|Year : 2016 | Volume
| Issue : 1 | Page : 6-13
Pre-emptive analgesia of ultrasound-guided pectoral nerve block II with dexmedetomidine–bupivacaine for controlling chronic pain after modified radical mastectomy
Ali M Ali Hassn1, Hala E Zanfaly1, Taha A Biomy2
1 Department of Anesthesia and Intensive Care, Faculty of Medicine, Zagazig University, Zagazig, Egypt
2 Department of General Surgery, Faculty of Medicine, Zagazig University, Zagazig, Egypt
|Date of Submission||01-Jun-2014|
|Date of Acceptance||09-Sep-2015|
|Date of Web Publication||15-Jun-2016|
Ali M Ali Hassn
Lecturer of Anesthesia and Intensive Care, Department of Anesthesia and Intensive Care, Faculty of Medicine, Zagazig University, Zagazig
Source of Support: None, Conflict of Interest: None
Background The term chronic pain refers to pain in and around the area of surgery lasting beyond 3 months after surgery when all other causes of pain, such as recurrence, have been ruled out. Persistent pain after treatment has a considerable negative influence on quality of life in breast cancer survivors.
Patients and methods Sixty female patients were enrolled for ultrasound-guided modified pectoral block. They were randomly assigned into two groups of 30 patients each: group C was administered 30 ml saline, and group BD was administered 30 ml 0.5% bupivacaine with dexmedetomidine 1 μg/kg. Pectoral block II was performed with ultrasound preoperatively and general anesthesia was induced after 15 min of assessment of the block in both groups. Patients were assessed for acute pain, chronic pain, and patient satisfaction.
Results A total of 60 female patients were randomized into two groups: group C (the control group) and group BD (the bupivacaine–dexmedetomidine group). Group BD showed highly significant reduction in intubation heart rate, intubation mean arterial blood pressure, intraoperative heart rate, intraoperative mean arterial blood pressure, and total fentanyl dose (μg) (76.1 ± 5.3 vs. 82.9 ± 4.6, P = 0.00007**; 75.2 ± 2.8 vs.77.5 ± 3.9, P = 0.01*; 76.2 ± 5.3 vs. 88.9 ± 6.3, P = 0.00**; 71.6 ± 8.06 vs.78.2 ± 7.03, P = 0.001**; and 107.76 ± 11.77 vs. 150.83 ± 26.6, P = 0.00**, respectively). Follow-up of patients for 6 months regularly for chronic pain, satisfaction, and need for analgesics revealed significant differences at 1 month, 3 months, and 6 months in group C in relation to group BD [1 month, 7 (23.3%) vs. 3 (10%) with P = 0.02*; 3 months, 11 (36.6%) vs. 6 (20%) with P = 0.03*; and 6 months, 16 (53.3%) vs. 8 (26.6%) with P = 0.002*].
Conclusion Reduced visual analogue scale was seen at the first 24 h postoperatively, with significant reduction in total postoperative analgesia and delayed rescue analgesia in the bupivacaine dexmedetomidine group (the BD group) in relation to the control group. This marked reduction in the severity of postoperative pain correlates with reduced chronic pain on follow-up of our patients with patient satisfaction, good sleep, and reduced analgesic need, which improves quality of life.
Keywords: postmastectomy pain, pre-emptive analgesia, ultrasound-guided Pecs II block
|How to cite this article:|
Ali Hassn AM, Zanfaly HE, Biomy TA. Pre-emptive analgesia of ultrasound-guided pectoral nerve block II with dexmedetomidine–bupivacaine for controlling chronic pain after modified radical mastectomy. Res Opin Anesth Intensive Care 2016;3:6-13
|How to cite this URL:|
Ali Hassn AM, Zanfaly HE, Biomy TA. Pre-emptive analgesia of ultrasound-guided pectoral nerve block II with dexmedetomidine–bupivacaine for controlling chronic pain after modified radical mastectomy. Res Opin Anesth Intensive Care [serial online] 2016 [cited 2017 Oct 17];3:6-13. Available from: http://www.roaic.eg.net/text.asp?2016/3/1/6/184078
| Introduction|| |
Breast cancer is the most common cancer in women worldwide, with more than one million new cases diagnosed every year . The prognosis has improved considerably over the past 30 years, and the 5-year overall survival of patients with a diagnosis of primary breast cancer has increased to about 85% ,. Consequently, the population of long-term survivors is increasing, emphasizing the need for knowledge on long-term sequelae.
