Dr. YK Amdekar discusses the different clinical presentations of oedema, the possible underlying causes, and approach to help deduce and reverse/manage the primary organ disease.

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Before you begin, take this quiz to test your knowledge on the basics of oedema.

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Back to basics

Oedema refers to increased collection of fluids in interstitial spaces including third space (pleural and peritoneal). It results from imbalance between pressures in intravascular and extravascular compartments. In health, two thirds of total body fluid is intracellular (part of extravascular compartment) and remaining is divided into intravascular (plasma and lymph), interstitial and small amount in transcellular space (ocular, cerebrospinal fluid, fluid in pleura, peritoneum and joint space). Transcellular fluid is static and not in balance with other compartments.

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Pressure between compartments

Intravascular pressure pushes fluid out of vessels. Mean arterial pressure is 70 to 90 mmHg, at arterial capillary end 30 mmHg and at venous end 10 mm Hg. Intravascular osmotic pressure pulls fluid into vessels. 19 mmHg pressure is exerted by albumen and 9 mmHg by cations in plasma. Interstitial osmotic pressure of 8 mmHg is contributed by interstitial albumen. Interstitial fluid also exerts negative pressure of 3 mmHg and helps in pulling the fluid into vessels.

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Net effect

Pressure at arterial capillary end (pushing out) is more than at venous end (pulling in). This difference results in leaking of fluid at arterial capillary end. However 90% of leaked fluid is reabsorbed at venous end because of large venous surface and big pores and remaining 10% is absorbed through lymphatics back into circulation. This is the way balance is maintained in health and no oedema results.

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Genesis of oedema

• It is clear from the above mentioned physiology that oedema results when there is imbalance in pressures; increase in hydrostatic pressure and decrease in osmotic pressure pushes fluid out of the intravascular compartment
• Oedema also results in case of capillary leak (as happens in dengue fever) and also due to lymphatic block (lymphedema)
• In renal conditions, fluid retention and excess of sodium leads to leakage into interstitial spaces and hence oedema results
• In case of protein malnutrition, decrease in albumen causes oedema and so also in liver disease in which excess fluid accumulates in the peritoneal cavity due to portal hypertension
• In congestive cardiac failure, oedema results due to increase in hydrostatic pressure
• Capillary leak also leads to fluid exuding out resulting in oedema and also fluid in pleural or peritoneal cavity
• Lymphatic obstruction as well as venous obstruction leads to localised oedema related to site of obstruction
• In angioedema, allergic inflammation leaks fluid locally out of the capillaries resulting in local oedema (sudden swelling of eyes or lips)

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Common causes of oedema

1. Renal: Acute nephritis and nephrotic syndrome presents with sudden onset of periorbital oedema. The patient typically complains of eyelid oedema noticed on waking up in the morning. This is because of acute onset oedema which is first visible in loose connective tissue around the eyes and venous congestion around the face during sleep makes it appear typically on waking up in the morning.
2. Angioedema: This is another condition where onset of oedema is sudden and so again noticed around the eyes.
3. Chronic liver disease: It presents with oedema feet and collection of fluid in the peritoneal cavity occurring due to slow decrease in albumen due to liver failing to produce it. As onset of oedema in the liver disease is slow; it manifests on dependent parts (feet and ascites- localised due to portal hypertension). In acute liver disease such as acute hepatitis, there is no oedema as half-life of albumen is 2 to 3 weeks and hence it takes that much time before oedema manifests.
4. Congestive cardiac failure: It presents with oedema feet as oedema develops slowly and so seen on dependent parts in an ambulant patient. In a non-ambulant patient, it may be seen on sacral areas- dependent parts of the body in lying down position. Though sacral oedema is not noticed by the patient.
5. Protein malnutrition (PEM): It presents as oedema feet as oedema is slow to develop due to poor intake of proteins or proteins not digested or absorbed.
6. Capillary leak syndrome: It presents with oedema in dependent parts due to slow leakage and also in serous cavities.
7. Lymphatic or venous obstruction: It occurs at a particular site, presents with localised oedema (say of one leg only) as against generalised oedema (both legs).
8. Myxedema is seen in hypothyroidism and Lipedema in morbid obese patient. Oedema is non-pitting in these conditions and so also in chronic lymphatic obstruction due to thickening of accumulated lymph (as in chronic filariasis).

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Clinical approach

Detailed history: Asses whether oedema is generalised or localised. Obviously causes would vary.

Onset of oedema: Acute onset oedema noticed around the eyes is mostly due to acute renal disease and also may be seen in angioedema (it is localised and with itching, redness). Slow onset of oedema is classical in other conditions such as liver, cardiac diseases, capillary leak and PEM.

Degree of oedema: Severe, sudden onset oedema is typical of nephrotic syndrome referred to as anasarca. Rarely it may be seen in late stages of other disorders in young children.

Urine output: Oliguria is seen in acute nephritis along with high colored urine due to hematuria. Oliguria may also appear in dehydrated state due to poor intake or loss of fluids as in diarrhoea and also seen in cardiac failure due to poor renal perfusion and in severe intravascular constriction due to massive oedema in liver disease or capillary leak.

High colored urine may be due to hematuria, jaundice and also concentrated urine due to dehydration.

Accompanying symptoms would pinpoint to a specific organ involvement such as jaundice in liver disease, breathlessness and palpitation in cardiac disease and irritability or lethargy in PEM.

Physical examination: It is necessary to confirm pitting oedema by transient pressure over a bony surface such as shin of tibia. Oedema is pitting in most conditions though it may be non-pitting in hypothyroidism and chronic lymphatic obstruction. Next is to make sure whether oedema is generalised or localised as causes vary.

State of health offers clue: Comfortable child with massive oedema is typical of nephrotic syndrome. Child is acutely sick looking in capillary leak syndrome while chronic sick look is seen in liver, cardiac diseases or in PEM.

Ascites is typical of chronic liver disease and may be seen in capillary leak along with pleural effusion.

Other signs such as systemic hypertension would suggest renal disease, jaundice and hepatomegaly in chronic liver disease, enlarged liver also in cardiac disorder due to congestive cardiac failure, cardiomegaly and heart murmur indicative of cardiac disease and signs of PEM denoting severe protein malnutrition.

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Investigations

Provisional diagnosis would help in ordering specific investigations. Urinalysis and biochemistry in renal disease, urine for bile salts and pigments and liver function tests in liver disease, chest X-ray, ECG and 2D echo cardiogram in cardiac disease are main investigations. Other tests would depend on primary conditions.

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Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.