ILD revisited print version.pptx

INTERSTITIAL LUNG
DISEASES
DR DEEPAK
SINGH
ASSO. Prof & HOD
GMC,
BHARATPUR

The interstitium Described by Weibel:-
 Peribronchovascular
interstitium and centrilobular
interstitium consist the
‘AXIAL FIBER SYSTEM’
 Subpleural interstitium and
interlobular septa consist the
‘PERIPHERAL FIBER
SYSTEM’
 Intralobular interstitium
equivalent to the ‘SEPTAL
FIBER SYSTEM’.
[ forms a mesh
around alveoli and
holds it in place]

PATHOGENESIS OF ILD’S
LARGELY UNKNOWN!!!- IDIOPATHIC
 Some understanding of the mechanism of
injury
 Initiating injuries are likely multiple=
 Inhaled
 Sensitization to allergens
 Circulatory
 With continued injury, “repair” process
continues with additional fibroproliferation, that
is unchecked

PATHOGENE
SIS
Epithelial cell apoptosis with loss of basement membrane
integrity:
Production of growth factors in response to alveolar epithelial
injury with hyperplastic type II cells and myofibroblast

 Heterogeneous group of more than 150 lung disorders
with variable degree of pulmonary fibrosis
 Incidence ranges from 1/3000-4000 per year in UK.
 Prevalence- 10 times that of clinically recognized disease-
tip of the iceberg disease.
 IPF -m/c - about 30 percent of new cases.
 Due to increasing numbers/use of cytotoxic drugs,
increased occurrence/detection of occupational lung
diseases and increasing life expectancy, as well as better
imaging, diagnostics and knowledge, the incidence of
these diseases is expected to rise

Events in pathogenesis
 Acute
 Edema, per se or a stage on the way to alveolar
edema
 Infection (e.g. mycoplasma)
 Inflammation
 Chronic
 Fibrosis, end stage of inflammation
 Often involves some degree of bronchiolitis.

ILD depends more on structural features
than functional assessment.
 Anatomical changes
 Histological
changes
 Malignant potential
 Mechanical
interference with
function
It’s the other way
round with airway
diseases-
functional
parameters will go
first
However, causes of
ILD may also cause
some airway
dysfunction.

Patterns of interstitial lung
disease

IIPs according to the ATS-ERS classification.

Syndromic diagnosis with
more common clinical
features
 Exertional dyspnea
 Bilateral diffuse infiltrates on chest radiograph
 Restrictive lung defects, ↓DLCO
 Abnormal (PAo2-Pao2)
 Absence of pulmonary infection and
neoplasia
 Histopathology: varied degrees of fibrosis
and inflammation, with or without evidence of
granulomatous or secondary vascular changes
in pulmonary parenchyma

Respiratory symptoms
Cough
 Raises possibility of
superimposed/ coexistent
airway disease
 1. RB-ILD
 2. Sarcoidosis
 3. H P
 4. LCH
 5. Lipoid pneumonia
Productive cough – long
standing IPF with traction
bronchiectasis
Exertional dyspnea
Chest pain
 Pleuritis – SLE , RA
& other CVD’s
 Pneumothorax
 Substernal chest
pain - sarcoidosis

Respiratory symptoms
(contd)
Wheezing
Airway diseases
 1. Churg-Strauss
 2. CEP
Endobronchial lesions
 1. Sarcoidosis
 2. Wegner’s
 3. Amyloidosis
Hemoptysis
 DAH (33% - no hemoptysis)
 LAM
 Tuberous sclerosis
 Pulmonary Veno-occlusive
disease
 Drugs such as D-pencillamine
Known case of ILD- R/o
1. Malignancy
2. Pulmonary embolism
3. Infection

Pulmonary signs
Crackles
 Velcro , end inspiratory,
predominantly bibasilar
 Common in many chronic
ILD
 80% of cases of IPF
 Less common in
granulomatous diseases
such as sarcoidosis,
 HP(25%)
Inspiratory squeaks
 Mid inspiratory, high
pitched
 Seen in Primary
bronchiolitis
 Airway centered
Clubbing
 Common – IPF (50%),
DIP(50%),
Asbestosis(43%),
chronic HP(some cases)
 Rare – RB-ILD
 Uncommon –
Sarcoidosis, Acute ILD,
COP, LIP, CVD-ILD
Cor pulmonale
 CVD- ILD (scleroderma)
 Veno occlusive diseases
 Advanced fibrosis
(IPF, vital capacity <50%,
DLCO <30%)

