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. Allergicreaction. Drug-induced.

10. Renal vasoconstriction

11. ADHNet result is an increase in hydrostatic pressure

13. Painless, pitting.

14. The presence of a heart disease: dyspnea, cardiac enlargement, hepatomegaly (tender).

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.

18. 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:

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.

24. Antihypertensive drugs: calcium channel blockers, alpha-adrenergic antagonists.

25. Steroid hormones.

26. Cyclosporine.

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

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.

44. Loopdiuretics.

46. GIT irritation.

47. Electrolytedisturbance: hypokalemia (except K-sparing).

48. Nephritis (exceptloopdiuretics).

51. Hypertension.

53. It decreasesrenalblood flow.

54. Causes hypercalcemia.

56. Hypertension.

57. Hypercalcemia.

59. Ototoxic deafness.

60. Hypocalcemia.

63. With steroids (because steroids cause Na and water retention).

64. Gout.

65. Diabetes mellitus.

66. Renal diseases (for thiazides).

67. Liver disease.

69. Essential hypertension.

71. Mental confusion and drowsiness.

73. Hyperkalemia.

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.