Dieulafoy disease = abnormally dilated submucosal vessels of pulmonary artery prone to hemorrhage

[Paul Georges Dieulafoy (1839–1911), chief of medical services at the Hôtel-Dieu, Paris, France]

2.   Bronchiectasis, mouthful (15%)

3.   Tuberculosis (Rasmussen aneurysm)

4.   Aspergillosis

5.   Abscess

6.   Cystic fibrosis

E.  CRYPTOGENIC (3–10–42%)

◊  6–10% of patients who smoke present with unresectable lung cancer within subsequent 3 years!


√  cluster of avidly enhancing “nodular” bronchial arteries in posterior mediastinum below level of aortic arch paralleling bronchial anatomy

√  abnormal bronchial arteries show tortuosity, dilatation, hypervascularity, neovascularity, aneurysms, shunts

N.B.:   multidetector CT mapping prior to angiography reduces the rate of catheterization failures and the number of patients needing surgical intervention!


√  vasodilated enlarged tortuous bronchial arteries → bronchial-to-pulmonary-artery shunting, hypervascularity, parenchymal staining

Prognosis:  50–100% mortality rate of conservatively treated massive hemoptysis; death usually from asphyxiation rather than from exsanguination

Rx:     transcatheter particulate embolization of bronchial aa. using polyvinyl alcohol (PVA) + Gelfoam® pledgets (effective in 70–95%; recurrent bleeding in 20–30%)

N.B.:   identify arteria radicularis (= artery of Adamkiewicz) at T5–L2 (in 75% T9–T12) to avoid postembolization transverse myelitis

DDx:  hematemesis (containing food particles, dark blood, acid pH)


=  intake of solid / liquid materials into the airways and lungs

Predisposing factors:

1.   Alcoholism (most common in adults)

2.   General anesthesia, loss of consciousness

3.   Structural abnormalities of pharynx / esophagus (congenital / acquired tracheoesophageal + tracheopulmonary fistula), laryngectomy

4.   Neuromuscular disorders

5.   Deglutition abnormalities


(a)  solids

›  foreign bodies

›  lentils

(b)  liquids

›  gastric acid = Mendelson syndrome

›  water = near drowning

›  barium, water-soluble contrast material

›  liquid paraffin / petroleum = acute exogenous lipoid pneumonia / fire-eater pneumonia

›  mineral oil / cod liver oil = chronic exogenous lipoid pneumonia

(c)  contaminated substances from oropharynx / GI tract

Acute Lower Airway Obstruction in Childhood

Location:  intrathoracic trachea + bronchi

(a)  infectious / inflammatory:

•  fever, cough, wheeze

›  < 2 years old:

1.   Bronchiolitis

√  bronchial wall thickening + hyperinflation

›  > 2 years old:

2.   Lower respiratory tract inflammation

√  bronchial wall thickening

3.   Reactive airways disease

√  bronchial wall thickening + hyperinflation

(b)  others:

1.   Aspirated foreign body


1.   Bronchogenic carcinoma

2.   Chronic bronchitis

3.   Centrilobular emphysema

4.   Panacinar emphysema with α-1 antitrypsin deficiency

5.   Smoking-related interstitial lung disease

›  Respiratory bronchiolitis ILD (RB-ILD)

›  Desquamative interstitial pneumonitis (DIP)

›  Pulmonary Langerhans cell histiocytosis (PLCH)

›  Idiopathic pulmonary fibrosis (IPF)


large particles reaching the tracheobronchial mucosa (pollens, certain fungi, some animal / insect epithelial emanations)

1.   Extrinsic asthma

2.   Hypersensitivity aspergillosis

3.   Bronchocentric granulomatosis

4.   Byssinosis in cotton-wool workers




small particles of < 5 µm reaching alveoli


Histopathologic manifestations:

(a)  Diffuse alveolar damage:

bleomycin, busulfan, carmustine, mitomycin, cyclophosphamide, melphalan, gold salts

(b)  Nonspecific interstitial pneumonia:

amiodarone, methotrexate, carmustine, chlorambucil

(c)  Bronchiolitis obliterans organizing pneumonia: gold salts, bleomycin, methotrexate, amiodarone, nitrofurantoin, penicillamine, sulfasalazine, cyclophosphamide

(d)  Eosinophilic pneumonia:

penicillamine, sulfasalazine, nitrofurantoin, nonsteroidal anti-inflammatory drugs, para-aminosalicylic acid

(e)  Pulmonary hemorrhage:

anticoagulants, amphotericin B, cytarabine (ara-C), penicillamine, cyclophosphamide

A.  CYTOTOXIC DRUGS (most important group)

1.   Cyclophosphamide

Use:   variety of malignancies, Wegener granulomatosis, glomerulonephritis

Toxicity:   after 2 weeks – 13 years (mean, 3.5 years), no relationship to dose / duration of therapy

Prognosis:   good after discontinuation of therapy

√  diffuse alveolar damage (most common)

√  nonspecific interstitial pneumonia

√  BOOP (least common)

2.   Busulfan = Myleran® (for CML)

Toxicity:   dose-dependent, after 3–4 years on the drug in 1–10%

√  diffuse linear pattern (occasionally reticulonodular / nodular pattern)

√  partial / complete clearing after withdrawal of drug

DDx:   Pneumocystis pneumonia, interstitial leukemic infiltrate

3.   Nitrosoureas = carmustine (BCNU), lomustine (CCNU)

Use:   CNS glioma, lymphoma, myeloma

Toxicity:   in 50% after doses > 1500 mg/m2; sensitivity increased after radiation Rx

√  diffuse alveolar damage (most common)

√  nonspecific interstitial pneumonia:

√  linear / finely nodular opacities (following treatment of 2–3 years)

√  high incidence of pneumothorax

4.   Bleomycin

Use:   squamous cell carcinoma of neck / cervix / vagina, Hodgkin lymphoma, testicular carcinoma

Toxicity:   at doses > 300 mg (in 3–6%); increased risk with age + radiation therapy + high oxygen concentrations

Prognosis:   death from respiratory failure within 3 months of onset of symptoms

√  diffuse alveolar damage (most common)

√  nonspecific interstitial pneumonia / BOOP:

√  subpleural linear / nodular opacities (5–30 mm) in lower lung zones occurring after 1–3 months following beginning of therapy

DDx:   metastases

5.   Taxoid derivatives = paclitaxel, docetaxel, gemcitabine, topotecan, vinorelbine

Use:   breast cancer, lung cancer, ovarian cancer

√  interstitial pneumonitis


1.   Amiodarone

=  triiodinated benzofuran

Use:   refractory ventricular tachyarrhythmia

Toxicity:   in 5–10%; risk increased with daily dose > 400 mg + in elderly

Prognosis:   good after discontinuation of drug

•  pulmonary insufficiency after 1–12 months in 14–18% on long-term therapy

√  nonspecific interstitial pneumonia (most common) + associated BOOP:

√  alveolar + interstitial infiltrates (chronic presentation)

