PULMONARY CONSOLIDATION

SYNDROMES

PULMONARY CONSOLIDATION SYNDROMES

Classification
Not retractile
1.Well delimitated
PNEUMONIAS
PULMONARY INFARCTION

2.Not well delimitated lung cancer

Or

Inflamatory / Not inflamatory

Retractile

I.
PULMONARY CONSOLIDATION
SYNDROME
CAUSED BY INFLAMMATORY PROCESS

PNEUMONIAS
BRONCHOPNEUMONIAS

CLASSIFICATION:
PNEUMONIAS:
-bacterial
-viral
-with atypical microorganisms

BACTERIAL PNEUMONIAS

PHYSICAL SIGNS IN PULMONARY

CONSOLIDATION
Increased tactile fremitus
Dulness to percussion
egophony and whispered pectoriloquy
Bronchial breath sounds
Rales or crackles
/absent intensity of breath sounds

Bacterial Pneumonias
The most common etiologies :
Pn. with S.pneumoniae (pneumococcus)
(Lobar Pn.)=typical lobar pneumonia
& The most common pneumonia
Pn. with Staphylococcus
Pn. with Streptococcus
Pn. with Klebsiela (Friendlander bacillus)
Pn. with Haemophilus influenzae

TYPICAL LOBAR PNEUMONIA

TYPICAL LOBAR PNEUMONIA

Etiology:

Streptococcus pneumoniae
= G+ diplo coccus

Involves 1 segment / pulmonary lobe

Evolution in 3 stages
1.Onset
2.Evolution
3.Resolution

ONSET-1

CHILLS sudden
Single rigor
Duration 15 30 minutes

followed by
high FEVER 390 400, constant
pyrexia

ONSET-2

Chest aching/pleuritic pain

1. Severe
2. Sharp/knifelike
3. Aggravated by each breath/by coughing
4. The patient is immobilized on the sick side
5. Localization: submammary area/basal
6. Results from inflamed parietal pleura
(e.g.: diaphragmatic pl. shoulder pain

children abdominal pain)

ONSET-3
COUGH irritative, hollow cough, at first
1 3 day
- Productive of
pinkish or adherent rusty sputum
containing fibrin and red cells

ONSET-4
PHYSICAL EXAMINATION

Warm teguments (febrile)

Severe state of health
Redness of face
herpes labialis ( whole face)

ONSET-5

RESPIRATORY SYSTEM EXAMINATION

INSPECTION - superficial respiration ( caused by chest
aching/pleuritic pain)

- polypnea
PALPATION normally transmitted tactile fremitus
PERCUSSION: discreet dullness
AUSCULTATION :

Initially: tonality and intensity of breath

sounds = bronchial breath sounds
timber changes = hardening of breath sounds

= fremitus, breath and voice sounds are transmitted as if

they came directly from the larynx and trachea

EVOLUTION
After 24 48 hours
Duration 7 10 days
Clinical presentation of consolidation syndrome

Sustained Fever
Dyspnea with inspiratory polypnea
Cyanosis
Sustained pleuritic pain of intensity
Coughing with rusty sputum yellowish (afterwards)
Redness of face (plethora of the cheek of affected side)
Jaundice ( hemolysis, impaired liver function)

EVOLUTION
THORAX EXAMINATION

Inspection : chest expansion

restricted motion of the affected
hemithorax

Palpation : tactile fremitus

Percussion : Dullness
Auscultation : bronchial breath sounds
surrounded by fine crepitant rales, instead of
vesicular breath sounds
(initially, fine crepitant rales dominate, being replaced
by tubular or bronchial breath sounds)

Resolution
Less well defined dullness

/ tubular

breath sounds disappear

Crepitant rales reappear
= other characters
coarse, unequal, mucous

Recovery in crisis
= sudden
Before AB / pt. died in crisis
The patient state of health is aggravated suddenly
Rapid temperature rise at 400
delirium

Abundant sweating

Fever normal
Normal pulse

Recovery in lisis
Without particular clinical signs
Apparent state of health is improving
Body temperature begins to fall
Cough diminishes, then disappears

LABORATORY FINDINGS
INFLAMATION: leukocytosis with
neutrophils, VSH, fibrinogen, CRP
BIOCHIMIE: indirect bil.,
creatinine, urea (oliguria)
SPUTUM:
-Bacteriological examination: Grams method, culture
=pneumococci
-Cellularity: red cells, alveolar cells, leucocytes

CONFIRMATION
X-ray of the chest
= triangular density
1. The base towards the pleura
2. The tip towards the hil
3. Subcostal intensity, homogenous
4. May occupy an entire segment / lobe

Strep. pneumoniae

pneumonia.
Right upper-lobe
consolidation
demonstrating a
pronounced air
bronchogram and absence
of
volume change.

Bacterial pneumonia. Pneumococci on sputum Gram stain.

Bacterial pneumonia.
A posteroanterior chest radiograph shows left lower pneumonia.
Sputum Gram stain showed gram-positive diplococci.

