The types and causes of oedema

Oedema may be generalised or localised and it results from factors disturbing the physiological control of body fluid.

Generalised oedema (Fig. 2.9). There are two principal causes of generalised oedema, hypoproteinaemiu and fluid overload. Clinically, these two causes can be distinguished because fluid overload usually results in a rise in JVP (p. 89). whereas the JVP is not elevated in hypoproteinaemia.

Hypoproteinaemia. The osmotic pressure is mostly due to the serum albumin so that a fall in the concentration of this protein predisposes to oedema. Hypoproteinaemia may arise for a variety of reasons:

• Kwashiorkor may develop when there is a selective inadequate intake of protein. This, and true famine, are the most important nutritional disorders in the world. Self-imposed dietary restrictions or pyloric obstruction with vomiting may also impair protein intake.

• Failure of digestion of dietary protein results from impairment of the exocrine secretion of the pancreas, as in chronic pancreatitis.

• Failure of absorption of the products of digestion may occur in conditions such as Crohn's disease or gluten enteropathy, or after extensive small bowel resection.

Ask about:

Cardiac causes (e.g. past history of rheumatic fever, breathlessness, palpitations) Malabsorption (e.g. stool odour, bulk and colour) Malnutrition Liver disease Rena! disease (e.g. diabetes, sore throat, colour of urine, frothing of urine)

Oedema Hornet Sting

Fig. 2.9 Generalised oedema checklist.

Fundal haemorrhage Periorbital oedema

Tonsils JVP

Cardiac size

Gynaecomastia and other signs of hepatic disease

Blood pressure Pleural effusion Spleen Liver

Ascites, bowel sounds

Clubbing, feukonychia Abdominal veins Genital oedema Hair distribution

Petechial haemorrhage Oedema

Fig. 2.9 Generalised oedema checklist.

Reduced synthesis of albumin is found in hepatocellular disease, including cirrhosis. When the portal venous pressure is high, ascites is a more prominent feature than dependent oedema.

Excessive loss of protein may occur in the urine in the nephrotic syndrome. The repeated removal of body fluids, especially ascites, will also aggravate depletion of protein. Uncommonly protein may be lost into the gut in protein-losing enteropathy, which occurs in a variety of gastrointestinal disorders.

In one patient several of these reasons may coexist. In addition, a low intravascular volume may cause secondary hypcraldosteronism via the renin-angiotensin system, promoting sodium retention and an increase in the oedema.

The cause of hypoproleinaemia can usually be identified from the history. The nephrotic syndrome can be excluded in the absence of heavy proteinuria and most patients with a hepatic cause will show the features either of hepatocellular failure (Fig. 5.14, p. 167) and/or of cirrhosis, which is associated with venous changcs, splenomegaly and ascites (p. 169).

Fluid overload. This may have a number of causes:

1. Cardiac causes. The causes of oedema in cardiac failure are multiple and are not fully understood.

Significant factors are:

• Impairment of renal blood flow. The reduction in renal blood flow, alteration in the pulsatile pattern of renal perfusion, and possibly alteration in the distribution of blood How within the kidney promote excessive reabsorption of salt and water - this is the main cause of 'cardiac' oedema.

• Increaseil venous pressure. There is a rise in venous pressure proximal to the failing chamber. In right-sided failure this can be detected by inspection of the neck (p. 88). In left-sided failure, pulmonary venous congestion may produce dyspnoea and cough and the auscultatory finding of crepitations in the lungs. However, the heights of the rises in venous pressure do not correlate with the degrees of oedema and the hydrostatic effect alone does not account for the fluid retention.

« The effect of aldosterone. In some cases secondary hyperaldosteronism occurs and contributes to the oedema.

« Antidiuretic hormone. There is evidence of increase in antidiuretic suhstances in the urine of some patients.

• Lymphatic factors. Lymphangiectasis, incompetent valves and poor lymph drainage have been demonstrated.

• Osmotic pressures. A combination of chronic passive congestion of the liver reducing albumin synthesis, a poor appetite and loss of protein into the oedema fluid and the urine may sometimes account for a significant drop in the concentration of the scrum albumin. The protein content of the interstitial fluid may rise to as much as 1 g/dl compared with 0.02 g/dl in normal interstitial fluid. This change has sometimes been interpreted as evidence for an increase in capillary permeability supposedly due to ischaemia, but it is unlikely to be mainly due to lymphatic failure.