√  focal homogeneous peripheral consolidation (acute presentation):

√  attenuation values of iodine ← incorporation of amiodarone into type II pneumocytes

√  pleural thickening (inflammation) adjacent to consolidation

√  associated high-attenuation of liver relative to spleen

2.   Gold salts

Use:   inflammatory arthritis

Toxicity:   in 1% within 2–6 months

•  mucocutaneous lesions (30%)

√  diffuse alveolar damage (common)

√  nonspecific interstitial pneumonia (common)

√  BOOP (less common)

3.   Methotrexate, procarbazine

Use:   lung cancer, breast cancer, head and neck epidermoid cancer, nonmetastatic osteosarcoma, advanced stage NHL, AML, recalcitrant psoriasis, severe rheumatoid arthritis, pemphigus

Toxicity:   in 5–10%; not dose-related

Prognosis:   usually self-limited despite continuation of therapy

•  blood eosinophilia (common)

√  nonspecific interstitial pneumonia (most common)

√  BOOP (less frequent)

√  linear / reticulonodular process (time delay of 12 days to 5 years, usually early)

√  acinar filling pattern (later)

√  transient hilar adenopathy + pleural effusion (on occasion)

DDx:   Pneumocystis pneumonia

4.   Nitrofurantoin (Macrodantin®)

Use:   urinary tract infection

Toxicity:   rare

•  positive for ANA + LE cells

(a)  acute disorder within 2 weeks of administration:

•  fever, dyspnea, cough

•  peripheral eosinophilia (more common)

Prognosis:   prompt resolution after withdrawal from drug

√  diffuse bilateral predominantly basal heterogeneous opacities

(b)  chronic reaction with interstitial fibrosis (less common)

•  insidious onset of dyspnea + cough

•  may not be associated with peripheral eosinophilia

√  nonspecific interstitial pneumonia (common)

√  bilateral basilar interstitial opacities


1.   Heroin, propoxyphene, methadone

Toxicity:   overdose followed by pulmonary edema in 30–40%

√  bilateral widespread airspace consolidation

√  aspiration pneumonia in 50–75%

2.   Salicylates

•  asthma

√  pulmonary edema (with chronic ingestion)

3.   Intravenous contrast material

√  pulmonary edema


=  subgroup of hematologic malignancies comprising 4 different types:

1.   Lymphoma (Non-Hodgkin Lymphoma)

>  30 subtypes of lymphoma

2.   Hodgkin disease

3.   Lymphocytic leukemias (acute or chronic)

4.   Plasma cell myeloma (multiple myeloma)


Disorders with Hepatic & Pulmonary Manifestations

1.   Alpha-1-antitrypsin deficiency

2.   Cystic fibrosis

3.   Hereditary hemorrhagic telangiectasia

4.   Autoimmune disease: primary biliary cirrhosis, rheumatoid arthritis, Hashimoto thyroiditis, Sjögren syndrome, scleroderma, sarcoidosis

5.   Drugs with toxic effects on lung and liver: methotrexate, phenytoin, amiodarone

Pulmonary-Renal Syndromes

1.   Wegener granulomatosis = granulomatosis with polyangiitis

2.   Goodpasture syndrome

3.   Systemic lupus erythematosus

4.   Mixed connective tissue disease

5.   Microscopic polyangiitis


=  abnormal accumulation of fluid in the extravascular compartments of the lung

Pathophysiology (Starling equation):

transcapillary flow dependent on

(1)  Hydrostatic pressure

(2)  Oncotic (= colloid osmotic) pressure

(3)  Capillary permeability (the endothelial cells are relatively impermeable to protein but remain permeable to water and solutes; the tight intercellular junctions of alveolar epithelium remain nearly impermeable to water and solutes)

Qfilt = Kfilt (HPiv – HPev) – t(OPiv – OPev)

Qfilt = amount of fluid filtered per unit area per unit time
HPiv = intravascular hydrostatic pressure
HPev = extravascular hydrostatic pressure
OPiv = intravascular oncotic pressure
OPev = extravascular oncotic pressure
Kfilt = conductance of capillary wall = water resistance of capillary endothelial cell junction
t = oncotic reflection coefficient = permeability of capillary membrane to macromolecules

Cause:   disturbed equilibrium of net flow Fnet between fluid transudation / exudation Qfilt and lymphatic absorption Qlymph

Fnet = Qfilt – Qlymph


(a)  cardiogenic (most common)


1.   Heart disease: left ventricular failure, mitral valve disease, left atrial myxoma

2.   Pulmonary venous disease: acute / chronic pulmonary embolism, primary venoocclusive disease, mediastinal fibrosis

3.   Pericardial disease: pericardial effusion, constrictive pericarditis (extremely rare)

4.   Drugs: antiarrhythmic drugs; drugs depressing myocardial contractility (beta-blocker)

(b)  noncardiogenic

1.   Renal failure

2.   Massive IV fluid overload

3.   Hyperosmolar fluid (eg, contrast medium)

(c)  neurogenic

? sympathetic venoconstriction in cerebrovascular accident, head injury, CNS tumor, postictal state


1.   Hypoproteinemia

2.   Transfusion of crystalloid fluid

3.   Rapid reexpansion of lung

Endothelial injury from

(a)  physical trauma: parenchymal contusion, radiation therapy

(b)  aspiration injury:

1.   Mendelson syndrome (gastric contents)

2.   Near drowning in sea water / fresh water

3.   Aspiration of hypertonic contrast media

(c)  inhalation injury:

1.   Nitrogen dioxide = silo-filler’s disease

2.   Smoke (pulmonary edema may be delayed by 24–48 hours)

3.   Sulfur dioxide, hydrocarbons, carbon monoxide, beryllium, cadmium, silica, dinitrogen tetroxide, oxygen, chlorine, phosgene, ammonia, organophosphates

(d)  injury via bloodstream

1.   Vessel occlusion: shock (trauma, sepsis, ARDS) or emboli (air, fat, amniotic fluid, thrombus)

2.   Circulating toxins: snake venom, paraquat

3.   Drugs: heroin, morphine, methadone, aspirin, phenylbutazone, nitrofurantoin, chlorothiazide

4.   Anaphylaxis: transfusion reaction, contrast medium reaction, penicillin

5.   Hypoxia: high altitude, acute large airway obstruction

mnemonic:   ABCDEFGHI – PRN




Drugs (heroin, nitrofurantoin, salicylates)

Exudative skin disorders

Fluid overload

Gram-negative shock

Heart failure

Intracranial condition

Polyarteritis nodosa

Renal disease

Near drowning

Atypical pulmonary edema = lung edema with an unusual radiologic appearance

Unusual form of pulmonary edema = lung edema from unusual causes

Increased Hydrostatic Pressure Edema

•  Pulmonary capillary wedge pressure (PCWP):

=  reflects left atrial pressure and correlates well with radiologic features of CHF + pulmonary venous HTN