Several studies have shown that persistent pain after treatment for breast cancer is a common problem, ranging between 25 and 60% depending on definition, measurement, and methods of treatment . The term chronic pain refers to pain in and around the area of surgery lasting beyond 3 months after surgery when all other causes of pain, such as recurrence, have been ruled out . Persistent pain after treatment has a considerable negative influence on quality of life in breast cancer survivors ,, and persistent pain in general has important economic consequences for the healthcare system ,,. Many potential preoperative, intraoperative, and postoperative risk factors for persistent pain after treatment for breast cancer have been proposed, including young age, pain elsewhere in the body, radiotherapy, and the extent of axillary surgery . Only few studies, however, have focused on persistent pain in patients for 5 or more years after primary surgery, leaving questions on the natural course of such pain ,,. After another common surgical procedure, groin hernia repair, persistent postoperative pain decreased from about 25% at 1 year after surgery to about 12% at 5 or more years after surgery ,. We found no study with long-term detailed longitudinal data on patients with and without pain after surgery.
The analgesia for breast reconstructive surgery can involve different degrees of nerve blocks. Blanco described different types of modifications to suit the type of surgery based on the affected tissues and nerves (Pecs I and Pecs II or modified Pecs). During breast expander and prosthesis insertions, the PMm (pectoralis Major and minor) is mainly involved. For tumorectomies, mastectomies, and sentinel node dissection, the intercostal nerves are the main nervous structures that we need to block. Finally, for complex reconstructions, the thoracodorsal nerve is also involved. The Pecs blocks (types I and II) are peripheral approaches based on good anatomical knowledge and on the use of ultrasound. They combine both motor and sensory nerve blocks that compare with wound infiltration techniques that only aim for sensory nerves. It is important to emphasize the advantages of Pecs: there is no sympathetic block that is associated with paravertebral and epidural blockades; opiates are not usually necessary; there could be less tumor recurrences; and it is a simple and fast-acting block. Injection in the fascial plane between the pectoralis muscles is not enough to reach the anterior branches of the intercostal nerves and they will not be reliably blocked; this is one of the main reasons for designing the Pecs II block. They obtain consistent anesthesia of the dermatomes from T2 to T4 with variable spread to T6. This is confirmed by the MRI study .
An understanding of the types of changes that occur in the nervous system after disease and injury is important, but the subject is immensely complicated. However, a basic appreciation of the mechanisms is useful for several reasons. First, if injury is responsible for initiating the changes in the nervous system then it is likely that subsequent surgery may make it worse by further winding up the nervous system. Given the complexity of the changes, it is unlikely that simple treatments such as nerve blocks will produce a long-term benefit. A multidimensional approach, involving the psychological dimension and physical and pharmacological treatments, will probably be required. An appreciation of the complexity of the mechanisms will also help to guide future studies ,.
The neural supply of the anatomical structures involved in breast surgery is not well understood when it comes to providing analgesia for perioperative pain relief. Thoracic epidural  and paravertebral ,, blocks became the gold standard techniques to achieve this goal, but not every anesthesiologist is comfortable performing these procedures. As an alternative for these techniques, a novel series of blocks were designed (Pecs I and Pecs II).
Dexmedetomidine is a novel highly selective α2-adrenergic receptor agonist. The α2: α1 activity ratio of dexmedetomidine is 1620 : 1 compared with 220 : 1 for clonidine. This results in a more specific and selective α2-adrenoceptor agonism. It can affect the brain and spinal cord α2-adrenergic receptor and inhibit neural discharge to produce sedative, analgesic, and anxiolytic effects. The locus coeruleus is a verified key part of the brain responsible for the regulation of arousal and sleep. Dexmedetomidine affects the brainstem locus coeruleus α2-adrenergic receptors and produces sedative, hypnotic, and anxiolytic effects. Compared with benzodiazepine, dexmedetomidine also reduces the movement of the stomach and intestines and inhibits glandular secretion, as well as reduces the incidence of postoperative nausea and vomiting. In addition, dexmedetomidine can inhibit sympathetic activity, reduce plasma epinephrine and norepinephrine levels, and maintain hemodynamic stability. The sedative effect of dexmedetomidine is unique in many ways, and has a dose-dependent manner . Moreover, dexmedetomidine is not addictive and has a very slight respiratory inhibition.
| Aim of the Study|| |
The aim of this study was to assess the efficacy and safety of pre-emptive analgesia with ultrasound-guided pectoral II block (modified pectoral block) to control long-term pain sequelae after modified radical mastectomy.
| Patients and Methods|| |
After written consent from the patients and Zagazig University ethical research committee approval, a prospective controlled study was carried out in Zagazig University Hospitals within 6 consecutive months, starting at December 2013. A total of 60 female patients of ASA physical status I or II between 26 and 60 years of age were included in the study. Exclusion criteria were local infection, deformities, coagulation abnormalities, morbid obesity (BMI ≥ 35 kg/m2), allergy to local anesthetics, patients' refusal, severe respiratory or cardiac disease, pre-existing renal, neurological disorders, hepatic insufficiency, and preoperative long-term analgesic administration. All patients were operated by the same surgeon using the same surgical approach. The surgeon and the anesthetist were blinded to the medication of the group.
