Odema types

1. IMPORTANT TYPES OF OEDEMA

2. EXAMPLES OF ODEMA:
1- Renal Oedema
2- Cardiac Oedema
3- Pulmonary Oedema
4- Cerebral Oedema
5- Myxoedema
6- Nutritional Oedema
7- Hepatic Oedema

3. RENAL OEDEMA
• Generalized oedema occurs in certain diseases
of renal origin
Eg:
 Oedema in Nephrotic Syndrome,
 Oedema in Nephritic Syndrome, and
 Oedema in Acute Tubular Injury.

4. 1. Oedema in Nephrotic Syndrome
DAMAGE TO THE RENAL GLOMERULUS (IN CHRONIC GLOMERULAR DISEASES)
LEAKAGE OF PROTEINS (ALBUMINS) THROUGH GLOMERULAR BASEMENT MEMBRANE
HEAVY PROTEINURIA (>1g/dl)
DECREASED PLASMA PROTEINS (Hypoalbuminaemia)
DECREASED PLASMA ONCOTIC PRESSURE
(PRIMARY REASON FOR ODEMA)
DECREASED PLASMA VOLUME
ACTIVATION OF RENIN-ANGIOTENSIN-
ALDOSTERONE MECHANISM
SODIUM, WATER RETENSIONNEPHROTIC OEDEMA

5. • The nephrotic oedema is classically more
severe, generalized and marked and is
present in the subcutaneous tissues as well as
in the visceral organs.

6. 2. Oedema in Nephritic Syndrome
GLOMERULONEPHRITIS (ACUTE, RAPIDLY PROGRESSIVE)
HEMATURIA (Hypovolaemia)
ACTIVATION OF RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
(PRIMARY REASON FOR OEDEMA)
EXCESSIVE REABSORPTION OF SODIUM AND WATER IN THE RENAL TUBULES
NEPHRITIC OEDEMA

7. • NOTE: in Nephritic syndrome the primary
reason behind the oedema is due to activation
of RENIN-ANGIOTENSIN-ALDOSTERONE
MECHANISM.
• However proteinuria (<0.5g/dl) which is
moderate in nephritic syndrome leads to mild
hypoproteinaemia and initiates oedema
formation secondarily.

8. •The degree of oedema is mild in nephritic oedema
•Usually observed in the loose connective tissues of the
body like face, genitalia, eyes.

10. 3. Oedema in Acute Tubular Injury
ACUTE TUBULAR INJURY

11. ACUTE TUBULAR INJURY
by shock or toxic chemicals
DAMAGED TUBULES LOSE THEIR CAPACITY FOR SELECTIVE
REABSORPTION AND CONCENTRATION OF THE GLOMERULAR
FILTRATE
EXCESSIVE RETENTION OF WATER AND ELECTROLYTES
GENERALISED ODEMA

12. CARDIAC OEDEMA
• Generalised oedema develops in right-sided
and congestive cardiac failure.
• Pathogenesis of cardiac oedema is explained
on the basis of the following mechanisms:
1- Due to Heart Failure
2- Due to Chronic hypoxia
3- Due to reduced Cardiac output.

13. 1- Due to Heart Failure
Heart Failure
Increased Central Venous Pressure
Increased Capillary Hydrostatic Pressure
Oedema

14. 2- Due to Chronic hypoxia
Chronic Hypoxia
Injury to the Capillary endothelium
Increased Capillary Permeability
Oedema

15. 3- Due to Reduced Cardiac output.
Reduced Cardiac Output
Hypovoleamia
Activation of Intrinsic-renal and Extra-renal Hormonal
Mechanisms & ADH Secretion
Sodium and Water Retention
Oedema

16. Pulmonary Oedema
• Acute pulmonary oedema is the most
important form of local oedema as it causes
serious functional impairment.
• However, it has special features and differs
from oedema elsewhere in that the fluid
accumulation is not only in the tissue space
but also in the pulmonary alveoli.

17. ETIOPATHOGENESIS :
• The hydrostatic pressure in the pulmonary
capillaries is much lower (average 10 mmHg).
• A normal plasma oncotic pressure prevents
the escape of fluid into the interstitial space
and lungs are normally free of oedema.
• However can Pulmonary oedema can result
from either:
- ELEVATION OF PULMONARY HYDROSTATIC
PRESSURE OR
- THE INCREASED CAPILLARY PERMEABILITY.
- HIGH ATITUDES

18. 1. Elevation in pulmonary hydrostatic pressure
(Haemodynamic oedema)
INCREASED PRESSURE IN PULMONARY VEINS WHICH IS
TRANSMITTED TO PULMONARY CAPILLARIES
LEFT HEART FAILURE (eg: due to Mitral Stenosis)
INCREASED PULMONARY CAPILLARY HYDROSTATIC PRESSURE
EXCESS FLUID GETS ACCUMULATED IN THE INTERSTITIUM
(INTERSTITIAL OEDEMA)
i.e., IN THE LOOSE TISSUES AROUND BRONCHIOLES,
ARTERIES AND IN THE LOBULAR SEPTA.

19. THICKENING OF THE ALVEOLAR MEMBRANE
(NO DISTURBANCE IN GASEOUS EXCHANGE UPTO THIS STAGE)
PROLONGED ELEVATION OF HYDROSTATIC PRESSURE AND INTERSTITIAL ODEMA
PRESSURE
ALVEOLAR MEMBRANE CELL DAMAGE
RUSH OF INTERSTITIAL FLUID INTO ALVEOLAR AIR SPACES
(ALVEOLAR ODEMA)
(SERIOUS DISTURBANCE TO THE LUNG FUNCTION)

20. INTERSTITIAL SPACE
INTERSTITIAL OEDEMA
ALVEOLAR MEMBRANE THICKENED ALVEOLAR MEMBRANE

21. ALVEOLAR OEDEMA

22. PULMONARY INFECTIONS/ INHALATION OF TOXIC
SUBSTANCES/ASPIRATION/HYPERSENSITIVITY TO DRUGS
ALVEOLO-CAPILLARY MEMBRANE DAMAGE
INCREASED VASCULAR PERMEABILITY
PLASMA PROTEINS LEAK OUT
INITIALLY INTO THE INTERSTITIUM
2. Increased vascular permeability (Irritant oedema)
ALVEOLAR OEDEMA
INTERSTITIAL OEDEMA
PLASMA PROTEINS LEAK OUT
LATER INTO THE ALVEOLI

23. 3. Acute high altitude oedema:
CLIMBING TO HIGH ALTITUDE SUDDENLY WITHOUT HALTS > 2500 METRES
HYPOXIA & SYMPATHETIC ACTIVATION DUE TO COLD AND
PHYSICAL WORK CAUSES VASOCONSTRICTION
VASOCONSTRICTION INCREASES PULMONARY CAPILLARY
HYDROSTATIC PRESSURE
PULMONARY OEDEMA