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Evaluation the Effects of Intravenous vs. Spinal Dexmedetomidine during Anesthesia for Cesarean Sections with Severe Pre-Eclampsia
ISSN: 2155-6148

Journal of Anesthesia & Clinical Research
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Evaluation the Effects of Intravenous vs. Spinal Dexmedetomidine during Anesthesia for Cesarean Sections with Severe Pre-Eclampsia

Ahmed Said Elgebaly*
Department of Anesthesia and Post-Surgical Intensive Care, Faculty of Medicine, Tanta University, Egypt
*Corresponding Author: Ahmed Said Elgebaly, Faculty of Medicine, Tanta University, Egypt, Tel: 01005121944, Email: [email protected]

Received Date: Dec 26, 2017 / Accepted Date: Jan 22, 2018 / Published Date: Jan 29, 2018

Abstract

Background: Side effects of low-dose spinal anesthesia with opioids and adjuvants raised the essential requirement to look for better alternatives like dexmedetomidine for patients with severe pre-eclampsia undergoing cesarean section to provide satisfactory spinal anesthesia and improve its outcomes.
Aim: Evaluate and compare effects of intravenous and intrathecal dexmedetomidine on duration of spinal block, postoperative analgesia and incidence of adverse effects in parturient with severe Pre-eclampsia undergo Caesarean section.
Settings and design: A prospective, double blind controlled randomized and comparative study.
Methods: Sixty ASA II patients were randomized into 3 groups: Group I: (control group) (n=30) each patient received intrathecal hyperbaric bupivacaine 10 mg with 3 mL total volume. Group II: (Intrathecal dexmedetomidine group) (n=0) each patient received dexmedetomidine 5 μg diluted i n 0.5 ml saline and hyperbaric bupivacaine 10 mg with 3 mL total volume. Group III: (Intravenous dexmedetomidine group) (n=30) each patient received intravenous dexmedetomidine started at a loading dose of 1 μg/kg diluted in 50 ml saline and administered within 10 min. as a loading dose, followed by maintenance at a dose of 0.4 μg/kg/h diluted in 200 ml saline till the end of surgery and hyperbaric bupivacaine 10 mg in 3 ml total volume. Primary outcome is the duration of spinal block while secondary outcomes are the postoperative analgesia and the incidence of side effects.
Results: Time (min) to sensory regression to s1 level in group I, II, III was (200.23 ± 3.25, 230.4 ± 2.5, 294.1 ± 15.1) respectively, showed significance increase in group III. Time to reach motor block Bromage 3 was (5.5 ± 0.2, 5.7 ± 0.9, 8.5 ± 0.3) in group I, II, III respectively, there was significance increase in group III. Time of regression to Bromage 0 was assessed as (170.5 ± 2.35, 190.6 ± 3.51, 249.2 ± 20.2) in groups I, II, III respectively, showed significance increase in group III. Onset of 1st post-operative analgesic dose was assessed in the study groups (242.23 ± 15.01, 270.15 ± 25.00, 371.25 ± 88.54), showed significance increase in group III. Side effects showed significance decrease in group III.
Conclusion: Intravenously administered dexmedetomidine prolonged the duration of sensory and motor blockade with reduced side effects.

Keywords: Dexmedetomidin; Intravenous; Intrathecal; Severe Pre-eclampsia

Introduction

Neuraxial blockade for patients with pre-eclampsia undergoing cesarean section is a safe and potent anesthetic technique [1]. Fast onset, higher level blockade, lower failure rates, and cost-effectiveness are main causes that make spinal block is the preferred technique although it has numerous side effects which my occur intra operative as hypotension, bradycardia, respiratory depression, short period of block and postoperative complications as nausea, vomiting, shivering, prurites paresthesia, post dural puncture headache (PDPH), allergy, and voiding difficulty shortness of postoperative analgesia [2].

