Peripheral edema: symptoms and causes

2021-03-15 12:00 AM

The main mechanism of peripheral subcutaneous oedema depends on increased hydrostatic pressure, decreased interstitial hydrostatic pressure, decreased plasma volume, increased interstitial fluid pressure, increased vascular permeability, lymphatic embolism.


An abnormal accumulation of fluid under the skin or in the body cavities, causing swelling or indentation of the skin when pressed.


Disease-related to peripheral oedema very much.

The main reasons can be named as:


Congestive heart failure.

Liver failure.

Nephrotic syndrome.

Renal failure.

Varicose veins.

Side effects of medications.



Reduced blood albumin.


Peripheral oedema in heart failure

Peripheral oedema in heart failure


Peripheral oedema in liver failure

Peripheral oedema in liver failure


Peripheral oedema in nephrotic syndrome.

Peripheral oedema in nephrotic syndrome.


The main mechanism of peripheral subcutaneous oedema depends on the histological structure of that tissue. Often, however, one or more of the following factors are present:

Increased capillary hydrostatic pressure (increased pressure to push fluid out of the lumen).

Reduces interstitial hydrostatic pressure (reduces the pressure to push fluid into the lumen).

Decreased plasma volume (reducing the protein that holds fluid in the vascular lumen).

Increased interstitial fluid pressure (increased proteins that pull fluid out of the lumen).

Increases vascular permeability.

Lymphatic occlusion - decreased drainage of fluid and protein from the interstitial tissue to normal circulation.

Mechanisms in heart failure

Increased intravenous hydrostatic pressure induces hydrocephalus in which fluid is pushed from the lumen into the interstitial space. This condition is common in right heart failure.

Factors driving this process include:

Increased plasma volume - Decreased cardiac output (including left or right heart failure) leads to decreased renal perfusion. In response to this condition, the RAAS system becomes activated and causes the body to retain water salts, increasing capillary and venous hydrostatic pressure.

Venous hypertension - ventricular failure causes increased end-systolic and/or a diastolic pressure - these pressures increase upstream to the atria and venous systems, increasing venous and capillary hydrostatic pressure.

Increased hydrostatic pressure pushes fluid out of the lumen into the surrounding tissue.

The lymphatic system does not drain all the re-absorbed fluid from the interstitial tissue and causes oedema.

Liver failure

Contrary to popular belief, the main factor causing oedema in liver disease is vasodilation in the spleen. Edema is not a consequence of the liver decreased protein synthesis, although it also contributes to oedema.

When the liver fails, NO and prostaglandin increase in the spleen. These substances dilate the spleen blood vessels, create more blood pools, reduce the effective circulation volume to the kidneys, increase the secretion of hormones in the kidneys that cause saltwater retention through the RAAS system, increasing hydrostatic pressure.

Nephrotic syndrome

The mechanism of oedema in nephrotic syndrome is not well understood. The main causes could be:

Losing a large amount of protein through the kidneys and reducing blood albumin, reducing plasma colloid pressure - due to too little protein to keep fluid in the lumen, resulting in fluid leaking out.

Reducing the circulating volume causes a hydrophilic response to increasing saltwater retention, thereby increasing capillary hydrostatic pressure to push fluid out of the lumen.

The decreased liver produces a protein that reduces plasma proteins.

Decreased atrial diuretic response (ANR) - is a normal response to fluid overload resulting in increased renal excretion of water salts.

Impaired renal function in kidney disease and nephrotic syndrome does not allow normal salt excretion, causing fluid retention. This may be the predominant mechanism in the case of non-decreased blood albumin.


Peripheral edema is a useful symptom when it is present; however, there is no unallocated heart failure oedema (sensitivity 10%, 93% specific) with only about 25% of heart failure patients under 70 years of age with oedema.

In liver failure, the presence of peripheral edema, and especially the abdominal state, predicts a bad prognosis.