Perioperative Intravenous Lidocaine Decreases the Incidence of Persistent Pain After Breast Surgery : The Clinical Journal of Pain

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Perioperative Intravenous Lidocaine Decreases the Incidence of Persistent Pain After Breast Surgery

Grigoras, Anca MD; Lee, Peter MD; Sattar, Faisal BSc; Shorten, George PhD

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The Clinical Journal oF Pain 28(7):p 567-572, September 2012. | DOI: 10.1097/AJP.0b013e31823b9cc8

Abstract

Objectives: 

Breast cancer surgery is associated with a high incidence of persistent postsurgical pain (PPSP). The aim of this study was to evaluate the impact of intravenous (IV) lidocaine on acute and PPSP, analgesic requirements, and sensation abnormalities in patients undergoing surgery for breast cancer.

Methods: 

Thirty-six patients participated in this randomized, double-blinded study. Before induction of general anesthesia, patients received a bolus of intravenous lidocaine 1.5 mg/kg followed by a continuous infusion of lidocaine 1.5 mg/kgh (lidocaine group) or an equal volume of saline (control group). The infusion was stopped 1 hour after the skin closure. Pain scores and analgesic consumption were recorded at 2, 4, 24 hours, and then daily for 1 week postoperatively. Three months later, patients were assessed for PPSP and secondary hyperalgesia.

Results: 

Two (11.8%) patients in the lidocaine group and 9 (47.4%) patients in the control group reported PPSP at 3 months follow-up (P=0.031). McGill Pain Questionnaire revealed greater present pain intensity-visual analog scale in the control group (14.6±22.5 vs. 2.6±7.5; P=0.025). Secondary hyperalgesia (area of hyperalgesia/length of surgical incision) was significantly less in the lidocaine group compared with control group (0.2±0.8 vs. 3.2±4.5 cm; P=0.002). The 2 groups were similar in terms of analgesic consumption during the early postoperative period.

Discussion: 

Intravenous perioperative lidocaine decreases the incidence and severity of PPSP after breast cancer surgery. Prevention of the induction of central hyperalgesia is a potential mechanism.

Copyright © 2012 Wolters Kluwer Health, Inc. All rights reserved.

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