Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 92-98

Dexmedetomidine versus ketorolac as adjuvants for intravenous regional anesthesia


Department of Anesthesiology, Al-Minia University, Minia, Egypt

Date of Submission14-Mar-2015
Date of Acceptance04-Sep-2015
Date of Web Publication17-Mar-2016

Correspondence Address:
Ahmed Hassanein
Department of Anesthesiology, Al-Minia University, Minia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.178886

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  Abstract 

Background
Multiple adjuvants have been added to improve the quality of intravenous regional anesthesia (IVRA). The aim of this study was to compare the effect of dexmedetomidine with that of ketorolac as an adjuvant for lidocaine IVRA as regards the onset and duration of sensory and motor blocks, intraoperative-postoperative pain, and intraoperative and postoperative analgesic requirement.
Patients and methods
This study was a prospective, randomized, double-blinded trial. Sixty patients scheduled for hand or forearm surgery were randomly divided into three equal groups (n = 20): group I was given 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 0.5 μg/kg of dexmedetomidine; group II was given 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 30 mg ketorolac; and group III was given 3 mg/kg of lidocaine 2% (maximum: 200 mg). In the three groups, 0.9% normal saline was added for a total volume of 40 ml. Sensory and motor block onset, recovery times, intraoperative and postoperative analgesic requirement, and hemodynamic variables were recorded and compared between the three groups.
Results
There was a significant reduction in sensory and motor onset, and prolonged sensory and motor duration in the dexmedetomidine group than in the ketorolac and the control group, and in the ketorolac group than in the control group (P < 0.001). There was improved tolerance to tourniquet and postoperative pain, with low levels of intraoperative and postoperative analgesic requirement in the dexmedetomidine group than in the ketorolac group followed by the control group.
Conclusion
We concluded that dexmedetomidine seems to be superior to ketorolac as an adjuvant to lidocaine in IVRA in terms of tourniquet pain and intraoperative and postoperative analgesic requirements.

Keywords: dexmedetomidine, intravenous regional anesthesia, ketorolac


How to cite this article:
Hassanein A. Dexmedetomidine versus ketorolac as adjuvants for intravenous regional anesthesia. Ain-Shams J Anaesthesiol 2016;9:92-8

How to cite this URL:
Hassanein A. Dexmedetomidine versus ketorolac as adjuvants for intravenous regional anesthesia. Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2019 Sep 15];9:92-8. Available from: http://www.asja.eg.net/text.asp?2016/9/1/92/178886


  Introduction Top


Intravenous regional anesthesia (IVRA) is a method of inducing anesthesia in a part of the limb with intravenous injection of a local anesthetic into an extremity isolated from the rest of the systemic circulation with a tourniquet to avoid effects of general anesthesia and upper airway instrumentation. It produces a rapid onset of anesthesia and skeletal muscle relaxation [1] . Lidocaine 0.5% is probably the local anesthetic most commonly chosen for this technique, because it is characterized by a rapid onset of action and topical anesthetic activity and intermediate duration of activity [2] . For procedures of longer duration, tourniquet pain is a limiting factor. It has been suggested that tourniquet pain may arise from ischemia of the peripheral neurons or nociceptors distal to the tourniquet or from nerve fiber activation directly under it. Moreover, mechanical trauma and tissue ischemia under or distal to the tourniquet lead to the release of inflammatory mediators and thus tourniquet pain [3] . Several agents have been used as adjuvants to local anesthetics in IVRA in an attempt to improve the tourniquet tolerance and postoperative analgesia and reduce the amount of local anesthetic used, such as opioids including morphine and fentanyl [4] , clonidine [5] , and ketorolac [3] , muscle relaxants such as cisatracurium [2] and ketamine [6] , and alkalinization by bicarbonate [7] . Dexmedetomidine is an α2-adrenoreceptor (AR) agonist that has been the subject of many anesthetic studies owing to its sedative and analgesic effects. It is approximately eight times more selective toward the α2-AR compared with clonidine. It decreases anesthetic requirements by up to 90% and induces analgesia in patients. Therefore, it is considered as a full agonist of the receptor (with more potent neurological and less cardiovascular effects). Its highly lipophilic nature allows rapid absorption into cerebrospinal fluid and binding to α2-AR of the spinal cord and α2A-AR of peripheral nerves. Dexmedetomidine has been successfully used in IVRA [8] . Ketorolac is the only NSAID that is approved for intravenous use and it acts by interference with the synthesis of inflammatory mediators [9] .

The aim of this work was to compare the effect of dexmedetomidine and ketorolac when added to lidocaine during IVRA.


