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Year : 2013  |  Volume : 3  |  Issue : 1  |  Page : 23-26

Comparison of hemodynamic response and vasopressor requirement following spinal anaesthesia between normotensive and severe preeclamptic women undergoing caesarean section: A prospective study

1 Department of Anaesthesiology, Burdwan Medical College, Burdwan, West Bengal, India
2 Department of Obstetrics and Gynaecology, Burdwan Medical College, Burdwan, West Bengal, India

Date of Web Publication1-Jul-2013

Correspondence Address:
Sarmila Ghosh
33, Panchanantala, Natagarh, Sodepur, Kolkata - 700 113, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4472.114286

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Background: Spinal anesthesia is the technique of choice in cesarean sections, but it is not widely accepted in severe pre-eclampsia due to fear of sudden and extensive sympathetic blockade. The aim of the present study was to compare the heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), phenyl ephrine requirement, and neonatal outcome between normotensive and severe pre-eclamptic women undergoing cesarean section under spinal anesthesia.
Materials and Methods: A total of 30 healthy (group 1) and 30 severe pre-eclamptic (BP > 160/110 mmHg) parturients (group 2) above 18 years of age, meeting inclusion criteria undergoing elective cesarean section, were included in the study. After preloading with 10 ml/kg of ringer lactate solution spinal anesthesia was administered with 12.5 mg of hyper baric bupivacaine. Also, SBP, DBP, MAP, and HR were recorded before spinal anesthesia and then at every 2-min interval after spinal block for the first 30 min and thereafter every 5 min until completion of surgery. Phenylephrine was administered in 50 μg bolus dose when MAP decreased below 30% of base line. Apgar score was noted 1 and 5 min after birth.
Results: The minimum SBP, DBP, and MAP recorded were lower in normotensive, and the difference between two groups was statistically significant. The mean phenylephrine requirement in the normotensive group (151.1 ± 70) was significantly greater (P < 0.0001) than that of pre-eclamptic group (48.3 ± 35). Apgar scores at 1 and 5 min after birth were comparable in both the groups.
Conclusion: Pre-eclamptics experienced less hypotension following subarachnoid block (SAB) than normotensives and required less phenylephrine with comparable fetal Apgar scores.

Keywords: Hypotension pre-eclampsia, phenylephrine, spinal anesthesia

How to cite this article:
Saha D, Ghosh S, Bhattacharyya S, Mallik S, Pal R, Niyogi M, Banerjee A. Comparison of hemodynamic response and vasopressor requirement following spinal anaesthesia between normotensive and severe preeclamptic women undergoing caesarean section: A prospective study. J Obstet Anaesth Crit Care 2013;3:23-6

How to cite this URL:
Saha D, Ghosh S, Bhattacharyya S, Mallik S, Pal R, Niyogi M, Banerjee A. Comparison of hemodynamic response and vasopressor requirement following spinal anaesthesia between normotensive and severe preeclamptic women undergoing caesarean section: A prospective study. J Obstet Anaesth Crit Care [serial online] 2013 [cited 2021 Aug 1];3:23-6. Available from: https://www.joacc.com/text.asp?2013/3/1/23/114286

  Introduction Top

Pregnancy induced hypertension constitutes major cause of morbidity and mortality in developing countries, and it is 5-10% of all pregnancies. [1] Although regional anesthesia (RA) in this group of parturients current clinical experience demonstrated relative safety of regional technique over general anesthesia (GA), among RA, epidural anesthesia (EA) has been the method of choice. However, spinal anesthesia has not yet been popular due to the common belief that the sudden and extensive sympathetic blockade following subarachnoid block (SAB) will result in severe hypotension that will endanger maternal and fetal safety. Recently, some studies challenged this view and suggested that SAB may in fact be an appropriate choice in pre-eclamptics. [2],[3] But, there are very few published information regarding the use of SAB in pre-eclamptics.

The present study was initiated to further validate the safety of SAB in pre-eclamptic parturients.