◊  In acute CHF radiologic features are delayed in onset and resolution

√  flow inversion = “cephalization of pulmonary vessels” is ONLY seen in longstanding left heart failure, NEVER in pulmonary edema of renal failure / overhydration / low oncotic pressure


√  smooth interlobular septal + peribronchovascular thickening

√  ground-glass opacities in a perihilar / dependent distribution, which may progress to consolidation

√  centrilobular ground-glass nodules

Interstitial Pulmonary Edema

=  1st phase of pressure edema with increase in quantity of extracellular fluid

Cause:    increase in mean transmural arterial pressure of 15–25 mmHg

√  mild enlargement of peribronchovascular spaces

√  appearance of Kerley lines

√  subpleural effusions

√  early loss of definition of subsegmental + segmental vessels

√  progressive blurring of vessels ← central migration of edema at lobar + hilar levels

√  small peripheral vessels difficult to identify ← decrease in lung radiolucency

◊  Often marked dissociation between clinical signs + symptoms + roentgenographic evidence

◊  Nothing differentiates it from other interstitial lesions

◊  Does not necessarily develop before alveolar pulmonary edema

◊  NOT typical for bacterial pneumonia

Alveolar Flooding Edema

=  2nd phase of pressure edema

Cause:    increase in mean transmural arterial pressure of > 25 mmHg ± pressure-induced damage to alveolar epithelium

√  tiny nodular / acinar areas of increased opacity

√  frank consolidation

Bat-Wing Edema (in < 10%)

=  central nongravitational distribution of alveolar edema

Cause:    rapidly developing severe cardiac failure (acute mitral insufficiency associated with papillary muscle rupture, massive MI, valve leaflet destruction by septic endocarditis) or renal failure

√  lung cortex spared from fluid (due to pumping effect of respiration / contractile property of alveolar septa / mucopolysaccharide-filled perivascular matrix)

Asymmetric Distribution of Pressure Edema

Cause:    morphologic lung changes in COPD, hemodynamics, patient position

√  lung apices spared (= lung emphysema in heavy smokers)

√  upper + middle portions of lung spared (= end-stage TB, sarcoidosis, asbestosis)

√  predominantly RUL involvement (= mitral regurgitation refluxes preferentially into right upper pulmonary vein)

√  anteroposterior gradient on CT in recumbent position

√  unilateral edema in lateral decubitus position

Pulmonary Edema with Acute Asthma

Cause:    air trapping maintains a positive intraalveolar pressure and thus decreases hydrostatic pressure gradient

Pathogenesis:   associated with severity of Müller maneuver

√  heterogeneous edema ← nonuniform airway obstruction

√  peribronchial cuffing

√  ill-defined vessels

√  enlarged ill-defined hila

√  patency of narrowed airways maintained ← high negative pleural pressure in forced inspiration

Postobstructive Pulmonary Edema

Cause:    following relief from an upper airway obstruction (impacted foreign body, laryngospasm, epiglottitis, strangulation)


(a)  forced inspiration causes a high negative intrathoracic pressure (Müller maneuver) and increases venous return

(b)  obstruction creates high positive intrathoracic pressure that impairs development of edema

√  septal lines, peribronchial cuffing

√  central alveolar edema

√  normal heart size

Prognosis:   resolution within 2–3 days

Edema with Pulmonary Embolism (< 10%)

Cause:    occlusion of pulmonary arterial bed causes redirection of blood flow and hypertension in uninvolved areas

√  areas of ground-glass attenuation

√  sharply demarcated from areas of transparency distal to occluded arteries

√  associated with dilated pulmonary arteries (70%)

Edema & Pulmonary Venoocclusive Disease

Cause:    organized thrombi in small veins causes an increase in peripheral resistance and hydrostatic pressure

•  rapidly progressive dyspnea, orthopnea ± hemoptysis

•  normal / low pulmonary capillary wedge pressure

√  enlarged pulmonary arteries

√  diffuse interstitial edema + numerous Kerley lines

√  peribronchial cuffing

√  dilated right ventricle

Permeability Edema

Heroin-induced Pulmonary Edema

Hx:  overdose of opiates (almost exclusively with heroin, rarely with cocaine / “crack”)

Frequency:   15% of cases of heroin overdose

Pathophysiology:   depression of medullary respiratory center leading to hypoxia + acidosis

√  widespread patchy bilateral airspace consolidations

√  ill-defined vessels + peribronchial cuffing

√  markedly asymmetric gravity-dependent distribution of edema (motionless recumbent position for hours / days)

√  resolution within 1 or 2 days in uncomplicated cases


(1)  Extensive crush injuries with associated muscle damage and ensuing renal insufficiency (from motionless recumbency)

(2)  Aspiration of gastric contents

Prognosis:   10% mortality rate

Edema following Administration of Cytokines

(a)  intravenous interleukin 2 (IL–2):

enhances tumoricidal activity of natural killer cells in metastatic melanoma + RCC

(b)  intraarterial tumor necrosis factor:

increases production + release of IL–2

Frequency:  in 75% of IL–2 therapy;
in 20% of tumor necrosis factor therapy;
in 25% of recombinant IL–2 therapy

Pathophysiology:   permeability disruption of capillary endothelial cells

•  12 mmHg increase in pulmonary capillary wedge pressure (= direct toxic effect on myocardium)

√  pulmonary edema 1–5 days after start of therapy:

√  bilateral symmetric interstitial edema with thickened septal lines

√  peribronchial cuffing (75%)

√  small pleural effusions (40%)

√  NO alveolar edema (unless associated cardiac insufficiency)

High-altitude Pulmonary Edema

Predisposed:   young males after rapid ascent to > 3,000 m

Cause:    prolonged exposure to low partial oxygen atmospheric pressure

Pathophysiology:   acute persistent hypoxia with endothelial leakage

•  prodromal acute mountain sickness

•  dyspnea at rest, cough with frothy pink sputum

•  neurologic disturbances ← brain edema

•  arterial oxygen levels as low as 38%

√  central interstitial pulmonary edema

√  peribronchial cuffing

√  ill-defined vessels

√  patchy airspace consolidation

Mixed Hydrostatic & Permeability Edema

Neurogenic Pulmonary Edema

Frequency:   in up to 50% of severe brain trauma, stroke, subarachnoid hemorrhage, status epilepticus

Pathophysiology:   modification in neurovegetative pathways causes sudden ↑ in pressure in pulmonary venules with reduced venous outflow

•  dyspnea, tachypnea, cyanosis shortly after brain insult + rapid disappearance

√  bilateral inhomogeneous / homogeneous airspace consolidations, in 50% affecting predominantly the apices, disappearing within 1–2 days

Dx:  by exclusion

DDx:  fluid overload, postextubation edema

Reperfusion Pulmonary Edema

Frequency:   in up to 90–100%

Cause:    pulmonary thrombendarterectomy for massive pulmonary embolism / for webs and segmental stenosis

Pathophysiology:   rapid increase in blood flow + pressure

•  dyspnea, tachypnea, cough during the first 24–48 hours after reperfusion

√  pulmonary edema within 2 days after surgery:

