You are on page 1of 92

ATELECTASIS

AND PULMONARY
INFECTION
Ella C. Lim, M.D., DPSP
ATELECTASIS
 The long of lung volume due to
inadequate expansion of the air
spaces (collapse).

 Types:
 Resorption Atelectasis
 Compression Atelectasis

 Atelectasis due to loss of


surfactant
ATELECTASIS

 Compression Atelectasis
 Air or fluid in the pleural cavity
under increased pressure (e.g.,
tension pneumothorax, effusion)
collapses small airways under the
pleura.

 Resorption Atelectasis
 Airway obstruction prevents air
from reaching the alveoli; May
RESORPTION ATELECTASIS
 Causes of obstruction:
 Mucous or mucoplurulent plug

 aspiration of foreign material

 bronchogenic carcinoma

 Cause of alveolar collapse:


 Lack of air

 Distal resorption of preexisting air

 Most common cause of fever 24-36


hours after surgery – develops into
ATELECTASIS due to Loss of
Surfactant
 Respiratory distress in newborns
 Causes of decreased surfactant in
fetal lungs:
 Prematurity

 Maternal diabetes

 Cesarean section

 Microscopic findings: collapsed


alveoli lined by hyaline membranes
derived from necrotic cellular debris
PULMONARY INFECTION

 Tuberculosis
 Pneumonia
 Other pulmonary
infections
TUBERCULOSIS

Epidemiology:
 Inhalation of the bacterium (droplet
infection)
Screening: PPD skin test – does not
distinguish active from inactive
disease
Primary TB
 initially localizes in a subpleural
location (upper part of the lower
lobes or lower part of the upper
TUBERCULOSIS
 Ghon complex – spread of infection
to hilar lymph nodes with caseous
necrosis in nodes
 Usually resolves – calcified
granuloma or area of scar tissue
(may be a nidus for reactivation TB)

Secondary (reactivation) TB
 Cavitary lesion involves one or both
apices in the upper lobes

TUBERCULOSIS

Complications of secondary
(reactivation) TB:
 Miliary spread in lungs – invasion into
the bronchus or lymphatics

 Systemic miliary spread – invasion of


pulmonary vein; kidneys is the most
common extrapulmonary site

 Massive hemoptysis, bronchiectasis,


TUBERCULOSIS

 Most common cause of TB in AIDS


patients:
Mycobacterium avium-
intracellulare
TUBERCULOSIS

                                                

                       
TUBERCULOSIS
 Ghon complex
 Calcified lymph nodes
 Subpleural nodule
 CXR & photo: Note a calcified, well-
circumscribed nodule in the left lung -
an old healed focus of primary
tuberculosis; characteristically
peripheral in location.
 Other calcified nodules can be seen in
the CXR in the left hilar region where
the clavicle appears to touch the arch
TUBERCULOSIS

 The peripheral and mediastinal


calcified nodules together form
the Ghon complex.

 What are the different stages of


pulmonary tuberculosis?
TUBERCULOSIS
 Primary pulmonary tuberculosis:
residuum of which is the Ghon
complex, usually asymptomatic.

 Secondary, or reactivation
tuberculosis: occurs years after
the primary infection, most
commonly involves the apex of
the lung - typically causes
caseous necrosis and cavitation.
TUBERCULOSIS

 Either of these types of


tuberculosis may become
progressive, that is, evolve into
miliary tuberculosis or
tuberculous bronchopneumonia.
TUBERCULOSIS

                                                

                       
TUBERCULOSIS
 Cystic cavities
 Patchy consolidation

Note:
 The cavities in the upper lobes -
pathologic & radiographic findings in
secondary, or reactivation
tuberculosis.
 Patchy consolidation is present in the
upper lobe - may represent either
superimposed bronchopneumonia or
progressive spread of tuberculosis.
TUBERCULOSIS

 How does the morphology of


tuberculosis differ in the
immunocompetent vs. the
immunosuppressed host?
TUBERCULOSIS
 Immunosuppressed patients -
more likely to have disseminated
infection involving lymph nodes,
blood, central nervous system,
and bowel.
 Less likely to have well-formed
granulomas
 More likely to consist of
histiocytes and necrosis.