  Materials and Methods Top

Following approval from institutional ethics committee, 60 non-laboring parturients of ASA (physical status I or II, age 18-30 years, weight 45-70 kg) carrying a singleton pregnancy and scheduled to have elective cesarean section were included in our study and written informed consent was taken in their own language from every parturient. Among them, 30 women were normotensive (Group I) and 30 were severe pre-eclamptic (Group II) having BP ≥ 160/110 requiring antihypertensive therapy (either nifedipine, 10-20 mg BD or TDS, or labetalol, 800-1200 mg in 2 to 3 divided doses). Parturients with cardiac disease, chronic hypertension, renal disease, diabetes mellitus, coagulopathy, and those who refused SAB were excluded from the study. All parturients were premedicated with oral ranitidine (150 mg) and oral metoclopramide (10 mg) 2 h prior to the surgery. In addition, in pre-eclamptic parturients, antihypertensive medication was continued. After establishing IV access with 18 G cannula prehydration was done with 10 ml/kg body weight of lactated ringer (RL) solution. Standard multichannel monitor was attached and baseline hemodynamic variables (HR, SBP, DBP, MAP) were recorded. Baseline BP was measured as the mean of the three readings taken 5 min after arrival in the operation theatre and before doing any invasive procedures.

After proper asepsis and draping, SAB was administered with 26G -spinal needle at L3-4 interspace in sitting posture with 12.5 mg hyperbaric 0.5% bupivacaine. Patient was then placed supine with a 10-cm wedge under the right buttock to prevent aortocaval compression. Infusion of RL was continued at the rate of 5 ml/kg/h. Surgery was allowed as soon as upper level of sensory block reached T 4 . Oxytocin 3 IU was given over 5 min immediately after delivery of the head of the baby and oxytocin infusion was continued at 0.16 IU/min for 12-18 h unless there is postpartum hemorrhage.

After SAB, SBP, DBP, MAP, and HR were recorded every 2 min for 30 min and every 5 min thereafter until completion of surgery. Hypotension (defined as MAP < 30% of the baseline) was treated with 50 μg phenylephrine IV bolus and dose was repeated at 5-min interval if required to maintain MAP within 30% of baseline. Bradycardia (HR < 60 beats/min) if associated with hypotension was treated with 0.6 mg IV atropine (maximum 1.8 mg). Lowest SBP, DBP, and MAP were noted for each patient and for the HR both the lowest and highest values were recorded. The total amount of phenylephrine consumed was also noted. Apgar score at 1 and 5 min, birth weight, and gestational age of the baby were also compared.

All the cases had adequate block for cesarean section and none of them had to be excluded from study due to inadequate block. All the pre-eclamptic parturientsts were stabilized by antihypertensive medication and did not have any clinical evidence of pulmonary edema.

Statistical analysis

Data was compiled in Microsoft Excel worksheet and student test was used to detect significant difference for difference of means and Chi-square test was used for difference of proportions. P < 0.05 was considered significant.

  Results Top

Parturients in the two groups were comparable regarding age, weight, height, and gestational age of fetus.

The baseline SBP, DBP, and MAP were higher in the pre-eclamptic group. The mean baseline HR was comparable between the two groups.

The SBP, DBP, and MAP all decreased from the baseline in both the groups following SAB, but minimum recorded SBP, DBP, and MAP in normotensive group were lower than the parturients with pre-eclmpsia, which was statistically significant [Figure 1],[Figure 2] and [Figure 3]. Percentage fall of DBP and MAP from the baseline was less in pre-eclamptic group as compared to the normotensive group, although this difference was not statistically significant between the two groups. Phenylephrine consumption was significantly less in pre-ecclamptic group as compared to the normotensive group [Figure 1].
Figure 1: Trend of SBP in two groups

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Figure 2: Trend of DBP in two groups

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Figure 3: Trend of MAP in two groups

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  Discussion Top

In past EA was preferred over SAB to be given to pre-eclamptics undergoing cesarean section due to the fear of sudden and extensive sympathetic block in them after SAB leading to dangerous hypotension compromising mother and fetus. Large volumes of intravenous fluids administered to treat this hypotension were another concern because of the possibility of developing iatrogenic pulmonary edema.