√  heterogeneous airspace consolidation, predominantly in areas distal to recanalized vessels

√  random distribution in up to 50%

Reexpansion Pulmonary Edema

Cause:    rapid reexpansion of a collapsed lung following evacuation of hydro-, hemo- or pneumothorax

Pathophysiology:   prolonged local hypoxic event, abrupt restoration of blood flow, sudden marked increase in intrapleural pressure, diffuse alveolar damage

•  frank respiratory insufficiency: cough, dyspnea, tachypnea, tachycardia, frothy pink sputum; may be asymptomatic

√  pulmonary edema within reexpanded entire lung within 1 hour (in 64%)

√  increase in severity within 24–48 hours with slow resolution over next 5–7 days

Prognosis:   20% mortality

Pulmonary Edema due to Air Embolism

Cause:    usually iatrogenic complication (neurosurgical procedure in sitting position, placement / manipulation of central venous line), rare in open / closed chest trauma

Pathophysiology:   embolized air bubbles cause mechanical obstruction of pulmonary microvasculature

•  sudden onset of chest pain, tachypnea, dyspnea

•  hypotension

√  air bubbles in right-sided cardiac chambers on echocardiography

√  interstitial edema

√  bilateral peripheral alveolar areas of increased opacity, predominantly at lung bases

Postpneumonectomy Pulmonary Edema

=  life-threatening complication in early postoperative period after pneumonectomy (rare in lobectomy / lung reduction surgery)

Frequency:   2.5–5%; R > L pneumonectomy

Risk factors:   excessive administration of fluid during surgery, transfusion of fresh frozen plasma, arrhythmia, marked postsurgical diuresis, low serum colloidal osmotic pressure

Pathophysiology:   increased capillary hydrostatic pressure, altered capillary permeability

•  marked dyspnea during first 2–3 postop days

√  ARDS-like picture

Prognosis:   very high mortality rate

Pulmonary Edema after Lung Transplantation

Frequency:   in up to 97% during first 3 days after surgery

Pathophysiology:   tissue hypoxia, disruption of pulmonary lymphatic drainage, lung denervation

√  progressive diffuse confluent areas of increased opacity, most pronounced on postop day 5

√  return to normal 2 weeks after surgery

Unilateral Pulmonary Edema

A.  IPSILATERAL = on side of preexisting abnormality

(a)  filling of airways

1.   Unilateral aspiration / pulmonary lavage

2.   Drowned lung (bronchial obstruction)

3.   Pulmonary contusion

(b)  increased pulmonary venous pressure

1.   Unilateral venous obstruction

2.   Prolonged lateral decubitus position

(c)  pulmonary arterial overload

1.   Systemic artery-to-pulmonary artery shunt (Waterston, Blalock-Taussig, Pott procedure)

2.   Rapid thoracentesis (rapid reexpansion)

B.  CONTRALATERAL = opposite to side of abnormality

(a)  pulmonary arterial obstruction

1.   Congenital absence / hypoplasia of pulmonary a.

2.   Unilateral arterial obstruction

3.   Pulmonary thromboembolism

(b)  loss of lung parenchyma

1.   Swyer-James syndrome

2.   Unilateral emphysema

3.   Lobectomy

4.   Pleural disease


PATHOGNOMONIC for mitral valve regurgitation

Pulmonary Edema with Cardiomegaly

1.   Cardiogenic

2.   Uremic (cardiomegaly ← pericardial effusion / hypertension)

Pulmonary Edema without Cardiomegaly

mnemonic:   U DOPA




Pulmonary hemorrhage

Acute myocardial infarction, Arrhythmia

Noncardiogenic Pulmonary Edema

mnemonic:   The alphabet

ARDS, Alveolar proteinosis, Aspiration, Anaphylaxis

Bleeding diathesis, Blood transfusion reaction

CNS (increased pressure, trauma, surgery, CVA, cancer)

Drowning (near), Drug reaction

Embolus (fat, thrombus)

Fluid overload, Foreign-body inhalation

Glomerulonephritis, Goodpasture syndrome, Gastrografin® aspiration

High altitude, Heroin, Hypoproteinemia

Inhalation (SO2, smoke, CO, cadmium, silica)

Narcotics, Nitrofurantoin

Oxygen toxicity


Rapid reexpansion of pneumothorax / removal of pleural effusion




“Classic” pneumonia pattern:

1. Lobar distribution: Streptococcus pneumoniae
2. Bulging fissure: Klebsiella
3. Pulmonary edema: Viral / Pneumocystis pneumonia
4. Pneumatocele: Staphylococcus
5. Alveolar nodules: Varicella, bronchogenic spread of TB



›  Normal host: S. pneumoniae, Mycoplasma, virus

›  Compromised host: S. pneumoniae


›  Normal host: Mycoplasma, virus, Streptococcus, Staphylococcus, S. pneumoniae

›  Compromised host: gram-negative, Streptococcus, Staphylococcus

›  Nosocomial: gram-negative, Pseudomonas, Klebsiella, Staphylococcus

›  Immunosuppressed: gram-negative, Staphylococcus, Nocardia, Legionella, Aspergillus, Phycomycetes


›  Normal host: virus (eg, influenza), Legionella

›  Compromised host: candidiasis, Pneumocystis, TB


›  Normal host: anaerobic (aspiration)

›  Compromised host: anaerobic (aspiration)


›  Noninfectious eosinophilic pneumonia


A.  Community-acquired pneumonia

Organism:   viruses, S. pneumoniae, Mycoplasma

Mortality:   10%

B.  Nosocomial pneumonia

[nosos, Greek = disease; kamnein, Greek = to suffer; nosocomium, Latin = hospital]

(a)  gram-negative organism (> 50%): Klebsiella pneumoniae, P. aeruginosa, E. coli, Enterobacter

(b)  gram-positive organism (10%): S. aureus, S. pneumoniae, H. influenzae


1.   Empyema

2.   Pulmonary abscess

3.   Cavitary necrosis

4.   Pneumatocele

5.   Pneumothorax

6.   Pyopneumothorax

7.   Bronchopleural fistula

Bacterial Pneumonia

Lobar Pneumonia


=  pathogens reach peripheral air space, incite exudation of watery edema into alveolar space, centrifugal spread via small airways, pores of Kohn + Lambert into adjacent lobules + segments

√  nonsegmental sublobar consolidation

√  round pneumonia (= uniform involvement of contiguous alveoli)

(a)  Streptococcus pneumoniae

(b)  Klebsiella pneumoniae (more aggressive); in immunocompromised + alcoholics

(c)  any pneumonia in children

(d)  atypical measles

√  expansion of lobe with bulging of fissures

√  lung necrosis with cavitation

√  lack of volume loss

DDx:  aspiration; pulmonary embolus

Lobular Pneumonia


=  combination of interstitial + alveolar disease (injury starts in airways, involves bronchovascular bundle, spills into alveoli, which may contain edema fluid, blood, leukocytes, hyaline membranes, organisms)


