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Anasarca
Sri Rama Surya Tez Kattula; Akshay Avula; Krishna M. Baradhi.

Author Information
Last Update: August 14, 2020.

Introduction
Edema is defined as a palpable swelling on the body produced by expansion of the interstitial
fluid volume. This accumulation of fluid in the interstitial space occurs as the capillary filtration
exceeds the amount of fluid take out by lymphatic drainage. When Edema is massive and
generalized, it is called anasarca. It is caused by a variety of clinical conditions like heart failure,
renal failure, liver failure, or problems with the lymphatic system. Edema usually becomes
clinically apparent as the interstitial volume exceeds 2.5 -3 liters.[1][2][3]

Etiology
The most common causes of anasarca seen by the clinician are heart failure, cirrhosis, renal
failure, and pregnancy. Other causes of anasarca are venous obstruction, burns, trauma,
malignancy etc.

Epidemiology
The epidemiology of anasarca is not studied yet, but it is one of the common complaints among
the patients admitted to the hospital. Anasarca is noted in high frequency in patients with organ
dysfunction especially in multi-organ dysfunction.

Pathophysiology
Edema develops as a response to an elevation in capillary hydraulic pressure, increased capillary
permeability, a lower plasma oncotic pressure, or a combination of these changes.
Edema also can be secondary to lymphatic obstruction leading to retained fluid in the interstitial
space. The following are the clinical conditions for the various mechanisms described.[4][5]

An elevation in capillary hydraulic pressure

Heart failure, kidney disease, early cirrhosis, pregnancy, drugs

Venous obstruction or insufficiency states like DVT, hepatic venous congestion

Increased capillary permeability

Burns, trauma, sepsis, allergic reactions, malignant ascites

Lymphatic obstruction

Malignancy, Post lymph node dissection

Hypoalbuminemia

Nephrotic syndrome, liver disease, malnutrition

As a first step, when the fluid moves from the vascular space to the interstitium, it reduces the
plasma volume. This reduces tissue perfusion. Poor tissue perfusion causes retention of sodium
and water by the kidneys. Some of the excess fluid gained will be retained in the intravascular
compartment. However, the alteration in capillary hemodynamics results in most of the retained
fluid entering the interstitium and, eventually, becoming apparent as edema.

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History and Physical

The history should include the timing of the edema, and position changes, and whether it is
unilateral or bilateral, and medication history as well as an assessment for systemic
diseases. Chronic accumulation of more generalized edema is caused by the onset or
exacerbation of systemic conditions such as congestive heart failure (CHF), renal disease, or
hepatic disease. Dependent edema caused by venous insufficiency is more likely to improve with
elevation and deteriorate with dependency. Edema associated with decreased plasma oncotic
pressure (e.g., malabsorption, liver failure, nephrotic syndrome) does not change with
dependency.

The physical examination can aid in establishing the diagnosis. The exam should be focused on
identifying the pattern of edema – peripheral vs. pulmonary edema, pitting vs. non-pitting edema,
and presence of jugular venous distension. Below are the exam findings of common clinical
conditions that can cause anasarca.

Patients with pulmonary edema complain primarily of dyspnea on exertion and orthopnea.
Physical examination usually reveals wet rales, possible diastolic gallop (S3), and heart
murmurs. Cardiac and renal disease are common causes of pulmonary edema. Peripheral edema
is usually detected by the presence of pitting after pressure is applied to the edematous area for at
least 5 seconds. Pitting reflects the movement of the excess interstitial water in response to
pressure. It is usually seen in dependent areas like lower extremities in ambulatory patients and
over the sacrum in patients who are bed-bound. Scrotal edema is also common in males.
Nonpitting edema suggests lymphatic obstruction or hypothyroidism. Acute onset of unexplained
unilateral leg edema should raise the possibility of deep vein thrombosis (DVT). Cirrhotic
patients can develop ascites and then edema in the lower extremities because of an increase in
venous pressure below the diseased liver. The presence of other signs of portal hypertension,
such as distended abdominal wall veins and splenomegaly, also is suggestive of a primary
hepatic disease.

Cause of edema can be determined by noting changes in skin temperature, color, and texture.
Acute DVT and cellulitis may produce increased warmth over the affected area. The deposition
of hemosiderin or chronic venous insufficiency often causes the skin to have a brawny, reddish
hue and commonly involves the medial malleolus. As venous insufficiency progresses, it can
result in lipodermatosclerosis which is associated with marked sclerotic and hyperpigmented
tissue and characterized by fibrosis and hemosiderin deposition that can lead to venous ulcers
over the medial malleolus. The ulcers may progress to deep, weeping erosions. Myxedema from
hypothyroidism presents with a generalized, dry, thick skin with nonpitting periorbital edema and
yellow to orange skin discoloration over the knees, elbows, palms, and soles. Pretibial
myxedema occurs in patients with thyroid disease and is characterized by bilateral, asymmetric,
nonpitting, scaly thickening and induration of the skin. These ulcers may be violaceous or
slightly pigmented (yellow-brown) and often have an orange-peel appearance. The most frequent
location of pretibial myxedema is over the lower legs, especially the pretibial areas or the dorsum
of the foot.