During the preanesthetic preparation, patients reported about pain by means of visual analogue scale (VAS) score rating in which 0 = no pain and 10 = worst imaginable pain. Oral diazepam 0.1 mg/kg was administered at night and midazolam 5 mg was administered intravenously 1 h preoperatively. Before induction of anesthesia, all patients received ultrasound-guided pectoral block II (modified pectoral nerve block). The patients were assigned into two groups of 30 patients each using a computer-generated random number assignment in sealed opaque envelopes: the control group (group C = 30) and the dexmedetomidine–bupivacaine group (group BD = 30).
On arrival at the operating room, monitoring lines were established for noninvasive blood pressure on the opposite side of surgery and for continuous ECG, EtCO2, and SpO2. Two sets of 30 ml syringes were prepared by one resident anesthesiologist who was not included in the study (group C syringes contained 30 ml saline and group BD syringes contained bupivacaine 0.5% and 1 μg/kg dexmedetomidine). The patient was placed supine under complete antiseptic condition and a cover sheath was used for the ultrasound probe with enough gel applied on the probe. A high-frequency linear probe was placed caudad to the lateral third of the clavicle to locate the axillary vessels under the pectoralis major and the subclavius muscle, and the first rib was identified. The probe was moved distally toward the axilla until the third rib was encountered. At this position, the pectoralis minor is above the serratus anterior, and the clavipectoral fascia continues into the axilla as Gerdy's ligament. Using an in-plane medial-to-lateral approach, 10 ml of diluted prepared solution was injected into the interfascial plane between the two pectoralis muscles and 20 ml was injected into the interfascial plane between the pectoralis minor and the serratus anterior muscle ([Figure 1]) The anesthesiologists were blinded to the contents of the syringes prepared in the study.
|Figure 1: Sonographic sequence to locate the local anesthesia injection point for the Pecs block. aa, axillary artery; av, axillary vein; pM, pectoralis major; pm, pectoralis minor; pl, pleura; r3/r4/r5, ribs 3/4/5; sm, serratus (anterior) muscle. NB. Bottom left: am, anteromedial; sm, superomedial.|
Click here to view
General anesthesia was induced with propofol 2–3 mg/kg, followed by cisatracurium 0.2 mg/kg, to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane 1.5% and cisatracurium 0.1 mg/kg when train of four equals 50%. Fentanyl boluses of 0.5 μg/kg were administered intravenously if heart rate (HR) and mean arterial blood pressure (MAP) increased more than 20% from the preoperative baseline. At the end of surgery, neuromuscular reversal was carried out with 0.07 mg/kg of neostigmine and 0.01 mg/kg of atropine, and tracheal extubation was performed on return of consciousness. Intraoperative ECG, SpO2, and noninvasive pressure were evaluated every 5 min. After extubation, the patient was transferred to the postanesthesia care unit where pain was assessed by a blinded observer using VAS until 24 h after surgery, and analgesia was given when VAS was 3 or greater in the form of 0.05 mg/kg of morphine. The patients were evaluated by questionnaire using 10 points scale to assess the patient satisfaction about the procedure 24 hours postoperatively (from 0 = not satisfied to 10 = fully satisfied). Sedation was assessed in the recovery room with Ramsay scores (1 = anxious or restless or both; 2 = cooperative, orientated, and tranquil; 3 = responding to commands; 4 = brisk response to stimulus; 5 = sluggish response to stimulus; and 6 = no response to stimulus) excessively high sedation levels with Ramsay 5 or 6; adequate sedation levels needing observation with Ramsay 2 to 4; inadequate or insufficient sedation levels with Ramsay 1.
At the time of discharge, we prescribed a regimen to control pain according to severity: oral ketorolac tab for mild-to-moderate pain, ketorolac 30 mg injection for agonizing pain. The patient was asked to communicate to us absence of pain.
Intercostobrachial nerve dissection and preservation by the surgeon were recorded intraoperatively ([Figure 2]).
|Figure 2: Intercostobrachial nerve preservation as performed by the surgeon during axillary dissection.|
Click here to view
Outcome criteria were recorded and compared:
- Demographic data (age, BMI, and ASA status).
- Operative time calculated from surgical incision until adhesive application to the wound.
- Preoperative MAP and HR.
- Intraoperative total fentanyl dose.
- MAP at induction, intubation, and at surgical incision.