Aim of researchers work to decrease spinal anesthesia complications is necessary for rehabilitation, rapid functional recovery, allowing patients to return to their usual activity quickly and improve patient satisfaction and surgeon opinion [3]. Intrathecal adjuvants are progressively used for better post-operative analgesia. Intrathecal opioids are used to potentiate post-operative pain management but their side effects have raised the essential requirement to look for better alternatives [4].

Several authors demonstrated that although intrathecal addition of a low dose of dexmedetomidine results in significant prolongation of the duration of the sensory and motor blockade added to spinal anesthetics [5]. But it has high incidence of spinal anesthesia complications such as nausea, vomiting, shivering, pruritus parenthesis, PDPH, allergy, total spinal anesthesia, and voiding difficulty.

Dexmedetomidine is a centrally acting α2-agonist with sedative and analgesic effects; it is near to clonidine but has much greater α2 to α1 binding affinity [6]. Stimulation of the brain and spinal cord receptors retards neuronal firing, causing hypotension, bradycardia, sedation, and analgesia [7]. Depressing the liberation of C-fiber transmitters and by hyperpolarization of postsynaptic dorsal horn neurons are the mechanisms of analgesic effect of dexmedetomidine. This antinociceptive action and safety of the use of dexmedetomidine on neonatal outcome is a very important issues which encourage us to use with spinal anesthesia either intravenously or intrathecally [8].

The aim of this study was to investigate and compare the effects of intravenous dexmedetomidine and when used as an additive to intrathecal 0.5% bupivacaine in decreasing the incidence of intra and post spinal anesthesia adverse effects and improving its quality (duration of spinal block, postoperative analgesia, hemodynamic stability and neonatal outcome) with mild pre-eclampsia undergo Caesarean section.

Patients and Methods

This prospective randomized blind study of one year duration was performed on 90 patients scheduled for elective lower segment Caesarean section (LSCS). After approval from ethical committee; an informed consent was taken from the patients. Any unexpected risk occurring during the course of the study was cleared to ethical committees in time. Each patient received an explanation to the purpose of the study. All patients identified by a coded number to ensure privacy. Female patients aged 18:42 years old with severe pre-eclampsia at least 36 weeks gestation scheduled for elective cesarean delivery were included.

Severe pre-eclampsia was defined as a systolic arterial blood pressure (SAP) of 160 mmHg or more or a diastolic arterial blood pressure (DAP) of 110 mmHg or more and proteinuria of 100 mg/dL or more. Patients with eclampsia, coagulopathy, placental abruption, severe fetal distress, contraindications to regional anesthesia or a history of allergy to local anaesthetics were excluded from the study. On arrival at the Operating Room, two peripheral venous cannulae and a urinary catheter were inserted and all the patients were preloaded with 10 ml/kg Lactated Ringer's solution.

Monitoring consisted of echocardiogram (ECG), pulse oximeter and non-invasive blood pressure recording. Ramsay's score was used to monitor the sedation levels. Intravenous hydralazine 5 mg was given to all patients at 20 min intervals, to decrease the DAP to about 90 mmHg, prior to the start of anesthesia.

Patients were randomly classified using sealed envelopes into 3 group: Group I: (Control group) (n=30) each patient received intrathecal hyperbaric bupivacaine 10 mg in 2.5 ml and 0.5 ml saline with 3 ml total volume and Continuous 50 ml saline infusion for 10 min followed by 200 ml saline infusion till end of surgery, Group II: (Intrathecal dexmedetomidine group) (n=30) each patient received dexmedetomidine 5 μg diluted in 0.5 ml saline and hyperbaric Bupivacaine 10 mg in 2.5 ml with 3 mL total volume and Continuous 50 ml saline infusion for 10 min followed by 200 ml saline infusion till end of surgery. Group III: Intravenous dexmedetomidine group (n=30) each patient received intravenous dexmedetomidine started at a loading dose of 1 mg/kg diluted in 50 ml saline and administered within 10 min as a loading dose, followed by maintenance at a dose of 0.4 mg/kg/h diluted in 200 ml saline till the end of surgery and hyperbaric Bupivacaine 10 mg in 2.5 ml total volume.