  Patients and methods Top


After obtaining approval of the Local Ethics Committee of Al-Minia University Hospital, 60 adult patients undergoing elective and emergency hand and forearm soft tissue surgeries (carpal tunnel, trigger finger, tendon release, cyst excision, lipoma, and cut tendon) under IVRA were enrolled from January 2013 to January 2014. All patients gave informed written consent. The study was carried out on ASA grade I and II patients of either sex between 18 and 80 years of age. We excluded patients with peripheral vascular disease, sickle cell anemia, psychiatric disorders, peripheral neuropathy, history of chronic pain or undergoing regular medication with analgesics, history of opioid dependence, patients who refused to participate, patients with known hypersensitivity to the drugs used in this study, and patients who had been treated with α methyldopa or clonidine. The patients were randomly allocated using a computer-generated sequence of random numbers and a sealed envelope technique. Study drugs were prepared by an anesthetist who did not participate in the operation; this study was conducted in a random double-blind manner (neither the administrator of the drug nor the patient knew the nature of drugs given). The patients were divided into three equal groups (n = 20 each group). In group I, IVRA was achieved with 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 0.5 μg/kg of dexmedetomidine (Precedex 200 μg/2 ml; Abbott, North Chicago, Illinois, USA) (the dexmedetomidine group). Group II received 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 30 mg of ketorolac (Ketolac 30 mg/2 ml; Amirya Pharma Ind., Egypt) (the ketorolac group). Group III received 3 mg/kg of lidocaine 2% (maximum: 200 mg) (the control group). In the three groups, 0.9% normal saline was added for a total volume of 40 ml, prepared in identical syringes by an anesthetist who was not involved in the study.

Anesthetic technique

All patients received a standard anesthetic plan, which included premedication with oral midazolam at 0.5 mg/kg given 0.5 h before operation. In the operating room, patients were connected to standard monitoring including ECG, noninvasive arterial blood pressure, and pulse oximetry (SpO 2 ) (Marquette Solar 8000 Patient Monitor; UK). An intravenous access was assured by inserting an intravenous wide bore cannula on the nonsurgical upper limb for fluid infusion and analgesic injection. Another intravenous cannula (22-G) was inserted in a distal vein of the diseased limb. A double upper arm tourniquet was used for IVRA; the upper arm was properly padded with web roll for patients' comfort and to avoid bruises due to pressure exerted by the cuff on the skin and soft tissue. With the patient in the supine position, the limb to be operated upon was elevated for 3 min at 90° above the patient's chest to passively empty the venous system and decrease the volume of blood in the arm. A wide Esmarch's rubber bandage was then applied from the fingertips to the distal tourniquet cuff. However, if the Esmarch's bandage was likely to cause intolerable pain to the patient (e.g. fractured limb) it was acceptable to simply elevate the arm for 3-4 min while applying firm digital pressure on the brachial artery to allow venous drainage from the limb without further arterial blood entering. The operative limb was exsanguinated with an Esmarch's bandage, and a pneumatic tourniquet was applied to the upper arm. The proximal cuff of the double cuff tourniquet was then inflated 100 mmHg above the premeasured systolic blood pressure (maximum: 250 mmHg). Circulatory isolation of the limb was confirmed by absence of pulse oximetry tracing in the ipsilateral index finger and absence of palpable radial pulsations in the same limb and then the Esmarch's bandage was removed. The local anesthetic containing solution was then slowly injected over 1 min through the cannula, on the operative limb, and then the cannula was removed. The times for tourniquet and drug administration were recorded. After administration of drugs, sensory block was assessed every 30 s and the onset of sensory block was evaluated using the pin prick method using a 22-G short beveled needle taken out at dermatomal distribution of the ulnar nerve (hypothenar eminence), the median nerve (thenar eminence), and the radial nerve (first web space). Onset of sensory block was defined as a decrease from baseline value; complete sensory block was defined as absence of sensation of pain at the surgical site. Moreover, motor block was assessed every minute and the onset of motor block was evaluated by asking the patient to flex and extend the wrist and fingers. Onset of motor block was defined as a decrease from baseline value; complete motor block was achieved when no voluntary movement was possible. After sensory block was achieved, distal cuff was inflated 100 mmHg above preoperative systolic pressure and proximal tourniquet was deflated and the operation was started. Tourniquet pain was assessed using the visual analogue scale (VAS) (0 = no pain, 10 = worst pain) at 0, 5, 10, 20, 40, and 60 min. Fentanyl 1 μg/kg was given if VAS was greater than 4. Onset of both surgical and tourniquet pain was recorded and total fentanyl requirements were also recorded. At the end of the surgery, the tourniquet was deflated using the cyclic deflation technique (tourniquet was deflated three times in a cyclic manner with 10 s of deflation separated by 1 min of reinflation). The tourniquet was not deflated before 20 min and was not shifted for more than 1.5 h. The patient was then transported to the post anesthesia care unite (PACU) for 3 h with continuous monitoring of hemodynamic and respiratory data. The patient was then discharged to the ward.

