Hrct interpretation radiology simplify tome

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HRCT Interpretation - Simplified Guide

Sources: Grainger & Allison's Diagnostic Radiology; Murray & Nadel's Textbook of Respiratory Medicine; Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics

1. What Is HRCT and Why It Matters

HRCT uses thin slices (1-2 mm) at high spatial resolution to image the lung parenchyma with far greater detail than a standard chest CT or plain radiograph. It has become the cornerstone of interstitial lung disease (ILD) evaluation because it:

Detects early disease that chest X-ray misses
Can suggest a specific histological diagnosis in certain cases
Distinguishes reversible (ground-glass, consolidation) from irreversible (fibrosis, honeycombing) changes
Guides biopsy site selection and treatment response monitoring

(Grainger & Allison's, p. 221)

2. The Four Main HRCT Patterns (Fleischner Glossary Framework)

All diffuse lung abnormalities on HRCT fall into one of four main buckets. Overlap between them is common.

Pattern	What You See	Think of
Reticular	Network of lines (fine or coarse)	ILD, fibrosis
Nodular	Discrete round opacities	Granulomas, infection, mets
Mosaic attenuation	Patchwork of light/dark areas	Air trapping, vascular disease
Cystic	Air-filled spaces with definable walls	LAM, LCH, emphysema

(Grainger & Allison's, p. 224)

3. Pattern Deep-Dives

A. Reticular Pattern

A reticular (net-like) pattern almost always represents significant ILD.

Types of reticulation:

Type	Appearance	Causes
Interlobular septal thickening - smooth	Clean straight lines at lung edges	Pulmonary edema, alveolar proteinosis
Interlobular septal thickening - irregular/beaded	Lumpy, nodular septa	Lymphangitic carcinomatosis, sarcoidosis
Intralobular lines	Fine lace-like net within the lobule	Fibrotic lung disease (IPF, NSIP)
Honeycombing	Stacked cystic air spaces with thick, irregular walls	End-stage fibrosis (UIP/IPF)

Key concept - honeycombing vs. reticulation: Honeycombing = cystic air spaces (3-10 mm) with thick fibrotic walls, typically subpleural and basal. It is the hallmark of UIP/IPF and signals irreversible disease. Distinguishing it from mere reticulation changes the diagnosis and prognosis.

Traction bronchiectasis often accompanies honeycombing - bronchi dragged outward by surrounding fibrosis, appearing as dilated, irregular airways in the periphery.

(Grainger & Allison's, p. 224; Murray & Nadel's, p. 470)

Interlobular septal thickening (A) and intralobular lines creating a reticular pattern (B)

Fig: (A) Smoothly thickened interlobular septa in metastatic breast carcinoma; (B) Intralobular lines in scleroderma creating a fine reticular (lace-like) pattern with mild peripheral bronchiolectasis.

B. Nodular Pattern

The single most useful step: classify nodules by their location within the secondary pulmonary lobule (SPL).

Secondary Pulmonary Lobule = the smallest unit of lung anatomy
  - Center: centrilobular artery + terminal bronchiole
  - Periphery: interlobular septa + subpleural lymphatics

Three nodule distributions:

1. Perilymphatic Nodules

Located along interlobular septa, subpleural surfaces, and peribronchovascular bundles
Fissure involvement is a KEY clue
Causes: Sarcoidosis (classic), lymphangitic carcinomatosis, silicosis

2. Random Nodules

Evenly scattered throughout the lung - no lobular pattern preference
Causes: Miliary TB, hematogenous metastases, fungal infection

3. Centrilobular Nodules

Located a few mm away from the pleura (important - they spare the pleural surface and fissures)
Can be well-defined or poorly defined
Tree-in-bud = centrilobular nodules with branching pattern = impacted small bronchioles
- Causes: Endobronchial infection (TB, NTM, bronchopneumonia), aspiration

Distribution	Spares Pleura?	Key Disease
Perilymphatic	No (affects it)	Sarcoidosis, lymphangitic ca
Random	No	Miliary TB, hematogenous mets
Centrilobular	YES	Hypersensitivity pneumonitis, bronchopneumonia

(Murray & Nadel's, p. 468-469)

C. Mosaic Attenuation Pattern

The lung looks like a patchwork quilt - alternating areas of different density.