Primary outcome is the duration of spinal block while secondary outcomes are the postoperative analgesia and the incidence of intraoperative side effects (All durations recorded considering the time of spinal injection as time zero).

The study drug solution was prepared by anesthetic nurse who was not being involved in the study or care of the patient. Both patient and anesthetist performed the block were blinded to the study drug.

Spinal anesthesia block was performed with the patient in sitting position, in which the patient sit on the border of the operating table with legs on stool, leaning forward arching his back. Under complete aseptic technique, iliac crest was palpated and thumb extended to meet the midline, feeling the expanse between L4-5.

Spinal anesthesia performed as follows: using a 25-G spinal (needle B Braun medical, Germany) the epidural space identified by the loss of resistance technique. The needle then was further advanced until cerebrospinal fluid flowed from the cannula without restriction. Immediately the prepared solution was injected.

Sensory block: Sensory testing was evaluated by loss of pinprick sensation to 23 G hypodermic needle and dermatomes levels was tested every 2 min until the highest level is stabilized by consecutive tests the mid clavicular line bilaterally and on achieving T7 sensory blockade level (which is halfway between the level of the xiphoid process and the level of the umbilicus). Surgery was allowed on skin incision, we told the patient about the various sensations that she would sense like stretching of muscles and compression on abdomen by the surgeon assistant for baby delivery. In case of failed neuraxial block and total spinal, patient was given general anesthesia and the case was excluded from the study.

The motor block was assessed according to the modified Bromage scale. Bromage 0 the patient is able to move the hip, knee and ankle, Bromage 1 the patient is unable to move the hip but is able to move the knee and ankle, Bromage 2, the patient is unable to move the hip and knee but able to move the ankle, Bromage 3, the patient is unable to move the hip, knee and ankle) When Bromage 3 is reached surgery was allowed.

Before baby delivery 15 IU oxytocin was given to the mother by the baby delivery as 5 I.U IV slowly bolus and 10 IU as infusion followed by measuring of blood pressure, observing and asking the surgeon about the tone of uterus.

Intraoperative: Heart rate, Arterial blood pressure and SpO2 were recorded in the following times at base line, immediate after spinal 5, 10, 15, 30 and 45 min during surgery. Time to achieve T7 sensory blockade was assessed by loss of pinprick sensation (onset of sensory blockade) from the time of injection. Time to reach motor block Bromage 3 was assessed according to the Modified Bromage scale (onset of motor blockade) from the time of injection.

Hypotension, defined as a decrease of systolic blood pressure by more than 30% from baseline or a fall below 90 mmHg, was treated with incremental IV doses of ephedrine 5 mg and IV fluid as required. Bradycardia, defined as heart rate <50 bpm, was treated with IV atropine 0.3-0.6 mg. Side effects as nausea, vomiting and pruritus recorded.

Postoperative: The regression time for Bromage 0 was recorded. Time to sensory regression to S1 level (which corresponds to lateral side of calcareous) was recorded. Sedation was recorded by Ramsay sedation score. The score, from 1 to 6, describes a patient as follows:

1. Anxious and agitated or restless, or both

2. Cooperative, oriented, and calm,

3. Responsive to commands only,

4. Exhibiting brisk response to light or loud auditory stimulus,

5. Exhibiting a sluggish response to light or loud auditory stimulus,

6. Unresponsive

The duration between the administration of spinal block and the first desire for supplemental analgesia (onset of 1st post-operative analgesic dose). First post-operative analgesic dose was 1 μg/kg intravenous fentanyl when VAS is 4 or more [visual analogue pain score (VAS) between 0 and 10{0=no pain, 10=most severe pain}] ,after that patient was assessed for pain relief every 10 min and increments of 0.5 μg/kg IV fentanyl was given until pain is relieved.