PARTICULAR FORMS
ABORTIVE FORMS
spontaneous healing without AB
THE ELDER PNEMUMONIA
discreet presentation, severe evolution
CHILD PNEUMONIA
abdominal pain, vomiting, meningeal signs
ALCHOOLICS
mental disorders, psychomotor agitation

EVOLUTION

NATURAL
-Death in crisis
-Complication

UNDER TREATMENT
-Immunocompetent
Youngers
= healing in 5-6 days
-Complications at
elders,
immunosuppressed

COMPLICATIONS
Sepsis bacteriemia:
pericarditis, endocarditis,
meningitis, brain abscess,
parotitis, nephritis,
Circulatory collapse
Abscess
Pleural effusion
- Early -parapneumonic
= sterile serocitrine effusion
-Late: metapneumonic
=usually, purulent fluid

STAPHYLOCOCCAL PNEUMONIA
May begin insidiously
Grave state of health
Clinical = dyspnea and cyanosis are the chief
symptoms
Remitent fever
Sputum may be bloody or frankly purulent
Physical signs: consolidated foci, dull areas,
bronchial respiration, fine crackles and coarse
crackles
X-ray = Multiple foci of patchy consolidation
pneumatoceles pneumotorax

= in fact, bronchopneumonia

PNEUMONIA WITH KLEBSIELLA PNEUMONIAE

(Friedlander)
Most frequently found in pts. with increased
susceptibility (chronic diseases, underfed persons)

Characteristic = severe state of health with

prostration, often with collapse septic
patients
Intense cyanosis and dyspnea
Sputum is thick, gelatinous, brick red, and
laced with pus
Consolidation syndrome is not often present
X-ray: densities that occupy more than one lobe,
often, an entire lung
Tendency to form abscess and to be a chronic form

TREATMENT-GENERAL PRINCIPLES
Oxygen
Hydration
Symptomatic (antipyretics,

anticoughing, drugs that fluidly sputum)

Complications treatment

ETIOLOGIC = ANTIBIOTICS

ETIOLOGICAL SPECIFIC treatment

if the etiological agent is identified + antibiogram

Strep.pneumoniae
Penicillin sensitive =
AMP iv, amox po, M, pen G iv, doxi, O Ceph
P resistant : FQ (moxi) / P ceph 3

H influenzae
-lactamase + : AM/CL, O Ceph 2/3, P Ceph 3
-Lactamase : AMP iv, amox po, TMP/SMX, M
Amp- ampiciline
AM/CL- augmentin
P Ceph 3- 3rd generation cephalosporin

FQ- fluoroquinolone ( Moxi- moxifloxacine)

Tmp/smx- trimetoprim/sulfametoxaxol

ATYPICAL INTERSTITIAL
PNEUMONIAS
(NON BACTERIAL)

ETIOLOGIES
commonly, viral,
Also with: chlamydia, mycoplasmae
CLINICAL MANIFESTIONS:
Fever
Cough with mucous expectoration or
mucopurulent
Bronchitis syndrome
Asthenia, nocturne diaphoresis

The pulmonary infiltrative processes

dont realize
parenchymatous consolidation
syndrome

CLINICAL DIAGNOSTIC
Significant epidemiological element
Suggested by the association of:
Rinitis
Erythematous angina
Bronchitis

There is a poor correlation between

clinical signs and X-ray chest

X-ray chest
Accentuated pattern
Linear and reticular densities
Hilar-basal,
uni or bilateral

Sometimes, the densities are micro- or

macronodular with transitory character

A 38-year-old patient with Mycoplasma pneumonia.

Chest radiograph shows a vague, ill-defined opacity

Measles pneumonia. An example of a widespread primary viral

pneumonia with extensive bilateral confluent consolidation.

BRONCHOPNEUMONIA

BRONCHOPNEUMONIAS
Anatomic and clinical syndrome caused by various diseases,
with unpredictable evolution, reserved prognosis
Affect extreme ages or immunodepressed persons
May be: primary / secondary
PRIMARY:
Children, elders, immunodepressed (microbial associations)
Secondary
-more commonly
-predisposing causes:
various pulmonary infections (microbial, viral)
Aspiration
Toxic substances inhalation

BRONCHOPNEUMONIAS
SYMPTOMS

discreet/ absent

with severe state of health

Untypical, insidious ONSET

Grave, severe STATE OF HEALTH
CHILLS, pleuritic pain may miss
Gradually increase of FEVER, it is
irregular, it increases each time a new
focus reappears, decreases at the end of
the disease

COUGH with mucopurulent sputum with

hemorrhagic striae
Intense central CYANOSIS (lips and
extremities)

DYSPNEA
with
Severe POLYPNEA (> 35respirations/min)
= on the first plane + suprasternal and
intercostal retraction and grunting (newborn)

/ or permanent dyspnea with

exacerbations

BRONCHOPNEUMONIAS
PHYSICAL SIGNS

Fluctuating

There is no correlation
between the gravity of
general signs+dyspnea
and physical signs
Varying with time and
location, changing the
characters from day to
day, sometimes in hours

They vary with the

degree of process
extension

PERCUSSION
Only in confluent bronchopneumonias,
there are dull areas that mimic lobar
pneumonia
Usually, foci are localized in inferior
lobes (exceptions: scarlet rash, barking
cough)

AUSCULTATION :
Bronchial breath sounds
= the expression of bronchitis
- Crackles surrounding the territory of
lobular focus

