SYNDROM OF CONSOLIDATED

PULMONARY TISSUE.
PNEUMONIA.
ATHELECTASIS.

Andrei Ichim
DEPARTMENT OF INTERNAL MEDICINE-SEMIOLOGY
 Patterns of Lung disorders:
Airway
– Bronchitis, Bronchiectasis, Bronchiolitis.
– Tumors / Cancer
Parenchyma
– Pneumonia.
– Lung abscess, TB
– Hyaline membrane dis (HMD & ARDS)
– Pneumoconiosis
– Tumors / Cancer
Pleura:
– Pleural effusion (TB)
– Tumors / Cancer
 Pathogenesis of Pulmonary
Infections
Entry:
Aspiration (ie Pneumococcus)
Inhalation (ie Mtb and viral pathogens)
Inoculation (contaminated equipment)
Colonization (in patients with COPD)
Hematogenous spread (patients with sepsis)
Direct spread (adjacent abscess)
 DEFINITION

Syndrom of consolidated pulmonary tissue is

characterized by increased lung attenuation
associated with obscuration of underlying
vessels and air bronchograms. It indicates filling
of the airspaces by fluid, cells, protein, or other
material
 Consolidation, bacterial pneumonia. CT shows increased
attenuation of the right upper lobe posteriorly with a few air
bronchograms and obliteration of vessels.
Pneumonia
 DEFINITION
Pneumonia is characterized by inflammation of the
alveoli and terminal airspaces in response to
invasion by an infectious agent introduced into the
lungs through hematogenous spread or inhalation.
The inflammatory cascade triggers the leakage of
plasma and the loss of surfactant, resulting in air
loss and consolidation. This is in contrast to
pneumonitis, which is caused by noninfectious
agents such as radiation or chemicals.
PNEUMONIA
 Conditions that allow pneumonia-causing
infectious organisms to circumvent the upper
airway defense mechanisms include the
following:
Intubation, tracheostomy, impaired cough reflex,
and aspiration: These conditions provide infectious
organisms with easier access to the alveoli and
terminal airspaces.
Ciliary dyskinesia, bronchial obstruction, viral
infection, cigarette smoke, and certain chemical
agents: These conditions create disruption in the
mucociliary blanket.
Conditions that allow pneumonia-causing
infectious organisms to circumvent the
upper airway defense mechanisms include
the following: (cont-d)
Anatomic abnormalities (eg, sequestrations),
gastric fluid aspiration or other causes of
noninfectious inflammation, altered pulmonary
blood flow, and pulmonary edema: These
conditions increase the predisposition for
pneumonia.
Immunodeficiency and immunosuppression:
These conditions increase predisposition for
pneumonia.
Initial descriptions of pneumonia focused
on the anatomic or pathologic appearance
of the lung, either by direct inspection
at autopsy or by its appearance under a
microscope.
ANATOMICAL CLASSIFICATION OF
PNEUMONIA
LOBAR PNEUMONIA
BRONCHOPNEUMONIA
INTERSTITIAL PNEUMONIA
 Lobar pneumonia is a form
of pneumonia that affects a large and
continuous area of the lobe of a lung.
It is one of the two anatomic
classifications of pneumonia (the other
being bronchopneumonia)
Multilobar pneumonia involves
more than one lobe, and it often
causes a more severe illness.
Bronchopneumonia or bronchial
pneumonia or "Bronchogenic
pneumonia"
is the acute inflammation of the walls of the
bronchioles. It is a type of pneumonia
characterised by multiple foci of isolated,
acute consolidation, affecting one or
more pulmonary lobes
Lobar & Bronchial
pneumonia
Bronchopneumonia is less likely
than lobar pneumonia to be
associated with Streptococcus
 Pathology

Macroscopically: Multiple foci of consolidation

are present in the basal lobes of the human
lung, often bilateral. These lesions are 2-
4 cm in diameter, grey-yellow, dry, often
centered on a bronchiole, are poorly delimited
and have the tendency to confluence,
especially in children.
 Pathology
Microscopically: A focus of inflammatory
condensation is centered on a bronchiole with
acute bronchiolitis (suppurative exudate - pus -
in the lumen and parietal inflammation).
Alveolar lumens surrounding the bronchiole are
filled with neutrophils ("leukocytic alveolitis").
Massive congestion is present. Inflammatory
foci are separated by normal, aerated
parenchyma.
Bronchopneumonia: focus of inflammatory condensation centred
by a bronchiole with acute bronchiolitis (suppurative exudate in
the lumen and parietal inflammation). Alveolar lumens surrounding
the bronchia are filled with neutrophils ("leukocytic alveolitis").
Inflammatory foci are separated by normal, aerated parenchyma.
Bronchopneumonia.
 Bronchopneumonia (detail) : central area of a focus of

inflammatory condensation - bronchiola with acute bronchiolitis.

