Why is it important that a patient comes to clinic because her eyelids are suddenly puffy or her legs are swollen?

Normal fluid homeostasis is critical to orderly cellular functioning, and although mild edema may be simply annoying, pulmonary or cerebral edema may be rapidly fatal.

I. Fluid distribution

~60% of lean body weight is water

~2/3 is intracellular

~1/3 is extracellular (mostly interstitial)

~5% of total body water is in blood plasma

2. Edema — increased fluid in the interstitial tissue spaces

1. Fluid collections in different body cavities may have various designations

Hydrothorax (pleural effusion)

Hydropericardium

Hydroperitoneum (usually called ascites)

Anasarca is severe, generalized edema with profound subcutaneous tissue swelling

 

2. Etiologies of Edema
   

   Categories of Edema — Table 5-1

   Increased Hydrostatic Pressure

   Reduced Plasma Osmotic Pressure

   Lymphatic Obstruction

   Sodium Retension

   Inflammation

   largely related to local increases in vascular permiability

   (Edema occurring in hydrodynamic derangements is usually a transudate: protein-poor, specific gravity < ~1.012 to 1.015, usually with few cells. Edema occurring in inflammatory conditions is usually an exudate: protein-rich, specific gravity >~1.015 to 1.020, often with inflammatory components such as leucocytes, fibrin, etc.) What are some examples of situations in which a transudate occurs versus an exudate?)

1. Increased Hydrostatic Pressure

1. Local

e.g., Impaired venous outflow, such as in deep venous thrombosis, or lower extremity inactivity with prolonged dependency

2. Generalized

1. Reduced Plasma Osmotic Pressure

1. Excessive loss or reduced synthesis of albumin (which is the serum protein most responsible for maintaining colloid osmotic pressure)

i. Nephrotic syndrome

Leaky glomerular capillary wall, albumin loss, and generalized edema

ii. Diffuse liver pathology or protein malnutrition

Reduced albumin synthesis

2. Decreased albumin leads to reduced plasma osmotic pressure, with subsequent net movement of fluid into interstitial tissues and resultant plasma volume contraction. In spite of sodium and water retention, plasma volume deficit cannot be corrected because low serum protein persists.

1. Lymphatic obstruction — usually localized; inflammatory versus neoplastic

1. Filariasis — elephantiasis
2. Carcinoma

1. Obstruction

1. Secondary to therapy — e.g., axillary node dissection at time of diagnosis (as with breast carcinoma) or post-irradiation

1. Increased hydrostatic pressure due to intravascular fluid volume expansion
2. Diminished vascular colloid osmotic pressure

 

C. Morphology of Edema

Usually recognized "grossly" rather than microscopically, in which edema is seen as subtle cell swelling with clearing and separation of extracellular matrix elements

 

1. Subcutaneous tissues

1. Diffuse distribution— e.g., renal dysfunction, nephrotic syndrome

 

i. Affects all parts of body equally

i. Initially may be more obvious in tissues with loose connective tissue matrix such as eyelids (periorbital edema)

2. More conspicuous in site of higher hydrostatic pressure — "dependent"

Prominent feature of congestive heart failure (particularly right heart failure)

3. "Pitting" edema versus “nonpitting edema”

1. Pulmonary edema

1. Typical in left heart failure, but also in renal failure, adult respiratory distress syndrome, infection (pneumonia), hypersensitivity reactions

 

1. Grossly, lungs are heavy with frothy, blood-tinged fluid that is mixture of air, edema fluid, and red blood cells

1. Brain edema

1. Localized to sites of injury

1. Abscess
2. Neoplasm

 

b. Generalized — brain is grossly swollen with narrowed sulci and distended, flattened gyri

1. Encephalitis
2. Hypertensive crises
3. Obstruction to venous outflow

1. Trauma may cause localized or generalized edema

1. Clinical correlations

2. Hyperemia and Congestion — local increased volume of blood in a particular tissue or area

1. Hyperemia — active process resulting from augmented tissue inflow because of arteriolar dilation; tissue is redder than surrounding areas

1. Skeletal muscle during exercise
2. Sites of inflammation

1. Congestion — passive process resulting from impaired outflow; systemic or local; tissue becomes blue-red (cyanotic), as worsening congestion leads to accumulation of deoxygenated hemoglobin

1. Systemic
2. Local

Congestion and edema commonly occur together: congestion of capillary beds is related to development of edema

Long-standing congestion (chronic passive congestion) results in stasis of poorly oxygenated blood and chronic hypoxia

1. May result in parenchymal cell degeneration, cell death, microscopic scarring
2. Capillary rupture may cause small hemorrhagic foci
3. Breakdown and phagocytosis of red cell debris may result in hemosiderin-laden macrophages

1. Morphology

Cut surfaces of affected tissues — hemorrhagic and wet

 

Pulmonary

1. Acute congestion — engorged alveolar capillaries, alveolar septal edema, intra-alveolar hemorrhage
2. Chronic congestion — thickened and/or fibrotic septae, hemosiderin-laden macrophages

Hepatic

1. Acute congestion — central vein/sinusoids distended with blood, may see central hepatocyte degeneration. Periportal hepatocytes suffer less severe hypoxia.
2. Chronic congestion — central regions of lobules grossly red-brown and slightly depressed (loss of cells)

Capillary bleeding can occur under conditions of chronic congestion.

1. Hemorrhage may be external or may be enclosed within a tissue. Accumulation of blood is called a hematoma.

B. Clinical significance

1.Depends on volume and rate of blood loss

2. Site of hemorrhage is also important

3. Loss of iron and subsequent iron-deficiency anemia may become a diagnostic consideration