Extra pulmonary symptoms
 Arthritis – Sarcoidosis and CVD’s
 Ocular – Sarcoidosis, CVD,s & HLA-B27 associated
diseases
 Skin and muscle - Polymyosistis
 Sicca syndrome – Sarcoidosis, Sjogrens and other
CVD
 GERD – IPF and Scleroderma
 Lower GI symptoms -- IBD
 Recurrent sinusitis- WG
 Neurological symptoms – Sarcoidosis, Vasculitis
 Epilepsy & mental retardation – Tuberous sclerosis
 Diabetes inspidus – Sarcoidosis, PLCH

 AGE
Age - 20-40 Years
 1. Sarcoidosis
 2. CTD associated ILD
 3. LAM
 4. PLCH
 5. Inherited forms of ILD
Age >50 Years
 1. IPF – appx 2/3 of pts
are >60 years old at time
of diagnosis
 SEX
Male predominance
 PLCH
 Pneumoconiosis
 Rheumatoid arthritis –
ILD
Female predominance
 LAM
 Hermansky-Pudlak
syndrome
 Collagen vascular
disorders

Family history
Autosomal dominant pattern
(with or without incomplete penetrance)
 IPF
 Sarcoidosis
 Neurofibromatosis
Autosomal recessive pattern
 Niemann-Pick disease
 Gaucher's disease
 Hermansky-Pudlak syndrome

Occupational history
Detailed history of occupation should be taken in all
patients.
 Pneumoconioses – miners
 Silicosis – sand blasters & granite workers.
 Asbestosis – welders, electricians, mechanics,
workers with brakes, shipyard workers.
 Berylliosis – aerospace, nuclear, computer &
electronic industries
 Dental worker’s pneumoconiosis – dental workers
 Hypersensitive pneumonitis – farm workers, poultry
workers, bird breeders
The degree of exposure, duration, latency of
exposure, and the use of protective devices
should be elicited

Environmental exposure history
 Air conditioners
 Humidifiers
 Hot tubs
 Evaporative cooling systems
 Passive exposure in the family

Smoking
Current or former
smokers
 1. RB-ILD (100%)
 2. LCH ( 90%)
 3. DIP (90%)
 4. IPF
 Active smoking –
increased
complications in
GPS
Never or former
smoker
1. Sarcoidosis
2. H P

PRESENTATION
Acute presentation (days to
weeks)
 Acute IIP
 Eosinophillic pneumonia
 Hypersensitive pneumonitis
 BOOP
 CVD associated
Sub-acute presentation (weeks
to months)
 Sarcoidosis
 Drug induced ILD
 Alveolar hemorrhage syndromes
 Sub Ac HP
 COP
 CV-ILD
Chronic presentation (months
to years)
 IPF
 Sarcoidosis
 PLCH
 NSIP
 Occupation related ILD’s
Episodic DPLD’S
 Eosinophillic pneumonia
 Hypersensitivity pneumonitis
 Vasculitides/pulmonary
hemorrhages
 Churg-Strauss syndrome
 COP

ILD-PULMONARY FUNCTION
TESTING
Good correlation between degree
of fibrosis and Degree of
inducible arterial hypoxemia
Exercise induced physiological
abnormalities
 ↓Work rate & maximum oxygen
consumption
 High minute ventilation at sub
maximal work
 ↓ Peak minute ventilation
 Failure of tidal volume to ↑ at
sub maximal work, with
disproportionate ↑ in
respiratory rates
Interstitial pattern on CXR with
obstructive pattern
 ILD superimposed with COPD
 LAM (65-78%)
 Sarcoidosis (>50%)
 PLCH (4-33%)

BAL- cellular profile
Lymphocytosis (>20% of
cellularity)
 Hypersensitive pneumonitis (60-80%)
 Sarcoidosis (acute – 40-60%)
 IPF (15-30%)
 Berylliosis
 Amiodorane
 PLCH
 Lymphoma/pseudolymphoma
Neutrophilia (>5% of cellularity)
 IPF (15-40%)
 COP (40-70%)
 Inorganic dust disease
 PLCH
 Hypersensitivity pneumonitis (early)
 Sarcoidosis (advanced)
Eosinophilia (>5% of
cellularity)
High count (>30%)
 1. TPE (40-70%)
 2. EP (>40%)
Mild to moderate count (5-30%)
 1. IPF (<10%)
 2. Sarcoidosis
 3. PLCH
 4. Drug induced
 5. CVD-ILD
Mast cells (>1%)
 1. Hypersensitivity
pneumonitis
 2. COP (±)
 3. Advanced sarcoidosis