 Although these two patterns of pneumonia,
lobar and lobular, are the classic anatomic
categories of bacterial pneumonia, in clinical
practice the types are difficult to apply, as the
patterns usually overlap. Bronchopneumonia
(lobular) often leads to lobar pneumonia as the
infection progresses. The same organism may
cause one type of pneumonia in one patient, and
another in a different patient. From the clinical
standpoint, far more important than distinguishing
the anatomical subtype of pneumonia, is
identifying its causative agent and accurately
assessing the extent of the disease.
 Lobar pneumonia
Lobar pneumonia usually has an acute
progression. Classically, the disease has
four pathomorfological stages:
Congestion in the first 24 hours
Red hepatisation or consolidation
Grey hepatisation
Resolution (complete recovery)
 LOBAR PNEUMONIA

If not treated, lobar pneumonia evolves in

four stages :
a. Congestion (first 2 days)
b. Red hepatisation (fibrinous alveolitis) (2nd
to 4th day)
c. Grey hepatisation (leukocytic alveolitis)
(4th to 8th day)
d. Resolution (after 8th day)
Leukocytic alveolitis is the 3rd phase of the lobar pneumonia.
Alveolar lumens are filled with leukocytic (suppurative) exudate
(neutrophils and macrophages, in order to remove the fibrin).
Alveolar walls are thickened due to capillary congestion and
edema.
Pneumonias – Classification
CAP • Community Acquired

HCAP • Health Care Associated

HAP • Hospital Acquired

ICUAP • ICU Acquired

VAP • Ventilator Acquired

Nosocomial
Pneumonias
A recently introduced type of
healthcare-associated
pneumonia (in patients living
outside the hospital who have
recently been in close contact with
the health care system) lies
between these two categories.
(community-acquired pneumonia
and hospital-acquired pneumonia).
 Community-Acquired Pneumonia
(CAP)
CAP occurs throughout the world and is a
leading cause of illness and death. Causes of
CAP include:
bacteria,
viruses,
fungi, and
parasites.
 CAP – The Two Types of
Presentations
Classical Atypical

Gradual & insidious onset

Sudden onset of CAP
High fever, shaking chills
Pleuritic chest pain, SOB
Productive cough
Rusty sputum, blood tinge
Poor general condition
High mortality up to 20% in
patients with bacteremia
S.pneumoniae causative
Low grade fever
Dry cough, No blood tinge
Good GC – Walking CAP
Low mortality 1-2%; except in
cases of Legionellosis
Mycoplasma, Chlamydiae,
Legionella, Ricketessiae,
Viruses are causative
CAP – Pathogenesis

Inhalation

Aspiration

Hematogenous
 Pathophysiology

The symptoms of CAP are the result of

both the invasion of the lungs
by microorganisms and the immune
system's response to the infection. The
mechanisms of infection are quite different
for viruses and the other microorganisms.
 Pathophysiology
Viruses
– Viruses must invade cells in order to reproduce. Typically, a
virus will reach the lungs by traveling in droplets through
the mouth and nose with inhalation. There, the virus invades
the cells lining the airways and the alveoli. This invasion
often leads to cell death either through direct killing by the
virus or by self-destruction through apoptosis. Further
damage to the lungs occurs when the immune system
responds to the infection. White blood cells, in
particular lymphocytes, are responsible for activating a
variety of chemicals (cytokines) which cause leaking of fluid
into the alveoli. The combination of cellular destruction and
fluid-filled alveoli interrupts the transportation of oxygen into
the bloodstream. In addition to the effects on the lungs,
many viruses affect other organs and can lead to illness
affecting many different bodily functions. Viruses also make
the body more susceptible to bacterial infection; for this
reason, bacterial pneumonia often complicates viral CAP.
 Pathophysiology
(con---d)
Bacteria and fungi
– Bacteria and fungi also typically enter the lung with inhalation, though
they can reach the lung through the bloodstream if other parts of the
body are infected. Often, bacteria live in parts of the upper respiratory
tract and are constantly being inhaled into the alveoli. Once inside the
alveoli, bacteria andfungi travel into the spaces between the cells and
also between adjacent alveoli through connecting pores. This invasion
triggers the immune system to respond by sending white blood cells
responsible for attacking microorganisms (neutrophils) to the lungs. The
neutrophils engulf and kill the offending organisms but also release
cytokines which result in a general activation of the immune system. This
results in the fever, chills, and fatigue common in CAP. The neutrophils,
bacteria, and fluid leaked from surrounding blood vessels fill the alveoli
and result in impaired oxygen transportation. Bacteria often travel from
the lung into the blood stream and can result in serious illness such
as septic shock, in which there is low blood pressure leading to damage
in multiple parts of the body including the brain, kidney, and heart.
 Pathophysiology
(con---d)
Parasites
– There are a variety of parasites which can
affect the lungs. In general, these parasites
enter the body through the skin or by being
swallowed. Once inside the body, these
parasites travel to the lungs, most often
through the blood. There, a similar
combination of cellular destruction and
immune response causes disruption of
oxygen transportation.
 CAP – Risk Factors for
Pneumonia
 Age
 Obesity; Exercise is protective
 Smoking, PVD
 Asthma, COPD
 Immuno-suppression, HIV
 Institutionalization, Old age homes etc
 Dementia

