Starling forces and oedema

The core idea: Starling forces

Water crosses the capillary wall under four forces.

• Net filtration pressure = (Pc − Pi) − σ(πc − πi), where σ is the reflection coefficient for protein.
• Worked example at the arterial end: Pc 35, Pi 0, πc 25, πi 3. Net = (35 − 0) − (25 − 3) = 13 mmHg outwards. Interstitial oncotic pressure pulls fluid out, so it adds to filtration.
• Across a whole bed, filtration slightly exceeds reabsorption; the excess (2–4 L/day) returns via lymphatics, which have many valves and are driven by muscle pumping and intrinsic contraction.
• Body fluid in a 70 kg man: total water about 42 L; ECF about 14 L, of which interstitial fluid is about 10.5 L and plasma about 3.5 L.
• The endothelial glycocalyx (a layer of glycoproteins on the luminal surface) is the real barrier to protein; when it is shed, σ falls and protein and fluid leak.

Types of capillary

• Myogenic autoregulation: arterioles constrict when stretched. In untreated hypertension this protects downstream capillaries, keeping foot capillary pressure near normal; amlodipine abolishes it by dilating arterioles, transmitting pressure into capillaries (ankle oedema that diuretics barely help).

Why oedema forms

• Chronic heart failure: raised venous pressure increases capillary hydrostatic pressure, and low output activates renin–angiotensin–aldosterone and ADH, retaining salt and water that sustain the oedema.
• Cirrhosis with ascites: splanchnic arterial vasodilatation (nitric oxide) creates arterial underfilling; low effective volume activates RAAS, sympathetic nerves and ADH, so the kidney retains sodium avidly (urine Na under 10 mmol/L). Hepatorenal syndrome is the extreme; NSAIDs remove protective renal prostaglandins.
• Post-operative saline overload: several litres of 0.9% saline dilute plasma proteins, lowering plasma oncotic pressure; albumin falls (38 to 27 g/L) with normal JVP and heart.
• Septic shock: inflammatory shedding of the endothelial glycocalyx lets albumin and fluid leak, so crystalloid boluses raise BP only briefly; start vasopressors early.
• ARDS (pancreatitis, sepsis): increased alveolar–capillary permeability with a normal wedge pressure (10 mmHg); diuretics do not treat the cause.
• Pre-eclampsia: systemic endothelial dysfunction (antiangiogenic factors) causes leak; facial and hand swelling.
• Ovarian hyperstimulation syndrome after hCG: VEGF-driven capillary leak; plasma volume is depleted (rising haematocrit, oliguria), so diuretics are wrong.
• Reperfusion after 8 hours of limb ischaemia: free radicals generated on reoxygenation damage endothelium, causing leak and compartment syndrome despite good pulses.
• Immobile limbs after stroke: loss of the calf muscle pump raises venous and capillary pressure in dependent legs; also a DVT risk.

Where oedema shows and why it pits

• Oedema collects in the dependent part: ankles when upright, the sacrum when bed-bound.
• In a child with nephrotic syndrome, oedema is most obvious around the eyes on waking: lax periorbital tissue and lying flat overnight.
• Pitting: firm pressure displaces free interstitial fluid, which flows back slowly. Non-pitting swelling has protein and glycosaminoglycans or fibrosis: lymphoedema, myxoedema, long-standing venous disease.
• Lymphoedema: congenital lymphatic hypoplasia (often familial) presents as painless swelling from birth; Stemmer sign (skin over the second toe cannot be pinched into a fold) distinguishes it from venous or cardiac oedema.

Exam trap Calcium channel blocker oedema comes from capillary pressure, not salt retention, so diuretics help little.

Safety factors against oedema

1. Interstitial pressure rises as fluid accumulates. 2. Lymph flow increases many-fold. 3. Extra filtration washes out interstitial protein, lowering πi.

• Raising plasma oncotic pressure reduces filtration and so reduces lymph flow; interstitial fluid formation increases with a decrease in plasma oncotic pressure.

Special beds

• Lung: low capillary pressure (7–10 mmHg); pulmonary oedema appears when wedge pressure exceeds about 25 mmHg. Kerley B lines are short horizontal lines at the bases reaching the pleura: fluid in the interlobular septa (also seen in lymphangitis carcinomatosa).
• Kidney: glomerular capillary pressure is high (about 50 mmHg) along its whole length, so it filters throughout.
• Brain: vasogenic oedema (leaky tumour vessels; finger-like white-matter oedema) responds to dexamethasone, which makes tumour vessels less leaky. Cytotoxic oedema in early infarction is cell swelling from Na+/K+ pump failure (restricted diffusion) and does not respond to steroids.
• After haemorrhage: capillary pressure falls and transcapillary refill draws interstitial fluid into the blood within hours, diluting Hb later.

Compartment syndrome

• Rising pressure in a closed fascial compartment collapses veins and capillaries first, so perfusion fails while distal pulses remain. The earliest and most reliable sign is pain out of proportion, worse on passive stretch of the compartment's muscles.
• Supports fasciotomy: delta pressure (diastolic BP minus compartment pressure) under 30 mmHg. Do not wait for measurement in an awake patient.

Remember Out: capillary pressure and interstitial protein. In: plasma albumin. Lymph mops up the rest.

Ascites and effusions

• Serum–ascites albumin gradient (SAAG) = serum albumin minus ascitic albumin (a subtraction). 11 g/L (1.1 g/dL) or more means portal hypertension: 28 − 8 = 20 g/L. Below 11 suggests peritoneal disease (TB, malignancy).
• Light's criteria: a pleural effusion is an exudate if fluid:serum protein is above 0.5, fluid:serum LDH above 0.6, or fluid LDH above two-thirds of the upper normal serum LDH.

How FCPS asks about this

• Net filtration with Pc 35, Pi 0, πc 25, πi 3: 13 mmHg outwards.
• Oedema in burns or sepsis: increased permeability (glycocalyx damage); in nephrotic syndrome: low oncotic pressure.
• Early plasma volume restoration after haemorrhage: transcapillary refill.
• Sodium retention in cirrhotic ascites: splanchnic arterial vasodilatation; SAAG 11 g/L or more means portal hypertension.
• Tumour oedema helped by dexamethasone: vasogenic, less leaky vessels; infarct swelling is cytotoxic.
• Earliest sign of compartment syndrome: pain on passive stretch; fasciotomy if delta pressure is under 30 mmHg.
• Kerley B lines: fluid in interlobular septa.