After that, the pain score was every 4 h in 24 h and fentanyl was given in a dose of 1 μg/kg when VAS is 4 or more. Any out breaking pain was treated with increments of fentanyl in a dose of 0.5 μg/kg. The total requirement of fentanyl was calculated in the different group. Fentanyl was stopped if patient becomes sedated (Ramsay score more than 2), has respiratory rate less than 9 bpm, or oxygen saturation less than 95%.

The neonatal outcome: Apgar scores at 1st and 5th min. and incidence of apgar score <7 was recorded. Patients were discharged from the PACU (Post Anesthesia Care Unit) after sensory regression to S1 dermatome and Bromage 0.

Statistics

The sample size was chosen after reviewing many randomized. Control studies on the same subject. The full detailed form is: SPSS 20, IBM, Armonk, NY, United States of America. Quantitative data were expressed as mean ± standard deviation (SD). Qualitative data were expressed as frequency and percentage. 1. Independent-samples t-test of significance was used when comparing between two means. 2. Chi-square (χ2) test of significance was used in order to compare proportions between two qualitative parameters.

Results

As regard age, weight and duration of surgery, there was no significant difference between both group; those data were recorded in (Table 1).

  Group I (n=30) Group II (n=30) Group III (n=30) p value
Age (years) 27.3 ± 5.2 25.6 ± 5.6 26.4 ± 4.7 0.325
Weight (kg) 61.9 ± 10.3 66.4 ± 11.9 63.7 ± 11.2 0.274
Duration of surgery (min) 36.8 ± 6.4 37.6 ± 5.9 38.6 ± 5.2 0.319
Data are represented as mean ± SD; P>0.05 is considered statistically non-significant compared with the other two groups.

Table 1: Patients' demographics.

The study as regard HR comparison between group in baseline, 5 min, 10 min, 15 min, 30 min, 45 min showed that, in group I there was decrease in mean value of HR at 15 min, 30 min, 45 min from (84.6 ± 6.3) to (72.6 ± 5.6), (71.4 ± 5.1), (70.3 ± 5.9) and also, in group II there was decrease in mean value of HR at 15 min, 30 min, 45 min from (83.4 ± 7.2) to (71.6 ± 6.1), (69.3 ± 5.2), (68.7 ± 5.4), there was no significance changes between group at baseline, 5 min, 10 min but at 15 min, 30 min, 45 min, there was significance decrease between group I and group III and also, between group II and group III while, between I, II there was no significance difference (Table 2).

Heart rate Group I (n=30) Group II (n=30) Group III (n=30) p value P1 P2 P3
Baseline 90.3 ± 7.8 89.4 ± 6.5 90.1 ± 6.3 0.523      
5 min 89.9 ± 5.9 88.4 ± 5.6 90.7 ± 6.1 0.489      
10 min 84.6 ± 6.3 83.4 ± 7.2 85.1 ± 6.8 0.369      
15 min 72.6 ± 5.6 71.6 ± 6.1 86.9 ± 6.7 0.001* 0.511 0.001* 0.001*
30 min 71.4 ± 5.1 69.3 ± 5.2 85.7 ± 6.2 0.001* 0.120 0.001* 0.001*
45 min 70.3 ± 5.9 68.7 ± 5.4 82.6 ± 6.1 0.001* 0.278 0.001* 0.001*
Data are represented as mean ± SD;  *P<0.05 is considered statistically significant compared with the other two groups.

Table 2: Comparison between group I, II, III in heart rate values.