ID Clinics 1998;12:723. Am J Med 1994;96:313

 Risk factors

Some people have an underlying problem

which increases their risk of getting an
infection. Some important situations are
covered below:
 Risk factors (con---d)
Obstruction
When part of the airway (bronchi) leading to the
alveoli is obstructed, the lung is not able to
clear fluid when it accumulates. This can lead to
infection of the fluid resulting in CAP. One
cause of obstruction, especially in young
children, is inhalation of a foreign object such
as a marble or toy. The object is lodged in the
small airways and pneumonia can form in the
trapped areas of lung. Another cause of
obstruction is lung cancer, which can grow into
the airways block the flow of air.
 Risk factors (con---d)
Lung disease
People with underlying lung disease are
more likely to develop CAP. Diseases such
as emphysema or habits such
as smoking result in more frequent and
more severe bouts of CAP. In children,
recurrent episodes of CAP may be the first
clue to diseases such as cystic
fibrosis or pulmonary sequestration.
Risk factors (con---d)
Immune problems
People who have immune system problems are
more likely to get CAP. People who
have AIDS are much more likely to develop CAP.
Other immune problems range from severe
immune deficiencies of childhood such
as Wiskott-Aldrich syndrome to less severe
deficiencies such as common variable
immunodeficiency
CAP – The Pathogens
40-60% - No causative agent identified
Involved
2-5% - Two are more agents identified

9%
4% S.pneumoniae
4% H.influenza
5% Chlamydia
Legionella spp
6%
S.aureus
56%
6% Mycoplasma
Gram Neg bacilli
10% Viruses
 ETIOLOGY
Infants:
Streptococcus agalactiae, also known as
Group B Streptococcus or GBS (50% of
cases of CAP in the first week of life ).
Listeria monocytogenes and tuberculosis.
herpes simplex virus ,
adenovirus, mumps, and enterovirus
 ETIOLOGY (con---d)
CAP in older infants:
Streptococcus pneumoniae, Escherichia
coli,Klebsiella pneumoniae, Moraxella
catarrhalis, and Staphylococcus aureus.
Common viruses include respiratory
syncytial
virus (RSV),metapneumovirus, adenovirus
, parainfluenza, influenza, and rhinovirus.
 Children
For the most part, children older than one
month of life are at risk for the same
microorganisms as adults.
Children less than five years are much less
likely to have pneumonia caused
by Mycoplasma pneumoniae, Chlamydophila
pneumoniae, or Legionella pneumophila.
older children and teenagers are more likely to
acquire Mycoplasma
pneumoniae and Chlamydophila
pneumoniae than adults.
 Streptococcus pneumonia
(Pneumococcus)
 Most common cause of CAP
 About 2/3 of CAP are due to S.pneumoniae
 These are gram positive diplococci
 Typical symptoms (e.g. malaise, shaking
chills fever, rusty sputum, pleuritic chest
pain, cough)
 Lobar infiltrate on CXR
 May be Immuno suppressed host
 25% will have bacteremia – serious effects
 CAP – Special Features –
Pathogen wise
Typical – S.pneumoniae, H.influenza, M.catarrhalis – Lungs
Blood tinged sputum - Pneumococcal, Klebsiella, Legionella
H.influenzae CAP has associated of pleural effusion
S.Pneumoniae – commonest – penicillin resistance problem
S.aureus, K.pneumoniae, P.aeruginosa – not in typical host
S.aureus causes CAP in post-viral influenza; Serious CAP
K.pneumoniae primarily in patients of chronic alcoholism
P.Aeruginosa causes CAP in pts with CSLD or CF, Nosocom
Aspiration CAP only is caused by multiple pathogens
Extra pulmonary manifestations only in Atypical CAP
 CAP – Risk Factors for

