Dyshydration and clinical significance of edema
Disruption of the body's water balance in pathological anatomy is called dyshydration. Normally, this balance is maintained only when water intake strictly equals output. Depending on the localization of the pathological process, intracellular and extracellular dyshydration are distinguished.
The development of edema has serious consequences for the entire organism:
- Organ changes: macroscopic increase in the volume of the edematous organ occurs.
- Serous cavities: their free capacity predictably decreases during massive fluid accumulation.
- Function: the normal work of edematous tissues and organs is invariably disrupted.
- Infection: accumulated edematous fluid is a favorable environment, which is why it easily becomes infected.
- Life threat: edema of the larynx, lungs, and brain is most dangerous for the patient, requiring emergency care.
Five factors of edema development
The pathogenesis of any edema consists of a combination of basic factors determining the disturbance of water exchange between vessels and tissues. There are a total of 5 such mechanisms:
- Hydrodynamic
- Lymphogenic
- Oncotic
- Osmotic
- Membranogenic
Below we will analyze in detail two of them, which play a crucial role in clinical practice and are a logical continuation of the study of mixed dystrophies.
Osmotic factor
Osmotic edema develops as a result of a pathological increase in osmotic pressure directly in the intercellular fluid. Important to remember: the osmotic pressure of blood plasma is a strict biological constant. Its decrease is never considered a cause of edema, as such a condition is simply incompatible with life.
The accumulation of ions and molecules in tissues (hyperosmia) causes fluid to be retained in the interstitium. This occurs for several reasons:
- Endocrine genesis (main cause): hypersecretion of hormones such as aldosterone and deoxycorticosterone causes massive retention of sodium ions ($Na^+$) in tissues, which inevitably leads to water retention.
- Microcirculation disorders: the washout of osmotically active metabolites (lactate, pyruvate) and various ions from tissues is reduced.
- Cell damage: during hypoxia and ischemia, cell membranes are damaged, and ions leave cells and accumulate in the intercellular space.
- Acidosis: the shift of the medium towards the acidic side leads to increased dissociation of salts.
Clinical significance: the osmotic factor plays a completely leading role in the development of nephritic and cardiac edema.
Membranogenic factor
This mechanism is entirely based on an increase in vascular wall permeability, which leads to the unhindered exit of fluid from microvessels directly into the interstitium.
The permeability of the vascular bed increases due to two main reasons:
- Action of biologically active substances (BAS): compounds such as histamine, serotonin, bradykinin, and prostaglandins act on the endothelium and physically increase interendothelial gaps.
- Direct endothelial damage: is the result of the aggressive impact of various physical, chemical, and biological factors on the vessel wall.
Clinical significance: the membranogenic factor is always initial (triggering) in the development of allergic, toxic, and angioneurotic edema.
Briefly: answers to topical questions
What is the mechanism of development of hydrodynamic edema?
The mechanism of development of hydrodynamic (mechanical) edema consists of an increase in effective hydrostatic pressure in the vessels of the microvasculature. This leads to a decrease in fluid reabsorption from tissues into the vessel and the transition of fluid into the interstitium.
Main causes of pressure elevation:
- Heart failure — increase in central venous pressure (left ventricular failure causes pulmonary edema, right ventricular failure causes generalized edema).
- Local venous outflow disturbance — blockage or compression of veins leading to local edema.
What is the mechanism of development of oncotic edema?
The mechanism of development of oncotic edema consists of a decrease in the effective oncotic suction force of blood plasma. Edema develops as a result of a decrease in blood oncotic pressure (hypoonquia) and/or its increase in intercellular fluid (hyperonquia).
A decrease in plasma oncotic pressure leads to two simultaneous processes:
- Increase in filtration volume — enhanced fluid exit from arterioles and precapillaries into the interstitium.
- Decrease in resorption — reduction of water return from the interstitium into postcapillaries and venules.
The main cause of blood hypoonquia is hypoalbuminemia occurring in starvation, liver failure, or protein loss in urine.
What is the mechanism of development of lymphogenic edema?
The mechanism of development of lymphogenic edema consists of a disruption of lymph formation and lymph outflow, which makes adequate fluid removal from tissues impossible.
The following pathogenetic mechanisms are distinguished:
- Mechanical obstacle — vessel blockage (thrombi, parasites, cancer emboli), their compression (scars, enlarged lymph nodes), or congenital anomalies.
- Venous congestion — an increase in central venous pressure impedes lymph outflow into the bloodstream (mechanical lymphatic insufficiency).
- Dynamic lymphatic insufficiency — enhanced lymph formation with limited capabilities for its outflow.
Prolonged outflow disturbance leads to fibrous changes and organ deformation (elephantiasis).
GLOOM is an acronym for remembering 5 pathogenesis factors: Hydrodynamic, Lymphogenic, Oncotic, Osmotic, Membranogenic.
Class and exam questions
Can a decrease in plasma osmotic pressure cause edema?
No. Plasma osmotic pressure is a strict constant. Its decrease is incompatible with life, so it is not a cause of edema development.
What is the main cause of tissue hyperosmolarity in edema?
The endocrine factor plays a leading role — hypersecretion of aldosterone and deoxycorticosterone, which leads to the retention of sodium and water in tissues.
In which conditions is the membranogenic factor the initiating one?
Increased vascular permeability initiates the development of allergic, toxic, and angioneurotic edema.
What else to study on this topic
- Hydrodynamic factor of edema development
- Lymphogenic factor of edema development
- Oncotic factor in the development of edema
- Intracellular and extracellular dyshydration
- Mixed dystrophies in the context of the pathogenesis of edema
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