Pulmonary

Edema

Pathophysiological Considerations
Manifestations on Chest Radiography

Kathryn Glassberg MS4

February 2006

Pulmonary Edema:
Overview

Pathophysiology : Edema as an end

result of a multitude of diverse insults
(not just heart failure vs. ARDS!)
Physiologic approach for radiologic
evaluation of edema
Hydrostatic edema
Permeability edema +/- diffuse alveolar
damage
Mixed permeability and hydrostatic edema

Pulmonary Edema

Edema occurs when physiologic resorption

of fluid via lymphatics is overwhelmed
Causes usually divided into hydrostatic
and increased capillary permeability, but
both mechanisms can occur in the same
patient!
Chest radiography, when combined with
clinical data, helps distinguish pathologic
cause in vast majority of cases

Causes of Pulmonary
1
Edema
Hydrostatic
Hydrostatic
Cardiac: Left
Left heart
heart failure
failure
Cardiac:

Noncardiac
Noncardiac

Increased transmural
transmural
Increased
capillary pressure
pressure
capillary

Lymphatic block:
block: lymphangitis,
lymphangitis,
Lymphatic
carcinomitosis, lymphangiectasia
lymphangiectasia
carcinomitosis,

Increased intracapillary
intracapillary pressure:
pressure:
Increased
neurogenic, hyperperfusion
hyperperfusion(high
(highaltitude,
altitude,
neurogenic,
postembolic, post
post transplant)
transplant)
postembolic,
Lowered extracapillary
extracapillary pressure:
pressure:
Lowered
reexpansionedema,
edema,
reexpansion
postglottic spasm
spasm
postglottic
Oncotic:nutritional,
nutritional,near-drowning
near-drowning
Oncotic:

Combined hemodynamic/oncotic:
hemodynamic/oncotic:
Combined
renalfailure,
failure, overhydration
overhydration
renal

Causes of Pulmonary
1
Edema
Increased capillary
capillary
Increased
permeability
permeability

Injury
Injury

Extracapillary (alveolar
(alveolar insult):
insult):
Extracapillary
Inhalation, aspiration,
aspiration, infection
infection
Inhalation,

Noninjury:
Noninjury:
Allergic, endocrine
endocrine
Allergic,
Intracapillary
Intracapillary
Trauma:
Trauma:
sepsis, hypotension,
hypotension,
sepsis,
Pancreatitis, DIC
DIC
Pancreatitis,
Embolism:
Embolism:
fat, air,
air, amniotic
amniotic fluid
fluid
fat,

Pathophysiology
overview2
Normally, excess
hydrostatic
transudate from
pulmonary
capillaries is
filtered into
peribronchovascul
ar lymphatics and
removed

Pathophysiology
overview2

In hydrostatic edema,
transudate
accumulates in the
interstitum initially,
only entering alveoli in
severe cases
In permeability edema
associated with diffuse
alveolar damage
(DAD), exudate fills
the interstitum and the
alveoli

Hydrostatic Edema

The lungs can accommodate

increases in fluid: the lymphatic
flow can increase 3-10x before
edema develops
Higher hydrostatic pressures
force fluid through endothelial
cell pores, but the tighter
junctions of epithelial cells
prevent fluid from entering
alveoli until pulmonary capillary
pressures reach ~ 40 mm Hg,
causing stress failure

Hydrostatic Edema:
radiologic manifestations3
Earliest sign: vascular indistinctness
Bronchial wall thickening/peribronchial
cuffing
Septal lines: Kerley A, B, C
Thickened fissures
Severe edema: dependent ground glass
opacities reflecting alveolar involvement
Often associated with bilateral
transudative pleural effusions

Hydrostatic Edema:
radiologic manifestations3

Cephalization or inversion not

specific for edema

Reflects chronic pulmonary venous changes

in patients with left-sided heart failure

Vascular pedicle width

patients with volume overload often have
widened vascular pedicles when compared
to previous studies
However, patients can certainly have
hydrostatic edema despite a narrow pedicle,
thus this sign can be misleading

Vascular indistinctness
Norm
al

Edema

Images courtesy of Dr. Marc Go

Vascular Indistinctness
Norm
al

Edema

Images courtesy of Dr. Marc Go

Peribronchial cuffing

Images shown
are pre- and
post-treatment
for hydrostatic
edema
Arrowheads
point to Kerley A
lines

Septal Lines

The presence of septal lines reflects fluid

accumulation between the lung lobules
Kerley lines
A: long, diagonal, central
B: short, horizontal, extend to lateral pleural
surfaces
C: reticular pattern of ~ 1 cm polygons
representing septal lines viewed on end (Ive
heard Dr. Kerley is the only one who has ever
really seen these)

Septal Lines
Septal lines
in a patient
with cardiac
failure

Septal Lines
Lateral view of
same patient
note fluid in
both fissures

Septal Lines
All three
Kerleys
claim to be
present;
can you
find them?

Septal Lines
Even in you
cant name
the lines, you
can see that
this patient
has severe
hydrostatic
edema in
need of
treatment!

A
B

C?