Fine and Coarse CRACKLES

Conclusion
Disparate zones of congestion
Bronchial vesicular sounds,
Fine bubbling rales, coarse
crepitants,
and dull areas

BRONCHOPNEUMONIAS
Chest X-ray
There is no correlation between clinical
presentation and Xray

Xray chest: multiple patchy opacities,

with irregular outlines and less well
limited
Sometimes, there are opacities more
dense

BRONCHOPNEUMONIAS
COMPLICATIONS
EARLY ONSET : LOCAL / GENERAL
LATE ONSET : bronchiectasis
E.g.:
Septic shock with tachycardia, hypotension,
collapse, renal failure,
failure heart failure
Hypoxemia with hypercapnia
Children: acute cor pulmonale
Prognosis was severe before antibiotics use improved
with etiological and complications treatment (supportive)

INFLAMATION: leukocytosis with

polymorphonuclears, VSH, fibrinogen, CRP
BIOCHIMIE: indirect bil.,
creatinine, urea (oliguria)
SPUTUM:
-Bacteriological examination: Gram method, culture
=pneumococ
-Celullarity: red cells, alveolar cells, leukocytes

Classification CS

Not retractile
Well delimitated
Not well delimitated
Retractile

PULMONARY INFARCTION
Consolidation syndrome caused by alveolar air
replacement with blood
Sudden occlusion of a part of pulmonary arterial tree
Predisposing factors (diseases that favor thrombosis
deep venous thrombosis)

PULMONARY INFARCTION
CLINICAL
CHEST PAIN
Pleuritic chest pain aggravated by cough/respiration
Lateral decubitus on the healthy side)

DYSPNEA
ANXIETY
HEMOPTOSYS after a few hours of chest pain
onset /
Or dry cough with pleural character

PULMONARY INFARCTION
Conjunctival jaundice
Lips cyanosis
Tachycardia
Fever
Sometimes, right heart failure signs

PULMONARY INFARCTION
SMALL INFARCT
Sub dullness

tactile fremitus

Coarse respiration
Pleural rub

PULMONARY INFARCTION
LARGE INFARCT
Sub dullness

tactile fremitus
Tubular breath sounds
Rales, fine crepitants
Pleural rub

Pleural effusion syndrome

PULMONARY INFARCTION
DIAGNOSTIC
The clinical manifestations of underlying
disease
X ray chest
Triangular density with the base towards
the pleura
dilated pulmonary artery

PULMONARY INFARCTION
TREATMENT
Of underlying disease
ANTICOAGULANT
HEPARINS (UFH, LMWH)
ORAL ANTICOAGULANTS

Classification

Not retractile
Well delimitated
Not well delimitated
Retractile

II.
PULMONARY
CONSOLIDATIONS CAUSED BY
TUMORAL PROCESSES

BRONCHOPULMONAR NEOPLASM
Association of syndromes
Retractile consolidation syndrome / non

retractile
Pleural effusion syndrome

Mediastinal pulmonary syndrome

Cavity syndrome

According to localization neo. are:

Hilar
Peripheral nodule
Lobar
Segmental

Consolidation pulmonary syndrome = Rare

CHIEF COMPLAINTS
COUGH
Irritation of X nerve

PAIN
Appears tardily
permanent, not related to the respiration

HEMOPTISYS
currant jelly aspect

DYSPNEA
If there is an involvement of principal bronchia

Physical signs
LOCALIZED BRONCHIC OBSTRUCTION SYNDROME

PARTIAL OBSTRUCTION
Localized wheezing
Local hyperresonance
Sibilants + localized bronchial breath sounds
tactile fremitus, vesicular breath sounds localized

TOTAL OBSTRUCTION
= Atelectasis
Dullness or flatness, without fremitus, absent breath sounds

COMPLICATION OF THE OBSTRUCTION

Repeated pneumonias in the same place
Abscesses

SDR. CAUSED BY LOCAL INVASION

THE INVASION OF MEDIASTINUM

Recurent N. = vocal cords palsy, hoarseness

Phrenic = diaphragm palsy, pain irradiated to neck
Esophagus = deglutition disorders
X nerve = Dyspnea, constipation
Cervical sympatic = Claude-Bernard- Horner sdr.
Trachea = stridor, dyspnea
Superior cave vein = turgescent jugulars, pelerine

Pleura = pleural effusion syndrome

Pericardium= pericardial effusion/ tamponade
Myocardium = arrhythmias
Towards the superior thoracic outlet = sdr.Pancoast

edema

( the 1st-2nd rib lysis)

SIGNS FROM
LYMPHATIC SPREAD

Ganglions:
hilar,
mediastinal,
supraclavicular

Carcinomatous lymphangitis
(dyspnea,

Respiratory failure)

HEMATOGENOUS SPREAD
liver, brain, SR, bone

SYSTEMIC SYNDROMES
weight
Fever
Endrocrine syndromes
Neurologic paraneoplastic syndromes= peripheral neuropathy
Myasthenic Eaton-Lambert syndrome, polymyositis
Rheumatic syndromes
Pierre Marie hypertrophic osteoarthropathy
Dermatological syndr.: dermatomyositis, achantosis nigricans
Migratory venous thromboplebitis (Trouseau)
Nonbacterial thrombotic (marantic) endocarditis
Hematologic manifestations: anemia, thrombocytopenia,
disseminated intravascular coagulation
Membranous glomerulopathy