The key question: which component is abnormal - the dark areas or the bright areas?

Pathological dark areas (increased black):
- Air trapping from small airway obstruction (confirm with expiratory CT - dark areas persist)
- Reduced blood flow from chronic vascular disease (e.g. CTEPH)
Pathological gray/bright areas:
- Increased interstitial density from inflammation or edema (the dark areas are actually normal)

Expiratory CT is the most useful discriminator - air trapping causes the dark areas to remain dark on expiration, while perfusion-related differences equalize.

(Grainger & Allison's, p. 224)

D. Cystic Pattern

Cysts = air-filled spaces with a definable wall (distinguishing them from emphysema which has no wall, and cavities which have thicker walls).

Disease	Cyst Features	Distribution	Clues
LAM (Lymphangioleiomyomatosis)	Thin-walled, round, uniform	Diffuse, bilateral	Young women, chylothorax
LCH (Langerhans Cell Histiocytosis)	Irregular/bizarre shapes, thick-walled early	Upper lobe predominant	Smoker + nodules also present
LIP (Lymphoid Interstitial Pneumonia)	Thin-walled, scattered	Perivascular	Sjögren's syndrome, HIV
Birt-Hogg-Dubé	Oblong, septated	Lower lobe, subpleural, paradiastinal	Renal tumors, skin fibrofolliculomas
Emphysema	No perceptible wall	Upper (centrilobular), lower (paraseptal)	Smoking history

(Murray & Nadel's, p. 474)

HRCT cystic patterns: LAM (A-B), LCH (C), follicular bronchiolitis (D), LIP/Sjögren (E), Birt-Hogg-Dubé (F-G)

Fig: Comparison of diffuse cystic diseases. Note that LAM cysts are round and uniform (A); LCH shows irregular thick-walled cysts AND nodules (C); Birt-Hogg-Dubé has characteristic lower-lobe, paradiastinal, oblong cysts (F-G).

4. Ground-Glass Opacity (GGO) - A Special Finding

GGO = hazy increased lung attenuation that does not obscure the underlying vessels (unlike consolidation, which does).

Key concept: GGO = potentially reversible. Honeycombing + reticulation = likely irreversible.

GGO alone	GGO + reticulation ("crazy paving")	GGO + traction bronchiectasis
Active alveolitis, DIP, HP, edema, drug reaction	Alveolar proteinosis, NSIP, Pneumocystis	Organizing phase - fibrosis setting in

Consolidation = complete air space replacement - vessels obscured. Causes: pneumonia, COP, AIP, malignancy, edema.
Crazy paving = GGO + smooth interlobular septal thickening = classic for pulmonary alveolar proteinosis (PAP), also Pneumocystis jirovecii, lipoid pneumonia.

(Murray & Nadel's, p. 474; Grainger & Allison's, p. 224)

5. Reading an HRCT Systematically - A 5-Step Approach

Step 1 - Distribution

Upper vs. lower lobe predominance?
Central (peribronchovascular) vs. peripheral (subpleural)?
Bilateral or unilateral?

Step 2 - Pattern

Assign to one of the 4 main patterns (reticular / nodular / mosaic / cystic)
Note GGO, consolidation, honeycombing if present

Step 3 - Nodule location (if nodules present)

Centrilobular / perilymphatic / random?

Step 4 - Associated findings

Traction bronchiectasis (fibrosis)
Lymphadenopathy (sarcoid, lymphoma, infection)
Pleural effusion / thickening
Air trapping on expiratory CT

Step 5 - Reversibility assessment

Reversible	Irreversible
Ground-glass opacity	Honeycombing
Consolidation	Coarse reticulation
Centrilobular nodules	Traction bronchiectasis
	Architectural distortion

(Grainger & Allison's, p. 225)