- Intercostobrachial nerve dissection and preservation in both groups (number of patients).
- VAS at 0, 6, 12, and 24 h postoperatively.
- Postoperative complications (hypotension, nausea, vomiting, respiratory depression, and sedation score).
- Total mean morphine dose administration during the first 24 h postoperatively in each group (mg) and first rescue analgesia.
- Patient satisfaction, chronic pain assessed with VAS as mild, moderate, and intolerable pain, and need for analgesics at 2 weeks, 3 months, and 6 months after hospital discharge (number of patients in each group).
- Length of hospital stay.
Data were collected by means of history taking and examination. Data were entered and analyzed using Microsoft Excel software. Data were then imported into Statistical Package for the Social Sciences (SPSS version 20.0, Chicago, Illinois: SPSS Inc., USA) (Statistical Package for the Social Sciences) software for analysis. According to the type of data, the following tests were used to test differences for significance. Differences between frequencies (qualitative variables) in groups were compared using the c 2-test. Differences between means (quantitative variables) in two parametric groups were compared using Student's t-test. A P value was set at less than 0.05 for significant results and at less than 0.001 for highly significant results.
| Results|| |
The groups were compared in terms of age, sex, weight, ASA status, and preoperative MAP and HR. There was no significant difference in terms of these characteristics ([Table 1]).
[Table 2] shows no differences between the two groups in duration of surgery, total operation time (min), induction HR (b/m), induction MAP (mmHg), and thoracolumbar nerve resection. Group BD showed highly significant reduction in intubation HR (b/m) (76.1 ± 5.3 vs. 82.9 ± 4.6 with P = 0.00007**), intubation MAP (mmHg) (75.2 ± 2.8 vs. 77.5 ± 3.9 with P = 0.01*), intraoperative HR (b/m) (76.2 ± 5.3 vs. 88.9 ± 6.3 with P = 0.00**), intraoperative MAP (mmHg) (71.6 ± 8.06 vs.78.2 ± 7.03 with P = 0.001**), and total fentanyl dose (μg) (107.76 ± 11.77 vs. 150.83 ± 26.6 with P = 0.00**) in comparison with group C.
[Table 3] shows highly significant differences in VAS at 0, 2, 6, 12, and 24 h during the postoperative period in group BD in relation to group C, with marked reduction in VAS 0 (1.45 ± 0.3 vs. 2.03 ± 0.4; P = 0.00**), VAS 2 h (4.75 ± 1.1 vs. 2.96 ± 0.7; P = 0.00**), VAS 6 h (3.82 ± 1.2 vs. 2.55 ± 0.9; P = 0.00001**), VAS 12 h (5.03 ± 1.3 vs. 2.67 ± 0.60; P = 00**), and VAS 24 h (4.79 ± 0.8 vs. 3.0 ± 0.70; P = 00**) and highly significant difference in first rescue analgesia in the postoperative care unit between group C and group BD (90.6 ± 16.9 vs. 240.1 ± 25.5; P = 0.00**).
|Table 3: Postoperative visual analogue scale at first rescue analgesia and total morphine dose during the first 24 h|
Click here to view
There were highly significant differences in postoperative results between group BD and group C as regards sedation [8 (26.6%) vs. 2 (6.6%) with P = 0.0006**], patient satisfaction [13 (43%) vs. 22 (73%) with P = 0.005*], nausea and vomiting [4 (13.3%) vs. 1 (3.3%) with P = 0.01*], respiratory depression [6 (20%) vs. 1 (3.3%) P = 0.0003**], and length of hospital stay (days) (3.53 ± 0.2 vs. 1.98 ± 0.13 with P = 0.00**) ([Table 4]).
On follow-up of patients for 6 months regularly for chronic pain, satisfaction, and need for analgesics, significant differences were found at 1 month, 3 months, and 6 months in group C in relation to group BD at 1 month [7 (23.3%) vs. 3 (10%) with P = 0.02*], 3 months [11 (36.6%) vs. 6 (20%) with P = 0.03*], and 6 months [16 (53.3%) vs. 8 (26.6%) with P = 0.002*] ([Table 5]).