TUBERCULOSIS

                                                

                       
TUBERCULOSIS
 Caseous necrosis

 Zone of epithelioid cells

 Large central area of caseous


necrosis - seen as granular pink
structureless material with complete
destruction of lung parenchyma

 Caseous material - surrounded by a


TUBERCULOSIS

 What are the causes of caseous


necrosis?
TUBERCULOSIS

 Causes of Caseous Necrosis:


 Tuberculosis

 Leprosy

 Fungal infections
FUNGAL PULMONARY INFECTION

 The differential diagnosis of


granuloma formation includes
histoplasmosis, blastomycosis, and
coccidioidomycosis.

 Special stains for these organisms


help differentiate the cause of the
granulomatous inflammation.
TUBERCULOSIS

 How does caseous necrosis differ


from coagulative necrosis under
the microscope?
TUBERCULOSIS

 In caseous necrosis, there is total


loss of tissue structure.

 In coagulative necrosis, cell


outlines are retained.
TUBERCULOSIS

                                                

                       
TUBERCULOSIS

 Caseous necrosis

 Zone of epithelioid cells

 Langhan’s Type Giant cell


TUBERCULOSIS

 Caseous necrosis - seen as pink


granular structureless material that
has destroyed the lung alveoli.

 Epithelioid cells - surrounding the


caseous material are elongated cells
with indistinct cell boundaries.
TUBERCULOSIS

 What is the origin of epithelioid


cells?
TUBERCULOSIS

 They are transformed


macrophages.
TUBERCULOSIS

 Is this lesion an example of


granulomatous inflammation or
granulation tissue?
TUBERCULOSIS

 This lesion is granulomatous


inflammation.
TUBERCULOSIS

                                                

                       
TUBERCULOSIS

 Reddish rods = acid-fast bacteria


(Mycobacterium tuberculosis)
seen within an area of caseous
necrosis.
TUBERCULOSIS CASE
 A 68-year-old man presented with
weight loss over a four-month period
and the recent onset of fever and
chills at night.

 Admission chest x-ray revealed an


irregular opacity of the right lung
with pleural effusion.

 Thoracocentesis was performed, and


cytologic examination of the pleural
TUBERCULOSIS CASE
 Abdominal CT revealed
hepatomegaly and diffuse
lymphadenopathy.

 The patient was treated with multiple


broad-spectrum antibiotics, but his
fever did not respond.

 His hospital course was also notable


for electrolyte imbalances, including
hyperkalemia and hyponatremia.
TUBERCULOSIS CASE

 Despite supportive care, the patient


expired on the fourth hospital day,
and an autopsy was performed.
TUBERCULOSIS

 Why do you think this patient


developed tuberculosis?

 Can this explain the other clinical


features in this patient?
TUBERCULOSIS
 Cancer patients are often
immunosuppressed. Most likely,
immunosuppression allowed
reactivation of some old focus of
TB in this patient after he
developed cancer.

 Disseminated TB could cause


lymphadenopathy and
hepatomegaly. Destruction of the
adrenal cortex by tuberculosis is
PNEUMONIA CASE

 A 45/M was found wandering


downtown with an alcohol breath
and coughing up thin, rusty
sputum.

 He was brought to ER and said he


was fine the day before but that
morning he had begun to shake
uncontrollably and felt alternately
cold then hot and sweaty. He said his
chest hurt when he breathed and
PNEUMONIA CASE
 The patient’s past medical history
included a hospital admission for
tuberculosis 10 years ago.
 Physical examination revealed a thin
male who was anxious and mildly
cyanotic.
 Other abnormal physical findings
included tachypnea and chest
splinting, accompanied by fine rales
and decreased breath sounds by
auscultation over the right lower
PNEUMONIA CASE
 His temperature was 39.2°C, but
his pulse was normal.
 WBC count was 16 x 103/µL (ref.
range 4.1-10.9 x 103/µL) with 70%
polys, 18% bands, and 12%
lymphocytes.
 Blood gases demonstrated hypoxia
and respiratory alkalosis.
 Sputum was collected for smear and
culture. A gram stain of the sputum
showed lancet-shaped, gram-positive
PNEUMONIA CASE
 The patient was admitted and
promptly begun on antibiotics and
oxygen therapy.

 However, he became progressively


more hypoxic, was placed in the ICU
on increasing concentrations of
oxygen, and expired 24 hours after
admission.

 During this time, both of the blood


PNEUMONIA

What predisposed this patient to


get pneumonia?
PNEUMONIA
 This patient is a chronic alcoholic,
probably malnourished and somewhat
immunosuppressed.