6. Quick-Reference: Common ILDs and Their HRCT Fingerprints

Disease	Pattern	Distribution	Key Feature
IPF (UIP)	Reticulation + honeycombing	Basal, subpleural, bilateral	Temporal heterogeneity; honeycomb
NSIP	GGO + fine reticulation	Basal, subpleural, bilateral	Subpleural sparing of ~1 cm
Sarcoidosis	Perilymphatic nodules	Upper/mid lobe, peribronchovascular	Fissure involvement; lymphadenopathy
Hypersensitivity pneumonitis (subacute)	Centrilobular nodules + GGO + air trapping	Upper/mid lobe	Mosaic attenuation; spares bases
COP	Consolidation ± GGO	Peripheral, peribronchial	Migratory; "reversed halo sign"
PAP	Crazy paving	Geographic/diffuse	GGO + smooth septa
LAM	Thin-walled cysts	Diffuse	Young woman; chylothorax
DIP	Diffuse GGO	Lower zone, peripheral	Smoker
RB-ILD	Centrilobular GGO nodules	Upper lobe	Smoker; air trapping
LCH	Nodules + irregular cysts	Upper lobe	Heavy smoker; cysts evolve from nodules
Miliary TB	Random nodules	Diffuse, uniform	Tiny (1-3 mm), no lobular pattern

7. Reversibility - The Clinically Crucial Axis

The whole point of HRCT over CXR is its ability to differentiate:

"Active" / treatable disease = GGO, consolidation, centrilobular nodules - these may improve with steroids/immunosuppression
"Fibrotic" / irreversible disease = honeycombing, traction bronchiectasis, architectural distortion - no recovery expected

This directly guides whether to offer treatment vs. transplant evaluation.

(Goldman-Cecil Medicine, p. 63)

Summary Mental Map

HRCT FINDING
    │
    ├── RETICULAR ──► Fine = NSIP/early IPF
    │                 Coarse + honeycomb = UIP/IPF (basal, subpleural)
    │                 Smooth septal thickening = Edema / Lymphangitic ca
    │
    ├── NODULAR ──► Perilymphatic = Sarcoidosis / Lymphangitic ca
    │               Random = Miliary TB / Hematogenous mets
    │               Centrilobular = HP / Bronchopneumonia / Tree-in-bud
    │
    ├── MOSAIC ──► Dark component abnormal = Air trapping / CTEPH
    │              Gray component abnormal = Infiltrative disease
    │              Confirm with EXPIRATORY CT
    │
    └── CYSTIC ──► Round, uniform, diffuse = LAM
                   Irregular, upper lobe + nodules = LCH
                   Lower lobe, paradiastinal = Birt-Hogg-Dubé
                   No wall = Emphysema

No shortcuts please , at least mention I. The bracket

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Here is the fully expanded guide with every abbreviation written out in full on first use, and the short form kept in brackets afterwards for reference.

High-Resolution Computed Tomography [HRCT] Interpretation - Complete Simplified Guide

Sources: Grainger & Allison's Diagnostic Radiology; Murray & Nadel's Textbook of Respiratory Medicine; Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics

1. What Is High-Resolution Computed Tomography [HRCT] and Why It Matters

High-Resolution Computed Tomography [HRCT] uses very thin slices (1-2 mm) and a high-spatial-frequency reconstruction algorithm to image the lung parenchyma in far greater detail than standard Computed Tomography [CT] or a plain chest radiograph.

It has become the cornerstone of Interstitial Lung Disease [ILD] evaluation because it:

Detects early disease that a chest X-ray misses
Can suggest a specific histological diagnosis in certain conditions
Distinguishes reversible changes (ground-glass opacity, consolidation) from irreversible changes (fibrosis, honeycombing)
Guides biopsy site selection and monitors response to treatment

The chest radiograph remains part of the initial assessment of Interstitial Lung Disease [ILD], but its pattern is often non-specific, observer variation is considerable, and it has low sensitivity for early disease. High-Resolution Computed Tomography [HRCT] has transformed this, enabling early detection and providing insights into disease reversibility and prognosis.

(Grainger & Allison's Diagnostic Radiology, p. 221)

2. The Lung Anatomy You Must Know First: The Secondary Pulmonary Lobule [SPL]

The Secondary Pulmonary Lobule [SPL] is the smallest discrete unit of lung anatomy visible on High-Resolution Computed Tomography [HRCT], roughly 1-2 cm in size and polyhedral in shape. Everything in HRCT interpretation anchors to it.

