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
Cardiac: Left heart failure
Noncardiac
Increased transmural
capillary pressure
Lymphatic block: lymphangitis,
carcinomitosis, lymphangiectasia
Increased intracapillary pressure:
neurogenic, hyperperfusion (high altitude,
postembolic, post transplant)
Lowered extracapillary pressure:
reexpansion edema,
postglottic spasm
Oncotic: nutritional, near-drowning
Combined hemodynamic/oncotic:
renal failure, overhydration
Causes of Pulmonary
1
Edema
Increased capillary
permeability
Injury
Extracapillary (alveolar insult):
Inhalation, aspiration, infection
Noninjury:
Allergic, endocrine
Intracapillary
“Trauma”:
sepsis, hypotension,
Pancreatitis, DIC
Embolism:
fat, air, amniotic fluid
Pathophysiology
2
overview
Normally, excess
hydrostatic transudate
from pulmonary
capillaries is filtered into
peribronchovascular
lymphatics and removed
Pathophysiology


2
overview
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


3
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
Norma
l
Edema
Images courtesy of Dr. Marc Gosselin
Vascular Indistinctness
Norma
l
Edema
Images courtesy of Dr. Marc Gosselin
Peribronchial cuffing


Images shown are preand post-treatment for
hydrostatic edema
Arrowheads point to
Kerley A lines
Septal


3
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 (I’ve 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
can’t name the
lines, you can
see that this
patient has
severe
hydrostatic
edema in need
of treatment!
A
B
C?
Evolving hydrostatic
33 year-old with
AML admitted for
renal failure and
fluid overload
4
edema
Evolving hydrostatic


Arrows indicate peribronchial cuffing
Note increasing size
of azygous vein
4
edema
Evolving hydrostatic


Arrowheads indicate
septal lines
Note ground-glass,
indicating alveolar
edema
4
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


3
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
bronchograms
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 overperfused and predisposed to edema
Higher pressures can result in some capillary
damage and stress failure
High-altitude pulmonary

Radiographs show
patchy ground glass with
a central distribution
favoring peribronchial
cuffing and vascular
indistinctness over septal
lines
3
edema
Neurogenic


3
Edema
Pathophysiology similar to HAPE– neural
mechanisms result in non-uniform
vasoconstriction
High protein content of fluid indicates capillary
leakage involved as well
Neurogenic


3
Edema
Classically, neurogenic edema has an upper lobe
predominance; however, it can present with any
pattern
Often clears rapidly, arguing for intact alveoli
Neurogenic


54 year-old woman
with intracranial
hemorrhage
Note upper lobe
predominance
4
Edema
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
4
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
1
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 Gosselin
“The condition of the capillary endothelium
and that of the alveolar epithelium are the
main determinants”3
References
1Milne
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.
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