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299© Springer International Publishing AG 2018
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-319-68379-9_18
Introduction
Edema is defined as palpable swelling caused by accumula-
tion of fluid in the interstitial space. Edema can be a localized
phenomenon, or when generalized throughout the body, it is
called anasarca. Different clinical conditions, including local-
ized conditions (e.g., venous and lymphatic disease) and sys-
temic conditions, such as cardiac, liver, and renal disease, can
cause edema. The etiology of edema can usually be deter-
mined by a careful history and a physical examination.
Routine labs can help rule out common conditions that cause
edema.
The Starling forces are involved in maintaining the bal-
ance between the intravascular space and the interstitial
space. Changes to this homeostasis can result in edema [1].
These physiologic forces include the gradient between the
intravascular and extravascular hydrostatic pressures and the
differences in oncotic pressure between the interstitial space
Chapter 18
Edema
Valerie Jorge Cabrera
V.J. Cabrera, MD (*)
Department of Internal Medicine, Section of Nephrology,
Yale University School of Medicine, Boardman Building 114, 330
Cedar Street, PO Box 208029, New Haven, CT 06520-8029, USA
e-mail: Valerie.cabrera@yale.edu
300
and plasma. The hydrostatic pressure within the capillaries
tends to drive fluid out of the capillaries, whereas the oncotic
pressure exerted within the capillaries tends to draw fluid
back. If the hydrostatic capillary pressure is increased or the
capillary oncotic pressure is diminished, a condition favoring
edema results. Conditions causing increased capillary perme-
ability, those affecting the electrolyte balance of the body
with sodium and chloride retention and decreased lymphatic
drainage, can also lead to edema.
Differential Diagnosis
Peripheral edema is a nonspecific finding common to a host
of diseases [2, 3]. The acute edema of a single limb (usually
defined as occurring for less than 72 h) should raise suspicion
for deep vein thrombosis, cellulitis, or a ruptured popliteal
cyst (Fig. 18.1). In those patients with history of recent trauma
or surgery, compartment syndrome should be considered.
There are two types of lower extremity edema, venous edema
and lymphedema. Chronic venous insufficiency is associated
with other chronic skin changes such as hyperpigmentation
and prominent veins. Lymphedema is usually non-pitting, and
the skin has a verrucous aspect. Lastly, obstruction by a
tumor or lymphadenopathy can lead to unilateral edema.
Edema related to systemic conditions is often subacute or
chronic and bilateral, affects the lower extremities, and on
occasion becomes generalized (Fig. 18.1). Certain clues can
orient to the etiology of edema. The presence of jugular
venous distention, positive hepatojugular reflux, an S3 gallop,
rales, and ascites are features of cardiac disease (e.g., conges-
tive heart failure, pulmonary hypertension). Jaundice, ascites,
and asterixis are seen with liver disease, and a frothy urine
could be a manifestation of underlying kidney disease.
Thyroid disease can result in generalized myxedema as seen
in hypothyroidism or pretibial myxedema as seen in hyper-
thyroidism. Idiopathic edema is a diagnosis of exclusion and
may occur in a cyclical fashion.
V.J. Cabrera
301
Key History and Physical Exam
The history should include details about the onset of edema
(acute or chronic), if unilateral or bilateral, if it involves the
upper extremities or lower extremities or is generalized, and
if it is positional (Fig. 18.2) [4]. Associated symptoms should
also be assessed, with emphasis on local skin changes and
presence or absence of pain. The clinician should also inquire
about the presence of other systemic symptoms such as fever,
chills, or weight loss as well as those suggestive of hypervol-
emia. The medication list, including over-the-counter
Fig. 18.1 Systemic and localized causes of edema
18. Edema
302
remedies, should be thoroughly reviewed given that commonly
used medications can be associated with edema (Table 18.1).
Physical examination should focus on evaluating the distri-
bution and severity of edema (Fig. 18.2) [4]. The physician
should evaluate for the presence or absence of pitting by
pressing with his or her finger continuously for 5 s. Pitting
refers to the movement of fluid in the interstitial space when
pressure is applied. The categorization of edema is based on
a scale of 1–4+, and it is useful to describe the distribution of
the pitting (e.g., pedal or pretibial). The Kaposi-Stemmer sign
refers to the inability to form a fold on the skin at the base of
second toe and is suggestive of lymphedema [2, 8]. The skin
should be thoroughly evaluated describing its color, tempera-
ture, and presence of ulcers or palpable vein cords. The sys-
Fig. 18.2 Key history and physical in the evaluation of edema
V.J. Cabrera
303
temic evaluation should include the evaluation for jugular
venous distention, hepatojugular reflux, rales on lung exami-
nation, sacral edema, and ascites.