(a)  Staphylococcus aureus, Pseudomonas pneumoniae: thrombosis of lobular artery branches with necrosis and cavitation

(b)  Streptococcus (pneumococcus), Klebsiella, Legionnaires’ bacillus, Bacillus proteus, E. coli, anaerobes (Bacteroides + Clostridia), Nocardia, actinomycosis

(c)  Mycoplasma

√  small fluffy ill-defined acinar nodules, which enlarge with time

√  lobar + segmental densities with volume loss from airway obstruction ← bronchial narrowing + mucus plugging

Atypical Bacterial Pneumonia

=  bacterial infection with radiographic appearance of viral pneumonia


(1)  Mycoplasma

(2)  Pertussis

(3)  Chlamydia trachomatis

Gram-negative Pneumonia

In 50% cause of nosocomial necrotizing pneumonias (including staphylococcal pneumonia)

Predisposed:   elderly, debilitated, diabetes, alcoholism, COPD, malignancy, bronchitis, gram-positive pneumonia, treatment with antibiotics, respirator therapy


1.   Klebsiella

2.   Pseudomonas

3.   E. coli

4.   Proteus

5.   Haemophilus

6.   Legionella

√  airspace consolidation (Klebsiella)

√  spongy appearance (Pseudomonas)

√  affecting dependent lobes (poor cough reflex without clearing of bronchial tree)

√  bilateral

√  cavitation common

Cx:   (1)   Exudate / empyema

(2)  Bronchopleural fistula

Mycotic Lung Infection


1.   Histoplasmosis

2.   Coccidioidomycosis

3.   Blastomycosis


1.   Aspergillosis

2.   Mucormycosis (phycomycosis)

3.   Candidiasis

Growth: (a) mycelial form
  (b) yeast form (depending on environment)

Source of contamination:

(a)  soil

(b)  growth in moist areas (apart from Coccidioides)

(c)  contaminated bird / bat excreta

Viral Lung Infection


[terms used in an attempt to differentiate from airspace pneumonia]

=  infection of bronchi + peribronchial tissues


◊  The cause of infection cannot be reliably ascertained from its imaging appearance!


(a)  Influenza A: more common during infancy, may lead to severe lower respiratory tract infection; mild URI in adults

1.   Avian flu (H5N1 subtype): 1997 Hong Kong; 60% fatality rate

2.   Swine influenza A (H1N1): 2009 in Mexico; pandemic; 1% fatality rate

(b)  Parainfluenza 1–4: common cause of seasonal URI

(c)  RSV = respiratory syncytial virus: most frequent viral cause of lower respiratory tract infection in infants

(d)  Human metapneumovirus (HMPV): clinically indistinguishable from RSV

(e)  Rubeola (measles): highly contagious; 1–36% mortality; febrile illness before / with onset of rash

(f)  Enterovirus, Coxsackie virus, ECHO virus: summertime URI

(g)  Human T-cell lymphotropic virus type 1 (HTLV-1): retrovirus associated with leukemia / lymphoma; transmission by sexual contact + blood transfusion + breast feeding

(h)  Hantavirus (hantavirus pulmonary syndrome): 1993 in southwestern USA

(i)  Coronavirus (SARS = severe acute respiratory syndrome): 2002 Guangdong Province / China; 10% mortality rate


(a)  Adenovirus: associated with Swyer-James-MacLeod syndrome in children

(b)  Herpes simplex virus: in immunocompromised

(c)  Varicella (chickenpox)-zoster virus: common in childhood; in 10% of adults; 2–5 days after rash

(d)  Cytomegalic inclusion virus: features suggestive of bronchopneumonia

(e)  Epstein-Barr virus

Path:  necrosis of ciliated epithelial cells, goblet cells, bronchial mucous glands with frequent involvement of peribronchial tissues + interlobular septa

Clinical syndromes:

1.   (Common) cold = mild upper respiratory tract symptoms ← tonsillopharyngitis, pharyngitis, epiglottitis, sinusitis, otitis media, conjunctivitis

•  sore throat, runny nose, congestion, sneezing, cough

•  headache, fever (milder than for influenza)

Cause:   > 200 different viruses other than influenza; Most common: rhinovirus (30–80%), coronavirus (15%), influenza virus (10–15%)

2.   Influenza

•  abrupt fever > 100° F (38° C), chills and sweats, headache, myalgias, malaise, fatigue, weakness

•  nasal congestion, sore throat, dry persistent cough

Cause:   influenza virus types A, B, C constantly changing (= antigenic drift + shift)

Viral Pneumonia in Childhood


tracheitis, bronchitis, bronchiolitis with peribronchial infiltrates → increased secretion of mucus + constriction of bronchi → narrowing of airways → increased resistance to air flow → air trapping → increase in residual volume; injury to alveolar cells with hyaline membranes; necrosis of alveolar walls with blood, edema, fibrin, macrophages within alveoli

Age:  most common cause of pneumonia in children < 5 years of age; adults have usually acquired immunity

•  retractions, tachypnea, air hunger, respiratory distress

Distribution:   usually bilateral

Accuracy of CXR:   92% NPV, 30% PPV

√  hyperaeration + air trapping (best indicator!):

√  depression of diaphragm on both views:

(a)  projects below anterior 6th rib

(b)  projects below posterior 8th/10th rib on lordotic view

(c)  loss of diaphragmatic dome on lateral view

√  increase in transverse diameter of chest

√  bowing of sternum upward + outward

√  increased anteroposterior diameter on lateral view

√  “dirty chest” = peribronchial cuffing + opacification:

√  symmetric parahilar peribronchial linear densities ← patchy atelectasis

√  bronchial wall thickening

√  interstitial pattern

√  segmental + subsegmental atelectasis with frequently changing distribution ← dislodgement of mucus plugs (common):

√  wedge-shaped / triangular densities

√  airspace pattern (50%) ← hemorrhagic edema

√  pleural effusion (20%)

√  hilar adenopathy (3%)

√  striking absence of pneumatoceles, lung abscess, pneumothorax

√  radiographic resolution lags 2–3 weeks behind clinical


(1)  Bacterial superinfection (child becomes toxic after a week of sickness, peripheral consolidations + air bronchograms + pleural effusion)


(2)  Bronchiectasis


(3)  Unilateral hyperlucent lung, bronchiolitis obliterans

◊  Atypical measles pneumonia does NOT show the typical radiographic findings of viral pneumonias!

Viral Pneumonia in Adulthood

Clinical groups:

(a)  atypical pneumonia in healthy host

(b)  viral pneumonia in immunocompromised host

Risk factors:   very young & old age, malnutrition, immunologic disorders


(a)  diffuse alveolar damage (intraalveolar edema, fibrin, variable cellular infiltrate with hyaline membrane)

(b)  intraalveolar hemorrhage

(c)  interstitial (intrapulmonary / airway) inflammatory cell infiltration


√  unilateral / patchy bilateral areas of consolidation

◊  Lobar consolidation is uncommon!