Secondary Pulmonary Lobule [SPL] anatomy:
  ┌─────────────────────────────────────────┐
  │  Center:                                │
  │    - Centrilobular artery               │
  │    - Terminal bronchiole                │
  │                                         │
  │  Periphery:                             │
  │    - Interlobular septa                 │
  │    - Subpleural lymphatics              │
  │    - Visceral pleural surface           │
  └─────────────────────────────────────────┘

The interstitium of the lung supports all these structures and includes:

The intralobular interstitium beneath the alveolar epithelium (inside the lobule)
The interlobular septa (walls between lobules)
The peribronchovascular interstitium (around airways and vessels)

Thickening of any of these compartments produces the patterns we read on High-Resolution Computed Tomography [HRCT].

3. The Four Main High-Resolution Computed Tomography [HRCT] Patterns

According to the Fleischner Society Glossary (the international standard terminology for chest imaging), all diffuse lung abnormalities on High-Resolution Computed Tomography [HRCT] can be broadly classified into four main patterns. Overlap between patterns is common.

Pattern	What You See	Broad Category of Disease
Reticular	Network of lines, fine or coarse	Interstitial Lung Disease [ILD], fibrosis
Nodular	Discrete round opacities	Granulomas, infection, metastases
Mosaic attenuation	Patchwork of light and dark areas	Air trapping, vascular disease, infiltration
Cystic	Air-filled spaces with definable walls	Lymphangioleiomyomatosis [LAM], Langerhans Cell Histiocytosis [LCH], emphysema

(Grainger & Allison's, p. 224)

4. Pattern 1 - The Reticular Pattern

A reticular (net-like) pattern on Computed Tomography [CT] almost always represents significant Interstitial Lung Disease [ILD].

What Causes It?

Morphologically, a reticular pattern is caused by:

Thickened intralobular or interlobular septa
Honeycombing (end-stage fibrotic destruction)

Types of Reticular Findings

A. Interlobular Septal Thickening

These are visible lines at the lung periphery outlining the lobule walls.

Appearance	Cause
Smooth septal thickening	Pulmonary edema, Pulmonary Alveolar Proteinosis [PAP]
Irregular / beaded septal thickening	Lymphangitis Carcinomatosa [LC], sarcoidosis (rare)

Numerous thickened interlobular septa indicate an extensive interstitial abnormality - caused by infiltration with fluid (e.g. pulmonary edema) or abnormal cells (e.g. Lymphangitis Carcinomatosa [LC]).

B. Intralobular Lines

Fine lines within the Secondary Pulmonary Lobule [SPL] separated by a few millimeters, creating a fine lace-like or net-like pattern. This is the hallmark of fibrotic lung disease - seen in Idiopathic Pulmonary Fibrosis [IPF] and Non-Specific Interstitial Pneumonia [NSIP].

C. Honeycombing

Severe pulmonary fibrosis produces a coarse reticular pattern made up of interlacing irregular linear opacities, eventually creating cystic air spaces (3-10 mm) surrounded by irregular, thick fibrotic walls - this is honeycombing.

Key features:

Subpleural and basal predominance
Stacked in layers ("stack of coins" appearance)
The defining feature for Usual Interstitial Pneumonia [UIP] / Idiopathic Pulmonary Fibrosis [IPF]
Represents irreversible destruction - no treatment can reverse it

D. Traction Bronchiectasis / Bronchiolectasis

The extensive fibrosis accompanying honeycombing distorts normal lung architecture, dragging the walls of segmental and subsegmental airways outward. This appears as dilated, irregular, non-tapering airways in the lung periphery. It is a marker of established fibrosis.

Interlobular septal thickening and intralobular reticular pattern

(A) Smoothly thickened interlobular septa in metastatic breast carcinoma. (B) Fine intralobular lines in scleroderma creating a reticular lace-like pattern - note mild peripheral bronchiolectasis.