LABORATORY
 Hemolytic Anaemia- SLE, MCTD, IPF, Sarcoid
 Thrombocytopenia- CVD, Sarcoid
 Leukopenia- CVD, Sarcoid
 Leukocytosis- HP
 Abnormal urinary sediment- SLE, GPS, WG, MPA
 Hypergammaglobulinemia- CVD, IPF, SS, WG,
MPA, LIP
 Hypogammaglobulinemia- LIP
 S. Immune complex- IPF, HP, RA, SLE, EG,WG
 S. ACE- Sarcoid, HP, LIP, ARDS, Silicosis.
 ↑ S. LDH- IPF, PAP, AIP

Chest x ray
 CXR is normal:--
in 10 to 15 % of symptomatic patients with
proven infiltrative lung disease
 In 30% of those with bronchiectasis
~ 60 % of patients with emphysema
 All previous radiology to be reviewed
A NORMAL CXR DOES NOT RULE
OUT THE PRESENCE OF DPLD

 Most common radiological abnormalities are
Reticular shadowing
Nodular
Mixed (alveolar filling + interstitial
markings)
 The correlation between the roentgenographic
pattern and the stage of disease is generally
poor.
 Only honeycombing (small cystic spaces)
correlates with pathologic findings and, when
present, portends a poor prognosis.
Chest x ray

Normal CXR may
be seen in-
 HP
 Sarcoidosis
 CTD’s
 Bronchiolitis
obliterans
 IPF (early stage)
 Asbestosis
 LAM
Alveolar opacities
 Pulm. hemorrhage
 Eosino.
pneumonia
 BOOP
 Lupus pneumonitis
 Alveolar
proteinosis

Consolidative (Alveolar) Pattern
Mechanism -ALVEOLAR FILLING
May be mimicked by alveolar collapse, as in
airway obstruction
Features:
 Fluffy, cloud-like, coalescent opacities
 Complete air bronchograms
 IF sharp edges – position or normal fissures
 Distribution: lobar

W. Granulomatosis
E. pneumonia
BOOP,
BAC
PAP,
Aspiration
Lymphoma
Lipoid Pneumonia
Sarcoidosis
Chronic Alveolar Infiltrates

Interstitial Infiltrates
 Linear or reticular
 Nodular
 Mixed
 Honeycomb
 Cysts and traction
bronchiectasis
 GGO
CXR CLUES

Peripheral lung zone predominance
 1. Eosino. pneumonia
 2. BOOP
Upper zone predominance
 1. Granulomatous – Sarcoidosis, LCH, Chronic HP
 2. Pneumoconiosis – Silicosis, berylliosis, CWP, hard metal disease
 3. Miscellaneous – RA, AS, CF, radiation pneumonitis, drugs (gold,
pencillamine)
Lower zone predominance
 1. IPF
 2. RA (UIP)
 3. Asbestosis
 4. Acute HP
Radiographic Patterns in ILD

Increased lung
volumes
 LAM
 LCH
 Sarcoidosis (stage 3)
 Chronic HP
 IPF and smoker
 Respiratory bronchiolitis
 Bronchiolitis obliterans
Pneumothorax
 LAM, LCH

Subsegmental migratory
infiltrates
 (CSS, ABPA, BOOP, TPE)
Recurrent infiltrates in same
location
 CEP (upper lobes/peripheral)
 Idiopathic BOOP
 Drug induced
 Realpse/recall radiation pneumonitis

Endstage or honey combing
 Upper zone predominance – Sarcoidosis,
LAM, LCH, Chronic HP.
 Lower zone predominance – IPF, Rheumatoid
arthritis (UIP), Asbestosis.

Classification of lung tissue patterns 6 classes of lung tissue
Healthy
Emphyse
Ground glass
Fibrosis
Micronodul
es
Macronodule

EXPIRATORY AIR
TRAPPING
Air trapping refers to the
abnormal retention of gas
within the lung following
expiration.

Ground glass
opacity
Presence of increased hazy
opacity within the lungs that is
not associated with obscured
underlying vessels (obscured
underlying vessels is known as
consolidation).
It can reflect minimal thickening of
the septal or alveolar
interstitium, thickening of
alveolar walls, or the presense
of cells or fluid filling the alveolar
spaces.