√  nodular opacities

√  bronchial wall thickening

√  small pleural effusion


√  disturbances of parenchymal attenuation:

√  patchy inhomogeneities = mosaic attenuation (= bronchiolar inflammation / cicatricial scarring → bronchiolar obstruction → alveolar hypoventilation):

√  area of decreased attenuation persists during expiration ← air trapping

√  lobular ground-glass opacities (= thickening of interstitium + partial filling of airspaces)

√  pulmonary consolidation:

√  patchy + poorly defined (bronchopneumonia)

√  focal + well defined (lobar pneumonia)

√  nodules < 10 mm

√  centrilobular micronodules

√  tree-in-bud of small airway disease

=  dilated centrilobular bronchioles, their lumina impacted with mucus / fluid / pus

√  widespread smooth interlobular septal thickening ± crazy paving pattern

√  bronchial ± bronchiolar wall thickening

Cx:  acute pneumonia with rapid progression to ARDS

Round Pneumonia


=  fairly spherical pneumonia caused by pyogenic organisms

Pathophysiology:   in young children only few intraalveolar pores of Kohn + bronchoalveolar channels of Lambert have developed to allow collateral air drift

Organism:  Haemophilus influenzae, Streptococcus, Pneumococcus

Age:     children >> adults

•  cough, chest pain, fever of ≥ 104° F (40° C)

Location:   always posterior, usually in lower lobes

√  spherical infiltrate with slightly fluffy borders + air bronchogram

√  triangular infiltrate abutting a pleural surface (usually seen on lateral view)

√  rapid change in size and shape

Cavitating Pneumonia

1.   Staphylococcus aureus

2.   Haemophilus influenzae

3.   S. pneumoniae

other gram-negative organisms (eg, Klebsiella)

Cavitating Opportunistic Infection

◊  Repeated infections in same patient are not necessarily due to same organism!


1.   Aspergillosis

2.   Nocardiosis

3.   Mucormycosis (= phycomycosis)


C.  TUBERCULOSIS (nummular form)


1.   Anaerobic organisms

DDx:  Metastatic disease in carcinoma / Hodgkin lymphoma

Recurrent Pneumonia in Childhood


1.   Immune deficiency

2.   Chronic granulomatous disease of childhood (males)

3.   Alpha 1-antitrypsin deficiency


1.   Gastroesophageal reflux

2.   H-type tracheoesophageal fistula

3.   Disorder of swallowing mechanism

4.   Esophageal obstruction, impacted esophageal foreign body


1.   Sequestration

2.   Bronchopulmonary dysplasia

3.   Cystic fibrosis

4.   Atopic asthma

5.   Bronchiolitis obliterans

6.   Sinusitis

7.   Bronchiectasis

8.   Ciliary dysmotility syndromes

9.   Pulmonary foreign body


Parenchymal Lung Disease on 1st Day of Life

◊  Radiographic findings overlap!

1.   Transient tachypnea of newborn

2.   Respiratory distress syndrome

3.   Neonatal pneumonia

4.   Meconium aspiration syndrome

5.   Prematurity with accelerated lung maturity (see below)

Air Leaks in Neonatal Chest

=  intrathoracic extra-alveolar gas

1.   Pulmonary interstitial emphysema

2.   Pneumomediastinum

3.   Pneumothorax

4.   Gas below visceral pleura

√  gas at lung base / against fissure

5.   Pneumopericardium

6.   Gas embolus to cardiac chambers / blood vessels

Mediastinal Shift & Abnormal Aeration in Neonate


1.   Congenital diaphragmatic hernia

2.   Chylothorax

3.   Cystic adenomatoid malformation


1.   Congenital lobar emphysema

2.   Persistent localized pulmonary interstitial emphysema

3.   Obstruction of mainstem bronchus (by anomalous or dilated vessel / cardiac chamber)

Pulmonary Infiltrates in Neonate

mnemonic:   I HEAR

Infection (pneumonia)




Respiratory distress syndrome

Reticulogranular Densities in Neonate

1.   Respiratory distress syndrome (90%): premature infant, inadequate surfactant

2.   Prematurity with Accelerated Lung Maturity (PALM)


premature infant with normal surfactant ← maternal steroid therapy / intrauterine stress

√  lung granularity (= almost clear chest)

√  small thymus (stress / steroids)

3.   Transient tachypnea of the newborn

4.   Neonatal group-B streptococcal pneumonia

5.   Idiopathic hypoglycemia

6.   Congestive heart failure

7.   Early pulmonary hemorrhage

8.   Infant of diabetic mother




1.   Lung agenesis-hypoplasia complex

2.   Congenital pulmonary airway malformation

3.   Congenital lobar overinflation / emphysema

4.   Bronchial atresia

5.   Bronchogenic cyst


1.   Absence of main pulmonary artery

2.   Pulmonary sling = Anomalous origin of left pulmonary a.

3.   Anomalous pulmonary venous drainage

4.   Pulmonary arterial / AV malformation


1.   Scimitar / hypogenetic lung / congenital pulmonary venolobar syndrome

2.   Bronchopulmonary sequestration

3.   Congenital pulmonary airway malformation = cystic adenomatoid malformation

Hypogenetic Lung Syndrome

=  collective name for congenital underdevelopment of one / more lobes of a lung separated into 3 forms:

1.   Pulmonary agenesis

=  complete absence of a lobe + its bronchus


√  missing bronchus + lobe(s)

2.   Pulmonary aplasia

=  rudimentary bronchus ending in blind pouch + absence of parenchyma + vessels

Incidence:   1÷10,000; R÷L = 1÷1


√  absence of ipsilateral pulmonary artery

√  bronchus terminates in dilated blind pouch

√  absence of ipsilateral pulmonary tissue

3.   Pulmonary hypoplasia

=  completely formed but congenitally small bronchus with rudimentary parenchyma + small vessels

Developmental causes:

resulting in intrauterine compression of chest

(a)  Idiopathic (rare)

(b)  Extrathoracic compression (= Potter syndrome)

1.   Oligohydramnios (renal agenesis, bilateral cystic renal disease, obstructive uropathy, premature rupture of membranes)

2.   Fetal ascites

(c)  Thoracic cage compression

1.   Thoracic bone dysplasia: Ellis-van Creveld, Jeune, thanatophoric dystrophy, severe achondroplasia

2.   Muscular disease

(d)  Intrathoracic compression

1.   Diaphragmatic defect

2.   Excess pleural fluid

3.   Large intrathoracic cyst / tumor


1.   Mass

=  any localized density not completely bordered by fissures / pleura

2.   Consolidative (alveolar) pattern

=  commonly produced by filling of air spaces with fluid (transudate / exudate) / cells / other material, ALSO by alveolar collapse, airway obstruction, confluent interstitial thickening

ground glass   =   hazy area of increased attenuation not obscuring bronchovascular structures

consolidation  =   marked increase in attenuation with obliteration of underlying anatomic features