(Grainger & Allison's, p. 224; Murray & Nadel's, p. 470)

5. Pattern 2 - The Nodular Pattern

A nodular pattern appears in both interstitial and airspace diseases. The most important step is to classify nodules by their location within the Secondary Pulmonary Lobule [SPL]. This single step generates the differential diagnosis.

The Three Nodule Distributions

Distribution 1 - Perilymphatic Nodules

Located along the interlobular septa, subpleural surfaces, and peribronchovascular bundles
Follow the path of lymphatic vessels
Involvement of the fissures is a key diagnostic clue - fissures are covered by visceral pleura which contains lymphatics, so nodules here are strongly perilymphatic
These nodules touch the pleura

Disease	Additional Clues
Sarcoidosis	Upper/mid lobe, bilateral hilar lymphadenopathy, peribronchovascular clustering
Lymphangitis Carcinomatosa [LC]	Unilateral possible, beaded septal thickening, history of known primary cancer
Silicosis / Coal Workers' Pneumoconiosis [CWP]	Upper lobe, subpleural and centrilobular regions, occupational history

Distribution 2 - Random Nodules

Scattered evenly and diffusely throughout both lungs with no preference for pleura or center
Defined by their broad, fairly uniform pattern - present throughout lung parenchyma in a roughly equal manner
They approach but also clearly contact the pleural surface (unlike centrilobular) and also appear centrally (unlike pure perilymphatic)

Disease	Additional Clues
Miliary Tuberculosis [TB]	1-3 mm tiny nodules, acute presentation, fever
Hematogenous metastases	Larger and variable-sized nodules, history of primary malignancy
Miliary fungal infection (histoplasmosis, coccidioidomycosis)	Travel/exposure history

Distribution 3 - Centrilobular Nodules

Located in the center of the Secondary Pulmonary Lobule [SPL], a few millimeters from the centrilobular artery and terminal bronchiole
Critically: they spare the pleural surface and fissures - this is the key distinguishing feature from perilymphatic nodules
Represent small airway or peribronchiolar disease

Sub-type	Disease	Additional Clues
Well-defined centrilobular nodules	Silicosis, Pulmonary Langerhans Cell Histiocytosis [PLCH], Coal Workers' Pneumoconiosis [CWP]	Occupational history, smoking
Poorly defined / ground-glass centrilobular nodules	Hypersensitivity Pneumonitis [HP], Respiratory Bronchiolitis-Interstitial Lung Disease [RB-ILD], pulmonary edema	Antigen exposure, smoking
Tree-in-bud pattern	Endobronchial infection (Tuberculosis [TB], Non-Tuberculous Mycobacteria [NTM], bacterial bronchopneumonia), aspiration	Centrilobular nodules + branching linear densities = impacted/inflamed small bronchioles

Side-by-Side Visual Comparison of Nodule Distributions

Comparison of perilymphatic, random, and centrilobular nodule distributions on HRCT

(A) Perilymphatic: nodules contact visceral pleural surfaces and interlobular septa - Lymphangitis Carcinomatosa [LC]. (B) Random: nodules diffusely and evenly distributed, some touching pleura, some central - hematogenous metastases. (C) Centrilobular: nodules approach but do not touch pleural surfaces - bronchopneumonia with tree-in-bud morphology.

(Murray & Nadel's, p. 468-469; Grainger & Allison's, p. 224)

6. Pattern 3 - Mosaic Attenuation Pattern

The lung looks like a patchwork quilt - alternating areas of different radiodensity with well-defined borders corresponding to interlobular septa.

The key question is: which component is abnormal?

The attenuation of a lung area depends on the amount of blood, parenchymal tissue, and air it contains. A mosaic pattern is the dominant abnormality in three completely different diseases:

Three Causes of Mosaic Attenuation

A. Small Airways Disease (obstructive)

The dark (low-attenuation) areas are abnormal - they contain too much air because diseased small airways trap it
Look for: bronchial wall thickening, associated bronchiectasis
Causes: Obliterative bronchiolitis [OB], Chronic Obstructive Pulmonary Disease [COPD], asthma, Cystic Fibrosis [CF]
Confirm with expiratory High-Resolution Computed Tomography [HRCT]: the dark areas remain dark (persist) on expiration because air cannot escape - called air trapping