Decision-Making/Treatment
Edema is a common manifestation of many disease states. In
those with unilateral edema concerning for DVT (Fig. 18.3), a
D-dimer and venous ultrasound can be part of the initial evalu-
ation depending on the level of clinical suspicion [9]. Tests
evaluating serum creatinine, liver function, and serum albumin
level along with urinalysis for proteinuria, presence of white
blood cells, red blood cells, and casts are useful initial labs in
patients with bilateral or generalized edema (Fig. 18.4).
Thyroid- stimulating hormone can also be included if there is
suspicion for thyroid disease. Duplex ultrasonography can also
reveal if there is chronic venous insufficiency and a transtho-
racic echocardiogram (TTE) could be obtained if history and
physical are concerning for heart failure. Ultrasound examina-
tion of the inferior vena cava diameter and collapsibility may
also provide information about hypervolemia.
By directing therapy at correcting the underlying capillary
hemodynamic disturbance, development of edema can be
stopped or reversed. Lifestyle and dietary modification in
conjunction with pharmacotherapy are useful in the long-
Table 18.1 Commonly used medications associated with edema [1,
5–7]
Category Examples
Antihypertensives Amlodipine, minoxidil
Corticosteroids Prednisone, fludrocortisone
Nonsteroidal anti-
inflammatory drugs (NSAIDs)
Ibuprofen
Antidiabetic drugs Pioglitazone
Others Estrogen/progesterone,
testosterone
18. Edema
304
Unilateral edema
Acute <72 hours
Clinical suspicion
for DVT
No: consider other
etiologies (cellulitis,
compartment syndrome,
ruptured popliteal cyst)
Yes
Intermediate/high
Check venous
ultrasond
If positive for
DVT: treat
If negative for
DVT: consider
other etiologies
Negative for DVT:
consider other
etiologies
If negative:
consider other
etiologies
If positive check
venous ultrasound
Positive for DVT:
treat
Check D-dimer
Low
Chronic ≥72 hours
Venous ulcers,
palpable venous
cords suggesting
venous
insufficiency
Check venous
ultrasound
Diagnose clinically.
Proceed with
pelvic imaging to
evaluate for tumor
or thrombosis
Skin thickenning,
positive Stemmer
sign consider
lymphedema
History of
malignancy,
trauma, or surgery
Fig. 18.3 Clinical approach for the patient presenting with unilateral edema
V.J. Cabrera
305
Edema
Bilateral or generalized
H&P suggestive of
systemic disease
Yes
Evaluate for heart
failure, liver cirrhosis,
renal or thyroid disease
Check chemistry, LFTs,
UA, serum albumin,
TSH, echocardiogram
based on clinical
suspicion
Diagnose/Treat
underlying disease
Use diuretics if
appropriate
Emphasize salt
restriction
Any potential culprit
medications
Yes: discontinue
No: consider venous
insufficiency
Check venous US
Positive for venous
insufficiency: treat
If negative consider
lymphedema. Diagnosis
is clinical
No
Fig. 18.4 Clinical approach for the patient presenting with bilateral or generalized edema
18. Edema
306
term management. For the common systemic causes, treat-
ment of the underlying condition is indicated. For those with
chronic venous insufficiency, mechanical therapies such as leg
elevation and compression stockings, as well as judicious
diuretic therapy, are useful, although caution should be taken
in those with peripheral arterial disease. Deep venous throm-
bosis is treated with anticoagulation therapy and cellulitis
with antibiotics. In medication-induced edema, the culprit
medication should be discontinued if possible, and in those
with heart failure, cirrhosis, and nephrotic syndrome, cautious
use of diuretics and salt restriction can be initiated.
Clinical Pearls
• A thorough history and physical examination are
essential.
• Chronic venous insufficiency and cellulitis have common
manifestations: peripheral edema, increase in skin tem-
perature, and erythema. Have in mind that cellulitis is usu-
ally a unilateral process.
Don’t Miss This!
• Deep vein thrombosis presents with acute limb swelling in
a patient with risk factors (e.g., immobilization,
malignancy).
• Compartment syndrome presents with acute limb swelling,
tense skin, and decreased peripheral pulses.
• Heart failure presents with peripheral edema ± pulmonary
edema, jugular venous distention, and ascites.
• Recheck medication list and do not forget over-the-coun-
ter medications: common things are common!
• Think of central venous stenosis causing upper extremity
edema in patients with history of central catheter
placement.
• Facial edema and dilated neck veins are findings of supe-
rior vena cava syndrome.
V.J. Cabrera
307
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18. Edema