 DIAGNOSTIC
Clinical suspicion confirmed Rx, CT,
bronchoscopy ( sputum), mediastinoscopy
TREATMENT

Chemotherapy
Surgery
Radiotherapy pre-surgery / palliative

RETRACTILE PULMONARY
CONSOLIDATIONS
ATELECTASIS
Classification

Not retractile
Well delimitated
Not well delimitated
Retractile

PULMONARY ATELECTASIS
Alveolar air resorption due to mechanical
causes (commonly bronchial obstruction)

Consolidation syndrome with the traction

of surrounding tissues/organs towards the
involved side
Most symptoms are related to onset
rapidity

PULMONARY ATELECTASIS
Lobar, segmental ATELECTASIS
Pain
Dry cough
Cyanosis

Small ATELECTASIS
=asymptomatic, occasional
finding on X-ray

PULMONARY ATELECTASIS
Affected hemithorax smaller in volume
Supraclavicular area depression on the involved side

Retraction of intercostal spaces

thorax expansion
Palpation: tactile fremitus / absent
Percussion : dullness
Ascultation: / absent breath sounds

PULMONARY ATELECTASIS
X-RAY
Homogenous density with concavity towards the

exterior

9 involves 1 segment, / one lobe,/ the entire lung

9 With a smaller extension than the respective region
(in normal conditions)

Narrow and oblique intercostal spaces

Mediastin shifted toward involved side
Ascended diaphragm
Inspiratory movement of mediastin toward the

involved side

Atelectasis. Left lower lobe collapse.

The opacity is in the posterior inferior location.

Atelectasis. Loss of volume on the left side; an elevated and silhouetted left
diaphragm; and an opacity behind the heart, called a sail sign,
are present.

Atelectasis. Left upper lobe collapse showing opacity contiguous

to the aortic knob, a smaller left hemithorax, and a mediastinal shift.

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.

DISORDERS
DISORDERS OF
OF THE
THE PLEURA
PLEURA

CLASSIFICATION
1.Pleuritic syndrome (dry)
2.Pleural effusion
3.Pleural fibrosis
4.Pneumothorax

Anatomy
1. Parietal pleura
- pleural space
- pleural fluid: 5 -20 ml

2. Visceral pleura
Both parietal and visceral membranes are smooth, glistening, and
semitransparent. Despite these similarities, the two membranes have
unique differences in anatomic architecture, innervation, pain fibers, blood
supply, lymphatic drainage, and function. For example, the visceral pleurae
contain no pain fibers and have a dual blood supply (bronchial and
pulmonary).
Parietal pleurae cover the inner surface of the thoracic cavity, including the
mediastinum, diaphragm, and ribs.
Visceral pleurae envelop all surfaces of the lungs, including the interlobar
fissures.
This lining is absent at the hilus, where pulmonary vessels, bronchi, and
nerves enter the lung tissue.
The mediastinum completely separates the right and left pleural spaces.

FUNCTION OF PLEURAL FLUID

is to provide a frictionless surface between
the two pleurae in response to changes in
lung volume with respiration.

Normally, pleural fluid:

spreads thinly over visceral and parietal pleurae
enters the pleural space from systemic
capillaries in the parietal pleurae
exits via parietal pleural stomas and lymphatics
facilitate movement between the lung and chest
wall

composition plasma but lower in protein (< 1.5 g/dL)

Characteristics of
Normal pleural fluid

clear ultrafiltrate of plasma

pH 7.60-7.64
protein content less than 2% (1-2 g/dL)
fewer than 1000 WBCs per cubic millimeter
glucose content similar to that of plasma
LDH level less than 50% of plasma
Na, K, Ca concentration similar to interstitial fluid

Symptoms:
- Pleuritic chest pain
- Dry cough
- Dyspnea

Signs:

- Pleural friction rub

- Particular signs - Pleural effusion syndrome
- Pleural fibrosis syndrome

PLEURITIC CHEST PAIN

Character : a vague discomfort OR sharp pain
Worsens by deep inhalation, chest expansion
Location: depending on affected pleura
indicates inflammation of the parietal pleura
usually felt over the inflamed site E.g.
9 Diaphragmatic pleura shoulder
9 Central pleura radiates back, neck, shoulder
9 intra-abdominal referred from irritation of lower 6 ic nerves

Special situations:
Miss in interlobar effusion
Continuous,
Continuous not influenced by respiration in:
Pleural tumor
Empyema
Massive Pleural effusion

PLEURITIC CHEST PAIN

Differential diagnosis
rib fracture = Fixed point location+ bone crepitation
Costochondritis local inflammation
Herpes zoster = pain on nerves + vesicles
Tracheobronchitis - burning over trachea + sputum
Angor pectoris
Pericarditis

PLEURITIC COUGH

dry, without sputum production

Irritative
Associated usually with pleuritic chest pain
DETERMINED by: Pleural irritation

