Today, I review, link to, and excerpt from Anasarca from StatPearls. Sri Rama Surya Tez Kattula; Akshay Avula; Krishna M. Baradhi1. Last Update: October 12, 2023.
All that follows is from the above resource.
Introduction
Anasarca is severe generalized fluid accumulation in the interstitial space. This generalized edema can result either when capillary filtration exceeds the fluid removed via lymphatic drainage, when intravascular hydrostatic pressure increases, when the permeability of the endothelial barrier increases, when oncotic pressure within the capillary decreases, or when oncotic pressure changes from low protein states. In contrast to peripheral edema, which is localized to specific areas, anasarca is characterized by massive and generalized swelling. Various clinical conditions can cause anasarca, including heart failure, renal failure, liver failure, or impairment of the lymphatic system. The presentation of anasarca in patients may vary, but it typically becomes clinically apparent when the interstitial volume exceeds 2.5 to 3L.[1][2][3] The characteristic feature is a significant accumulation of fluid in the interstitial spaces, resulting in noticeable swelling in multiple body areas, including the legs, arms, face, abdomen, and elsewhere.
Anasarca is not a standalone disease but rather a symptom of an underlying medical condition, primarily diagnosed through clinical evaluation. While diagnostic tests can aid in assessing the extent and areas of swelling, their primary purpose is to identify the root cause. Treatment typically involves the use of diuretics and addressing the underlying cause. Therefore, it is crucial to diagnose and treat the underlying condition promptly.[4]
Etiology
Anasarca is a condition characterized by severe generalized edema of the body. Due to various underlying pathologies, the etiology can be varied. It usually occurs due to the shift in the Starling forces that regulate fluid movement between blood vessels and the interstitium. A multitude of conditions can potentially lead to anasarca, including the following:
Epidemiology
Research on the precise occurrence of anasarca is quite scarce. Peripheral edema, a more commonly observed clinical condition, is estimated to affect roughly 20% of adults aged >50 years.[4] In contrast, one study reported that the incidence of anasarca in postoperative patients undergoing abdominal surgery was approximately 29.87%.[10]
Pathophysiology
The primary pathophysiological mechanisms underlying anasarca involve several factors: an elevation in capillary hydrostatic pressure, increased capillary permeability, a lower plasma oncotic pressure, lymphatic obstruction, or a combination of these. These mechanisms collectively lead to severe fluid retention in the interstitial space. Conditions that can cause increased capillary hydrostatic pressure include heart failure, kidney disease, early cirrhosis, pregnancy, medications (eg, amlodipine), or conditions characterized by venous obstruction or insufficiencies, such as deep venous thrombosis or hepatic venous congestion. Increased capillary permeability may result from burns, trauma, sepsis, allergic reactions, or malignant ascites. Hypoalbuminemia, which causes decreased plasma oncotic pressure, is associated with conditions like nephrotic syndrome, liver disease, and malnutrition, while malignancy and lymphatic dissection can lead to lymphatic obstruction.[11][12]
The physiologic abnormalities underlying anasarca stem from an imbalance in the forces that regulate fluid movement between vasculature and surrounding tissues, resulting in widespread fluid accumulation in the interstitial spaces throughout the body. Plasma oncotic pressure is primarily determined by the osmotic pressure exerted by blood proteins, especially albumin, in the blood vessels.[13] These proteins help retain fluid within the vessels, preventing excessive leakage into the tissues. Conditions that lead to low levels of plasma proteins can lead to decreased oncotic pressure and fluid retention in tissues. Another mechanism contributing to severe edema is an increase in vascular hydrostatic pressure. Reduced capillary hydrostatic or interstitial oncotic pressure favors fluid movement into the capillaries, known as absorption. However, when capillary hydrostatic or interstitial oncotic pressure rises, fluid shifts out of capillaries, a process called filtration. Additionally, an increase in the permeability of capillary walls can also lead to an increased outflow of fluid and proteins.[14]
As a result of these pathophysiological mechanisms, fluid moves from the vascular space to the interstitium, reducing plasma volume. This decrease in tissue perfusion triggers renal retention of sodium and water, setting off a cascade of effects that worsen interstitial fluid retention. Some excess fluid gained will be retained in the intravascular compartment, but the alteration in capillary hemodynamics causes most of the retained fluid to enter the interstitium, eventually becoming apparent as edema or anasarca.
History and Physical
Clinical Presentation
Anasarca is extensive and generalized fluid accumulation in various body tissues, which may affect multiple areas, including subcutaneous tissues, lungs, abdomen, and extremities. The clinical presentation of anasarca can include the following:
The patient’s history should be comprehensive, including medical, surgical, and medication history. Some medications (eg, amlodipine), postsurgical complications, and comorbidities can result in edema.[19] Clinicians should also inquire about the history of anasarca, including symptom onset and duration, affected areas, associated pain, and positional effects (eg, improvement of edema with elevation). Other symptoms (eg, dyspnea, chest pain) should be included in a detailed history, along with the onset or exacerbation of systemic conditions (eg, congestive heart failure, renal disease, or hepatic disease) that can cause chronic fluid accumulation. An accurate symptom history can help guide clinicians to the correct underlying etiology. For example, venous insufficiency causing dependent edema is often observed to improve with elevation. Conversely, edema caused by decreased plasma oncotic pressure associated with malabsorption or nephrotic syndrome does not improve with positional changes. Therefore, obtaining a careful history can help exclude differential diagnoses.[4]
Physical Examination
Anasarca is primarily diagnosed through characteristic findings on physical examination. Vital signs may reflect conditions secondary to fluid overload (eg, tachycardia, tachypnea, decreased oxygen saturation).[20] Physical examination should focus on identifying the edema pattern, such as peripheral versus generalized and pitting versus nonpitting edema. Clinical findings can also aid in establishing the underlying etiology, which will help guide management. For instance, pitting reflects the movement of excess interstitial water in response to pressure, usually seen in dependent areas, typically the lower extremities in ambulatory patients, and over the sacrum in bed-bound patients. Nonpitting edema more commonly suggests lymphatic obstruction or myxedema associated with hypothyroidism. Ascites suggest a primary hepatic disease, while signs of volume overload or heart failure may indicate cardiovascular-associated anasarca.[4] The following are common exam findings with anasarca:
Evaluation
The primary focus of anasarca evaluation is identifying the underlying cause and excluding differential diagnoses. Clinicians from various specialties (eg, cardiology, nephrology, gastroenterology, and oncology) frequently must collaborate to determine the primary etiology because multiple organ systems (eg, urinary, cardiovascular, and respiratory) are affected simultaneously.[22] Assessment may include the following studies to diagnose potential etiologies leading to anasarca.
Laboratory Studies
Imaging Studies
