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.
The presence of a heart disease: dyspnea, cardiac enlargement, hepatomegaly (tender).
There can be an elevated jugular venous pressure.
Oedema of renal origin
Nephrotic syndrome is defined as a glomerular disease that results in proteinuria(urinary protein loss of ≥ 3.5 gm/day), hypoproteinemia, oedema, and hyperlipidemia.
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.
Oedema of renal origin Characteristics of oedema of renal origin:
Mainly due to hypoalbuminemia and salt/water retention.
- Associated with hematuria, proteinuria, hypertension and impaired renal functions. - Associated with: puffiness of the face and prominent in the periorbital areas.
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:
Liver cirrhosis is defined as increased fibrous tissue in the liver associated with regeneration of focal areas of damaged liver parenchyma.
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.
Oedema of hepatic origin Characteristics of oedema of hepatic origin: - Clinical evidence of hepatic disease as spider angioma , jaundice , ascites (refractory to treatment).
Drug-induced oedema Some drugs can lead to oedema as:
Mechanism of action Thiazides(acts mainly on proximal part of distal convoluted tubule). Inhibits active reabsorption of Na and Clin the cortical diluting segment of the ascending loop of Henle. K-sparing diuretics Inhibits Na/K exchange in the late distal convoluted and collecting tubule Loop diuretics Inhibit exchange of Na/K/Cl in the thick segment of the ascending loop of Henle Loop of Henle Collecting tubule
Concomitant use withamiloride and triamterene hyperkalemia.
Diuretic resistance Development of resistance to the action of diureticscanoccur due to: - Neurohormonalactivation. - ReboundNa+uptakeaftervolumeloss. - Hypertrophy of distal nephron. - Reduced tubular secretion(renal failure, NSAIDs). - Decreased renal perfusion (low output). - Alteredabsorption of thediuretic. - Noncompliancewithdrugs.