DYSPNEA in pleural syndromes

Progressive
Generated by pain
Associated tachypnea
Associated with large effusion installed rapidly
It indicates a large effusion (usually not <500 mL)
Displaces mediastinum, if exceeds 2000 ml
Pleural effusion compresses the lung
Interferes with diaphragmatic musculature activity
Reduces vital capacity (VC)
Hypoxemia that do not respond to oxygen administration

SIGN - PHYSICAL EXAMINATION

Pleural friction rub

Corresponding to the pain location

Intensity maximum on posterior axillary line
Present throughout respiratory cycle
Loudest at end inspiration and early expiration
Great variability
Seldom present
When present, best heard over the area of pleural
inflammation, over posterior inferior aspect
of thoracic cage, or over inferior lateral anterior
surface of thoracic cage
Described as a rubbing or grating (eg, leather rubbing
on leather), harsh, dry, and scratchy sound that
disappears with breath holding

Pleural effusions
DEFINITION
Pleural effusion is defined as an abnormal
accumulation of fluid in the pleural space.
Excess fluid results from the disruption of
the equilibrium that exists across pleural
membranes.

Frequency
annual incidence: 320 per 100,000 people

Mortality/Morbidity
directly related to cause, stage of disease, and
biochemical findings in the pleural fluid.

Sex
M = F (incidence equal between the sexes)
Exception: some causes with sex predilection

Age
Pleural effusions usually occur in adults.

MECHANISMS OF PLEURAL EFFUSION:

1. Altered permeability of the pleural membranes
2. Reduction in intravascular oncotic pressure
3. Increased capillary permeability or vascular disruption
4. Increased capillary hydrostatic pressure in the systemic
and/or pulmonary circulation
5. Reduction of pressure in pleural space; lung unable to expand
6. Inability of the lung to expand (e.g., extensive atelectasis, mesothelioma)
7. Decreased lymphatic drainage or complete blockage, including thoracic
duct obstruction or rupture
8. Increased fluid in peritoneal cavity, with migration across the diaphragm
via the lymphatics
9. Movement of fluid from pulmonary edema across the visceral pleura
10. Persistent increase in pleural fluid oncotic pressure from an existing pleural
effusion, causing accumulation of further fluid
11. Iatrogenic causes

Pleural effusions

Causes multiple
Classification:
1.Transudates
2. Exudates

Pleural effusions

CLINICAL ASPECT
ASPECT -CLINICAL

History

1. Manifestations related to the underlying disease process

2. Dyspnea
Most common clinical symptom at presentation
Can be determined by other underlying lung disease
3. Chest pain
Intensity: May be mild or severe
Character: Typically sharp or stabbing
Localized to the chest wall or referred to the ipsilateral
shoulder or upper abdomen because of diaphragmatic involvement
Exacerbated by deep inspiration
Diminishes in intensity as the effusion increases in size
Offers etiological clue:
transudates do not cause direct pleural irritation

Pleural effusions

CLINICAL ASPECT
ASPECT -CLINICAL

Physical findings

are variable
depend on the volume of the pleural effusion
undetectable for effusions smaller than 300 mL
EFFUSION LARGER THAN 300 ML
1. Dullness or decreased resonance to percussion
2. Diminished or inaudible breath sounds
3. Decreased tactile fremitus
4. Egophony
5. Pleural friction rub
6. Asymmetric expansion of thoracic cage,
with lagging expansion on the affected side (i.e., Hoover sign)
7. Mediastinum shift

 Egophony
("e" to "a" changes) at the most superior aspect of the pleural effusion
(This finding signifies atelectasis and consolidation caused by
compression of lung parenchyma with subsequent decrease in gas
content per unit volume.)

Pleural friction rub

Present throughout respiratory cycle
Loudest at end inspiration and early expiration
Seldom present
Best heard over the area of pleural inflammation, over posterior inferior
aspect of thoracic cage, or over inferior lateral anterior surface of
thoracic cage

Pleural effusions

Physical findings
findings
Physical
For small,
small, medium
medium and
and large
large effusion
effusion
For

Small pleural effusion (under 500 ml)

DULL AREA
Posterior only (usual)
Basal
3- 4 cm high
dullness upper limit = Horizontal line
Not mobile with respiration
Diferential diagnosis with:

Ascended diaphragm ( perform Hirtz maneuver)

Atelectasis (dullness with increased tactile fremitus)

Small effusion

Posteroanterior upright chest radiograph shows

isolated left sided pleural effusion
and loss of left lateral costophrenic angle.

Small pleural effusion

Pseudotumor

Pseudotumors represent an accumulation of

fluid between interlobar fissures or fluid encapsulated
by adhesions.