As regard MAP comparison between group at baseline, 5 min, 10 min, 15 min, 30 min, 45 min shows ,in group I there was decrease in mean value of MAP at 15 min, 30 min, 45 min from (82.4 ± 8.1) to (68.4 ± 8.6), (67.4 ± 7.9) (65.6 ± 6.8) and also in group II there was decrease in mean value of MAP at 15 min, 30 min, 45 min from (80.9 ± 7.6) to (66.9 ± 9.1), ( 66.1 ± 8.6), (64.3 ± 5.9), there was no significance changes between group I, II, III at baseline, 5 min, 10 min but at 15 min, 30 min, 45 min, there was significance decrease between group I and group III and also between group II and group III while between I, II there was no significance difference (Table 3).

MAP  Group I (n=30) Group II (n=30) Group III (n=30) p value P1 P2 P3
Baseline 89.7 ± 8.9 91.4 ± 7.6 90.6 ± 8.1 0.415      
5 min 88.6 ± 7.9 86.4 ± 7.1 87.7 ± 6.8 0.349      
10 min 82.4 ± 8.1 80.9 ± 7.6 81.3 ± 7.9 0.319      
15 min 68.4 ± 8.6 66.9 ± 9.1 81.6 ± 8.7 0.001* 0.514 0.001* 0.001*
30 min 67.4 ± 7.9 66.1 ± 8.6 80.6 ± 7.4 0.001* 0.544 0.001* 0.001*
45 min 65.6 ± 6.8 64.3 ± 5.9 81.8 ± 5.5 0.001* 0.432 0.001* 0.001*
Data are represented as mean ± SD; *P<0.05 is considered statistically significant compared with the other two groups.

Table 3: Comparison between group I, II, III in MAP values.

Comparison between group as regard SpO2 values at baseline, 5 min, 10 min, 15 min, 30 min, 45 min, shows there was no significant difference between all groups during all period of study (Table 4).

SPO2 Group I (n=30) Group II (n=30) Group III (n=30) p value
Baseline 96.7 ± 6.5 94.6 ± 7.2 95.3 ± 7.5 0.365
5 min 97.4 ± 8.3 95.7 ± 7.3 97.9 ± 7.8 0.381
10 min 98.5 ± 6.7 97.6 ± 6.3 96.9 ± 7.1 0.326
15 min 96.8 ± 6.3 98.5 ± 7.2 97.4 ± 6.8 0.412
30 min 97.3 ± 7.1 96.5 ± 7.2 98.8 ± 6.8 0.285
45 min 96.3 ± 7.4 97.8 ± 6.8 96.9 ± 7.1 0.397
Data are represented as mean ± SD; P>0.05   is considered statistically non-significant compared with the other two groups.

Table 4: Comparison between groups I, II, III in SPO2 values.

Comparison between group as regard time to achieve T7 sensory blockade shows delay in group III (5.9 ± 0.9) and was (2.3 ± 0.7, 2.6 ± 0.6) in group I and II. There were no significant changes between group I, II but there was significance increase in group III when compared to group I, II. While the time to sensory regression to S1 level was (200.23 ± 3.25, 230.4 ± 2.5, 294.1 ± 15.1) in group I, II, III respectively, so intergroup comparison shows significant decrease between (I, II), (II, III), (I, III).

The time to reach motor block Bromage 3 was assessed in group I, II, III and it was (5.5 ± 0.2, 5.7 ± 0.9, 8.5 ± 0.3). There were no significance changes between groups I, II but there was significance increase in group III when compared to group I, II.

The time of regression to Bromage 0 was assessed in group I, II, III and it was (170.5 ± 2.35), (190.6 ± 3.51), (249.2 ± 20.2), so intergroup comparison shows significance decrease between (I, II), (II, III), (I, III). The time interval between the administration of spinal block and the first request for supplemental analgesia (onset of 1st post-operative analgesic dose) was assessed in group I, II, III and it was (242.23 ± 15.01, 270.15 ± 25.00, 371.25 ± 88.54), so intergroup comparison shows significant decrease between (I, II), (II, III), (I, III) (Table 5).

