Open AccessSympathetic nerve damage as a potential cause of lymphoedema after axillary dissection for breast cancer
Author(s) -
Bennett Britton T. M.,
Wallace S. M. L.,
Wilkinson I. B.,
Mortimer P. S.,
Peters A. M.,
Purushotham A. D.
Publication year - 2009
Publication title -
british journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.202
H-Index - 201
eISSN - 1365-2168
pISSN - 0007-1323
DOI - 10.1002/bjs.6660
Subject(s) - medicine , forearm , lymphedema , breast cancer , axillary lymph node dissection , dissection (medical) , surgery , vascular resistance , anesthesia , hemodynamics , cancer , sentinel lymph node
Background: The physiological disturbances leading to lymphoedema after breast cancer surgery are poorly understood. Damage to sympathetic nerves during axillary lymph node dissection (ALND), leading to increased capillary fluid filtration, was investigated as a possible contributory factor. Methods: The integrity of the upper limb sympathetic nervous system was tested in 36 patients before, and 3 and 12 months after ALND. Forearm vascular resistance (FVR), calculated from forearm blood flow and mean systemic arterial pressure, was measured before and after exposure to lower‐body negative pressure. Forearm venous compliance was measured using 99m Tc‐labelled autologous erythrocytes and radionuclide plethysmography before and after cold water immersion of the feet. Results: There were clear changes in FVR and venous compliance in response to sympathetic stimulation but no differences attributable to surgery or between the nine patients who developed lymphoedema and the 27 who did not; nor were there differences between the two arms. There was a trend towards lower preoperative FVR in patients who developed lymphoedema. Conclusion: Lymphoedema is not the result of sympathetic nerve damage sustained during ALND. Preoperative FVR may help predict who will get lymphoedema following this surgery. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.