| Discussion|| |
Postoperative sensations reported by patients can be transient or long-lasting, and can include pain, phantom sensations, and sensory loss or changes. Chronic pain can be a source of considerable disability and psychological distress. In patients undergoing diagnostic studies, surgical procedures, and other treatments for breast cancer, persisting pain is an additional burden for individuals already suffering from many psychosocial and medical stressors . Attributed to the aid of ulrasound (US) and understanding of the neural supply of the anterior chest wall and breast, the gate for Pecs block was opened. A novel interfascial plane block was recently described by Blanco. On the basis of anatomical structure, this block was initially performed as Pecs I block and then it was modified as Pecs II block to suit the extent of surgery. For instance, during breast expander and prosthesis insertion, Pecs I block is enough as the pectoralis major muscle is mainly affected. Meanwhile, Pecs II block favors mastectomy and axillary clearance, as long thoracic and thoracodorsal nerves are involved . The neural supply includes three distinguished groups: the lateral pectoral nerve (C5–C7) lying between the pectoralis major muscle and the pectoralis minor muscle and the medial pectoral nerve (C8–C1) running under the pectoralis minor muscle, both supplying to the pectoralis muscle; the spinal nerves (T2–T6) running in the plane between the intercostal muscles and constituting the lateral and anterior branches to supply the chest wall; and the long thoracic nerve (C5–C7) and the thoracodorsal nerve (C6–C8), which supply to the serratus anterior and latissimus dorsi muscle, respectively. In fact, wound infiltration and field block with local anesthetic were described after breast surgery, but with varying results ,,. Therefore, deposition of local anesthetic drugs under real-time US into the fascial planes of the above-described group of muscles is easy and would be accurate to provide better results.
Reduced VAS was observed during the first 24 h postoperatively, with significant reduction in total postoperative analgesia and delayed rescue analgesia in the bupivacaine dexmedetomidine group (the BD group) in relation to the control group. This marked reduction in the severity of postoperative pain correlates with reduced chronic pain on follow-up of our patients, with patient satisfaction, good sleep, and reduced analgesic need, which improves quality of life. All these results correlate with those of Kehlet ,, who have recently reported that persistent postoperative pain development correlates well with the intensity of acute postoperative pain; therefore, early and adequate treatment may be important in preventing or ameliorating the development of chronic postoperative pain ,.
The term preventive analgesia was introduced to emphasize the fact that central neuroplasticity is induced by preoperative, intraoperative, and postoperative nociceptive inputs. Thus, the goal of preventive analgesia is to reduce the central sensitization that arises from noxious inputs experienced throughout the entire perioperative period and not just from those occurring during the surgical incision. Pre-emptive treatment should be directed at the periphery, along the sensory axons, and along the central neurons. This can be accomplished with the use of NSAIDs, acetaminophen, local anesthetics, α2 agonists (e.g. clonidine), α2-d ligands (e.g. gabapentin and pregabalin), ketamine, and opioids, either alone or in combination. Effective preventive analgesic techniques may be useful not only for reducing acute pain but also for reducing chronic postoperative pain and disability .
Pre-emptive analgesia was intended to prevent the establishment of central sensitization caused by incisional and inflammatory injuries. The pre-emptive effects of administering a 72-h epidural infusion of mepivacaine, beginning before surgery, were compared with a postoperative epidural mepivacaine infusion in 70 patients who underwent thoracotomy. Follow-up at 3 and 6 months showed a significant reduction in the incidence of chronic post-thoracotomy pain in the group of patients who received the epidural before surgery . Similarly, other authors have found satisfying results with preoperatively initiated thoracic epidural analgesia in controlling post-thoracotomy pain in the acute-term and long-term period; they found decreased incidence and intensity of chronic pain when compared with postoperative epidural or intravenous analgesia . Dexmedetomidine is a relatively new, highly selective central α2 agonist. Dexmedetomidine, when used as an adjunct, can reduce postoperative morphine consumption in various surgical settings using various routes such as intravenous. In a recent study, the authors found that the addition of dexmedetomidine to intravenous patient controlled analgesia (PCA) morphine resulted in superior analgesia, significant morphine sparing, and less morphine-induced nausea, while it was devoid of additional sedation and untoward hemodynamic changes .
Considering that the frequency of postoperative nausea and vomiting (PONV) after breast surgery under general anesthesia is relatively high , the lower incidence of PONV in the Pecs group in comparison with the control group in the current study is another advantage. Perhaps, the use of propofol  and avoidance of nitrous oxide  have some effects, but lower morphine consumption in the Pecs group may play another role.
Follow-up of patients over 6 months postoperatively for chronic pain revealed reduction in group BD, with marked patient satisfaction, normal sleep, and reduced need for analgesia. This was mostly attributed to pre-emptive and preventive analgesia as the key to prevent chronic pain and acute postoperative pain, and this was seen in our study by the marked reduction in VAS at the first 24 h and reduced opioids. This correlates with following studies.
