Water Imbalance and Classification of Edema
Changes in body fluid volume follow two main scenarios: hypohydration (water output exceeds intake, resulting in exicosis) and hyperhydration (positive water balance).
When fluid excessively accumulates in tissues or cavities, edema occurs. Based on prevalence, edema is divided into localized (one limb or organ) and generalized. Depending on localization, specific pathological anatomy terms are used:
- Anasarca — diffuse infiltration of fluid into the intercellular spaces of the skin and subcutaneous tissue.
- Dropsy — accumulation of transudate in body cavities. This includes ascites (abdominal cavity), hydrothorax (pleural cavity), and hydropericardium (pericardial cavity).
Based on distribution level, edema can be extracellular (most common) and intracellular. The latter is extremely dangerous: due to osmotic or oncotic pressure gradients, the cell swells, which can result in the rupture of its membrane (sarcolemma / cytolemma) and cell death.
Pathogenesis of Edema: Three Main Factors
The mechanism of fluid retention in tissues depends on the leading pathogenetic factor:
- Hydrodynamic (mechanical) factor. Occurs when hydrostatic pressure rises in the venous end of the capillary. Fluid cannot be reabsorbed back into the vascular bed. A clear example is heart failure. Left ventricular failure leads to pulmonary edema, while right ventricular failure increases pressure in the systemic circulation, causing generalized "congestive" edema.
- Lymphogenic factor. Associated with mechanical obstruction to lymphatic drainage (thrombi, parasites, cancer emboli, scars) or dynamic insufficiency when too much lymph is produced (as in starvation). Prolonged lymph stasis stimulates irreversible fibrotic changes, leading to organ deformation (elephantiasis).
- Oncotic factor. Based on blood hypoonquia — a drop in the concentration of plasma proteins (specifically albumins). Blood loses its ability to retain water, filtration pressure rises, and fluid rushes into tissues. This is the initiating mechanism in nephrotic (protein lost in urine), hepatic (impaired synthesis), and nutritional edema. Such edema is generalized and rapidly appears in areas with low tissue pressure — in loose connective tissue.
Sodium Metabolism Disorders
Sodium determines the plasma osmotic pressure and extracellular fluid volume.
- Hyponatremia occurs with aldosterone deficiency (hypocorticism), kidney diseases, heavy sweating, severe diarrhea, or hemodilution (blood dilution). A drop in plasma osmotic pressure forces water to move inside cells, causing cellular edema. Patients complain of muscle weakness, falling blood pressure, sensory disturbances, and gastrointestinal dysfunction.
- Hypernatremia is a consequence of aldosterone excess (Conn's syndrome) or excessive administration of hypertonic solutions. Cells lose water, while the circulating blood volume increases. Vascular sensitivity to adrenaline and angiotensin II rises, leading to hypertension, seizures, and increased neuromuscular excitability.
Potassium and Copper Metabolism Disorders
Potassium is critical for normal tissue excitability.
- Hypokalemia sharply reduces neuromuscular excitability. General adynamia and muscle hypotonia develop, and reflexes are suppressed. Smooth muscle atonia (flatulence, bladder weakness), vomiting, and cardiac arrhythmias are characteristic.
- Hyperkalemia often accompanies renal failure, endocrinopathies, massive tissue breakdown (shock, hemolysis, destruction of proteins and glycogen), and metabolic acidosis. It causes bradycardia, arterial hypotension, painful spastic contractions of the gastrointestinal tract, and characteristic ECG changes (peaked T waves).
- A noteworthy genetic disorder is Wilson's disease (hepatolenticular degeneration), an autosomal recessive pathology. Due to a defect in copper excretion into bile and reduced production of ceruloplasmin, the toxic metal is deposited in target organs: hepatocytes and basal ganglia of the brain. About 1% of healthy people are hidden heterozygous carriers.