Ground glass opacity
•FAVORS
MILD/ACTIVE
PROCESS

Ground Glass Pattern
 HP
 PCP
pneumonia
 DIP
 NSIP
 PAP
 DAH
 Fluid

GGO and cavitary nodule in Systemic lupus
erythematosus due to cytomegalovirus and aspergillosis.

Ground-glass opacity on HRCT
:
PCP pneumonia.
Pulmonary hemorrhage.

Ground-glass opacity on HRCT:
Hypersensitivity pneumonitis
Nodular ground glass

MOSAIC PERFUSION
Mosaic perfusion
refers to areas of
decreased attenuation
which results from
regional differences
in lung perfusion
seen on inspiration
film secondary to
pulmonary vascular
disease. Often with
mosaic perfusion, the
pulmonary arteries will
be reduced in size in
the lucent lung field.

CRAZY PAVING
Alveolar
proteinosis
Pulmonary edema
GGO with Septal thickening

(a) Geographic areas of GGO with interlobular septal thickening.
(b) Photomicrograph (original magnification, 250; H&E stain) shows
acute intraalveolar hemorrhage.

Traction bronchiectasis
In patients with pulmonary fibrosis and peribronchovascular interstitial
thickening, often the dilatation of the bronchi is caused by traction by the
surrounding fibrosis. This is referred to as traction bronchiectasis

INTERLOBULAR SEPTAL THICKENING

Interlobular septal thickening:
differential diagnostic
considerations
Smooth
Pulmonary edema
Pulmonary alveolar proteinosis
Lymphangitic carcinomatosis
Pulmonary hemorrhage
Infections (especially subacute)
PCP pneumonia
Amyloidosis
Lymphoproliferative disease
Nodular
Lymphangitic
carcinomatosis
Sarcoidosis
LIP
Amyloidosis
Lymphoproliferative
diseases
Irregular
Chronic HP
Sarcoidosis
Pneumoconiosis:
Asbestosis
Silicosis/CWP

Irregular interlobular septal thicke
in a patient with pulmonary fibros
Smooth interlobular septal
thickening: Pulmonary edema.

Nodular interlobular septal
thickening: lymphangitic
carcinomatosis

INTRALOBULAR SEPTAL
THICKENING
 Thickening of the interstitium within the SPL
 IPF, NSIP,
 Asbestosis,
 CVD-ILD,
 chronic HP.

HONEYCOMBING
Honeycombing
suggests extensive
lung fibrosis with
alveolar destruction.
thick-walled, air-filled
cysts, usually
between the size of
3mm to 1cm in
diameter

Diseases with
fibrosis/honeycombing
 IPF, DIP, LIP, NSIP/fibrosis
 Systemic CVD
 Chronic drug reactions
 Pneumoconioses
 Sarcoidosis
 Pulmonary LCH
 Chronic aspiration
 Chronic granulomatous infections
 Chronic HP

Common causes of the organising
pneumonia pattern
 Organising Alveolar
Damage
 HP
 Organising infectious
pneumonias in:
– COPD
– bronchiectasis
– cystic fibrosis
– aspiration
pneumonia
 Drug and toxin
reactions
 CVD
 Eosinophilic
pneumonia
 COP
 Peripheral reaction
around:
– abscesses
– infarcts
– WG lesions

Pulmonary Edema producing Kerley
lines

(1) Bronchiolocentric
(2) Angiocentric
1+2= Centrilobular
(3) Lymphatic, and
(4) Random
Nodule distributions with in SPL

Diagnostic utility of nodule distribution relative to the secondary
pulmonary lobule
Nodule
distribution
on HRCT
Relevant secondary
pulmonary lobular
anatomic structures
Representative diseases
Centrilobula
r
Centrilobular artery and
bronchus
Infectious bronchiolitis,
diffuse panbronchiolitis,
HP,
Respiratory bronchiolitis,
LIP,
Pulmonary edema,
Vasculitis,
Plexogenic lesions of PHTN,
Metastatic neoplasms
Perilymphati
c
Interlobular septa,
subpleural interstitium,
Sarcoidosis,
lymphangitic
carcinomatosis,
Amyloidosis
Random All structures of the lobule Hematogenously
disseminated

Centrilobular nodules with tree-in-bud
opacity: diagnostic considerations
 Bacterial pneumonia with infectious bronchiolitis
 Typical & atypical mycobacterial infections
 Aspiration,
 ABPA, Cystic fibrosis,
 Diffuse panbronchoilitis
 Endobrochial neoplasms (particularly BAC CA)
 RB – ILD, COP
 Silicosis & coal-worker’s pneumoconiosis
 LCH
 Vasculitis & Pulmonary edema