 Alcoholics are also prone to aspirate


bacteria-laden secretions from the
upper respiratory tract during an
alcoholic bout.

 Impaired mucociliary clearance and


defective phagocytic functions of
PNEUMONIA

 What accounts for the rusty


sputum in this case?
PNEUMONIA

 The sputum is composed of the


exudate in the alveoli; it is rusty
because of the red cells in the
exudate.
PNEUMONIA

 Community Acquired Pneumonia


(CAP)
 Typical

 Atypical

 Nosocomial Pneumonia (hospital-


acquired)
TCA PNEUMONIA
 Risk factors:
 Splenic dysfunction

 Immunodeficiency (old age, AIDS)

 BRONCHOPNEUMONIA

 LOBAR PNEUMONIA
PNEUMONIA

What is the most common


pathogen causing typical
community-acquired pneumonia?
PNEUMONIA

 Streptococcus
pneumoniae
PNEUMONIA

 What are the complications of


pneumonia?
Complications of PNEUMONIA

 Abscess formation
 Empyema

 organization with subsequent


fibrosis (excessive scar tissue)
 bacteremic dissemination
(sepsis)
PNEUMONIA
CLINICAL FINDINGS:
 Sudden onset of symptoms: high
fever w/ productive cough
 Signs of consolidation (alveolar
infiltrate): dullness to percussion ;
increased vocal tactile fremitus

LABORATORY FINDINGS:
 Positive gram stain, neutrophilic
leukocytosis
PNEUMONIA

                                                

                       
PNEUMONIA

 Cardiac silhouette
 Infiltrate
 Note: The usual angle between
the right heart border and the
right diaphragm has been lost.
 Diffuse infiltrate extends to the
fissure between the right middle
and right lower lobes.
 This is a lobar pneumonic
PNEUMONIA

 What would bronchopneumonia


look like radiographically?
PNEUMONIA

 Bronchopneumonia tends to be
patchy, although, if severe, even
bronchopneumonia may become
confluent and involve an entire
lobe of lung.
BRONCHOPNEUMONIA

                                                

                       
BRONCHOPNEUMONIA
 Bronchopneumonia
 Abscess

 There is extensive involvement of the


anterior aspect of the lung by
bronchopneumonia.
 Bronchopneumonia - patchy
consolidation and follows the
distribution of the bronchi and
bronchioles.
BRONCHOPNEUMONIA

 Begins as ACUTE BRONCHITIS and


spreads locally into the lungs

 Usually involves the LOWER LOBES


or RIGHT MIDDLE LOBE

 Microabscesses in areas of
consolidation
BRONCHOPNEUMONIA

 What organisms are particularly


associated with abscess
formation?
BRONCHOPNEUMONIA

 Staphylococcus aureus
 Klebsiella pneumoniae

 type 3 Pneumococcus.
BRONCHOPNEUMONIA

                                                

                       
BRONCHOPNEUMONIA

 Bronchopneumonia
 Normal Lung

 Note: the focal distribution of the


inflammatory process in
bronchopneumonia.
 The inflammation is in a bronchiolar
distribution - there is abundant
inflammation within and surrounding
the bronchioles. Some normal areas
Lungs, LOBAR PNEUMONIA

                                                

                       
PNEUMONIA
 Bronchopneumonia is patchy
 Lobar pneumonia is diffuse, complete
or almost complete consolidation of a
lung lobe
 See contrast between the stages of
red hepatization (right) and gray
hepatization (left).
 The lower lobes are expanded

 Red hepatization stage - the gross


appearance reflects the microscopic
features of congestion and
PNEUMONIA

 Gray hepatization stage -


congestion becomes less
prominent and red blood cells
that have exited into the alveoli
lyse, leaving behind the
fibrinosuppurative exudate.
LOBAR PNEUMONIA

                                                

                       
LOBAR PNEUMONIA
 Congested alveolar septa
 Interstitial pneumonitis

 The alveolar spaces are filled with


neutrophils (PMNs) and a fibrinous
exudate. The alveolar septa are
easily demarcated because of
congestion with red cells. Because of
the alveolar exudate, the lung
becomes airless (solid). This is called
consolidation.
INTERSTITIAL PNEUMONITIS

 Interstitial pneumonitis - the typical


inflammatory response to viruses and
mycoplasma, is very different from
acute bacterial pneumonia.