Evaluation
Routine labs tests like a comprehensive metabolic panel can help assess renal function, albumin,
and liver function tests. Urinalysis must be obtained in all children with edema. Dipstick testing
principally detects albumin and need additional protein sulfosalicylic acid precipitation test
(SAS) to detect globulins and Bence-Jones proteins. Urine protein/creatinine ratio or 24-hr urine
for protein can obviate the need for SAS testing. The finding of a markedly positive dipstick for
protein in combination with hypoalbuminemia and clinical edema is virtually diagnostic of a
nephrotic syndrome. Brain natriuretic peptide measurement can give clues to underlying CHF.
Albumin and liver function tests can aid in diagnosing liver cirrhosis. Chest radiography is
helpful in detecting cardiac failure, pulmonary edema, and pleural effusions. Because of safety,
ease of use, and the information provided, the most commonly used radiographic technique in
patients presenting with renal disease is renal ultrasonography. Ultrasonography allows the
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clinician to characterize kidney size and assess for cystic renal disease and hydronephrosis.
Cardiac echocardiography can evaluate ventricular function, assess for the presence of a
pericardial effusion, and aid in the diagnosis of cardiac disease.[6][7]

Echocardiography to evaluate pulmonary arterial pressures is recommended for patients with

obstructive sleep apnea and edema. Venous ultrasonography is the imaging of choice in the
evaluation of suspected DVT. Duplex ultrasonography also can be used to confirm a chronic
venous insufficiency. Magnetic resonance angiography with venography of the lower extremity
and pelvis can be used to evaluate for intrinsic or extrinsic pelvic or thigh DVT. Left iliac vein
compression by the right iliac artery (May-Thurner syndrome) should be suspected in women
who are 18 and 30 years of age and present with edema of the left lower extremity.
Lymphoscintigraphy is the method of choice for evaluating lymphedema when the diagnosis
cannot be made clinically. MRI may aid in the diagnosis of musculoskeletal etiologies like a
gastrocnemius tear or popliteal cyst. T1-weighted magnetic resonance lymphangiography can
visualize the lymphatic channels when lymphedema is suspected.

Treatment / Management
Management of edema is guided by the underlying etiology. This commonly includes chronic
venous insufficiency, lymphedema, DVT, and medication-induced edema. Pulmonary edema is
the only form of generalized edema that is life-threatening and requires immediate therapy. In all
other edematous states, removal of the excess fluid can proceed more slowly as it is not acutely
life-threatening to the patient. In patients with generalized edema due to heart failure, the
nephrotic syndrome, or primary sodium retention, the edema fluid can be mobilized rapidly. In
patients with anasarca, removing 2 to 3 liters or more of edema fluid in 24 hours can ordinarily
be accomplished without a clinically significant reduction in plasma volume. In patients with
localized edema due to venous or lymphatic obstruction or malignant ascites, diuretic therapy
can lead to volume depletion. Diuretic therapy in generalized edematous states is usually begun
with a loop diuretic, such as furosemide. In patients with cirrhosis, the combination
of spironolactone and a loop diuretic is the preferred initial diuretic regimen to prevent
hypokalemia. As hypokalemia predisposes to increased production of ammonia. Higher doses of
diuretics may be required in patients with nephrotic syndrome. Some cases of idiopathic edema
are diuretic-induced, and the initial approach in patients with idiopathic edema who are already
on diuretics is to stop the diuretics for at least 2 to 3 weeks and encourage sodium restriction in
diet. The mainstays of therapy of lower-extremity edema due to venous insufficiency are
mechanical therapies, including leg elevation and compression stockings with 20 to 30 mmHg
for mild edema and 30 to 40 mmHg for severe edema complicated by ulceration. Compression
therapy is contraindicated in patients with a peripheral arterial disease. Local skin and wound
care of venous ulcers is essential in preventing secondary cellulitis and dermatitis. Eczematous
(stasis) dermatitis, characterized by dry, inflamed, scaling skin overlying superficial varicose
veins, often occurs in patients with chronic venous insufficiency. Treatment includes daily
hydration with emollients and short courses of topical steroid creams for the severely inflamed
skin. Primary lymphedema treatment involves complex decongestive physiotherapy, including
manual lymphatic massage and multilayer bandages. The first goal is the improvement of fluid
resorption and continue until achieving the maximum therapeutic response. The maintenance
phase of treatment includes compression stockings at 30 to 40 mmHg. Pneumatic compression
devices can be used to augment standard therapies. Surgical debulking or bypass procedures are
limited to severe refractory cases. Diuretics are not demonstrated to be effective in the treatment
of lymphedema.

Differential Diagnosis

Acute edema blister

Acute kidney injury

Acute myeloid leukemia

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Chronic kidney disease

Congestive heart failure

IgA nephropathy

Liver cirrhosis

Membranoproliferative glomerulonephritis

Pericardial effusion

Ventricular septum defect

Prognosis
Prognosis of anasarca depends on the underlying etiology. Reversible causes may carry favorable
outcomes, whereas irreversible etiologies and malignancies have a poor prognosis. However in
most of the situations, by the time anasarca has developed, the underlying problem has
progressed beyond cure.

Complications
If left untreated, common complications include, but not limited to skin ulcerations, skin
infections, dyspnea, congestive heart failure, and death.

Enhancing Healthcare Team Outcomes

Anasarca is a serious condition leading to generalized accumulation of fluid in the body. Because
there are many causes of anasarca, it is best managed by an interprofessional team of healthcare
workers. The nurse practitioner, physician assistant and primary care giver should refer these
patients to an internist because in many cases, admission is required to determine the diagnosis.
A team approach for management is necessary with support of nurses and
pharmacists. The outcomes of patients with anasarca is guarded, for those with failing organs, the
mortality rates are very high. Even benign causes can require long-term admission and recovery
is a very slow process.

Continuing Education / Review Questions

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References
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