SW17 ORE 1. Surgery and radiotherapy to axillary lymph nodes during breast cancer treatment is often followed, commonly years later, by chronic postmastectomy oedema (PMO). PMO is considered a 'high protein' oedema due to reduced axillary lymph drainage. Since oedema formation also depends on fluid input (capillary filtration), we studied the Starling pressures in the affected and contralateral arm. Colloid osmotic pressure was measured in patient serum (7rp) and interstitial fluid (i1). Subcutis fluid was collected from PMO arms by both wick and aspiration methods, and from the control arm by the wick method only. Interstitial hydraulic pressure (Pi) was measured by the wick-in-needle method. 2. Oedema iT was 19-2 + 4-1 cmH20 (n = 13, wick) to 16-3 + 4.4 cmH20 (n = 41, aspirate;difference not significant; means + S.D. throughout). This was significantly lower than rit in the control arm (21-4 + 3-8 cmH2O, n = 14, P < 0.01, analysis of variance). Also, there was a negative correlation between oedema 7Ti and the percentage increase in arm volume(correlation coefficient r = -0 35, P < 0'05) in contrast to conventional expectation.3. Oedema Pi (1P9 + 2-0 cmH20, n = 28) exceeded the subatmospheric control Pi (-2-8 + 3 0 cmH20; P < 0-01). Venous and arterial pressures were normal but 7rp was subnormal (31-1 + 2-7 cmH20, n= 47).4. Net pressure opposing capillary blood pressure, P., was calculated as Pi + ao (7rp -7it) for a reflection coefficient, C., of 0 90-0 99. P0 in the control arm, 6-2-8-5 cmH2O, was less than antecubital venous pressure, 10-5 cmH20. This provides no support for the traditional view that venous capillaries in the arm are in a state of continuous fluid reabsorption.5. In the PMO arm, PO was raised to 15-0 + 4-6 cmH2O (n = 28, P < 0.01, ANOVA) and correlated positively with increase in arm volume (r = 0-41, P < 0 05). A rise in P0 will reduce filtration rate if capillary pressure is unaltered, which should raise interstitial protein concentration and 7Ti -whereas 7iT actually decreased. Possible explanations include a rise in capillary pressure. The pathophysiology of postmastectomy oedema evidently involves additional mechanisms besides lymphatic damage.Chronic oedema of the arm is a common and distressing late complication of successful treatment of breast cancer. Its origin seems, on the face of it, obvious, namely that axillary lymph node extirpation and/or axillary radiotherapy impairs lymph drainage from the arm. Since interstitial protein drainage is also thought to be reduced, the oedema is classified as a 'high protein lymphoedema'. Lymphangiography reveals dilated lymphatic vessels in the arm and a collateral lymphatic system around obstructions (Clodius, 1977;McIvor & O'Connell, 1978). Lymphangiographic medium moves along the lymphatic vessels at reduced velocity, but flow (velocity x cross-sectional area) has never been measured. It is not known why the chronic postmastectomy oedema (PMO) often arises years after the initial nodal trauma.Lymphatic drainage is clearly abnormal in PMO, b...