3.   Interstitial pattern

4.   Vascular pattern

(a)  increased vessel size: CHF, pulmonary arterial hypertension, shunt vascularity, lymphangitic carcinomatosis

(b)  decreased vessel size: emphysema, thromboembolism

5.   Bronchial pattern

√  wall thickening: bronchitis, asthma, bronchiectasis

√  density without air bronchogram (= complete airway obstruction)

√  lucency of air trapping (= partial airway obstruction with ball-valve mechanism)


Classic appearance of airspace consolidation:

mnemonic:   A2BC3

√  Acinar rosettes: rounded poorly defined nodules of acinus size (6–10 mm), best seen at periphery of opacity

√  Air alveologram / bronchogram

√  Butterfly / bat-wing distribution: perihilar / bibasilar

√  Coalescent / confluent cloudlike ill-defined opacities

√  Consolidation in diffuse, perihilar / bibasilar, segmental / lobar, multifocal / lobular distribution

√  Changes occur rapidly (labile / fleeting)


√  poorly marginated densities within primary lobule (up to 1 cm in size)

√  rapid coalescence with neighboring lesions in segmental distribution

√  predominantly central location with sparing of subpleural zones

√  air bronchograms

Diffuse Airspace Disease

=  alveoli filled with


1.   Lobar pneumonia

2.   Bronchopneumonia: especially gram-negative organisms

3.   Unusual pneumonia

(a)  viral: extensive hemorrhagic edema especially in immunocompromised patient with hematologic malignancy + transplant

(b)  Pneumocystis

(c)  fungal: Aspergillus, Candida, Cryptococcus, Phycomycetes

(d)  tuberculosis

4.   Complication of pneumonia = lung abscess


1.   Trauma: contusion

2.   Pulmonary embolism, thromboembolism

3.   Bleeding diathesis: leukemia, hemophilia, anticoagulants, DIC, immune thrombocytopenia (ITP)

4.   Vasculitis:

Wegener granulomatosis, Goodpasture syndrome, SLE, mucormycosis, aspergillosis, Rocky Mountain spotted fever, infectious mononucleosis

5.   Idiopathic pulmonary hemosiderosis

6.   Bleeding metastasis: eg, choriocarcinoma


1.   Cardiac edema

2.   Neurogenic edema

3.   Hypoproteinemia

4.   Fluid overload

5.   Renal failure

6.   Radiotherapy

7.   Shock

8.   Toxic inhalation

9.   Drug reaction

10.   Drowning

11.   Aspiration

12.   Adult respiratory distress syndrome


1.   Phospholipoprotein: Pulmonary alveolar proteinosis

2.   Mucus plugging


(a)  malignant: bronchioloalveolar cell carcinoma, lymphoma

(b)  T4 lymphocytes: sarcoidosis

(c)  Neutrophils: infection

(d)  Eosinophils: eosinophilic pneumonia

(e)  Plasma cells, mast cells: hypersensitivity pneumonitis

simulating airspace disease, eg, “alveolar sarcoid”

mnemonic:   AIRSPACED


Inhalation, Inflammatory

Renal (uremia)


Proteinosis (alveolar)

Alveolar cell carcinoma

Congestive (CHF)


Drug reaction, Drowning

Air-space Opacification in Trauma


1.   Pulmonary contusion

2.   Pulmonary laceration

3.   Aspiration pneumonia

4.   Atelectasis ← splinting / mucous plug

5.   Pulmonary edema: cardiogenic / noncardiogenic

B.  SUBACUTE PHASE (> 24 hours) add

1.   Fat embolism

2.   Adult respiratory distress syndrome

Localized Airspace Disease

mnemonic:   4P’s & TAIL


Pulmonary edema

Pulmonary contusion

Pulmonary interstitial edema


Alveolar cell carcinoma



Acute Alveolar Infiltrate

mnemonic:   I 2 CHANGE FAST






Near drowning

Goodpasture syndrome



Allergic sensitivity

Shock lung


Chronic Alveolar Infiltrate

mnemonic:   STALLAG



Alveolar cell carcinoma


Lipoid pneumonia

Alveolar proteinosis

Goodpasture syndrome

CT Angiogram Sign

=  homogeneous low attenuation of lung consolidation, which allows vessels to be clearly seen

1.   Lobar bronchioloalveolar cell carcinoma

2.   Lobar pneumonia

3.   Pulmonary lymphoma

4.   Extrinsic lipid pneumonia

5.   Pulmonary infarction

6.   Pulmonary edema

Migratory / Fleeting Pulmonary Opacities

1.   Simple pulmonary eosinophilia

2.   Pulmonary hemorrhage

3.   Pulmonary vasculitis

4.   Cryptogenic organizing pneumonia

5.   Recurrent aspiration / infection


=  thickening of lung interstices (= interlobular septa)


1.   Lymphangitic carcinomatosis

2.   Congenital pulmonary lymphangiectasia

3.   Pulmonary edema

4.   Alveolar proteinosis

B.  PULMONARY VEINS (↑ pulmonary venous pressure)

1.   Left ventricular failure

2.   Venous obstructive disease


1.   Interstitial edema

2.   Chronic interstitial pneumonia

3.   Pneumoconioses

4.   Collagen-vascular disease

5.   Interstitial fibrosis

6.   Amyloid

7.   Tumor infiltration within connective tissue

8.   Desmoplastic reaction to tumor

Path:   stereotypical inflammatory response of alveolar wall to injury

(a)  acute phase: fluid + inflammatory cells exude into alveolar space, mononuclear cells accumulate in edematous alveolar wall

(b)  organizing phase: hyperplasia of type II pneumocytes attempt to regenerate alveolar epithelium, fibroblasts deposit collagen

(c)  chronic stage: dense collagenous fibrous tissue remodels normal pulmonary architecture

Characterizing criteria:

(a)  distribution:

›  vertical distribution: upper / lower lung zones

›  horizontal distribution : axial (core) / parenchymal (middle) / peripheral compartment

(b)  volume loss

(c)  time course

(d)  interstitial lung pattern

Classification scheme:

A.  Interstitial pneumonia

1.   Usual interstitial pneumonia (UIP)

2.   Nonspecific interstitial pneumonia (NSIP)

3.   Acute interstitial pneumonia (AIP)

4.   Alveolar macrophage pneumonia (AMP) = desquamative interstitial pneumonia (DIP)

5.   Bronchiolitis obliterans organizing pneumonia

B.  Diffuse infiltrative disease with granulomas

1.   Sarcoidosis

2.   Hypersensitivity pneumonitis

C.  Lymphocytic interstitial pneumonia (LIP)

D.  Pneumoconiosis

E.  Interstitial lung disease with cysts

1.   Langerhans cell histiocytosis

2.   Lymphangioleiomyomatosis

F.  Interstitial lung disease with interlobular septal thickening

1.   Lymphangitic carcinomatosis

2.   Interstitial pulmonary edema

3.   Alveolar proteinosis

G.  Eosinophilic syndrome

H.  Pulmonary hemorrhage

I.  Vasculitis

Interstitial Lung Pattern on CXR


(a)  Kerley lines = septal lines = thickened connective septa

Path:   accumulation of fluid / tissue

√  Kerley A lines = relatively long fine linear shadows in upper lungs, deep within lung parenchyma radiating from hila