Evolving hydrostatic
edema4
33 year-old
with AML
admitted for
renal failure
and fluid
overload

Evolving hydrostatic
edema4

Arrows indicate
peri-bronchial
cuffing
Note increasing
size of azygous
vein

Evolving hydrostatic
edema4

Arrowheads
indicate septal
lines
Note groundglass,
indicating
alveolar edema

Permeability Edema

multiple insults can cause increased

pulmonary vessel permeability
resulting in leakage of fluid AND
protein
In its most severe form, the disease
is a combination of vessel
permeability and DAD, leading to the
acute respiratory distress syndrome
(ARDS)

ARDS pathology

Acutely, exudative
edema in the
alveoli causes
hyaline membrane
formation
Type II epithelial
cells then
proliferate and,
usually, fibrosis
occurs

ARDS: Radiologic
manifestations3

Patchy, diffuse ground glass opacities

Pattern of opacification does not change
with position change, as the exudates are
trapped in alveoli
Septal lines, peribronchial cuffing, and
thick fissures are usually ABSENT
In severe cases, air bronchograms can be
seen
Good rule of thumb: presence of ET tube!

ARDS: Radiologic
manifestations3
Caution: While a normal sized heart
and narrow vascular pedicle are
helpful signs, neither is specific for
injury edema

ARDS

Patchy
diffuse
ground glass
Air
bronchogram
s
ET tube

Permeability Edema
without DAD3

Seen in IL-2 therapy for metastatic

disease, hantavirus pulmonary
syndrome
Severe capillary permeability without
alveolar involvement
Radiographically, resembles
hydrostatic edema (septal lines,
peribronchial cuffing) because
alveolar epithelium remains intact

Mixed hydrostatic and

permeability edema

High-altitude pulmonary edema

Neurogenic edema
Reexpansion and post-obstructive

High-altitude pulmonary
edema (HAPE)3

Hypoxia causes non-uniform

pulmonary vasoconstriction, leaving
other lung units over-perfused and
predisposed to edema
Higher pressures can result in some
capillary damage and stress failure

High-altitude pulmonary
edema3

Radiographs show
patchy ground
glass with a
central distribution
favoring
peribronchial
cuffing and
vascular
indistinctness over
septal lines

Neurogenic Edema

Pathophysiology similar to HAPE

neural mechanisms result in nonuniform vasoconstriction
High protein content of fluid
indicates capillary leakage involved
as well

Neurogenic Edema

Classically, neurogenic edema has an

upper lobe predominance; however,
it can present with any pattern
Often clears rapidly, arguing for
intact alveoli

Neurogenic Edema

54 year-old
woman with
intracranial
hemorrhage
Note upper
lobe
predominance

Reexpansion and
Postobstructive Edema3

Both occur in setting of high negative

pleural pressure
Reexpansion: usually seen as localized
lung injury, with alveolar filling and
exudative fluid, arguing for increased
permeability as a cause
Postobstructive: pattern usually
hydrostatic, secondary to increased
central blood volume caused by the relief
of obstruction

Reexpansion Edema4

Right pneumothorax

One-hour post chest-tube placement

Postobstructive Edema

Postextubation Laryngospasm: note

central distribution and
peribronchial cuffing.

Conclusions

Hydrostatic Edema is characterized by

Permeability Edema with DAD (ARDS) is

characterized by

Vascular indistinctness
Peribronchial cuffing
Septal lines/fissure thickening

Diffuse, patchy ground glass opacities

Air bronchograms

Overlap is seen in pathophysiology, thus

can be reflected in the radiograph

Summary Table

Hydrostatic

Permeability
with DAD

Heart size

Often enlarged

Usually not
enlarged

Septal Lines

Common

Absent

Peribronchial
cuffs

Common

Not common

Air
bronchograms

Not common

Very common

Regional
distribution

Even or central

Patchy or
peripheral

Hydrostatic and
Permeability Edema

Images courtesy of Dr. Marc Go

The condition of the capillary

endothelium and that of the
alveolar epithelium are the main
determinants3

References
Milne ENC and Massimo P. Reading the Chest
Radiograph: A Physiologic Approach. Mosby, 1993.
2Ware LB and Matthay MA. Acute pulmonary edema.
The New England Journal of Medicine. 2005; 353:
2788-96.
3Ketai LH and Godwin JD. A new view of pulmonary
edema and acute respiratory distress syndrome.
Journal of Thoracic Imaging. 1998; 13: 147-171.
4Gluecker T. Capasso P. Schnyder P. Gudinchet F.
Schaller MD. Revelly JP. Chiolero R. Vock P. Wicky
S. Clinical and radiologic features of pulmonary
edema. Radiographics. 19(6):1507-31; discussion
1532-3, 1999 Nov-Dec.
1

References

Images taken from:

myweb.lsbu.ac.uk/ ~dirt/museum/p6-71.html

www.bcm.edu/.../cases/ pediatric/text/7a-desc.htm
http://www.hcoa.org/hcoacme/chf-cme/chf00030.htm
http://www-medlib.med.utah.edu/WebPath/LUNGHTML/LUNG131.html
http://www-medlib.med.utah.edu/WebPath/LUNGHTML/LUNG133.html
http://www.lumen.luc.edu/lumen/MedEd/MEDICINE/PULMONAR/CXR/atlas/images/
310a1.jpg
www.high-altitude-medicine.com/ AMS-medical.html
Sherman SC. Reexpansion pulmonary edema: a case report and review of the
current literature. Journal of Emergency Medicine. Jan 2003; 24(1): 23-7.

Thanks to Dr. Marc Gosselin for

images, insights