Pleural effusions

Physical findings
findings
Physical
For small,
small, medium
medium and
and large
large effusion
effusion
For

Medium pleural effusion (800- 1200 ml)

DULL AREA
Posterior

Upper limit :
the tip of scapula,
Damoiseau line = parabolic line of which the
highest point is on the middle axillary line

Anterior:

Dullness up to the 5th rib

With every 500 ml accumulation dullness
increases with one intercostal space
When dullness is up to the 1st rib = 3000 ml fluid
Traube area disappears when fluid reaches 800 ml
Mediastinal shift (usually >1000 mL)

Damoiseau-Ellis line
Also known as:
Damoiseaus curve
Ellis sign
Ellis-Damoiseau line
Ellis-Damoiseaus parabolic curve
Garlands curve
Associated persons:
Louis Hyacinthe Cleste Damoiseau
Calvin Ellis
George Minott Garland

Bibliography:
* L. H. C. Damoiseau:
Recherches cliniques sur plusieurs points du diagnostic
des panchements.
Extrait des Archives gnrales de mdecine, Paris, 1844.
Du diagnostic et du traitement de la plresie. Paris, 1845.
* C. Ellis:
The line of dulness in pleurite effusion.
Boston Medical and Surgical Journal, 1874, 90: 13-14.
The curved line of pleuritic effusion.
Boston Medical and Surgical Journal, 1876, 95: 689-697

Description:
The upper limit of the percutatory demonstrable upper limit of a
pleuritic exudate. A characteristic parabolic line of which the
highest point is in the middle axillary line.
Garlands curve is entered as Garlands triangle under George Minott Garland,
American internist, 1848-1926.

PA chest radiography shows an opacity (E) in the lower left hemithorax

with obliteration of the left hemidiaphragm and curvilinear upper margin
consistent with effusion.
Note the extension of the fluid into the left major fissure (arrow)
and mediastinal shift to the right.

Pleural effusions

CLINICAL ASPECT
ASPECT -- Physical
Physical findings
findings
CLINICAL

Large pleural effusion (2000 ml)

Dull area greater then previous

Infraclavicular tympanitic
Subclavicular tympanitic
Mediastinal shift
Seen only with massive effusions (usually >1000 mL)
Chest radiographies displacement of trachea and
mediastinum to the contralateral side of the pleural
effusion
(In contrast with complete atelectasis of the ipsilateral lung,
when the trachea deviates toward the affected side and is
most commonly seen with complete obstruction of ipsilateral
mainstem bronchus caused by bronchogenic carcinoma.)

Large pleural effusion

Loculated collections
Parietal collection
Diminished respiratory movement
Diminished tactile fremitus
Interlobar collection
Suspended dullness in medium part of axila
Without pain
Diaphragmatic collection
Pain by phrenic nerve irritation

Dry pleuritic syndrome

Pleuritic chest pain

Cough not productive, irritative
Pleural friction rub
RX: + / - diminished diaphragmatic movement

Pleural effusions
Detection
1. Physical examination
2. Chest x-ray
3. Ultrasonography can be used to detect as little as 5-50 mL
of pleural fluid, with 100% sensitivity for effusions of 100 mL or
more.

4. Chest CT scanning
5. Thoracentesis
6. Evaluation of pleural fluid to determine cause

Chest x-ray
blunting of the costophrenic angle and/or sulci
(sharp angle between the diaphragm and rib cage)
blunting becomes more pronounced as fluid accumulates
an upwardly concave meniscus seems to ascend the
lateral chest wall; this is called the meniscus sign.
Clues indicating pleural effusion include
generalized homogenous opacity
diffuse haziness as the fluid forms layers posteriorly
visibility of pulmonary vessels through the haziness,
absence of air bronchogram.
Diaphragmatic inversion because of the weight of the
pleural effusion on the left side. The superior border of the
diaphragm become upwardly concave, and paradoxical movement
occurs with respiration; the diaphragm rises with respiration and falls
with expiration. When the pleural fluid is removed, the diaphragm
assumes its normal shape.

Chest x-ray

Upright posteroanterior or anteroposterior rg may not show lateral

costophrenic angle blunting until 250-500 mL of fluid is present.
Haziness is less apparent as it progresses cephalad.
Lateral radiographs show blunting of the posterior costophrenic angle
and the posterior gutter when as little as 175-200 mL of fluid is present.
Bilateral decubitus rg. are recommended, with larger effusions.
They provide clues to exclude a loculated effusion and underlying
pulmonary lesion or pulmonary thickening and can depict as little as 510 mL of fluid.
Recumbent (supine views) usually are obtained in critically ill patients.
Findings may include costophrenic angle blunting (earliest finding),
generalized homogenous opacity, obliteration of the diaphragmatic
silhouette, decreased visibility of the lower-lobe vasculature, widened
minor fissure, apical capping, and hemidiaphragmatic elevation.

Posteroanterior radiographs may depict the following:

Flattening of the medial diaphragmatic aspect, with gradual upward
and lateral inclination from the cardiac shadow; lateral displacement
of the diaphragmatic dome apex (middle or inner hemithoracic third
to lateral third)
Change of the normal, domelike diaphragmatic curve to a
hockey-stick shape
Sharp diaphragmatic sloping toward the lateral costophrenic angle
Hemidiaphragm elevation
Increased distance (>2.0 cm) between the gastric fundus air bubble
and superior right hemidiaphragmatic margin
Absence of lower-lobe vessels normally present below the diaphragm
Lateral radiographs may depict sharp angulation of the anterior
diaphragmatic portion (ie, Rock of Gibraltar or middle-lobe step sign).