  Group I (n=30) Group II (n=30) Group III (n=30) p value P1 P2 P3
Time to achieve T7 sensory blockade 2.3 ± 0.7 2.6 ± 0.6 5.9 ± 0.9 0.001* 0.082 0.001* 0.001*
Time to sensory regression to S1 level 200.23 ± 3.25 230.4 ± 2.5 294.1 ± 15.1 0.001* 0.001* 0.001* 0.001*
Time to reach motor block Bromage 3 was assessed 5.5 ± 0.2 5.7 ± 0.9 8.5 ± 0.3 0.001* 0.241 0.001* 0.001*
The time of regression to Bromage 0 170.5 ± 2.35 190.6 ± 3.51 249.2 ± 20.2 0.001* 0.001* 0.001* 0.001*
The time interval between the administration of spinal block and the first request for supplemental analgesia (onset of 1st post-operative analgesic dose). 242.23 ± 15.01 270.15 ± 25.00 371.25 ± 88.54 0.001* 0.001* 0.001* 0.001*
Data are represented as mean ± SD; *P<0.05 is considered statistically significant compared with the other two groups.

Table 5: Comparison between group as regard time to achieve T7 sensory, regression to s1, Time to reach motor block, time of regression, time interval between the administration of spinal block and the first request for analgesia.

Comparison between group as regard Ramsay sedation score, Apgar scores, the total requirement of fentanyl in μg (in 24 h). There were no significance changes between groups in Ramsay sedation score, Apgar scores. The total requirement of fentanyl in μg (in 24 h) in group I, II, III was (996.3 ± 134.2, 917.4 ± 130.8, 658.7 ± 123.9), intergroup comparison shows significance decrease between (I, II), (II, III), (I, III) (Table 6).

  Group I (n=30) Group II (n=30) Group III (n=30) P value P1 P2 P3
Ramsay sedation score 1 (1-1) 1 (1-1) 1 (0-1)        
Apgar scores 10 (9-10) 10 (9-10) 10 (9-10)        
The total   requirement of fentanyl in µg (in 24 h) 996.3 ± 134.2 917.4 ± 130.8 658.7 ± 123.9 0.001* 0.024* 0.001* 0.001*
Data are represented as mean ± SD; *P<0.05 is considered statistically significant compared with the other two groups.

Table 6: Comparison between group as regard Ramsay sedation score, Apgar scores and total requirement of fentanyl.

Comparison between studied group as regard side effects (Nausea, vomiting, shivering and prurites, hypotension, bradycardia, respiratory depression paresthesia, PDPH and voiding difficulty), there were significance decrease in group III in side effects (Table 7).

Side effect Group I (n=30) Group II (n=30) Group III (n=30) p value
Nausea, vomiting  2 (6.7%) 3 (10%) 1 (3.3%) 0.001*
Shivering  3 (10%) 2 (6.7%) 1 (3.3%) 0.001*
Prurites 1 (3.3%) 1 (3.3%) 0 (0%) 0.001*
Voiding difficulty 2 (6.7%) 2 (6.7%) 1 (3.3%) 0.001*
Respiratory depression 2 (6.7%) 2 (6.7%) 1 (3.3%) 0.001*
Paresthesia, (PDPH) 3 (10%) 3 (10%) 2 (6.7%) 0.001*
Incidence of back and waist pain 3 (10%) 3 (10%) 2 (6.7%) 0.001*
Data are represented as n (%); P<0.05 is considered statistically significant compared with the other two groups.

Table 7: Comparison between studied groups as regard side effects.

Discussion

The present study has found that the intravenous dexmedetomidine started at a loading dose of 1 μg/kg administered within 10 min as a loading dose, followed by maintenance at a dose of 0.4 μg/kg/h for spinal anesthesia significantly prolongs the duration of spinal block as a primary outcome where the time to sensory regression to S1 level was (200.23 ± 3.25, 230.4 ± 2.5, 294.1 ± 15.1) in group I, II, III respectively, so intergroup comparison showed significance decrease between (I, II), (II, III), (I, III) and the time of regression to Bromage 0 was (170.5 ± 2.35, 190.6 ± 3.51, 249.2 ± 20.2) in group I, II, III and also the intergroup comparison showed significant decrease between (I, II), (II, III), (I, III).