Since then, several authors have compared the efficacy of SAB and EA in severe pre-eclamptics and found comparable hemodynamic effects in both the groups with similar fetal outcomes. Vishalputra et al., [4] compared the hemodynamic effect of SAB and EA in severe pre-eclamptics and found episodes of significant hypotension (SBP < 100 mmHg) were transient in both the groups with comparable neonatal outcome. Thus, they concluded that the use of SAB in severe preeclampsia was safe. Chiu et al., [5] in a study in 2004 found similar safety of SAB in pre-eclamptics. Another study by Hood et al., [2] found that parturients who had SAB required more fluid as compared to epidural group without any adverse sequel like pulmonary edema. Therefore, SAB was chosen as an acceptable technique to perform in severe pre-eclampsia due to its virtue of simplicity, rapidity, cost effectiveness, and intensity of block.

In this study, we compared the hemodynamic effect and vasopressor requirement after SAB between normotensive parturients and severe pre-eclamptics undergoing cesarean section. After establishing SAB, blood pressure decreased in both the groups from the baseline, but the minimum SBP, DBP, and MAP recorded during the observation period were always higher in the pre-eclamptic group (118.8 ± 6.36, 71.2 ± 12.16, 74.2 ± 7.34, respectively) in comparison with normotensive group (91.9 ± 16.9, 48.76 ± 12.72, 53.7 ± 6.36, respectively), which was are statistically significant difference (P < 0.0001). The percentage of fall of DBP and MAP calculated from the baseline was also less in the pre-ecalmptic group (34.5% and 33% in normotensive as opposed to 30.3% and 32.3% in pre-eclamptics, respectively). Pre-eclamptics needed significantly less phenylephrine to treat hypotension (151.1 ± 70 μg in normotensive and 48.3 ± 35.35 μg in pre-eclamptics), which is statistically significant (P < 0.0001) [Figure 4].
Figure 4: Phenylephrine consumption in two groups

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The study results corroborates with the study of Aya et al., in 2003 [6] comparing the incidence and severity of hypotension and ephedrine consumption in 30 pre-eclamptics and 30 healthy parturients. They found that SAB induced hypotension was 6 times less in pre-eclamptics group and they required significantly less ephedrine to treat it.

Other studies too have reported similar results. [7],[8]

In a recent study, Dyer et al., [9] observed the hemodynamic responses to SAB for cesaren delivery in 15 severe pre-eclamptic parturients and used the beat-to-beat monitoring of cardiac output (CO) for this purpose. The effect to phenylephrine on CO was also observed. They concluded that the changes in CO after SAB in severe pre-eclamptics were insignificant, and the reduction in MAP was easily restored by phenylephrine without any decrease in maternal CO.

This reduced incidence of hypotension after SAB in severe pre-eclamptics was initially attributed to be due to the lower gestational age in the parturients studied, with a small uterine mass and less aortocaval compression. However, this hypothesis was rejected after the study of Aya et al., [10] which compared the incidence and severity of hypotension between severe pre-eclamptics (n = 65) and parturients with preterm pregnancy (n = 71) undergoing SAB for cesarean delivery and concluded that small uterine mass was unrelated to the hypotension, and the probable reason behind the less fall in blood pressure was altered vascular response mainly due to humoral factors.

In normal pregnancy, increased synthesis of endogenous vasodilators like prostaglandins (PGs) and nitric oxide (NO) produces a vasodilated state, and there appears an increased dependence on sympathetic vasoconstriction for control of vascular tone. This explains the sudden and excessive hypotension after sympathetic blockade produced by SAB in them. [10]

In pre-eclampsia, vascular endothelial damage occurs, which produces increased amount of endogenous vasopressors like thromboxane and endothelin that are responsible in maintaining vessel tone. Sympathetic block following SAB does not alter this vascular response, limiting the excessive fall of BP in pre-eclamptics. [6],[11],[12],[13]

In normal pregnancy, there is reduced sensitivity to exogenous vasoconstrictors leading to increased vasopressor requirement to reverse the hypotensive effect after SAB. In preeclampsia, there is an increased sensitivity to vasoconstrictor agents, and less vasopressor is required. [7]

Even with varying incidence of hypotension and IV phenylephrine to treat it, we found comparable and good neonatal outcome in both the groups in respect to Apgar score at 5 min after birth and birth weight of the newborn.