Thoracentesis

Thoracentesis (also known as thoracocentesis or pleural tap)

is an invasive procedure to remove fluid or air from the pleural space for diagnostic
or therapeutic purposes. A cannula, or hollow needle, is carefully introduced into
the thorax, generally after administration of local anesthesia.
The procedure was first described in 1852.
The recommended location varies depending upon the source.
Some sources recommend the midaxillary line, in the sixth, seventh, or eighth
intercostal space.
http://picasaweb.google.com/clinicalcases/ThoracentesisAStepByStepProcedureGuide#

Empyema
= purulent pleural effusions
present on X-ray of 20-60% of patients
with bacterial pneumonia
often solves with antibiotic therapy
Risk factors: aspiration,
immunocompromised patients

Empyema
Exudative stage: free flowing pleural fluid, very
amenable to treatment with closed tube drainage
Fibrinopurulent stage: formation of fibrin strands
through the pleural fluid resulting in loculations, makes
adequate drainage with single chest tube unlikely
Organizational stage: fibrosis is much more extensive
forming a pleural peel that restricts expansion even if
fluid can be evacuated

Empyema
Decubitus films will be helpful in determining
if fluid is freely flowing or loculated
Pleural fluid that is gross pus with positive
cultures or gram stain is considered
empyema along with other findings: pH<7.1,
glucose<40 and LDH>1000

Empyema
Treatment:
- drainage of pus by chest tube reexpansion
of lung
- eradication of the infection.
Treatment of organizational stage requires
surgical intervention with removal of the
fibrous peel

Pneumothorax
DEFINITION
= the presence of air within the pleural space resulting
in collapse of the lung on the affected side
- it is considered one of the most common forms of
thoracic disease.

Pneumothorax
Classification
1. Spontaneous pneumothorax
Primary
Secondary
2. Traumatic pneumothorax
Resulting from direct (blunt) chest trauma
Resulting from penetrating chest trauma
3. Iatrogenic pneumothorax
Resulting from biopsy procedure
Resulting from therapeutic procedures
4. Catamenial pneumothorax
5. Pneumothorax in AIDS

Pneumothorax
History
Acute onset of chest pain
- Severe and/or stabbing pain, radiating to ipsilateral
shoulder and increasing with inspiration (pleuritic)
Sudden shortness of breath
# Anxiety, cough, and vague presenting symptoms (e.g.,
general malaise, fatigue) are less commonly observed.
# Dyspnea tends to be more severe with secondary
spontaneous pneumothoraces because of decreased lung
reserve.

Pneumothorax

Physical
General appearance
Diaphoretic
Splinting chest wall to relieve pleuritic pain
Cyanotic (with tension pneumothoraces)
Vital signs
Tachypnea
Tachycardia (most common finding) - If faster than 135 (bpm),
tension pneumothorax is likely.
Pulsus paradoxus
Hypotension (often with tension pneumothorax)
Asymmetric lung expansion - Mediastinal and tracheal shift to the
contralateral side with a large tension pneumothorax
Distant or absent breath sounds
Hyperresonance on percussion
Decreased tactile fremitus
Cardiovascular - Jugular venous distension (tension pneumothorax)
Neurologic - Altered mental status

Pneumothorax
Pulmonary Signs

Physical

Mild pneumothotax no obvious signs

Voluminous on the affected side appear
Fullness of the chest
Wide intercostal spaces
Diminished respiratory movement
Diminished or no vocal fremitus or resonance
Trachea and heart displace toward the healthy side
Tympanic sound on percussion
Liver dullness edge displaces downward when pneumothorax
is on the right side.
Breath sound is diminished or disappeared on the affected side
Coin sign is positive.

Small spontaneous primary pneumothorax.

Pneumothorax

A large right-sided pneumothorax has occurred from a rupture of a subpleural bleb.

Pneumothorax

A true pneumothorax line. Note that the visceral pleural line is observed clearly,
with the absence of vascular marking beyond the pleural line.

Pneumothorax

Pneumomediastinum from barotrauma may

result in tension pneumothorax and obstructive shock.

Table and pictures

A dull sound due to pleural effusion is usually located at

its highest point at the axillar line. On chest radiograph,
the dull sound represents the highest point of the EllisDamoiseau line. At the paravertebral line, just at the
border of the lung, an area with lesser dullness at the
side of the effusion may be heard (Figure). This has been
named the Garlands triangle. On the contralateral side,
an area of dullness over the normal lung (Groccos
triangle) may be detected.