The intensity of acute pain immediately before or after surgery is strongly associated with the incidence and intensity of subsequent chronic postsurgical pain after amputation, breast surgery, thoracotomy, and herniorrhaphy. Thus, suppression of this afferent nociceptive traffic by means of appropriate analgesic strategies, in addition to reduction of postoperative pain, may suppress the development of chronic pain after surgery. The association between intensity of acute postoperative pain and development of chronic pain after surgery implies that inadequate perioperative and postoperative analgesia may constitute a significant factor. Thus, in this context, effective pain management should be considered as an essential component of anesthesia and perioperative medicine. Various surveys have estimated the percentage of patients who experience pain after surgery to range between 30 and 80%, and, of these patients, the majority (more than 80%) report the intensity as moderate, severe, or extreme . Traditionally, opioid analgesics have been considered as the mainstay of management of moderate-to-severe postoperative pain. Advantages of these drugs include their established efficacy, wide availability, experience with their use, and relative ease of administration. However, side effects such as respiratory depression and hypoxemia, nausea and vomiting, sedation, and delayed recovery of bowel function are limitations of their use. The emerging recognition of opioid-induced hyperalgesia is an additional drawback; it has been shown that repeated administration of opioids intraoperatively induce an acute state of tolerance, hyperalgesia, or both ,,,. The pathophysiology of opioid-induced hyperalgesia is complex, but the phenomena of peripheral and central sensitization may be highly pertinent. Mechanisms related to N-methyl-d-aspartate receptor activation and translocation of the protein kinase C (PKC) in dorsal horn neurons have been implicated in the development of persisting pain, hyperalgesia, and tolerance to opioid analgesia. Opioid receptor activation results in stimulation of PKC, which phosphorylates several target proteins, including the N-methyl-d-aspartate receptor, with subsequent downstream activation of a series of cascades that mediate central sensitization and hyperalgesia. PKC stimulation has also been implicated in the process of acute tolerance to opioid analgesia. In contrast, attempts aiming to improve postoperative analgesia with nonopioid analgesics and techniques, result in opioid sparing effect, reduced side effects and morbidity, improved patient satisfaction, and decreased length of hospitalization or stay in the recovery period ,,.
In our randomized double-blinded study, we found a significant reduction in hemodynamic responses to intubation and intraoperative opioid consumption, as well as reduced hemodynamic responses to surgical incision in the bupivacaine dexmedetomidine group. Similar to clonidine, dexmedetomidine probably produces peripheral analgesic effects by inhibiting the transmission of nerve signals through the Ad and C-fibers and stimulating the release of enkephalin-like substances in the peripheral regions. Analgesic effects of clonidine are due to their combination with the analgesic route of opioids ,.
In a study by Carpenter et al. , two patients who had only a lumpectomy, with no axillary dissection, developed postmastectomy pain syndrome, and in four women the intercostobrachial nerve was spared. Several studies on breast surgery have studied the effect of preserving the intercostobrachial nerve. In a prospective randomized, controlled trial, Abdullah et al.  studied the effect of preserving or sacrificing the intercostobrachial nerve during axillary clearance. They found that, for a variety of reasons, it was not always possible to preserve the nerve. Although there was a significant difference in pain, numbness, and altered sensations at discharge, there was no significant difference between the groups at 3 months. However, as expected, the incidence of sensory deficit was less in the preservation group. At 3 months, symptoms had worsened in both groups, particularly in the group in which nerves were preserved. Two patients with objective sensory loss had no symptoms, whereas eight patients with sensory symptoms had no objective sensory deficit. Other studies have shown similar results . Gottrup and colleagues found that patients in both groups showed decreased sensitivity to thermal and pinprick stimuli on the affected side. Pressure pain threshold on the affected side was decreased in the pain group, but not in the pain-free group. The main finding was that repetitive pinprick stimulation around the scar in the pain group produced increased evoked pain intensity, sometimes called wind-up hyperalgesia. The magnitude of the evoked pain correlated with spontaneous pain intensity. The authors concluded that this indicated central sensitization .
Dexmedetomidine reduces total intraoperative and postoperative doses of opioids when added to bupivacaine in modified Pecs block, as well as reduces sympathetic stimulation to intubation and surgical stimulation. These findings correlate with those of a study by Esmaoglu et al. , who added dexmedetomidine to levobupivacaine for axillary brachial plexus block and showed that it shortens the onset time of both sensory and motor block and prolongs the duration of block and the duration of postoperative analgesia.
| Conclusion|| |
Pre-emptive ultrasound-guided pectoral nerve block II controls acute postoperative pain and opioid consumption, resulting in reduced chronic pain and thus improving the quality of life and avoiding repeated hospital readmission. Moreover, the high quality and accuracy of ultrasound guidance improves results and provides safety.
| Acknowledgements|| |
Conflicts of interest
There are no conflicts of interest.
| References|| |
Cronin-Fenton DP, Norgaard M, Jacobsen J, Garne JP, Ewertz M, Lash TL, Sorensen HT. Comorbidity and survival of Danish breast cancer patients from 1995 to 2005. Br J Cancer 2007; 96:1462–1468.