Also, we found that the addition of intrathecal dexmedetomidine to bupivacaine significantly reduced the onset time of spinal block compared intravenous dexmedetomidine, where the time to achieve T7 sensory blockade in group III was (5.9 ± 0.9) and was (2.3 ± 0.7, 2.6 ± 0.6) in group I and II, while the time to reach motor block Bromage 3 was (5.5 ± 0.2, 5.7 ± 0.9, 8.5 ± 0.3) in group I, II, III respectively. There was significant delay in the onset time for sensory block in compared intravenous dexmedetomidine group.

Our results in agreement with Kamuran Elcıcek and his colleagues [9] who found that intravenously administered dexmedetomidine prolonged the duration of sensorial and motor blockade, provided sufficient sedation, and had few side effects.

The use of α2 adrenoreceptor agonists as an adjuvant to local anesthetics in spinal anesthesia has been studied by Kanazi and his colleagues, they found that dexmedetomidine (3 μg) or clonidine (30 μg), when added to intrathecal bupivacaine for patients undergoing transurethral resection of prostate or bladder tumor under spinal anesthesia, produces a near prolongation in the time of the motor and sensory block and lesser onset of both motor and sensory block with steady hemodynamic condition and lack of sedation [10].

Gupta et al. [11] found that intrathecal dexmedetomidine is associated with prolonged motor and sensory block, hemodynamic stability, and reduced demand for rescue analgesics in 24 h as compared to fentanyl.

Xiao-Yin et al. [12] found that the use of dexmedetomidine including intravenous and intrathecal could statistically significantly prolong the duration of sensory and motor block and the time to first request for postoperative analgesia. There was no increased risk of the side effects and the occurrence of hypotension, but the risk of bradycardia increased.

The postoperative analgesic consumption which is a secondary outcome significantly decreased in patients of group III (intravenous dexmedetomidine) when compared with intrathecal dexmedetomidine (5 μg) and control group, also there was significant reduction in postoperative analgesic consumption in group II when compared with group I, it was (996.3 ± 134.2, 917.4 ± 130.8, 658.7 ± 123.9) in group I, II, III respectively.

Also, this study has found that the time interval between the administration of spinal block and the first request for supplemental analgesia (onset of 1st post-operative analgesic dose) was (242.23 ± 15.01, 270.15 ± 25.00, 371.25 ± 88.54) in group I, II, III and the intergroup comparison showed significant decrease between (I, II), (II, III), (I, III) [10,11].

We found that the addition of (intravenous dexmedetomidine) to spinal anaesthesia did not affect the patients' hemodynamics compared with other two groups. While dexmedetomidine stimulation of the brain and spinal cord receptors reduces neuronal firing, causing hypotension, bradycardia, sedation, and analgesia [5,6]. Also, there was no significant change between group I, II, III in Ramsay sedation score and Apgar scores in our study, despite the fact that (intravenous dexmedetomidine) increases the incidence of confusion and drowsiness in eclamptic patients. We preferred to use sedation score and SpO2 as the measures of respiratory depression over respiratory rate. Therefore, hemodynamic depression after intrathecal and intravenous dexmedetomidine need attentive monitoring of pulse rate, blood pressure and level of sedation.

Conclusion

Intravenously administered dexmedetomidine prolonged the duration of sensory and motor blockade with reduced side effects.

References

Citation: Elgebaly AS (2018) Evaluation the Effects of Intravenous vs. Spinal Dexmedetomidine during Anesthesia for Cesarean Sections with Severe Pre-Eclampsia. J Anesth Clin Res 9: 801. DOI: 10.4172/2155-6148.1000801

Copyright: © 2018 Elgebaly AS. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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