√  Kerley B lines = short horizontally oriented peripheral lines extending + perpendicular to pleura in costophrenic angles + retrosternal clear space

(b)  reticulations

=  innumerable interlacing linear opacities suggesting a mesh / network

√  Kerley C lines = fine “spider web / lacelike” polygonal opacities distributed primarily in a peripheral / subpleural location

Path:   pulmonary fibrosis (lower lobes), hypersensitivity pneumonitis (upper lobes)

√  thick linear opacities in a central / perihilar distribution

Path:   (a)   dilated thick-walled bronchi of bronchiectasis

(b)  cysts of lymphangioleiomyomatosis / tuberous sclerosis


=  small well-defined innumerable uniform 3–5-mm nodules with even distribution

Path:   diffuse metastatic disease, infectious granulomatous disease (TB, fungal), noninfectious granulomatous disease (pneumoconioses, sarcoidosis, eosinophilic granuloma)

3.   DESTRUCTIVE FORM = honeycomb lung

Signs of Acute Interstitial Disease

√  peribronchial cuffing = thickened bronchial wall + peribronchial sheath (when viewed end on)

√  thickening of interlobular fissures

√  Kerley lines

√  perihilar haze = blurring of hilar shadows

√  blurring of pulmonary vascular markings

√  increased density at lung bases

√  small pleural effusions

Signs of Chronic Interstitial Disease

◊  HRCT ~ 60% more sensitive than CXR

√  irregular visceral pleural surface

√  reticulations:

√  fine reticulations

=  early potentially reversible / minimal irreversible alveolar septal abnormality

(1)  Idiopathic pulmonary fibrosis (basilar predominance)

√  coarse reticulations

in 75% related to environmental disease, sarcoidosis, collagen-vascular disorders, chronic interstitial pneumonia

√  nodularity:

in 90% related to infectious / noninfectious granulomatous process, metastatic malignancy, pneumoconioses, amyloidosis

√  linearity:

(1)  Cardiogenic / noncardiogenic interstitial pulmonary edema

√  symmetric linearity

(2)  Lymphangitic malignancy

√  asymmetric linearity

(3)  Diffuse bronchial wall disorders: cystic fibrosis, bronchiectasis, hypersensitivity asthma

√  honeycombing

=  usually subpleural clustered cystic air spaces < 1 cm in diameter with thick well-defined walls set off against a background of increased lung density (end-stage lung)

Distribution of Interstitial Disease

Perihilar Interstitial Lung Disease

(a)  acute rapidly changing

1.   Pulmonary edema

2.   Pneumocystis pneumonitis

3.   Early extrinsic allergic alveolitis

(b)  chronic slowly progressive

1.   Lymphangitic carcinomatosis:
often unilateral, associated with adenopathy, pleural effusion

Peripheral Interstitial Lung Disease

(a)  acute rapidly changing

1.   Interstitial pulmonary edema with Kerley B lines (most common)

2.   Active fibrosing alveolitis

(b)  chronic slowly progressive

1.   Secondary pulmonary hemosiderosis

Upper Interstitial Lung Disease

(a)  chronic slowly progressive ± volume loss

1.   Postprimary TB (common)

2.   Silicosis (common)

(b)  chronic slowly progressive with volume loss

1.   Sarcoidosis (common)

2.   Ankylosing spondylitis (rare)

3.   Sulfa drugs (rare)

(c)  chronic slowly progressive without volume loss

1.   Extrinsic allergic alveolitis

2.   Eosinophilic granuloma

3.   Aspiration pneumonia

4.   Postradiation pneumonitis

5.   Recurrent Pneumocystis carinii pneumonia (PCP) under aerosolized pentamidine prophylaxis

mnemonic:   SHIRT CAP




Radiation therapy

Tuberculosis (postprimary)

Chronic extrinsic alveolitis

Ankylosing spondylitis

Progressive massive fibrosis

Chronic Diffuse Infiltrative Lung Disease


Prevalence:   up to 15% of pulmonary conditions

Cause:  > 200 described disorders; in only 25–30% known / established etiology; 15–20 diseases comprise > 90% of cases

•  dyspnea (primary complaint)

•  dry basilar rales / crackles that fail to clear with coughing


◊  Difficult to characterize due to similar findings

◊  Differentiation into alveolar + interstitial disease is unreliable as “interstitial disease” invariably involves alveoli + vice versa

√  ± nonspecific abnormality

mnemonic:   HIDE FACTS

Hamman-Rich, Hemosiderosis

Infection, Irradiation, Idiopathic

Dust, Drugs

Eosinophilic granuloma, Edema

Fungal, Farmer’s lung

Aspiration (oil), Arthritis (rheumatoid, ankylosing spondylitis)

Collagen vascular disease

Tumor, TB, Tuberous sclerosis

Sarcoidosis, Scleroderma

Zonal Predilection of Chronic Diffuse Parenchymal Lung Disease (DPLD)


=  zone with higher oxygen tension and pH, but less efficient lymphatic drainage

(a)  inhalational disease

1.  Silicosis

2.  Coal worker pneumoconiosis

3.  Extrinsic allergic alveolitis

4.  Aspiration pneumonia

(b)  granulomatous disease

1.  Sarcoidosis

2.  Langerhans cell histiocytosis (EG)

3.  Postprimary TB (common)

(c)  others

1.  Cystic fibrosis

2.  Ankylosing spondylitis

3.  Chronic interstitial pneumonia

4.  Sulfa drugs (rare)

5.  Radiation pneumonitis

6.  Recurrent Pneumocystis carinii pneumonia (PCP) under aerosolized pentamidine prophylaxis

mnemonic:   CASSET

Cystic fibrosis

Ankylosing spondylitis



Eosinophilic granuloma

Tuberculosis, fungus


lower lung zone = zone with greater ventilation, perfusion, and lymphatic drainage

1.   Idiopathic pulmonary fibrosis: usual interstitial pneumonia (common)

2.   Lymphangitic carcinomatosis

3.   Collagen vascular disease: scleroderma (common)

4.   Asbestosis (posterior aspect of lung base)

5.   Lymphangioleiomyomatosis

6.   Chronic aspiration pneumonia with fibrosis (often regional + unilateral)

mnemonic:   BAD LASS RIF




Lymphangitic spread




Rheumatoid arthritis

Idiopathic pulmonary fibrosis


Compartmental Predilection of Chronic DPLD


=  peribronchial vascular bundles + lymphatics

1.   Sarcoidosis

2.   Lymphangitic carcinomatosis

3.   Lymphoma

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Jun 29, 2017 | Posted by in GENERAL RADIOLOGY | Comments Off on CHEST

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