The following parameters were recorded:

  1. Tourniquet duration (min);
  2. Hemodynamics, including noninvasive arterial blood pressure, heart rate (HR), and SpO 2 , preoperatively, after inflation of tourniquet, and after administration of drugs (5, 10, 20, 40, and 60 min);
  3. Onset of sensory block (min) using the pinprick test;
  4. Sensory recovery time (min) - the time elapsed after tourniquet deflation until recovery of sensory pain;
  5. Onset of motor block (min), evaluated by asking the patient to flex and extend the wrist and fingers;
  6. Motor recovery time (min) (the time elapsed after tourniquet deflation to movement of fingers);
  7. Tourniquet pain (evaluated using VAS);
  8. Intraoperative analgesia (fentanyl 1 μg/kg);
  9. Postoperative pain (evaluated using VAS);
  10. Postoperative analgesic requirement - total amount of diclofenac (75 mg intramuscular) postoperatively; and
  11. Adverse effects such as nausea, vomiting, arrhythmia (ventricular and atrial), hypotension, tinnitus, and metallic taste.
Statistical analysis

On the basis of the data provided in previous studies [10],[11] on ketorolac as adjuvants for IVRA, we determined that, to detect 15% difference in analgesic requirement, a sample size of 20 patients in each group will permit a power of 80% and type I error probability of null hypothesis at 0.05.

Data were analyzed using SPSS (version 13 for Windows; SPSS Inc., Chicago, Illinois, USA) software. Quantitative data were presented as mean ± SD, whereas qualitative data were presented as frequency distribution. The χ2 , Krusksal-Wallis, and Mann-Whitney tests were used to test the significant differences of qualitative (noncategorical) data between the studied groups, whereas the analysis of variance test and the post-hoc test were used to test the significant difference of quantitative data between the studied groups. The paired t-test was used to test the follow-up of quantitative data in each group. A P value of less than 0.05 was considered as a cutoff value for significance.


  Results Top


The study included 60 patients, 20 in each group, who were scheduled for elective hand or forearm soft tissue surgery. All allocated patients completed the study. As regards age, sex, weight, ASA classification, operative time, and tourniquet time, the results were similar among the groups [Table 1].
Table 1 Demographic data, operative time, and tourniquet time in the three groups

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As regards the onset and duration of sensory block, group I (the dexmedetomidine group) showed a significant rapid onset (5.1 ± 1.4 min) compared with group II (the ketorolac group) and group III (the control group), which showed longer time (6 ± 2.1 and 8.6 ± 1.9 min, respectively; P < 0.001). Moreover, the sensory duration was longer in group I (the dexmedetomidine group) (10.7 ± 1.03 min) than in group II (the ketorolac group) (6.2 ± 1.6 min), whereas group III (the control group) showed the shortest sensory duration (3.8 ± 1.2 min) (P < 0.001). Onset of motor block was significantly shorter in group I (the dexmedetomidine group) (8.2 ± 1.1 min), followed by group II (the ketorolac group) (11.3 ± 3.4 min) and group III (the control group) (15.7 ± 3.1 min) (P < 0.005). Furthermore, motor offset time was longer in group I (12.1 ± 1.6 min) than in group II (10.9 ± 2.2 min), but without statistical significance (P = 0.9). However, the motor offset time was significantly longer in groups I and II than in group III (the control group) (5.1 ± 1.2 min) (P = 0.001) [Table 2].
Table 2 Comparison of the mean ± SD of the onset and duration times of sensory and motor block (min)

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As regards tourniquet pain, there was more stability in pain score value throughout operative time in group I (the dexmedetomidine group) than in group II (the ketorolac group) and group III (the control group). There was a significant difference in values of the VAS scores for tourniquet pain at 10 min between group I (the dexmedetomidine group) and group II (the ketorolac group) and group I and group III (the control group) after tourniquet inflation (P = 0.001 and 0.001, respectively). There was a statistically significant difference in the VAS scores for tourniquet pain at 30 min between group I (the dexmedetomidine group) and group II (the ketorolac group) and group I (the dexmedetomidine group) and group III (the control group) (P = 0.011 and 0.006, respectively) [Table 3].
Table 3 Comparison of mean tourniquet pain in the three groups