Perilymphatic nodules:
diagnostic considerations
Nodules in a perilymphatic distribution are
frequently associated with nodular thickening
of the bronchovascular bundles .
Another sign helpful in assessing the
perilymphatic distribution is the presence of
subpleural nodules in relation to the interlobar
fissures.
 Sarcoidosis,
 Amyloidosis
 Lymphangitic Carcinomatosis
 lymphocytic Interstitial pneumonia

Perilymphatic nodules- sarcoidosis

Sarcoidosis- Demonstrating septal beading (arrows)
and nodules abutting bronchovascular bundles
.

Random nodules: diagnostic considerations
 Hematogenous metastases
 Miliary TB & fungal infection
 Disseminated viral infection
 Silicosis or coal- worker’s Pneumoconiosis
 LCH

Random nodules- miliary tb
Both centrilobular and perilymphatic

Large nodules
 Masses
 Amyloidosis
 Churg-Strauss syndrome
 Langerhans cell
histiocytosis
 Rounded atelectasis,
asbestos
 Sarcoidosis
 Silicosis
 Wegener’s granulomatosis
 (Lymphoma, metastatic

Nodules with peripheral halo
Due to hemorrhage
 Invasive pulmonary aspergillosis
 Wegener granulomatosis
 Metastatic angiosarcoma
 Kaposi sarcoma
Nonhemorrhagic nodules
Bronchioloalveolar carcinoma
Metastases from carcinoma of the colon

Cysts or Cyst Like
LAM Bronchiectasis
E
EG

Conditions associated with DAD
 Infections (viral, fungal, bacterial, parasitic)
 Toxic inhalants
 Drug reactions
 Shock
 Collagen vascular diseases
 Radiation reactions (acute)
 Acute allergic reactions (eg, hypersensitivity
pneumonitis)
 Alveolar haemorrhage syndromes
 Idiopathic disease (acute interstitial pneumonia)

Causes of DAH
 Goodpasture syndrome (anti-GBM antibody)
 Vasculitides (esp. WG)
 Mitral stenosis
 IgA nephropathy
 Behcet syndrome
 Certain Collagen vascular diseases (esp. SLE)
 HIV infection
 Anti-phospholipid syndrome
 Pulm. veno-occlusive disease
 Idiopathic pulmonary haemosiderosis
 Drug reactions (toxic reactions and anticoagulants)
 Acute lung allograft rejection

 KEY HISTOLOGIC FEATURES- IIP’S
 UIP – Honey combing, fibrosis with prominent
fibroblastic foci
 NSIP – Variable interstitial fibrosis and inflammation
 DIP – Intra-alveolar macrophage accumulation
 RB-ILD – Peri-bronchiolar macrophage accumulation
 AIP(DAD) – Diffuse alveolar damage with hyaline
formation
 LIP – Infiltration of interstitium and alveolar spaces of
lung by lymphocytes, plasma cells and
lymphoreticular elements

UIP*-Chronic progressive dyspnoea and cough, in a
old male
Key Histologic Features
 Dense fibrosis and “honeycomb”
 Fibroblastic foci typically scattered at the edges of dense scars
 Patchy lung involvement, temporal heterogenity.
 Frequent basal, subpleural and paraseptal distribution
Pertinent Negative Findings
 Lack of active lesions of other interstitial diseases (i.e., sarcoidosis or
LCH)
 Lack of marked interstitial chronic inflammation
 Granulomas: inconspicuous or absent
 Lack of substantial inorganic dust deposits, i.e., asbestos bodies (except
for carbon black pigment)
 Lack of marked eosinophilia

NSIP- M:F =1
Both- Mild to moderate interstitial chronic
inflammation
Cellular pattern†
 Type II pneumocyte hyperplasia in areas of
inflammation
Fibrosing pattern†
 Dense or loose interstitial fibrosis lacking the
temporal heterogeneity pattern and patchy
features of UIP
 Lung architecture may appear lost on examination
of H&E-stained sections, but relatively preserved

LIP- 30-50’S, predominantly females
 Diffuse interstitial infiltration of involved areas
 Predominantly alveolar septal distribution
 Infiltrates comprise mostly T lymphocytes, plasma cells, and
macrophages
 Lymphoid hyperplasia (MALT hyperplasia)—frequent
 Lack of tracking along lymphatic routes (bronchovascular bundles,
pleura, and interlobular septa),
 Lack of extensive pleural involvement or lymph node involvement
 progression to lymphomas a major concern
 Organizing pneumonia, inconspicuous or absent
 Lack of necrotizing granulomas
 Autoimmune disorder or immunodeficiency should be ruled out.