Mouridsen HT, Bjerre KD, Christiansen P, Jensen MB, Moller S. Improvement of prognosis in breast cancer in Denmark 1977–2006, based on the nationwide reporting to the DBCG Registry. Acta Oncol 2008; 47:525–536.
Tryggvadottir L, Gislum M, Bray F, Klint A, Hakulinen T, Storm HH, Engholm G. Trends in the survival of patients diagnosed with breast cancer in the Nordic countries 1964–2003 followed up to the end of 2006. Acta Oncol 2010; 49:624–631.
Andersen KG, Kehlet H. Persistent pain after breast cancer treatment: a critical review of risk factors and strategies for prevention. J Pain 2011; 12:725–746.
Merskey H, Bogduk H, eds. Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms
. 2nd ed. International Association for the Study of Pain 909 NE 43rd St., Suite 306 Seattle, WA 98105 USA: IASP Press; 1994.
Macdonald L, Bruce J, Scott NW, Smith WC, Chambers WA. Long-term follow-up of breast cancer survivors with post-mastectomy pain syndrome. Br J Cancer 2005; 92:225–230.
Peuckmann V, Ekholm O, Rasmussen NK, Groenvold M, Christiansen P, Moller S, et al
. Chronic pain and other sequelae in long-term breast cancer survivors: nationwide survey in Denmark. Eur J Pain 2009; 13:478–485.
Smith BH, Hopton JL, Chambers WA. Chronic pain in primary care. Fam Pract 1999; 16:475–482.
Blyth FM, March LM, Brnabic AJ, Cousins MJ. Chronic pain and frequent use of health care. Pain 2004; 111:51–58.
Blyth FM, March LM, Cousins MJ. Chronic pain-related disability and use of analgesia and health services in a Sydney community. Med J Aust 2003; 179:84–87.
Deimling GT, Sterns S, Bowman KF, Kahana B. The health of older-adult, long-term cancer survivors. Cancer Nurs 2005; 28:415–424.
Aasvang EK, Bay-Nielsen M, Kehlet H. Pain and functional impairment 6 years after inguinal herniorrhaphy. Hernia 2006; 10:316–321.
Grant AM, Scott NW, O'Dwyer PJ. Five-year follow-up of a randomized trial to assess pain and numbness after laparoscopic or open repair of groin hernia. Br J Surg 2004; 91:1570–1574.
Blanco R. The 'pecs block': a novel technique for providing analgesia after breast surgery. Anaesthesia 2011; 66:847–848.
Villanueva L, Dickenson AH, Ollat H. The pain system in normal and pathological states
. Seattle: IASP Press; 2004. 115.
Wilder-Smith OH, Tassonyi E, Senly C, Otten P, Arendt-Nielsen L. Surgical pain is followed not only by spinal sensitization but also by supraspinalantinociception. Br J Anaesth 1996; 76:816–821.
Klein SM, Bergh A, Steele SM, Georgiade GS, Greengrass RA. Thoracic paravertebral block for breast surgery. Anesth Analg 2000; 90:1402–1405.
Schnabel A, Reichl SU, Kranke P, Pogatzki-Zahn EM, Zahn PK. Efficacy and safety of paravertebral blocks in breast surgery: a meta-analysis of randomized controlled trials. Br J Anaesth 2010; 105:842–852.
Norum HM, Breivik H. Thoracic paravertebral blockade and thoracic epidural analgesia: two extremes of a continuum. Anesth Analg 2011; 112:990.
Tahiri Y, Tran DQ, Bouteaud J, Xu L, Lalonde D, Luc M, Nikolis A. General anaesthesia versus thoracic paravertebral block for breast surgery: a meta-analysis. J Plast Reconstr Aesthet Surg 2011; 64:1261–1269.
Okamoto T, Mori T, Takeda T, Tokunaga M, Yuki N, Arimura S, et al
. Dexmedetomidine is an excellent sedative for voice monitoring surgery. Masui 2012; 61:542–545.
Kuehn T, Klauss W, Darsow M, Regele S, Flock F, Maiterth C, et al.
Long-term morbidity following axillary dissection in breast cancer patients – clinical assessment, significance for life quality and the impact of demographic, oncologic and therapeutic factors. Breast Cancer Res Treat 2000; 64:275–286.
Apfelbaum JL, Chen C, Mehta SS, Gan TJ. Postoperative pain experience: results from a national survey suggest postoperative pain continues to be undermanaged. Anesth Analg 2003; 97:534–540.
