Odema

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Oedema

Edema (American English) or Oedema (British English), formerly known as dropsy or hydropsy, is an abnormal accumulation of fluid beneath the skin, or in one or more cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause edema.

Five factors can contribute to the formation of edema. It may be facilitated by increased hydrostatic pressure or reduced oncotic pressure within blood vessels, increased blood vessel wall permeability as in inflammation, obstruction of fluid clearance via the lymphatic or changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.[1]

Mechanism

Generation of interstitial fluid is regulated by the forces of the Starling equation.[2] Hydrostatic pressure within blood vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood plasma and tissue. As a result the oncotic pressure of the higher level of protein in the plasma tends to suck water back into the blood vessels from the tissue. It is often not appreciated that the Starling equation does not indicate a balance between these forces. The hydrostatic force must always win, and there must always be leakage of fluid out of the vessel because otherwise there can be no oncotic gradient. Starling's equation states that the rate of leakage of fluid is determined by the difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with a fall in reflection coefficient.

Changes in the variables in Starling's equation can contribute to the formation of edema either by an increase in hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in vessel wall permeability. The latter has two effects. It allows water to flow more freely and it reduces the oncotic pressure difference by allowing protein to leave the vessel more easily.

A rise in hydrostatic pressure occurs in cardiac failure. A fall in oncotic pressure occurs in nephrotic syndrome and liver failure. An increase in permeability occurs in inflammation. It is commonly taught that these facts explain the occurrence of edema in these conditions. However, it has been known since the 1950s that the situation is more complex and it is still far from completely understood[3].

The variation in hydrostatic pressure in the vessels in the feet as compared to the face is about a metre of water. In the case of human feet, the Starling forces are always a long way out of balance. In severe heart failure the change in central venous pressure is tiny in comparison and cannot explain why edema of the feet develops simply through an effect on capillary leakage. Three other factors may be involved. If the central venous pressure rises to equal that of the thoracic lymph duct then clearance of fluid from the tissue will be impeded (see below). That is to say the edema may actually be caused by a change in output of fluid from the tissue, as much as input to the tissue. Secondly, severe heart failure is one of the most exhausting conditions there is. The sufferers tend to spend what little effort they can make trying to breathe with edematous lungs. They tend to sit up to make breathing easier and their feet hang immobile on the floor. Immobility is perhaps the commonest of all causes of edema, because clearance of fluid via the lymphatics needs muscle action. Thirdly, in severe heart failure endocrine and neural changes alter the way tissues are perfused in ways that are not fully understood.

Although a low plasma oncotic pressure is widely cited for the edema of nephrotic syndrome, most physicians note that the edema may occur before there is any significant loss of protein in the urine or fall in plasma protein level. Fortunately there is another explanation available. Most forms of nephrotic syndrome are due to biochemical and structural changes in the basement membrane of capillaries in the kidney glomerulae, and these changes occur, if to a lesser degree, in the vessels of most other tissues of the body. Thus the resulting increase in permeability that leads to protein in the urine can explain the edema if all other vessels are more permeable as well.

Abnormal removal of interstitial fluid is caused by failure of the lymphatic system. This may be due to obstruction from, for example, pressure from a cancer or enlarged lymph nodes, destruction of lymph vessels by radiotherapy, or infiltration of the lymphatics by infection (such as elephantiasis). It is most commonly due to a failure of the pumping action of muscles due to immobility, most strikingly in conditions such as multiple sclerosis, or paraplegia. Lymphatic return of fluid is also dependent on a pumping action of structures known as lymph hearts. It has been suggested that the edema that occurs in some people following use of aspirin-like cyclo-oxygenase inhibitors such as ibuprofen or indomethacin may be due to inhibition of lymph heart action.

In myxedema and a variety of other rarer conditions edema is due to an increased tendency of the tissue to hold water within its extracellular space. In myxedema this is because of an increase in hydrophilic carbohydrate-rich molecules (perhaps mostly hyaluronan) deposited in the tissue matrix. Edema forms more easily in dependent areas in the elderly (sitting in chairs at home or on aeroplanes) and this is not well understood. Estrogens alter body weight in part through changes in tissue water content. There may be a variety of poorly understood situations in which transfer of water from tissue matrix to lymphatics is impaired because of changes in the hydrophilicity of the tissue or failure of the 'wicking' function of terminal lymphatic capillaries.


Organ-specific edema

Edema will occur in specific organs as part of inflammation, as in pharyngitis, tendonitis or pancreatitis, for instance. Certain organs develop edema through tissue specific mechanisms. Examples of edema in specific organs:

  • Cerebral edema is extracellular fluid accumulation in the brain. It can occur in toxic or abnormal metabolic states and conditions such as systemic lupus. It causes drowsiness or loss of consciousness.
  • Pulmonary edema occurs when the pressure in blood vessels in the lung is raised because of obstruction to removal of blood via the pulmonary veins. This is usually due to failure of the left ventricle of the heart. It can also occur in altitude sickness or on inhalation of toxic chemicals. Pulmonary edema produces shortness of breath. Pleural effusions may occur when fluid also accumulates in the pleural cavity.
  • Edema may also be found in the cornea of the eye with glaucoma, severe conjunctivitis or keratitis or after surgery. It may produce coloured haloes around bright lights.

Causes of edema which are generalized to the whole body can cause edema in multiple organs and peripherally. For example, severe heart failure can cause pulmonary edema, pleural effusions, ascites and peripheral edema, the last of which effects can also derive from less serious causes.[4]

Common appearances of cutaneous edema are observed with mosquito bites, bee stings (wheal and flare), and skin contact with certain plants such as Poison Ivy or Western Poison Oak,[5] the latter of which are termed contact dermatitis.

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