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Generalized oedema
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  • 1. Clinical approach to a patient with generalized oedema
  • 2. Introduction
    Oedemaisdefined as the accumulation of abnormallyexcessfluid in the interstitialspaces.
    It canbeclassified as eithergeneralized or localized. (In thispresentationwewilldiscussgeneralizedoedema).
    Oedemacanalsobeclassified as pitting and non-pitting.
  • 3. 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
  • 4. Mechanisms maintaining Interstitial Fluid Volume
    [Oncotic pressure = osmotic pressure created by plasma protein molecules (P) that are impermeable across the capillary membrane].
  • 5. 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.
  • 6. 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.
  • 7. 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.
  • 8. To sum up…
    The causes of generalizedoedema are:
    Cardiac cause: Congestive heartfailure.
    Renal cause: Nephrotic syndrome.
    Hepatic cause: Livercirrhosis.
    Nutritional cause: Malnutrition.
  • 9. Oedema of cardiac origin
    • In congestive heart failure, there is an increase in the central venous pressure.
    Besides, there is a decrease in renal perfusion which leads to:
    Net result is an increase in hydrostatic pressure
  • 12. Oedema of cardiac origin
    Characteristics of oedema of cardiac origin:
    - Occurs in the lower extremities.
    • Symmetrical location.
    • 13. Painless, pitting.
    • 14. The presence of a heart disease: dyspnea, cardiac enlargement, hepatomegaly (tender).
    • 15. 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.
    • 16. Hypoalbuminemia due to urinary protein losses favors fluid movement from the intravascular to the interstitial compartment and exacerbates oedema formation in the nephrotic syndrome.
    • 17. 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.
  • 18. Cardiac / Renal disease
    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.
    Other signs:
  • 19. Oedema of hepatic origin
    • Liver cirrhosis is defined as increased fibrous tissue in the liver associated with regeneration of focal areas of damaged liver parenchyma.
    • 20. 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.
    • 21. This, in turn, can cause sodium retention and oedema formation.
    • 22. 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).
  • 23. Drug-induced oedema
    Some drugs can lead to oedema as:
    • Non-steroidal inflammatory drugs.
    • 24. Antihypertensive drugs: calcium channel blockers, alpha-adrenergic antagonists.
    • 25. Steroid hormones.
    • 26. Cyclosporine.
    • 27. Growth hormone.
  • Investigations
    • Urine Analysis
    • 28. Heavy proteinuria with nephrotic syndrome.
    • 29. FBC
    • 30. Hb decreased in malabsorption.
    • 31. U&Es
    • 32. Elevated urea and creatinine in renal failure.
    • 33. LFTs
    • 34. Abnormal in liver disease.
  • Investigations
    • Serum Albumin
    • 35. Decreased with nephrotic syndrome, liver disease, malabsorption & malnutrition.
    • 36. Renal Biopsy
    • 37. To determine the cause of nephrotic syndrome in adults.
    • 38. Echocardiography
    • 39. Liver Biopsy
    • 40. Faecal Fat Estimation
    • 41. Increased in malabsorption.
    • 42. Lymphangiography
  • Treatment of generalized oedema
    Treatment of the underlying cause.
    Decrease sodium and water intake.
    Increaseexcretion of sodium and water by the use of diuretics and bedrest.
    Fluid restriction:
    • An edema forming patient typically loses little sodium from his/her body - about 15 mEq/day in urine, sweat and stool combined.
    • 43. Thus restricting dietary salt often does not decrease oedema, it only prevents edema from becoming worse.
  • Diuretics
    These are drugsthatincrease the volume of urine.
    Diuretics in common use include:
    • Thiazidediuretics.
    • 44. Loopdiuretics.
    • 45. Potassium-sparingdiuretics.
    Common sideeffects to anydiuretic:
    • Allergy.
    • 46. GIT irritation.
    • 47. Electrolytedisturbance: hypokalemia (except K-sparing).
    • 48. Nephritis (exceptloopdiuretics).
    • 49. Specificsideeffects to each type.
  • 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
  • 50. Thiazide diuretics
    • Oedema (cardiac, hepatic, renal). It is the drug of choice in mild and moderate congestive heartfailure.
    • 51. Hypertension.
    • 52. Idiopathichypercalcuria.
    • Hypokalemia, hyponatremia, hyperuricemia, hyperglycemia, hyperlipidemia.
    • 53. It decreasesrenalblood flow.
    • 54. Causes hypercalcemia.
    • 55. Blood dyscriasis.
  • Loop diuretics
    • Oedema (cardiac, hepatic, renal). It is for Emergency use. In pulmonaryoedema, cerebraloedema, refractoryoedema.
    • 56. Hypertension.
    • 57. Hypercalcemia.
    • 58. Acute renalfailure.
  • Loop diuretics
    • Hypokalemia, hyponatremia, hyperuricemia, hyperglycemia, hyperlipidemia.
    • 59. Ototoxic deafness.
    • 60. Hypocalcemia.
    • 61. Blood dyscriasis.
    There are twophenomenonsthat are known to occur:
    • Rebound phenomenon: a decrease in sodium excretion below baseline after the effect of the loop diuretic has worn off. Volume depletion activates the sodium retaining mechanisms.
    • 62. Braking phenomenon
  • Contraindications to the use of thiazides and loop diuretics
    In the following conditions, it is contraindicated to use thiazides and loop diuretics:
    • Digitalis toxicity.
    • 63. With steroids (because steroids cause Na and water retention).
    • 64. Gout.
    • 65. Diabetes mellitus.
    • 66. Renal diseases (for thiazides).
    • 67. Liver disease.
    • 68. Pregnancy.
  • Potassium-sparing diuretics
    Spironolactoneis an aldosteroneantagonist.
    • Refractoryoedema (in combinationwithotherdiuretics): hyperaldosteronism, nephroticoedema, Livercirrhosis + ascites.
    • 69. Essential hypertension.
    • 70. Instead of thiazides and loopdiureticswhenthey are contraindicated.
  • Potassium-sparing diuretics
    • Gynecomastia and impotence in males. Irregular menstruation and ovulation in females.
    • 71. Mental confusion and drowsiness.
    • 72. Hyperkalemia.
    • Renalinsufficiency.
    • 73. Hyperkalemia.
    • 74. 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.
  • 75. Managing diuretic resistance
    • Restrict sodium and water intake.
    • 76. Increase dose (individual dose, frequency, i.v.).
    • 77. Combine: furosemide + thiazide/spironolactone/metolazone.
    • 78. Dopamine (increase cardiac output).
    • 79. Reduce dose of ACE inhibitors.
    • 80. Ultrafiltration.
  • Thankyou