Edema

Edema is the abnormal accumulation of fluid in the interstitial spaces of tissues (or body cavities). About 60% of lean body weight is water; only ~5% circulates as plasma, and 15% exists as interstitial fluid. When fluid shifts out of the vasculature and exceeds lymphatic drainage capacity, edema results.

Body Fluid Compartments (Normal)

Compartment	% Body Weight
Intracellular fluid	~40%
Extracellular fluid	~20%
- Plasma	~5%
- Interstitial fluid	~15%

Pathophysiology - The Starling Forces

Fluid movement across capillary walls is governed by opposing forces:

Capillary hydrostatic pressure - pushes fluid out of vessels
Plasma colloid osmotic pressure (mainly albumin) - pulls fluid into vessels

Normally, net outflow at the arteriolar end is nearly balanced by reabsorption at the venular end. The small residual filtrate is returned to circulation via lymphatics. Edema occurs when this balance is disturbed:

Factors influencing fluid movement across capillary walls - showing how increased hydrostatic pressure or decreased plasma osmotic pressure causes fluid leak into the interstitium and inadequate lymphatic resorption leads to edema

FIG. 3.2 - Robbins & Kumar Basic Pathology

Causes of Edema

1. Increased Hydrostatic Pressure

Impaired venous return raises capillary hydrostatic pressure, forcing fluid into the interstitium.

Examples:

Congestive heart failure (CHF) - systemic venous hypertension; triggers secondary hyperaldosteronism via RAAS, worsening Na+/H2O retention
Deep venous thrombosis - localized to affected limb
Constrictive pericarditis, hepatic cirrhosis (portal hypertension)
Venous obstruction by external compression or mass
Prolonged dependency of limbs with inactivity

2. Reduced Plasma Osmotic Pressure (Hypoproteinemia)

Albumin provides ~50% of plasma colloid osmotic pressure. A fall in albumin below ~2.5 g/dL significantly impairs fluid resorption.

Causes of low albumin:

Nephrotic syndrome - urinary albumin loss; most important cause of albuminuria
Cirrhosis - reduced hepatic synthesis
Protein malnutrition (e.g., kwashiorkor)
Protein-losing enteropathy

Low albumin → reduced intravascular volume → renal hypoperfusion → secondary hyperaldosteronism → more Na+/H2O retention → worsens edema (a vicious cycle)

3. Lymphatic Obstruction (Lymphedema)

Blockage of lymphatic drainage prevents removal of normal interstitial filtrate, causing protein-rich edema (lymphedema).

Examples:

Filariasis (Wuchereria bancrofti) - fibrosis of inguinal lymphatics causing "elephantiasis" of lower limb/genitalia
Breast cancer - lymphatic invasion causes peau d'orange (orange peel) skin
Post-mastectomy/radiation - axillary lymph node disruption causes arm lymphedema

4. Increased Vascular Permeability

Inflammatory mediators (histamine, bradykinin, cytokines) damage endothelium, allowing protein-rich fluid to leak out (exudate).

Examples: Acute inflammation, burns, sepsis, anaphylaxis

5. Sodium and Water Retention

Primary renal sodium retention expands intravascular volume and raises hydrostatic pressure.

Examples: Acute renal failure, post-streptococcal glomerulonephritis

Systemic Edema Pathways

Pathways leading to systemic edema - heart failure activates RAAS and raises capillary hydrostatic pressure; renal failure retains Na+/H2O; malnutrition, hepatic failure, and nephrotic syndrome reduce plasma albumin - all converging on edema

FIG. 3.3 - Robbins & Kumar Basic Pathology

Fluid Type: Transudate vs. Exudate

Feature	Transudate	Exudate
Mechanism	↑ hydrostatic pressure or ↓ osmotic pressure	↑ vascular permeability
Protein content	Low (protein-poor)	High (protein-rich)
Causes	CHF, nephrotic syndrome, cirrhosis	Inflammation, infection, malignancy
Specific gravity	<1.012	>1.020

Special Forms of Edema

Term	Definition
Anasarca	Severe, generalized edema with profound subcutaneous swelling and fluid in body cavities
Hydrothorax	Fluid in the pleural cavity
Hydropericardium	Fluid in the pericardial cavity
Ascites / Hydroperitoneum	Fluid in the peritoneal cavity
Pulmonary edema	Fluid in lung interstitium/alveoli; causes dyspnea, orthopnea
Cerebral edema	Dangerous - increases intracranial pressure; vasogenic (BBB disruption) or cytotoxic (cell swelling)
Pitting edema	Subcutaneous edema that retains an indentation when pressed; typical in cardiac/renal edema
Non-pitting edema	Lymphedema or myxedema (hypothyroidism); does not pit because of high protein/mucopolysaccharide content

Morphology

Edema is recognized grossly as tissue swelling. Microscopically, it appears as clearing and separation of extracellular matrix elements. The most clinically significant sites:

Subcutaneous edema - pitting in dependent areas (ankles in ambulatory patients, sacrum in bedridden patients)
Pulmonary edema - frothy pink fluid, heavy lungs; impairs gas exchange
Cerebral edema - brain herniates through foramen magnum; life-threatening

Clinical Approach (Harrison's Framework)

Localized or generalized?
- Localized → identify local cause (DVT, inflammation, lymphatic obstruction)
- Generalized → proceed below
Hypoalbuminemia present? (albumin <3.0 g/dL)?
- Yes → evaluate for cirrhosis, malnutrition, nephrotic syndrome
Evidence of heart failure?
- Assess for elevated JVP, S3 gallop, pulmonary rales, leg edema
Urine output?
- Oliguria/anuria → renal failure

Treatment Principles

The primary goal is treating the underlying disorder. General measures:

Dietary sodium restriction - limits fluid retention
Diuretics (loop diuretics like furosemide; thiazides) - promote renal Na+/water excretion
Aldosterone antagonists (spironolactone) - particularly useful in CHF and cirrhosis with secondary hyperaldosteronism
Leg elevation - reduces gravitational hydrostatic pressure
Compression stockings - for lymphedema and venous insufficiency
Treat underlying cause - optimize cardiac function, correct hypoalbuminemia, treat infections causing lymphedema

Sources:

Robbins & Kumar Basic Pathology, pp. 79-81 (Edema - causes, mechanisms, morphology)
Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 43 (Edema summary)
Harrison's Principles of Internal Medicine 22E, p. 326 (Clinical approach)
Ganong's Review of Medical Physiology, p. 16 (Fluid compartments and edema)

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