Hospitalization
Older, Unemployed, Unmarried
 Recurrent common cold
 Asthma, COPD; Steroid or bronchodilator
use
 Chronic diseases, Diabetes, CHF,
Neoplasia
 Amount of smoking
 Alcohol is NOT related to increased risk
for hospitalization
ID Clinics 1998;12:723. Am J Med 1994;96:313
CAP – Risk Factors for Mortality
 Age > 65
 Bacteremia (for S. pneumoniae)
 S. aureus, MRSA ,
Pseudomonas
 Extent of radiographic changes
 Degree of immuno-suppression
 Amount of alcohol consumption
ID Clinics 1998;12:723. Am J Med 1994;96:313
 Community Acquired
Pneumonia (CAP)
 Definition
… an acute infection of the pulmonary parenchyma
that is associated with some symptoms of acute
infection, accompanied by the presence of an
acute infiltrate on a chest radiograph, or
auscultatory findings consistent with pneumonia,
in a patient not hospitalized or residing in a long
term care facility for > 14 days before onset of
symptoms.

.
Lobar pneumonia, leukocytic
alveolitis.
Gram stain demonstrating gram-positive cocci in pairs and
chains and (B) culture positive for Streptococcus
pneumoniae.
Streptococcus pneumoniae
Community-acquired pneumonia

Community-acquired pneumonia (CAP)

is a disease in which individuals who have
not recently been hospitalized develop
an infection of the lungs (pneumonia).
CAP is a common illness and can affect
people of all ages.
 Complains
coughing that produces greenish or
yellow sputum
a high fever that may be accompanied with
sweating, chills, and uncontrollable shaking
sharp or stabbing chest pain
rapid, shallow breathing that is often painful
dyspnea or dyspnoea (problems breathing)
Less common symptoms include:
the coughing up of blood (hemoptysis)
headaches (including migraine headaches)
loss of appetite
excessive fatigue
blueness of the skin (cyanosis)
nausea
vomiting
diarrhea
joint pain (arthralgia)
muscle aches (myalgia)
 Clinical findings:
General state (status, condition) – more often
grave or very grave
Consciousness - in some patient's confusion
or disorientation may predominate in elderly or
alcoholic.
Posture – forced – on the affected side.
Color of the skin – in severe hypoxemic
patients may be cyanotic or hyperemia in high
fever, presence herpes labialis.
 Pulmonary system:
in the Ist stadium:
decreased respiratory excursion on the affected
side because of pleuretic pain,
vocal fremitus – decreased
percussion – dullness with tympanic sound
ausculatation - decreased vesicular breathing,
unpronounsed crepitation crackles (high-
pitched, end-respiratory crackles, originating
from fluid-filled alveoli, that are often increased
by, or heard only after coughing)
 Pulmonary system:
in the IInd stadium:
a. vocal fremitus – increased
b. percussion – dull sound
c. auscultation - pathological bronchial
breathing, pleural rub,
 Pulmonary system:
in the IIIrd stadium:
a. vocal fremitus slightly increased and
returns to normal
b. percussion – steadily returns to normal
c. occurs bronchovesicular breathing and
later normal vesicular breathing,
crepitation, moist crackles
 Heart system:
Tachycardia when fever is present
Decreased arterial pressure
Signs of myocarditis
 Pneumonia Diagnosis:
Routine laboratory tests: CBC, electrolytes,
hepatic enzymes) are of little value in
determining the etiology of pneumonia, but may
have prognostic significance and influence the
decision to hospitalization. Should be
considered in patients who may need
hospitalization, >65 yr, or with coexisting illness.
All admitted patients should have oxygen
saturation assessed by oximetry
CAP – Gram’s Stain of Sputum
Good sputum samples is obtained only
from 39%
83% show only one predominant
S. H.
Efficiency of test organism
pneumoniae influenza

Sensitivity 57 % 82 %

Specificity 97 % 99 %
Positive Predictive
Value
95 % 93 %
Negative Predictive
Value
71 % 96 %
Pathogens Retrieved from
Blood Culture
5% S.pneumoni
11% ae
Enterobacte
16% ria
Staph.aureu
s
68%
Others
 CAP – Value of Chest
Radiograph
• Usually needed to establish
diagnosis
• It is a prognostic indicator
• To rule out other disorders
• May help in etiological
diagnosis