B. Chronic Occlusive Vascular Disease

The dark areas are abnormal - they are underperfused because pulmonary vessels are blocked
The lung hypoperfusion causes reflex hypoxic vasoconstriction and bronchodilatation in that area
Look for: enlarged pulmonary trunk, abnormal artery-to-bronchus ratio (>1), no air trapping on expiratory High-Resolution Computed Tomography [HRCT]
Cause: Chronic Thromboembolic Pulmonary Hypertension [CTEPH]

C. Infiltrative Lung Disease

The gray/bright areas are abnormal - they contain increased interstitial or alveolar material
The dark areas are actually normal lung
Borders between areas may be less well-defined than in vascular causes
No vascular caliber differences are present
Causes: subacute Hypersensitivity Pneumonitis [HP], Acute Respiratory Distress Syndrome [ARDS], Non-Specific Interstitial Pneumonia [NSIP]

Summary Table

Cause	Abnormal Component	Expiratory High-Resolution Computed Tomography [HRCT]	Clue
Small airways disease	Dark areas	Air trapping persists	Bronchial wall thickening
Chronic Thromboembolic Pulmonary Hypertension [CTEPH]	Dark areas	No air trapping	Enlarged pulmonary trunk
Infiltrative lung disease	Gray/bright areas	Equalizes	Ground-glass opacity pattern

(Grainger & Allison's, p. 224)

7. Pattern 4 - The Cystic Pattern

Cysts on High-Resolution Computed Tomography [HRCT] are defined as air-filled spaces with a clearly definable, perceptible wall (even if thin). This distinguishes them from:

Emphysema: areas of low attenuation with NO perceptible wall
Cavities: thick-walled (>4 mm) air spaces inside a solid lesion
Bullae: >1 cm air spaces, usually in emphysema

Disease	Full Name	Cyst Morphology	Distribution	Key Clinical Clues
Lymphangioleiomyomatosis [LAM]	Lymphangioleiomyomatosis	Thin-walled, round, uniform in size	Diffuse, bilateral, no zonal predominance	Young women; chylothorax; may have Tuberous Sclerosis Complex [TSC]
Pulmonary Langerhans Cell Histiocytosis [PLCH]	Pulmonary Langerhans Cell Histiocytosis	Bizarre/irregular shapes, variable wall thickness; early lesions are nodules that cavitate	Upper and mid lobe predominant, spares Costophrenic [CP] angles	Heavy smoker; nodules coexist with cysts
Lymphoid Interstitial Pneumonia [LIP]	Lymphoid Interstitial Pneumonia	Thin-walled, uniform, peribronchovascular	Mid-lung, not predominantly subpleural	Sjögren Syndrome [SjS], Human Immunodeficiency Virus [HIV] infection
Birt-Hogg-Dubé Syndrome [BHD]	Birt-Hogg-Dubé Syndrome	Oblong, septated, unusual shapes	Lower lobe, subpleural, paradiastinal	Renal tumors, skin fibrofolliculomas
Emphysema	Emphysema	NO perceptible wall - just areas of low attenuation	Centrilobular: upper lobe; Panlobular: lower lobe; Paraseptal: subpleural	Smoking history; Chronic Obstructive Pulmonary Disease [COPD]

Diffuse cystic patterns: Lymphangioleiomyomatosis [LAM] (A-B), Pulmonary Langerhans Cell Histiocytosis [PLCH] (C), Follicular Bronchiolitis (D), Lymphoid Interstitial Pneumonia [LIP] (E), Birt-Hogg-Dubé Syndrome [BHD] (F-G)

(A) Extensive Lymphangioleiomyomatosis [LAM] with uniform, round, thin-walled cysts. (C) Pulmonary Langerhans Cell Histiocytosis [PLCH] with irregular, thick-walled upper lobe cysts AND nodules. (F-G) Birt-Hogg-Dubé Syndrome [BHD] with lower-lobe, paradiastinal, oblong cysts.

(Murray & Nadel's, p. 474)

8. Ground-Glass Opacity [GGO] - The Most Common Finding Explained

Ground-Glass Opacity [GGO] = a hazy, increased lung opacity that does not obscure the underlying pulmonary vessels or bronchial walls (if it does obscure them, it becomes consolidation).

