Pathophysiology
Edema
Fluid leaks into tissue when Starling forces tip — hydrostatic, oncotic, lymphatic, permeability
Edema is excess interstitial fluid. Starling's equation governs flow across capillary walls — net filtration depends on hydrostatic pressure (pushing out), oncotic pressure (pulling in), and capillary permeability. Normally lymphatics return ~3 L/day to the circulation. Edema appears when filtration exceeds lymphatic capacity. Four mechanisms: increased hydrostatic pressure (heart failure, venous obstruction), decreased oncotic pressure (cirrhosis, nephrotic syndrome — albumin <2.5 g/dL), increased permeability (sepsis, burns, allergic reactions), or lymphatic obstruction (filariasis, post-mastectomy). Pitting edema indicates protein-poor fluid; non-pitting suggests lymphedema or myxedema. Anasarca = generalized edema. Classic exam: 1+ to 4+ pitting graded by depression depth.
- EquationStarling's law of capillary exchange (1896)
- Driving forceHydrostatic minus oncotic pressure
- Normal albumin3.5-5.0 g/dL; edema risk <2.5
- Lymph flow~3 L/day returned to subclavian vein
- Pitting threshold~3 kg interstitial fluid before visible
- Pulmonary edemaWedge pressure >18 mmHg
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Why edema matters
- Heart failure staging. Severity tracks with diuretic response and prognosis.
- Liver disease. Ascites marks decompensated cirrhosis.
- Kidney disease. Nephrotic edema signals >3.5 g/day proteinuria.
- Sepsis resuscitation. Capillary leak warns against over-resuscitation.
- Drug effects. Calcium channel blockers, NSAIDs, glitazones cause edema.
- Lymphedema. Post-mastectomy or filariasis needs compression, not diuretics.
- Pregnancy. Distinguishes physiologic from preeclampsia (with hypertension and proteinuria).
Common misconceptions
- All edema responds to diuretics. Lymphedema worsens with diuretics; needs compression.
- Albumin infusion fixes hypoalbuminemia. Effect transient; treat underlying cause.
- Bilateral leg edema is always heart failure. Could be venous insufficiency, lymphedema, hypoalbuminemia, drug-induced.
- Diuretics first in cirrhosis. Sodium restriction is foundation; diuretics second-line.
- Non-pitting edema is benign. Myxedema coma carries 40% mortality; lymphedema risks cellulitis.
- Edema means fluid overload. In sepsis, intravascular volume can be low while interstitium is wet.
Frequently asked questions
What are Starling forces?
Four pressures across the capillary wall. Capillary hydrostatic pressure (Pc, ~32 mmHg arterial end, 15 mmHg venous) pushes fluid out. Interstitial hydrostatic (Pi, near 0) opposes. Plasma oncotic (πp, ~25 mmHg from albumin) pulls in. Interstitial oncotic (πi, ~5 mmHg) pulls out. Net filtration = Kf × [(Pc − Pi) − σ(πp − πi)]. Filter at arterial end, reabsorb at venous end; lymphatics drain the excess.
Why does heart failure cause leg edema?
Right-sided failure raises systemic venous pressure. Capillary hydrostatic pressure rises, filtration exceeds reabsorption, fluid pools dependently — ankles, sacrum if bedbound. Left-sided failure raises pulmonary venous and capillary pressure causing pulmonary edema. Treat with loop diuretics (furosemide 40 mg IV), nitrates, ACE inhibitors. Compression stockings help peripheral edema; do not use in active heart failure decompensation.
How does cirrhosis cause ascites?
Two mechanisms. Portal hypertension raises splanchnic capillary pressure. Liver fails to make albumin (hypoalbuminemia <2.5 g/dL), dropping plasma oncotic pressure. Splanchnic vasodilation activates RAAS, retaining sodium and water. Treat with sodium restriction (<2 g/day), spironolactone 100 mg + furosemide 40 mg ratio 100:40, paracentesis for tense ascites. SBP prophylaxis with norfloxacin if ascitic fluid protein <1.5 g/dL.
What is nephrotic syndrome edema?
Glomerular damage allows protein loss >3.5 g/day. Hypoalbuminemia drops oncotic pressure. Edema is generalized, periorbital in morning, dependent in evening. Causes — minimal change disease (children), focal segmental glomerulosclerosis, membranous nephropathy, diabetes. Treat underlying cause (steroids for minimal change), ACE inhibitors to reduce proteinuria, statins for hyperlipidemia, anticoagulation if albumin <2 g/dL.
When is edema dangerous?
Pulmonary edema is a medical emergency — pink frothy sputum, crackles, SpO2 falling. Treat with oxygen, sit upright, IV furosemide, nitroglycerin, BiPAP, address underlying cause. Cerebral edema raises intracranial pressure — Cushing's triad of bradycardia, hypertension, irregular respiration is preterminal. Mannitol or hypertonic saline, head of bed elevation, hyperventilation as bridge. Angioedema can obstruct airway — epinephrine 0.3 mg IM if anaphylactic; icatibant for hereditary.
How do you tell pitting from non-pitting?
Press 5 seconds with thumb. Pitting = depression remains, low-protein fluid (heart failure, hypoalbuminemia, renal failure). Non-pitting = no depression, high-protein. Lymphedema (post-cancer surgery, filariasis) is non-pitting and Stemmer sign positive (can't tent skin over second toe). Myxedema in hypothyroidism is non-pitting due to glycosaminoglycan deposits. Lipedema is non-pitting fat distribution, spares feet.
What about idiopathic edema?
Cyclic edema in women without identifiable cause. Often related to upright posture, salt intake, oral contraceptives, and possibly chronic diuretic use causing rebound retention. Treat — discontinue diuretics, weight-based salt restriction, support stockings, weight loss. Spironolactone may help. Rule out heart failure, kidney disease, liver disease, hypothyroidism, lymphedema first.