 Clinical presentation of IP -
nonproductive cough, fever, and
malaise. Pathologically, there is a
lymphoplasmacytic infiltrate in the
alveolar septa. Note the absence of
inflammatory cells in the alveolar
LOBAR PNEUMONIA

What are the components of the


inflammatory reaction to
bacteria?
LOBAR PNEUMONIA

 Bacteria typically cause acute


inflammation, characterized by
congestion, formation of an
exudate, and a
polymorphonuclear infiltrate.
LOBAR PNEUMONIA

 While viral pneumonitis is usually


self-limited, some patients
develop pulmonary
complications secondary to viral
pneumonitis. What are these?
LOBAR PNEUMONIA

 The most common complications


of viral pneumonitis are:
 secondary bacterial pneumonia
and
 diffuse alveolar damage
ATYPICAL COMMUNITY-
ACQUIRED PNEUMONIA
 Usually involves school-age children
& young adults
 Occurs in crowded conditions
(school, prison, slums)

 Most often caused by Mycoplasma


pneumoniae
 Other pathogens: Chlamydia
pneumoniae, C. trachomatis, RSV,
Influenza viruses, adenovirus
ATYPICAL COMMUNITY-
ACQUIRED PNEUMONIA
 Patchy interstitial pneumonia –
mononuclear infiltrate; alveolar
spaces usually free of exudate (no
signs of consolidation)

CLINICAL FINDINGS:
 Insidious onset with low grade fever

 Flu-like symptoms – pharyngitis,


laryngitis, mildly productive cough
HOSPITAL-ACQUIRED PNEUMONIA

 Associated with severe underlying


disease, antibiotic therapy,
immunosuppression, respirators, and
indwelling venous catheters

 Gram-negative bacteria (e.g., E. coli,


Pseudomonas aeruginosa) & gram-
positive bacteria (e.g.,
Staphylococcus aureus)
PNEUMONIA in the
IMMUNOCOMPROMISED

 Usually in AIDS patients and in bone


marrow transplantation
 Common opportunistic infections:
 CMV, Pneumocystis carinii
SYSTEMIC FUNGAL
RESPIRATORY INFECTIONS
 Usually produces a granulomatous
inflammatory reaction with or
without caseation

 Most common systemic fungal


infection – Histoplasma capsulatum

 Fungal respiratory pathogens:


Candida albicans, Aspergillus
fumigatus, Coccidioides immitis,
FUNGAL PNEUMONIA

                                                                

                          
FUNGAL PNEUMONIA

 Right middle lobe


 Intravascular thrombi
 Infarct w/ hyperemic border

 Diffuse consolidation and


vascular thrombosis with
infarction of surrounding
parenchyma of the right middle
lobe of the lung.
FUNGAL PNEUMONIA

What are the mechanisms of


pulmonary damage in
immunocompromised patients
with fungal infection?
FUNGAL PNEUMONIA

 Patients with fungal pneumonia


may have pulmonary damage
from vascular occlusion by the
fungus, resulting in ischemic
necrosis, or from direct invasion
by and host reaction to the
organism.
FUNGAL PNEUMONIA

                                                

                       
FUNGAL PNEUMONIA
 Pulmonary arterial wall
 Fungal hyphae

 This fungus is causing pulmonary


damage by occluding a major
arterial branch, resulting in a
surrounding infarct.
 Aspergillus and fungi of the
Mucorales group are the most
likely to produce this type of
FUNGAL PNEUMONIA

Aside from the lungs, what are


the other two sites in the body
frequently infected by Mucor?
FUNGAL PNEUMONIA

Paranasal sinuses with extension


to the brain (rhinocerebral
Mucor).
LUNG ABSCESS
Etiology:
 Aspiration of oropharyngeal material
(e.g., carious teeth, infected sinus or
tonsillar material)
 Complication of bacterial pneumonia

Gross findings:
 Vary in size and location
 Those due to aspiration are primarily
on the RIGHT side of the lung
 Most common aspiration site –
LUNG ABSCESS
Clinical Findings:
 Spiking fever with productive cough –
foul smelling sputum due to
anaerobes (e.g., Fusobacterium)
 CXR – cavitation with air-fluid level

Aspiration sites in the lungs:


 Standing or sitting position –
posterobasal segment of the right
lower lobe (RLL)
The End

You might also like