In conclusion, in the present study, hypotension following spinal anesthesia administered for cesarean section was significantly less in severe pre-eclamptics than in healthy pregnant women.

In addition, phenylephrine requirements were also less in pre-eclamptic parturients and neonatal outcome was comparable between the two groups.

  Acknowledgement Top

Dr. Mohan Chandra Mondol, Associate Professor, NBMCH, Darjeeling, India.

  References Top

1.Pritchard JA, MacDonald PC. Hypertensive disorders in pregnancy. In: Pritchard JA, Macdonald PC, editors. Williams Obstetrics. 15 th ed. New York: Appleton Century Crofts; 1976. p. 551-812.  Back to cited text no. 1
2.Hood DD, Curry R. Spinal versus epidural anaesthesia for Caesarean section in severely preeclampticpatients. A retrospective survey. Anesthesiology 1999;90:1276-82.  Back to cited text no. 2
3.Sharwood-Smith G, Clark V, Watson E. Regional anaesthesia for caesarean section in severe preeclampsia: Spinal anaesthesia is the preferred choice. Int J Obstet Anesth 1999;8:85-9.  Back to cited text no. 3
4.Visalyaputra S, Rodanant O, Somboonviboon W, Tantivitayatan K, Thienthog S, Saengchote W. Spinal versus epidural anesthesia for cesarean delivery in severe preeclampsia: A prospective randomized, multicenter study. Anesth Analg 2005;101:862-8.  Back to cited text no. 4
5.Chiu IU, Mansor M, Ng KP, Chan YK. Retrospective review of spinal versus epidural anaesthesia for caesarean section in preeclamptic patients. Int J Obstet Anesth 2003;12:17-23.  Back to cited text no. 5
6.Aya AG, Mangin R, Vialles N, Ferrer JM, Robert C, Ripart J, et al. Patients with severe preeclampsia experience less hypotension during spinal anesthesia for elective cesarean delivery than healthy parturients: A prospective cohort comparison. Anesth Analg 2003;97:867-72.  Back to cited text no. 6
7.Clark VA, Smith SG, Stewart AV. Ephedrine requirements are reduced during spinal anaesthesia for caesarean section in pre-eclampsia. Int J Obstet Anaesth 2005;14:9-13.  Back to cited text no. 7
8.Ishrat HM, Raja AT. Spinal anaesthesia in pre-eclamptic parturient-prospective cohort study. Internet J Anaesthesiol 2007;14:ISSN1092-406.  Back to cited text no. 8
9.Dyer RA, Piercy JL, Reed AR, Lombard CJ, Schoeman LK, James MF. Hemodynamic changes associated with spinal anaesthesia for caesarean delivery in severe pre-eclampsia. Anesthesiology 2008;108:802-11.  Back to cited text no. 9
10.Aya AG, Vialles N, Tanoubi I, Mangin R, Ferrer JM, Robert C, et al. Spinal anaesthesia-induced hypotension: A risk comparison between patients with severe pre-eclampsia and healthy women undergoing preterm caesarean delivery. Anesth Analg 2005;101:869-75.  Back to cited text no. 10
11.Santos AC, Birnbach DJ. Spinal anesthesia in the parturient with severe preeclampsia: time for reconsideration. Anesth Analg 2003;97:621-2.  Back to cited text no. 11
12.Khalil RA, Granger JP. Vascular mechanisms of increased arterial pressure in preeclampsia: Lessons from animal models. Am J Physiol-Reg I 2002;283:R29-45.  Back to cited text no. 12
13.Redman CW, Sargent IL. Pre-eclampsia, the placenta and the maternal systemic inflammatory response: A review. Placenta 2003;24(Suppl A):S21-7.  Back to cited text no. 13


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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