenital cystic
adenomatoid malformation

27. 6-staging
• GOLD classifications Global Initiative for Chronic
chronic bstructive pulmonary disease
• Stage1 :FEV1>80% OF NORMAL
• STAGE2 :FEV1 50-80%
• STAGE3 :FEV1 30-50%
• STAGE4;FEV1 <30%

28. 7-Complications
1-Pneumothorax
2-Pulmonary
hypertension
3-Corpulmonale
4-Respiratory failure
5-Recurrent infections
• 6-bronchiectasis

29. 8-Management
• 1-PREVENTIVE
Vaccine (influenza , pneumococcal)
• 2-MEDICAL
A-Oxygen{IN RESPIRATORY DISTRESS}
B-intubation{in respiratory failure,PO2 <60%,PCO2>50%}
C-Bronchodilatos :
• Short acting B-Agonist{salbutamol 100-200mcg inhalation}
• , Anticholinergic{ipratropium20-40mcg inhalation}
• Long acting B-Agonist {salmetrol 25-50mcg inhalation}
C-Steroid{budesnide 100-200mcg inhalation}
D-Antibiotics : IN Acute Exacerbation
E –Diuretics (Cor Pulmonale )
F-Mucolytics
• 3-SURGICAL : in
(CLE,BULLOUS EMPHYSEMA,SUBCUTANEOUS EMPHYSEMA)

30. α1-AT deficiency Emphysema
• α1-antitrypsin (α-AT):glycoprotein
• Site of synthesis :liver ,macrophage
• Action :α1-AT and other serum antiproteases help inactivate
proteolytic enzymes released from dead bacteria or leukocytes
in the lung
• Deficiency :of these antiproteases leads to an
• 1-accumulation of proteolytic enzymes in the lung, resulting in
destruction of pulmonary tissue with subsequent development
of emphysema
• 2-polymerized mutant protein in the lungs,liver may be pro-
inflammatory

32. PRESENTATION
• 1- In adult : chronic pulmonary symptoms as :
wheezes ,dyspnea ,cough.
• 2- In child: jaundice ,abdominal distension , bleeding
and cirrhosis
*A1AT deficiency remains undiagnosed in many patients.
Thus, testing should be performed for all patients with
1-COPD.
2- asthma with irreversible air-flow obstruction.
3-unexplained liver disease.
4-necrotizing panniculitis.

34. Investigations
• 1- Chest X-ray and CT
2-Lung function test may be normal in young
children but may show air flow obstruction
and increased lung volume
3-Liver function test : raised transaminase,
impaired PT and PC , low serum albumin (in
cirrhosis)
4-serum immunoassay of alpha 1 anti trypsin

35. Treatment
• 1-Enzyme replacement Therapy :
A-Purified blood derived human enzyme
*Dose;60 mgl kglweek IV
*Goal : level of 80 mg/dL is prtective for emphysema
*Results :in the appearance of the transfused
antiprotease in pulmonary lavage fluid
B-Recombinant

36. • 2-Supportive :
A-Treatment of pulmonary infection.
B- Routine use of pneumococcal
and influenza vaccines.
C- Bronchodilators.
D-Avoid smoking.
• 3-LUNG TRANSPLANTATION

37. Atelectasis

38. Atelectasis
Definition : the incomplete expansion or
complete collapse of air-bearing tissue, absorption of
air contained in the alveoli,
Causes :

39. Pleural effusion, pneumothorax,
intrathoracic tumors, diaphragmatic
hernia
External compression on the
pulmonary parenchyma
Enlarged lymph node, tumor, cardiac
enlargement, foreign body, mucoid plug,
broncholithiasis
Endobronchial obstruction
completely obstructing the
ingress of air
Foreign body, granulomatous tissue,
tumor, secretions, including mucous
plugs,bronchiectasis, pulmonary abscess,
asthma,chronic bronchitis, acute
laryngotracheobronchitis
Intraluminal obstruction of a
bronchus
Bronchiolitis, interstitial pneumonitis,
asthma
Intrabronchiolar obstruction
Neuromuscular abnormalities, osseous
deformities, overly restrictive casts and
surgical ,dressings, defective movement
of the diaphragm, or restriction of
respiratory effort
Respiratory compromise or
paralysis