Johansson A, Axelson J, Ingvar C, Luttropp H-H, Lundberg J. Preoperative ropivacaine infiltration in breast surgery. Acta Anaesthesiol Scand 2000; 44:1093–1098.
Johansson A, Kornfalt J, Nordin L, Svensson L, Ingvar C, Lundberg J. Wound infiltration with ropivacaine and fentanyl: effects on postoperative pain and PONV after breast surgery. J Clin Anesth 2003; 15:113–118.
Carpenter JS, Sloan P, Andrykowski MA, et al
. Risk factors for pain after mastectomy/lumpectomy. Cancer Pract 1999; 7:66–70.
Abdullah TI, Iddon J, Barr L, Baildam AD, Bundred NJ. Prospective randomized controlled trial of preservation of the intercostobrachial nerve during axillary node clearance for breast cancer. Br J Surg 1998; 85: 1443–1445.
Poleshuck EL, Katz J, Andrus CH, Hogan LA, Jung BF, Kulick DI, Dworkin RH. Risk factors for chronic pain following breast cancer surgery: a prospective study. J Pain 2006; 7:626–634.
Obata H, Saito S, Fujita N. Epidural block with mepivacaine before surgery reduces long-term post-thoracotomy pain. Can J Anaesth 1999; 46: 1127–1132.
Sentürk M, Ozcan PE, Talu GK, Kiyan E, Camci E, Ozyalcin S, et al
. The effects of three different analgesia techniques on long-term postthoracotomy pain. Anesth Analg 2002; 94:11–15.
Dholakia C, Beverstein G, Garren M, Nemergut C, et al
. The impact of perioperative dexmedetomidine infusion on postoperative narcotic use and duration of stay after laparoscopic bariatric surgery. J Gastrointest Surg 2007; 11:1556–1559.
Hammas B, Thorn SE, Wattwil M. Superior prolonged antiemetic prophylaxis with a four-drug multimodal regimen: comparison with propofol or placebo. Acta Anaesthesiol Scand 2002; 46:232–237.
Jokela RM, Kangas-Saarela TA, Valanne JV, Koivuranta MK, Ranta PO, Alahuhta SM. Postoperative nausea and vomiting after sevoflurane with or without ondansetron compared with propofol in female patients undergoing breast surgery. Anesth Analg 2000; 91:1062–1065.
Gan TJ, Meyer T, Apfel CC, Chung F, Davis PJ, Eubanks S, et al
., Department of Anesthesiology, Duke University Medical Center Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003; 97:62–71.
Chia YY, Liu K, Wang JJ, Kuo MC, Ho ST. Intraoperative high dose fentanyl induces postoperative fentanyl tolerance. Can J Anaesth 1999; 46:872–877.
Guignard B, Bossard AE, Coste C, Sessler DI, Lebrault C, Alfonsi P, et al.
Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology 2000; 93:409–417.
Li X, Angst MS, Clark JD. Opioid-induced hyperalgesia and incisional pain. Anesth Analg 2001; 93:204–209.
Vinik HR, Kissin I. Rapid development of tolerance to analgesia during remifentanil infusion in humans. Anesth Analg 1998; 86:1307–1311.
Law PY, Wong YH, Loh HH. Molecular mechanisms and regulation of opioid receptor signalling. Annu Rev Pharmacol Toxicol 2000; 40: 389–430.
Butterworth JFV, Strichartz GR. The alpha2 adrenergicagonists clonidine and gunafacine produce tonic and phasic block of conduction in rat sciatic nerve fibres. Anaesth Analg 1993; 76:295–301.
Nakamura M, Ferreira SH. Peripheral analgesic action of clonidine: mediation by release of endogenous enkephalin-like substances. Eur J Pharmacol 1988; 146:223–228.
Ueda H, Inoue M, Matsumoto T. Protein kinase C-mediated inhibition of mu-opioid receptor internalization and its involvement in the development of acute tolerance to peripheral mu-agonist analgesia. J Neurosci 2001; 21:2967–2973.
Ueda H, Inoue M, Mizuno K. New approaches to study the development of morphine tolerance and dependence. Life Sci 2003; 74:313–320.
Salmon RJ, Ansquer Y, Asselain B. Preservation versus section of intercostal-brachial nerve (IBN) in axillary dissection for breast cancer – a prospective randomized trial. Eur J Surg Oncol 1998; 24:158–161.
Gottrup H, Andersen J, Arendt-Nielsen L, Jensen TS. Psychophysical examination in patients with post-mastectomy pain. Pain 2000; 87: 275–284.
Esmaoglu A, Yegenoglu F, Akin A, Turk CY. Dexmedetomidine added to levobupivacaine prolongs axillary brachial plexus block. Anesth Analg 2010; 111:1548–1551.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]