RBILD and DIP (90-100% smoking)
 Uniform involvement of lung parenchyma
 Pigment-laden macrophages in and surrounding respiratory
bronchioles (RBILD) and diffusely throughout alveoli (DIP).
 Mild to moderate fibrotic thickening of alveolar septa
 Mild interstitial chronic inflammation (lymphoid aggregates)
 Dense and extensive fibrosis
 Honeycomb
 Smooth muscle proliferation
 Fibroblastic foci and organizing pneumonia
 Eosinophils

ORGANIZING PNEUMONIA
PATTERN- M:F=1
Acute to subacute, dyspnea, cough, and fever.
 Intraluminal organizing fibrosis in distal airspaces (bronchioles, alveolar
ducts, and alveoli)
 Patchy distribution
 Preservation of lung architecture
 Uniform temporal appearance
 Mild interstitial chronic inflammation
 Lack of interstitial fibrosis (except for incidental scars or apical fibrosis)
 Absence of granulomas, neutrophils, and eosionphils
 Absence of abscess, necrosis,
 Absence of vasculitis
 Lack of hyaline membranes or prominent airspace fibrin

AIP- M:F=1
 Acute to subacute dyspnea, cough, with rapid
progression to respiratory failure.
 No identifiable cause of acute lung injury.
 Evidence of diffuse alveolar damage on
surgical lung biopsy.
 Unclear response to medical therapy, poor
prognosis, may be recurrent.

 The classification of IIPs is based on histologic criteria,
but those histologic patterns are closely associated with
imaging patterns that correlate well with histologic
findings.
 The key role of the radiologist is to identify patients
with UIP and differentiate them from patients with
other IIPs, because UIP has a substantially poorer
prognosis than other IIPs.
 In all patients suspected to have IIPs who do not show
the typical clinical and radiologic features of UIP,
surgical lung biopsy should be performed.
 Biopsy specimens should always be obtained from
more than one lobe,
 NSIP is an area of diagnostic uncertainty, and the
term NSIP should be considered a provisional diagnosis

Indications for performing a
lung biopsy
1. To provide a specific diagnosis- IN CASE OF DOUBT
 Especially in a patient with atypical or progressive symptoms
and signs
 Normal chest x-ray or atypical radiographic features
 Unexplained extra pulmonary manifestations
 Unexplained pulmonary hypertension or cardiomegaly
 Rapid clinical deterioration or sudden change in radiographic
appearance.
2. To exclude neoplastic and infectious processes that
occasionally mimic chronic, progressive interstitial disease.
3. To assess disease activity.
4. To identify a more treatable process than originally suspected.
5. To establish a definitive diagnosis and predict prognosis before

Trans bronchial biopsy
Initial procedure of choice, especially when in peribronchovascular
areas
1. Sarcoidosis
 Diagnostic yield – 75-89% if diffuse infiltrates are there
 44-66% if no parenchymal lesion on CXR
 Endobronchial biopsy – 45-77%
2. Lymphangitic carcinomatosis
3. Eosinophilic pneumonia
4. Goodpasture's syndrome
5. Pulmonary Langerhans cell histiocytosis
 Is diagnostic if an infectious agent or maligancy is detected.
 Presence of giant cell granulomas are diagnostic of heavy

ILD- OPEN LUNG BIOPSY
 Indications -<65 yrs of age
when diagnosis is unclear
 H/o fever, wt loss, sweats and
hemoptysis
 Family h/o familial ILD or IPF
 H/o pneumothorax
 F/s/o vasculitis
 Atypical radiographic picture
 Unexplained pulmonary HTN
 Unexplained cardiomegaly
 Rapid progression or new
onset rapid deterioration
Relative contraindications
to this procedure include:
 Serious cardiovascular
disease
 X ray evidence of diffuse,
end-stage disease, eg,
"honeycombing"
 Severe pulmonary
dysfunction or other major
operative risks (especially
in the elderly population)
 High likelihood that an
adequate sized biopsy
from multiple sites, usually
from two lobes, will not be
obtained

ILD revisited print version.pptx

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