inspection
Chest appearance

Respiratory movement

Consolidation

Symmetrical

Diminished on the
affected side

Emphysema

Barrel-shaped

Diminished on both
sides

Atelectasis

Denting of the affected side

Diminished on the
affected side

Pleural effusion

Fullness of the affected side

Diminished or
disappeared on the
affected side

Thickened
pleura

Denting of the affected side

Diminished on the
affected side

pneumothorax

Fullness of the affected side

Diminished or
disappeared on the
affected side

palpation
Trachea location

Vocal fremitus

Consolidation

Central

Increased on the
affected side

Emphysema

Central

Diminished on both
sides

Atelectasis

Deviate toward the

affected side

Diminished or
disappeared

Pleural effusion

Deviate toward the

normal side

Diminished or
disappeared

Thickened
pleura

Deviate toward the

affected side

Diminished

pneumothorax

Deviate toward the

normal side

Diminish or disappeared

Percussion

Auscultation

Note

Breath sound

rale

Vocal resonance

Consolidation

Dullness or
flatness

Bronchial
breath sound

Moist rale

Strengthened

Emphysema

Hyper
resonance

Diminished

Always
without

Diminished

Atelectasis

Dullness

Disappeared or
diminished

Without

Disappeared or
diminished

Pleural
effusion

Flatness

Diminished or
disappeared

Without

Diminished or
disappeared

Thickened
pleura

Dullness

Diminished

Without

Diminished

pneumothorax

Tympany

Diminished or
disappeared

Without

Diminished or
disappeared

Inspection

Palpation

Percussion

Auscultation

Chest
appearance

Respiratory
movement

Trachea
location

Vocal fremitus

Note

Breath sound

rale

Vocal
resonance

Consolidation

Symmetrical

Diminished on
the affected side

Central

Increased on
the affected
side

Dullness or
flatness

Bronchial breath
sound

Moist
rale

Strengthened

Emphysema

Barrel-shaped

Diminished on
both sides

Central

Diminished on
both sides

Hyper
resonance

Diminished

Always
without

Diminished

Atelectasis

Denting of the
affected side

Diminished on
the affected side

Deviate
toward the
affected side

Diminished or
disappeared

Dullness

Disappeared or
diminished

Without

Disappeared or
diminished

Pleural
effusion

Fullness of the
affected side

Diminished or
disappeared on
the affected side

Deviate
toward the
normal side

Diminished or
disappeared

Flatness

Diminished or
disappeared

Without

Diminished or
disappeared

Thickened
pleura

Denting of the
affected side

Diminished on
the affected side

Deviate
toward the
affected side

Diminished

Dullness

Diminished

Without

Diminished

pneumothorax

Fullness of the
affected side

Diminished or
disappeared on
the affected side

Deviate
toward the
normal side

Diminish or
disappeared

Tympany

Diminished or
disappeared

Without

Diminished or
disappeared

Right middle-lobe atelectasis

in a 70-year-old female with
chronic obstructive lung
disease. (A) The frontal chest
radiograph shows minimal
blurring of the right heart
border. (B) The lateral chest
radiograph shows that the
right middle lobe is
completely collapsed. The
depressed minor fissure
(arrows), and the anteriorly
displaced major fissure
(arrowheads) are almost
apposed.

45-year-old man with left upper-lobe collapse due to endobronchial sarcoidosis.

(A) The chest radiograph shows hazy opacity over the left chest, with obscuration of the
left heart border. The apex of the left lung appears lucent because it is occupied by the s
uperior segment of the hyperinflated left lower lobe. The aortic arch is sharply outlined
by the hyperinflated left lower lobe. (B) The lateral view shows the hyperinflated left
lower lobe interfacing anteriorly with the collapsed left upper lobe along the major fissure
(arrows). (C) An axial CT scan shows the complete left lower-lobe collapse, and
endobronchial obstruction of the left upper-lobe bronchus (arrow). No extrinsic
component is shown.

Bilateral lower-lobe collapse,

presumed due to mucoid impaction,
in a 63-year-old man following
abdominal surgery. (A) The frontal
chest radiograph shows the
triangular outlines of the collapsed
lower lobes (sail sign) (arrows).
Both hila are depressed. The medial
portions of the diaphragm are
obscured. The collapsed left lower
lobe is almost exactly superimposed
on the heart. (B) A lateral chest
radiograph shows the collapsed
lobes overlying the spine (arrows).
The posterior portions of both
hemidiaphragms are obscured.

Combined right middle and right lowerlobe collapse in a 66-year-old woman

with breathlessness following
abdominal surgery. The frontal chest
radiograph shows combined right
middle lobe and right lower-lobe
collapse. Arrows indicate the minor
fissure. Arrowheads indicate the major
fissure. The multilobar collapse
simulates a right pleural effusion, but
the marked inferior hilar displacement,
the marked depression of the right
major fissure, and the ipsilateral
mediastinal shift are important clues
that this is a volume-losing process. A
decubitus view showed only minimal
right pleural fluid

Strep. pneumoniae pneumonia.

Bilateral lower-zone consolidation (arrows). Although
pneumococcal pneumonia is typically unifocal, multifocal
involvement is not uncommon.

Strep. pneumoniae

pneumonia.
Very extensive
consolidation affecting
more than one lobe in
the right lung. The
central lucency is due to
cavitation an unusual
feature in pneumococcal
pneumonia.

Staph. aureus pneumonia.

This cavitary pneumonia

was
a community-acquired
infection occurring two
weeks after an influenza
A infection.

Staph. aureus pneumonia

pneumatoceles.
Appearances following
incomplete resolution of a
staphylococcal pneumonia.
There are several thin-walled
cysts consistent with
pneumatoceles. Such
pneumatoceles are common in
children but unusual in adults.

Staph. aureus

infection in a drug
abuser.
Multiple disseminated
nodular
consolidations,
confluent in the right
lower zone; several
have cavitated. The
appearances are
typical of
haematogenous
dissemination.

Gram-negative
pneumonia
(Haemophilus
influenzae)
showing a typical
bronchopneumonic
pattern of
heterogeneous localized
consolidation. Such
infections are commonly
basal.

Legionella pneumophila pneumonia. While the unilateral lowerzone peripheral consolidation is a typical appearance, it completely
lacks specificity. Apparent cavitation was spurious.