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As regards the number of patients who needed fentanyl, there was a significant difference between group I (the dexmedetomidine group) and group II (the ketorolac group) (P = 0.029) and between group I (the dexmedetomidine group) and group III (the control group) (P < 0.001). However, there was no significant difference between group II (the ketorolac group) and group III (the control group) [Figure 1].
Figure 1: Comparison between the studied groups with regard to percentage of patients who needed fentanyl. Group I, dexmedetomidine group, group II, ketorolac group, and group III, control group

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As regards postoperative pain in the studied groups [Table 4], there was a significant difference in the VAS scores postoperatively at 10 min, 30 min, and 12 h between group I (the dexmedetomidine group) and group II (the ketorolac group) (P < 0.001), as well as between group I (the dexmedetomidine group) and group III (the control group). There was a statistically significant difference in the VAS scores postoperatively at 10 and 30 min (P < 0.001) and at 2, 6, and 12 h (P = 0.003, 0.001, and 0.002, respectively) between group II (the ketorolac group) and group III (the control group). There was a significant difference in the VAS scores postoperatively at 10 min, 6 h, and 12 h (P = 0.015, 0.010, and 0.001, respectively).
Table 4 Comparison of mean postoperative pain in the three groups

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As regards time (min) to first request of diclofenac [Table 5], there was a significant difference between group I (the dexmedetomidine group) (longer time) and both group II (the ketorolac group) (shorter time) and group III (the control group) (shortest time) (P = 0.001 and <0.001, respectively). However, there was no significant difference between group II (the ketorolac group) and group III (the control group) (P = 0.061). As regards total amount of diclofenac consumption, there was a significant difference between group I (the dexmedetomidine group) (less analgesic requirement at 12 h postoperatively) and both group II (the ketorolac group) and group III (the control group) (P = 0.033 and <0.001, respectively), and a significant statistical difference between group II (the ketorolac group) and group III (the control group) (P = 0.005). There was no hypotension, bradycardia, hypoxia, tinnitus, or vomiting in any of the groups.
Table 5 Comparison of mean time (h), frequency, and total amount of diclofenac (mg) administered in the three groups

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  Discussion Top


Surgical trauma results in postoperative pain by means of direct mechanical damage to nerve endings, as well as release of endogenous chemical mediators, leading to the activation of nociceptors. If these pain pathways are pharmacologically blocked before surgical trauma, the changes can be diminished or abolished. IVRA, a venous technique founded by August Gustav Bier in 1908 and so called the Bier's block [12] , acts by anesthetizing the peripheral nerve endings and also the nerve trunks. Hence, by the end of surgery, when the tourniquet is released, there is very little amount of the drug left in the vessels and cannot produce toxic side effects if washed into the systemic circulation. Dexmedetomidine has been involved in various applications and procedures with multiple delivery routes. The peripheral analgesic effects of dexmedetomidine that can potentiate local anesthetics are carried by a2-AR agonists. It causes hyperpolarization of noradrenergic fibers, which inhibits neuronal firing in the locus ceruleus, resulting in inhibition of norepinephrine release. These effects result in modulation of nociceptive neurotransmission causing analgesia [13] . Ketorolac is a NSAID that interferes with the synthesis of pain mediators at the site of trauma by suppression of cyclooxygenase (COX) enzymes, and so interferes with the arachidonic acid pathway. Increased levels of prostaglandine E (PGE) and I2 at the site of surgery stimulate the nociceptors, and so ketorolac suppresses these mediators by inhibiting both COX-1 and COX-2 [14] . Because of these advantages offered by dexmedetomidine and ketorolac, we decided to compare the effects of these drugs as adjuvants of IVRA.

Our study included patients undergoing hand and forearm soft tissue surgeries. The patients were divided into three equal groups (n = 20). Group I received 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 0.5 μg/kg of dexmedetomidine. Group II received 3 mg/kg of lidocaine 2% (maximum: 200 mg) + 30 mg ketorolac. Group III received 3 mg/kg of lidocaine 2% (maximum: 200 mg). In the three groups, 0.9% normal saline was added for a total volume of 40 ml. Our study showed a significant reduction in sensory and motor onset, and prolonged sensory and motor offset in the dexmedetomidine group than in the ketorolac group and the control group, and in the ketorolac group than in the control group. There was improved tolerance to tourniquet and postoperative pain, with low levels of intraoperative and postoperative analgesic requirement in the dexmedetomidine group than in the ketorolac group and lastly the control group.

