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Clinical approach to a patient with generalized oedema
Introduction Oedemaisdefined as the accumulation of abnormallyexcessfluid in the interstitialspaces. It canbeclassified as eithergeneralized or localized. (In thispresentationwewilldiscussgeneralizedoedema). Oedemacanalsobeclassified as pitting and non-pitting.
Mechanisms maintaining Interstitial Fluid Volume The volume of interstitial fluid is determined by Starling's law:  Hydrostatic pressure - Oncotic pressure                              =       Net fluid movement out of capillary into the interstitium
Mechanisms maintaining Interstitial Fluid Volume [Oncotic pressure = osmotic pressure created by plasma protein molecules (P) that are impermeable across the capillary membrane].
Etiology of generalized oedema Decreased plasma oncotic pressure: due to depletion of plasma proteins. This occurs in nephrotic syndrome, liver failure and malnutrition. Obstruction of lymphatic flow: this occurs in congestive heart failure.
Etiology of generalized oedema 3. Increased small vessel permeability: due to release of chemical mediators. Plasma proteins (P) leave the circulation and draws more water in the interstitial spaces. This occurs in allergic reactions as anaphylaxis, asthma, hay fever.
Etiology of generalized oedema 4. Increased hydrostatic pressure: this causes more water to be driven outwards in the interstitial spaces. This occurs in congestive heart failure, liver cirrhosis, renal disease.
To sum up…             The causes of generalizedoedema are: Cardiac cause: Congestive heartfailure. Renal cause: Nephrotic syndrome. Hepatic cause: Livercirrhosis. Nutritional cause: Malnutrition. Allergicreaction. Drug-induced.
Oedema of cardiac origin ,[object Object],    Besides, there is a decrease in renal perfusion which leads to: ,[object Object]
     Renal vasoconstriction
      ADHNet result is an increase in hydrostatic pressure
Oedema of cardiac origin Characteristics of oedema of cardiac origin: -  Occurs in the lower extremities. ,[object Object]
Painless, pitting.
The presence of a heart disease: dyspnea, cardiac enlargement, hepatomegaly (tender).
There can be an elevated jugular venous pressure.,[object Object]
Hypoalbuminemia due to urinary protein losses favors fluid movement from the intravascular to the interstitial compartment and exacerbates oedema formation in the nephrotic syndrome.
In some patients, urinary protein loss and hypoalbuminemia can be so severe that plasma volume becomes reduced, leading to renal hypoperfusion and further stimulating sodium and water retention.,[object Object]
Cardiac / Renal disease Cardiac  Renal Starts from the lower part of the body. Slow progression. Signs of heart failure: cardiac enlargement, venous distension, hepatomegaly. Starts from the face and periorbital areas. Quick progression. Proteinuria, hypertension, impaired renal function tests. Location: Progression: Other signs:
Oedema of hepatic origin ,[object Object]
If severe, scarring and distortion of normal liver architecture can lead to marked hepatic dysfunction. This leads to a decrease in plasma protein production from the liver.
This, in turn, can cause sodium retention and oedema formation.
It appears that the damaged liver fails to degrade or overproduces vasodilating factors. This activates compensatory mechanisms such as sympathetic nerves and the renin-angiotensin-aldosterone system.,[object Object]
Drug-induced oedema Some drugs can lead to oedema as: ,[object Object]
Antihypertensive drugs: calcium channel blockers, alpha-adrenergic antagonists.
Steroid hormones.
Cyclosporine.
Growth hormone.,[object Object]
Heavy proteinuria with nephrotic syndrome.
FBC
Hb decreased in malabsorption.

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Generalized oedema