At a microscopic level, Ground-Glass Opacity [GGO] results from:

Partial filling of the air spaces
Thickening of the interstitium
Or both simultaneously
Essentially: subtotal displacement of air from the lung

Ground-Glass Opacity [GGO] can reflect active (potentially reversible) disease or early fibrosis below the spatial resolution of High-Resolution Computed Tomography [HRCT].

Reading Ground-Glass Opacity [GGO] in Context

Ground-Glass Opacity [GGO] Pattern	Interpretation	Key Diseases
Pure Ground-Glass Opacity [GGO] alone	Active alveolitis, likely reversible	Hypersensitivity Pneumonitis [HP], Desquamative Interstitial Pneumonia [DIP], pulmonary edema, drug reaction
Ground-Glass Opacity [GGO] + smooth interlobular septal thickening = "Crazy Paving"	Combined airspace and septal involvement	Pulmonary Alveolar Proteinosis [PAP] (classic), Pneumocystis jirovecii Pneumonia [PJP], lipoid pneumonia
Ground-Glass Opacity [GGO] + traction bronchiectasis	Organizing/fibrotic phase - less reversible	Non-Specific Interstitial Pneumonia [NSIP], Acute Interstitial Pneumonia [AIP] (organizing phase)
Ground-Glass Opacity [GGO] + coarse reticulation + architectural distortion	Likely early fibrosis masquerading as Ground-Glass Opacity [GGO]	Idiopathic Pulmonary Fibrosis [IPF] (fibrotic Non-Specific Interstitial Pneumonia [NSIP] overlap)
Bilateral diffuse Ground-Glass Opacity [GGO] + consolidation (dependent)	Diffuse Alveolar Damage [DAD]	Acute Respiratory Distress Syndrome [ARDS], Acute Interstitial Pneumonia [AIP]

Consolidation vs. Ground-Glass Opacity [GGO]

Feature	Ground-Glass Opacity [GGO]	Consolidation
Vessels visible?	Yes	No (obscured)
Air bronchograms?	No	Yes (often)
Reversibility	Often reversible	Variable
Typical cause	Alveolitis, early edema	Pneumonia, Cryptogenic Organizing Pneumonia [COP], edema, malignancy

(Murray & Nadel's, p. 474; Grainger & Allison's, p. 225)

9. The Idiopathic Interstitial Pneumonias [IIPs] and Their High-Resolution Computed Tomography [HRCT] Fingerprints

The Idiopathic Interstitial Pneumonias [IIPs] are a group of disorders with no known cause, each with a distinct histological and radiological appearance. The 2013 American Thoracic Society [ATS] / European Respiratory Society [ERS] consensus classification requires a multidisciplinary team approach - clinicians, radiologists, and pathologists together.

Usual Interstitial Pneumonia [UIP] / Idiopathic Pulmonary Fibrosis [IPF]

Idiopathic Pulmonary Fibrosis [IPF] is applied when the clinical, imaging, and (when available) histological features all show a pattern of Usual Interstitial Pneumonia [UIP]. However, the Usual Interstitial Pneumonia [UIP] pattern can also be secondary to Connective Tissue Disease [CTD] (especially Rheumatoid Arthritis [RA]), Chronic Hypersensitivity Pneumonitis [HP], asbestosis, and drugs.

High-Resolution Computed Tomography [HRCT] features of Usual Interstitial Pneumonia [UIP]:

Reticulation (fine intralobular lines) - bilateral
Honeycombing - subpleural, basal predominant
Traction bronchiectasis - within fibrotic areas
Temporal heterogeneity - areas of different stages of fibrosis (fresh fibroblastic foci next to dense scar) in the same scan - this is unique to Usual Interstitial Pneumonia [UIP] and is macroscopically depicted by High-Resolution Computed Tomography [HRCT]
Subpleural and basilar predominance is required for a "definite Usual Interstitial Pneumonia [UIP]" diagnosis on High-Resolution Computed Tomography [HRCT]
Ground-Glass Opacity [GGO] is minimal and always less than the reticulation