Vp 6: Oedema

Front 1

Oedema

Back 1

Increased accumulation of fluid (only a clinical sign)

Expansion of the interstitial fluid compartment

Front 2

Dependent oedema

Back 2

The fluid tends to sink with gravity so that the ventral abdomen and limbs are mainly affected

Front 3

Pitting Oedema

Back 3

Severe diffuse s/c oedema, a finger pushed into the expanded interstitium leaves an indentation

Front 4

Hydrothorax

Back 4

Accumulation of oedema in pleural cavity.

Front 5

Hydropericardium

Back 5

Accumulation of oedema fluid in pericardial sac.

Front 6

Ascites

Back 6

Accumulation of oedema fluid in the peritoneal cavity.

Front 7

Anascara

Back 7

Severe, generalised oedema involving cavities in subcutis.

Front 8

Starling equilibrium

Back 8

At rest, the hydrostatic pressure forces fluid out of the arteriolar end of the capillary to the tissue spaces. At the venous end, the hydrostatic pressure has decreased and osmotic pressure of plasma proteins exceeds venous hydrostatic pressure. Fluid is reabsorbed.

Front 9

Three major factors controlling Starling Equilibrium..

Back 9

a. A Functioning cirulatory system

b. A functional lymphatic system

c. Serum albumin levels

Front 10

4 Main mechanisms that underpin oedema

Back 10

a. Increase in blood hydrostatic pressure

b. Increase vascular permeability

c. Decrease in plasma colloidal-osmotic pressure

d. Lymphatic obstruction

Front 11

Increased blood hydrostatic pressure

Back 11

Due to an increase in venous pressure rather than arterial.

2 types:

1. General (L sided heart failure--> pulmonary oedema; R sided heart failure--> generalised oedema)

2. Local (thrombus, tumour)

Front 12

Increased vascular permeability

Back 12

Oedema of inflammation!!

Opening of interendothelial gaps, allowing leakage of plasma protiens, as well as inflammatory cells.

Front 13

Decreased plasma colloidal osmotic pressure

Back 13

A measure of the colloidal solutes to draw water towards them (mainly ALBUMIN).

Hypoalbumenia causes decreased plasma colloid osmotic pressure.

Front 14

How does hypoalbumenia arise?

Back 14

1. Inadequate albumin production (starvation, chronic liver disease)

2. Net loss of albumin (glomerular disease, loss via GIT)

*tends to result in generalised oedema

Front 15

Lymphatic obstruction

Back 15

Leads to oedema.

Almost always localised because underlying lesion is localised.

Front 16

Pulmonary oedema

Back 16

Alveoli are kept dry as a result of normal fluid dynamics.

2 causes of pulmonary oedema:

1. haemodynamic

2. microvascular injury

Front 17

Haemodynamic cause of pulmonary oedema

Back 17

Due to increased hydrostatic pressure, secondary to L sided heart failure. Blood pushes back to lungs!

Front 18

Microvascular injury cause of pulmonary oedema

Back 18

Capillaries in the pulmonary vascular bed are damaged (broken endothelial cells).

Front 19

Pathogenesis of pulmonary oedema

Back 19

1. Fluid exceeds capacity of lymphatic drainage

2. Fluid accumulates in interlobular septa, perivascular and peri-airway connective tissue

3. Alveolar walls fill with fluid

4. Alveolar spaces fill with fluid

Front 20

What does pulmonary oedema look grossly?

Back 20

Lungs are heavy, wet, exuding red tinged fluid on cut section.

Front 21

Transudate

Back 21

Clear, pale yellow

Thin serous

0.05-0.5% protein, albumin

No coagulatoin, no fibrinogen

Low specific gravity

Low cell content

Underlying cause: all but inflammation

Front 22

Exudate

Back 22

Dark yellow, red or brown, cloudy/opaque

Viscous

Usually 2-4% protein

Coagulation, Fibrinogen present

High Specific gravity

High cell content (macrophages, lymphocytes, neutrophils)

Underlying cause: Usually inflammation

Front 23

Clinical consequences of oedema

Back 23

In brain and lungs can be fatal.

Cerebral oedema--> respiratory problems!

Pulmonary oedema--> hypoxia!