J Chr Dis 1984;37:215-25

 Infiltrate Patterns and
Pathogens
CXR Pattern Possible Pathogens
S.pneumo, Kleb, H. influ, Gram
Lobar
Neg
Patchy Atypicals, Viral, Legionella

Interstitial Viral, PCP, Legionella

Anerobes, Kleb, TB, S.aureus,
Cavitatory
Fungi
Large effusion Staph, Anaerobes, Klebsiella
Right lower lobe consolidation in a
patient with bacterial pneumonia.
A patient with bacterial pneumonia (same patient as in the prededing image) a few days
later. This radiograph reveals progression of pneumonia into the right middle lobe and

the development of a large parapneumonic pleural effusion.

Chest x-ray showing increased shadowing
in right lung (left side of image).
Right middle zone consolidation
 CAP – Complications
 Hypotension and septic shock
 3-5% Pleural effusion; Clear fluid + pus cells
 1% Empyema thoracis pus in the pleural space
 Lung abscess – destruction of lung - CSLD
 Single (aspiration) anaerobes, Pseudomonas
 Multiple (metastatic) Staphylococcus aureus
 Septicemia – Brain abscess, Liver Abscess
 Multiple Pyemic Abscesses
 Atelectasis

The term atelectasis is derived from the

Greek words ateles and ektasis, which
mean incomplete expansion.
Atelectasis is defined as diminished
volume affecting all or part of a lung.
Pulmonary atelectasis is one of the most
commonly encountered abnormalities in
chest radiology findings.
 Atelectasis
Atelectasis is divided physiologically into
obstructive and nonobstructive causes
Patterns of lobar atelectasis as seen on
CXRs are presented in the image below
 Obstructive atelectasis
Obstructive atelectasis is the most
common type and results from
reabsorption of gas from the alveoli when
communication between the alveoli and
the trachea is obstructed. The obstruction
can occur at the level of the larger or
smaller bronchus.
 Anterior view of lungs suffering from atelectasis
caused by obstruction An occlusion can be seen in
right Eparteral bronchus
 Pathophysiology
of obstructive atelectasis
Following obstruction of a bronchus, the
circulating blood absorbs the gas in the
peripheral alveoli, leading to retraction of
the lung and an airless state within a few
hours. In the early stages, blood perfuses
the airless lung; this results in ventilation-
perfusion mismatch and arterial
hypoxemia.
 Pathophysiology
of obstructive atelectasis
A filling of the alveolar spaces with
secretions and cells may occur, thereby
preventing complete collapse of the
atelectatic lung. The uninvolved
surrounding lung tissue distends,
displacing the surrounding structures. The
heart and mediastinum shift toward the
atelectatic area, the diaphragm is
elevated, and the chest wall flattens.
 Pathophysiology
of obstructive atelectasis
If the obstruction is removed, any
complicating postobstructive infection
subsides and the lung returns to its normal
state. If the obstruction is persistent and
infection continues to be present, fibrosis
develops and the lung becomes
bronchiectatic.
 Obstructive atelectasis
Causes of obstructive atelectasis include
foreign body,
tumor, and
mucous plugging.
 Obstructive atelectasis
The rate at which atelectasis develops and the extent
of atelectasis depend on several factors, including the
extent of collateral ventilation that is present and the
composition of inspired gas. Obstruction of a lobar
bronchus is likely to produce lobar atelectasis;
obstruction of a segmental bronchus is likely to
produce segmental atelectasis. Because of the
collateral ventilation without a lobe or between
segments, the pattern of atelectasis often depends on
collateral ventilation, which is provided by the pores of
Kohn and the canals of Lambert.
Nonobstructive atelectasis
Nonobstructive atelectasis can be caused
by loss of contact between the parietal and
visceral pleurae, compression, loss of
surfactant, and replacement of
parenchymal tissue by scarring or
infiltrative disease.
 Nonobstructive atelectasis
Relaxation or passive atelectasis results
when a pleural effusion or a pneumothorax
eliminates contact between the parietal and
visceral pleurae. Generally, the uniform
elasticity of a normal lung leads to preservation
of shape even when volume is decreased. The
different lobes also function differently, eg, the
middle and lower lobes collapse more than the
upper lobe in the presence of pleural effusion,
while the upper lobe may be affected more by
pneumothorax.
Relaxation atelectasis is caused by the
following:

Pleural effusion
Pneumothorax
A large emphysematous bulla
Nonobstructive atelectasis
Compression atelectasis occurs from any
space-occupying lesion of the thorax
compressing the lung and forcing air out of the
alveoli. The mechanism is similar to relaxation
atelectasis.
Compression atelectasis is caused by the
following:
Chest wall, pleural, or intraparenchymal masses
Loculated collections of pleural fluid
Anterior view of lungs suffering from
atelectasis caused by compression
of lung tissue
Nonobstructive atelectasis
Adhesive atelectasis results from
surfactant deficiency. Surfactant normally
reduces the surface tension of the alveoli,
thereby decreasing the tendency of these
structures to collapse. Decreased
production or inactivation of surfactant
leads to alveolar instability and collapse.
This is observed particularly in acute
respiratory distress syndrome (ARDS) and
similar disorders.
Adhesive atelectasis is caused by
the following:
Hyaline membrane disease
Acute respiratory distress syndrome
Smoke inhalation
Cardiac bypass surgery
Uremia
Prolonged shallow breathing
 Nonobstructive atelectasis
Cicatrization atelectasis results from
diminution of volume as a sequela of severe
parenchymal scarring and is usually caused by
granulomatous disease or necrotizing
pneumonia.
Cicatrization atelectasis is caused by the
following:
Idiopathic pulmonary fibrosis
Chronic tuberculosis
Fungal infections
Radiation fibrosis
Nonobstructive atelectasis
Replacement atelectasis occurs when the
alveoli of an entire lobe are filled by tumor
(eg, bronchioalveolar cell carcinoma),
resulting in loss of volume.
Replacement atelectasis is caused by
alveoli filled by tumor or fluid.
Resorptive atelectasis is caused by the
following:
•Bronchogenic carcinoma
•Bronchial obstruction from metastatic neoplasm
(eg, adenocarcinoma of breast or thyroid,
hypernephroma, melanoma)
•Inflammatory etiology (eg, tuberculosis, fungal
infection)
•Aspirated foreign body
•Mucous plug
•Malpositioned endotracheal tube
•Extrinsic compression of an airway by neoplasm,
lymphadenopathy, aortic aneurysm, or cardiac
enlargement
 Physical examination
The physical examination findings show:
Chest excursion in the area is reduced or
absent.
The trachea and the heart are deviated toward
the affected side
diminished or absent vocal fremitus
dullness to percussion over the involved area
and
diminished or absent breath sounds.
 History
of the disease
Most symptoms and signs are determined by the
rapidity with which the bronchial occlusion occurs, the
size of the lung area affected, and the presence or
absence of complicating infection.
Rapid bronchial occlusion with a large area of lung
collapse causes pain on the affected side, sudden
onset of dyspnea, and cyanosis. Hypotension,
tachycardia, fever, and shock may also occur.
Slowly developing atelectasis may be asymptomatic
or may cause only minor symptoms. Middle lobe
syndrome often is asymptomatic, although irritation in
the right middle and right lower lobe bronchi may
cause a severe, hacking, nonproductive cough.
 Laboratory Studies

Atelectasis of a significant size results in

hypoxemia as measured on arterial blood
gas determinations. Arterial blood gas
evaluation shows that despite hypoxemia,
the PaCO2 level is usually normal or low
as a result of the increased ventilation.
 Imaging Studies
Chest radiographs and CT scans show direct
and indirect signs of lobar collapse.
Direct signs include displacement of fissures
and opacification of the collapsed lobe.
Indirect signs include displacement of the hilum,
mediastinal shift toward the side of collapse,
loss of volume on ipsilateral hemithorax,
elevation of ipsilateral diaphragm, crowding of
the ribs, compensatory hyperlucency of the
remaining lobes, and silhouetting of the
diaphragm or the heart border.
 Imaging Studies
Complete atelectasis of an entire lung is
characterized as follows:
Complete collapse of a lung leads to
opacification of the entire hemithorax and
an ipsilateral shift of the mediastinum.
The mediastinal shift separates atelectasis
from massive pleural effusion.
 Complete atelectasis of the left lung. Mediastinal
displacement, opacification, and loss of volume are
present in the left hemithorax.
Complete right lung atelectasis.
Atelectasis. Right upper lobe
collapse
 Complications

Acute pneumonia
Bronchiectasis
Hypoxemia and respiratory failure
Postobstructive drowning of the lung
Sepsis
Pleural effusion and empyema