Canonical Question
Body Fluids
Master answer
Interstitial oedema occurs due to increased permeation of fluid from intravascular to interstitial spaces, and inability of the lymphatics to reabsorb this additional fluid
Starling Forces
- The NET flux across the membrane is the balance of hydrostatic pressure and oncotic pressure, as defined by the Classic Starling Equation:
\[J_v={\kappa \; ([P_{capil} – P_{interstit}] – \sigma \; [\pi_{plasma} – \pi_{interstit}])}\]
where
Jv is the trans endothelial solvent filtration volume per second
( [ Pc – Pi ] – σ [ πp – πi ] ) is the net driving force
P = hydrostatic pressure
π = oncotic pressure
σ = Staverman’s reflection coefficient ie. Permeability of membrane to protein
κ = filtration constant = LpS = Hydraulic conductivity x Surface Area
\[P_{cap} \; \propto \; {{Post-capil\;resist} \over {Pre-capil \; resist}}\]
- Typically quoted values for the variables in the classic Starling equation:
| Hydrostatic pressure | Oncotic pressure |
|---|---|
| Pressure moving fluid | pressure exerted by proteins which draw water into and keep it within a compartment |
| Pc ~35 → 15mmHg (Arterial → venous) Capillary hydrostatic pressure Pressure moving fluid out of capillary | πp ~ 20mmHg Plasma oncotic pressure Pressure keeping fluid within capillary |
| Pif = 5mmHg Interstitial hydrostatic pressure Pressure moving fluid into capillary | πif ~ 0mmHg Interstitial fluid oncotic pressure Pressure keeping fluid out of capillary |
- In general,
- at the arterial end of capillary NFP is positive (filtration) +10mmHg
- At the venous end NFP is negative (absorption) -10mmHg
- Approx. 24L fluid filtered / day
- 85% reabsorbed into capillaries
- Rest reabsorbed via lymphatics (~3.5L/day) = Net fluid loss from filtration
Tissue Interstitial Oedema
| Increased κ promotes oedema | – Inflammation |
| Increased Pc promotes oedema | Increased resistance to venous return – Diastolic HF – Increased R atrial pressures – Venous obstruction (DVT, mass) – Loss of one way valves – Loss of veno-muscular pump (in bed-bound patients) |
| Increased intravascular volume – Activation of RAAS in CHF, cirrhosis, nephrotic syndrome – Crystalloid administration in ICU | |
| Gravity and posture – Lower limbs if standing – Sacrum if supine | |
| Decreased πc promotes oedema | – Hepatic failure and decreased plasma proteins – Nephrotic syndrome |
| Endothelial glycocalyx – damage promotes oedema | – Glycoprotein layer on inner surface of capillaries which sequester plasma proteins |
| Decreased lymphatic flow promotes oedema | Obstruction – Compression – Tumour – Infection – filariasis |
| Increased Pi inhibits oedema | – Compression stockings – Deep sea diving, increased atmospheric pressure |
Sakurai / JC 2020
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2011A Q18 | Explain the physiological processes involved in the development of tissue interstitial oedema. | historical_member | — |