2. Renal causes. In acute glomerulonephritis, the cause of the fluid retention is not fully understood. There is an expansion of the circulating fluid volume as well as the extracellular space, due at least in part to increased tubular reahsorption of sodium and consequent reduction in urine volume. Should normal fluid intake be maintained, oedema results. 3. Iatrogenic. Excessive fluid replacement, especially if given intravenously, will result in fluid overload. The danger is greatest in infants and young children. The same mechanism can operate if oral intake is unrestricted when urine production is diminished or absent in renal failure.

Localised oedema. This may be due to venous, lymphatic, inflammatory or allergic causcs.

Venous causes. External pressure upon a vein, venous thrombosis or incompetence of the valves due to previous thrombosis may each contribute to a rise in capillary pressure. A common example is deep thrombosis in the leg veins. Venous return will also be impaired if the normal pumping action of the muscles is diminished or absent. Accordingly oedema may occur in an immobile bedridden

Lymphangiectasia Post Radical Mastectomy
Fig. 2.10 Lymphoedema ol the right arm. This patient had been treated with a simple mastectomy of the left breast and a radical mastectomy with radiotherapy on the right side.

patient, in a paralysed limb or even in a normal person sitting for long periods, as, for example, during air travel.

Lymphatic causes. The small quantity of albumin filtered at the capillary is normally removed through the lymphatics. In the presence of lymphatic obstruction, the water and solutes are reabsorbed into the capillaries as the tissue pressure rises, but the protein remains until its concentration approaches that in the blood. Ultimately, fibrous

Wasp Interstitial
Fig. 2.11 Anglo-oedema El following wasp sling and E after treatment.

tissues proliferate in the interstitial spaces and the whole part becomes hard and no longer pits on pressure. Lymphatic oedema (lymphoedema) is common in some tropical countries owing to lymphatic obstruction by filarial worms. One or both legs, the female breast, or the external genitalia in either sex. arc the parts most frequently involved. The skin of the affected area may eventually become very thick and rough - elephantiasis. Lymphoedema is comparatively rare in Britain. It may be due to congenital lymphangiectasia or hypoplasia of the lymph vessels of the legs (Milroy's disease), recurrent lymphangitis (resulting in fibrosis of lymphatics) or may affect an arm after radical mastectomy and/or irradiation for carcinoma of the breast (Fig. 2.10).

Inflammatory causes. Damage to tissues hy injury, infection. ischaemia or chemicals such as uric acid results in liberation of histamine, bradykinin and other factors which cause vasodilatation and an increase in capillary permeability. The inflammatory exudate has a high protein content. The resulting oedema is accompanied by the classical signs of inflammation, namely redness, heat and pain. Testing for pitting on pressure in inflammatory oedema causes pain and should be avoided.

Allergic causes. Increased capillary permeability occurs in allergic conditions, hut in contrast to inflammation, there is no pain, there is less redness and the exudate, which has a high protein content, contains eosinophil cells rather than polymorphs and red cells. Angio-oedema is a specific example of allergic oedema: it is particularly prone to affect Ihe facc and lips. The swelling develops rapidly, and it is pale or faintly pink in colour. The condition may be life-threatening if the tongue and glottis are affected (Fig. 2.11A and Bi.



A 27-year-old female was admitted to casualty with sudden severe swelling of the lips and periorbital region immediately following a wasp sting (Fig. 2.11 A). The patient had been stung by a wasp some 10 years previously with marked swelling on her arm at the site of the sting.

On this present occasion, she had increasing difficulty with breathing with evidence ol stridor. Pulflness was also present around her eyes, 1 ml (1 mg) of 1:1000 adrenaline was given subcutaneously. 4 mg chlorpheniramine orally and 100 mg hydrocortisone intravenously were also given, Her breathlessness Improved rapidly and Ihe facial features settled to normal within 6 hours (Fig. 2,1 IB).

Learning points

• An anaphylactic reaction may occur following initial sensitisation by an antigen.

• Early treatment is the safest way of aborting a life-threatening reaction; this patient has been taught how to give sell-medication should she be stung again.

• Dehydration in an adult only becomes clinically apparent after substantial fluid loss,

• The JVP is useful In distinguishing between the oedema of fluid overload and that of hypoproteinaemia.

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