Memis et al. [15] studied the effect of adding dexmedetomidine to lidocaine for IVRA on 30 patients in two groups, group L and group LD. IVRA was achieved using 3 mg/kg of lidocaine 2% diluted with saline to a total dose of 40 ml in the lidocaine group or 0.5 μg/kg of dexmedetomidine plus 3 mg/kg of lidocaine 2% diluted with saline to a total dose of 40 ml in the dexmedetomidine group. Their study is in agreement with our study; they reported that there was a significant reduction in the onset of sensory and motor block in the dexmedetomidine group (P < 0.05), as well as in the delayed recovery of sensory and motor block in the dexmedetomidine group (P < 0.001). Kaygusuz et al. [16] studied addition of dexmedetomidine to levobupivacaine for an axillary brachial plexus block on 64 patients with ASA I/II who were scheduled to undergo forearm and hand surgery. They found that sensory and motor block onset time was shorter in group D than in group L (P < 0.05). Sensory and motor block duration and time to first analgesic use were significantly longer in group D (P < 0.01), and the total need for analgesics was also lower in group D (P < 0.05). Intraoperative VAS for sensory block was significantly lower in group D (P < 0.05). The 12-h postoperative VAS value was also lower in group D (P < 0.05).

Steinberg et al. [17] showed a decreased incidence of intraoperative tourniquet pain in the ketorolac (60 mg) group. This coincides with our results, but lower dose is preferred to avoid appearance of side effects. In contrast to our study, a study by Goel et al. [18] with 30 mg ketorolac showed a nonsignificant reduction in the incidence of tourniquet pain; this may be attributed to the type of operation used.

We can conclude that the addition of 0.5 μg/kg of dexmedetomidine or ketorolac 30 mg to IVRA with 0.5% lignocaine has provided an added advantage of intraoperative analgesia, postoperative pain relief, and preemptive analgesia without side effects. When we compared both drugs, dexmedetomidine showed better preemptive analgesic property at the doses compared, by reducing the total number of analgesics required in the first 12 h.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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2.
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Reuben SS, Steinberg RB, Maciolek H, Manikantan P. An evaluation of the analgesic efficacy of intravenous regional anesthesia with lidocaine and ketorolac using a forearm versus upper arm tourniquet. Anesth Analg 2002; 95:457-460.  Back to cited text no. 3
    
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Tverskoy M, Oren M, Vaskovich M, Dashkovsky I, Kissin I. Ketamine enhances local anesthetic and analgesic effects of bupivacaine by peripheral mechanism: a study in postoperative patients. Neurosci Lett 1996; 215:5-8.  Back to cited text no. 6
    
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Lavin PA, Henderson CL, Vaghadia H. Non-alkalinized and alkalinized 2-chloroprocaine vs lidocaine for intravenous regional anesthesia during outpatient hand surgery. Can J Anaesth 1999; 46:939-945.  Back to cited text no. 7
    
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Kol IO, Ozturk H, Kaygusuz K, Gursoy S, Comert B, Mimaroglu C. Addition of dexmedetomidine or lornoxicam to prilocaine in intravenous regional anaesthesia for hand or forearm surgery: a randomized controlled study. Clin Drug Investig 2009; 29:121-129.  Back to cited text no. 8
    
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Bigat Z, Boztug N, Hadimioglu N, Cete N, Coskunfirat N, Ertok E. Does dexamethasone improve the quality of intravenous regional anesthesia and analgesia? A randomized, controlled clinical study, Anesth Analg 2006; 102:605-609.  Back to cited text no. 11
    
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Carollo DS, Nossaman BD, Ramadhyani U. Dexmedetomidine: a review of clinical applications. Curr Opin Anaesthesiol 2008; 21:457-461.  Back to cited text no. 13
    
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Santini G, Patrignani P, Sciulli MG, Seta F, Tacconelli S, Panara MR, et al. The human pharmacology of monocyte cyclooxygenase 2 inhibition by cortisol and synthetic glucocorticoids. Clin Pharmacol Ther 2001; 70:475-483.  Back to cited text no. 14
    
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Memis D, Turan A, Karamanhoglu B, Pamukçu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004; 98:835-840.  Back to cited text no. 15
    
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Kaygusuz K, Kol IO, Duger C, Gursoy S, Ozturk H, Kayacan U, et al. Effects of adding dexmedetomidine to levobupivacaine in axillary brachial plexus block. Curr Ther Res Clin Exp 2012; 73:103-111.  Back to cited text no. 16
    
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Steinberg RB, Reuben SS, Gardner G. The dose-response relationship of ketorolac as a component of intravenous regional anesthesia with lidocaine. Anesth Analg 1998; 86:791-793.  Back to cited text no. 17
    
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