40. Clinical Manifestation
1-SYMPTOMS
*Small area is likely to be asymptomatic
*Large area dyspnea accompanied by, tachycardia, cough, and
often cyanosis occurs. Chest pain if obstruction is removed, the
symptoms disappear rapidly.
2-SIGNS:
A- Inspection :tachypnea,cyanosis,flat chest over affected side
B- Percussion :dullness if large area
C- Auscultation : decreased breath sound

41. DIAGNOSIS
•
The diagnosis of atelectasis can usually be
established by :
1-chest radiographic examination showing :
a-Typical findings include volume loss and displacement of fissures
b-Atypical presentations a mass like opacity
c-Massive
Typical findings include elevation of the diaphragm,
narrowing of the intercostal spaces, and displacement of
the mediastinal structures and heart toward the affected side
2-CT CHEST
3-Bronchoscopic examination

42. Differential Diagnosis
1-Partial Unilateral Opacity
(Consolidation , Nodule)

43. 2-UNILATERAL OPAQUE HEMITHORAX
•(Consolidation , Effusion )

44. TREATMENT
1-Oxygen therapy is indicated when there is dyspnea or
desaturation.
2-Measures to facilitate expansion
Frequent changes in the child’s position, deep breathing, and
chest physiotherapy may be beneficial . Vigorous cough
3-Continuous positive airway pressure (CPAP) may improve
atelectasis.

45. • 4-Bronchoscopic INDICATION
1- Atelectasis is the result of a foreign body or any
other bronchial obstruction that can be relieved.
2- For bilateral atelectasis, bronchoscopic aspiration
should also be performed immediately.
3- It is also indicated when an isolated area of
atelectasis persists for several weeks

46. • 5-Lobectomy indication :
Bronchiectasis , chronic atelectasis , lung nodule

47. 6-Other lines:
A- Effusion, Pnemothorax :must be removed
B-Cystic fibrosis :
Recombinant human DNase (rhDNase),
which is approved only for the
treatment of cystic fibrosis, without cystic
fibrosis who have persistent atelectasis

48. C - Bronchial asthma
• bronchodilator and corticosteroid treatment may
• accelerate atelectasis clearance
D - Neuromuscular disease
• Several devices and treatments are available to assist
these patients, including intermittent positive pressure
breathing,
a mechanical insuffltor-exsuffltor, and noninvasive
bilateral positive pressure ventilation via nasal mask or
full-face mask.

49. 7- Prevention:
Incidence of postoperative pulmonary atlectasis
reduced by:
• 1-adequate ventilation during anesthesia
• 2-post op. frequent change of position,aspiration of
secretion
• 3-encourage child to breathe deeply,cough
• 4-AVOID tight thoracic or abdominal binders

50. Prognosis
• 1-re expansion of atlectatic area if obstruction
is removed
• 2-secondary infection as impaired mucocilary
clearance lead to bronchiectasis ,pulmonary
abscess
• 3-asthmatic patient with atlectasis have an
increased incidence of right middle lobe
syndrome

51. CASE STUDY
• Male patient ,normal delivery,3days old, 3kg,developped
yellowish discolouration of skin,sclera was diagnosed as
physiological jaundice .1mon later,the jaundice became more
deep with bloody stool , haematemsis, abdominal
distension.He was admitted to hepatology unit.
• On examination wt 2.7kg,jaundice,mild hepatomegally
otherwise normal
• Investigation:AST 600,ALT 750,Total bilirubin level 19mg/dl
direct 9mg,indirect 10 ,TORCH negative,hepatitis marker
negative
• Abdominal US early cirrhotic change.liver biopsy :distorted
architecture with regenerative nodules<cirrhosis>
• Band ligation was done and he was discharged

52. He developped recurrent attacks of haemtemsis
,was admitted for band ligation
• At age of 6y ,he began to complain of difficult
of breathing,chronic cough saught medical
advice and was diagnosed as
bronchopneumonia
• 1mon later he developped acute dyspnea
,cyanosis transferred to emergency
department

53. • 1-what to be done first?
• 2-what is differential diagnosis?