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Anesth Analg 2004;98:815-821 © 2004 International Anesthesia Research Society doi: 10.1213/01.ANE.0000099782.78002.30
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Abstract |
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In a randomized, double-blinded, controlled trial, we investigated the prophylactic infusion of IV phenylephrine for the prevention of hypotension during spinal anesthesia for cesarean delivery. Immediately after intrathecal injection, phenylephrine was infused at 100 µg/min (n = 26) for 3 min. From that point until delivery, phenylephrine was infused at 100 µg/min whenever systolic arterial blood pressure (SAP), measured each minute, was less than baseline. A control group (n = 24) received IV bolus phenylephrine 100 µg after each measurement of SAP <80% of baseline. Phenylephrine infusion decreased the incidence (6 [23%] of 26 versus 21 [88%] of 24; P < 0.0001), frequency, and magnitude (median minimum SAP, 106 mm Hg; interquartile range, 95–111 mm Hg; versus median, 80 mm Hg; range, 73–93 mm Hg; P < 0.0001) of hypotension compared with control. Heart rate was significantly slower over time in the infusion group compared with the control group (P < 0.0001). Despite a large total dose of phenylephrine administered to the infusion group compared with the control group (median, 1260 µg; interquartile range, 1010–1640 µg; versus median, 450 µg; interquartile range, 300–750 µg; P < 0.0001), umbilical cord blood gases and Apgar scores were similar. One patient in each group had umbilical arterial pH <7.2. Prophylactic phenylephrine infusion is a simple, safe, and effective method of maintaining arterial blood pressure during spinal anesthesia for cesarean delivery.
IMPLICATIONS: In patients receiving spinal anesthesia for elective cesarean delivery, a prophylactic infusion of phenylephrine 100 µg/min decreased the incidence, frequency, and magnitude of hypotension with equivalent neonatal outcome compared with a control group receiving IV bolus phenylephrine.
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Introduction |
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Spinal anesthesia for cesarean delivery may be associated with hypotension and fetal acidosis (1,2). Many different strategies have been investigated for the prevention of hypotension (usually defined as a decrease in systolic arterial blood pressure [SAP] by more than 20%–30% or to <90–100 mm Hg), but few have proven to be consistently reliable. Previously, we described the use of IV infusions of
agonists to maintain maternal SAP (3–5). In those studies, however, the infusion was withheld until after maternal SAP started to decrease, and in some cases there were marked initial periods of hypotension (5). Our recent clinical experience suggested that starting a prophylactic vasopressor infusion immediately after the induction of anesthesia was more effective for reducing both the incidence and frequency of hypotension. However, one concern of this technique is that relatively large doses of vasopressor are likely to be used. Although large doses of drugs such as phenylephrine and metaraminol are likely to be very effective at maintaining maternal SAP, they may potentially cause detrimental effects on fetal acid-base status because of adverse effects on uteroplacental blood flow. In this study, we investigated the use of a prophylactic infusion of phenylephrine 100 µg/min started immediately after the induction of spinal anesthesia. A control group received phenylephrine given by a more conventional method in which 100-µg IV boluses were given as treatment for episodes of hypotension. Our hypothesis was that there would be no detrimental effect on fetal acid-base status despite the likelihood that large doses of phenylephrine would be given when administered by infusion (3–5). The main outcome measurement was umbilical arterial (UA) cord blood pH, which is the variable most often measured as an index of fetal acid-base status (6).
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Methods |
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After obtaining approval from the Clinical Research Ethics Committee of the Chinese University of Hong Kong, we recruited 50 ASA physical status I and II women with term singleton pregnancies scheduled for elective cesarean delivery under spinal anesthesia. All patients gave written, informed consent. Patients with preexisting or pregnancy-induced hypertension, cardiovascular or cerebrovascular disease, known fetal abnormalities, or contraindications to spinal anesthesia were excluded.
According to routine practice at our institution, patients were premedicated with famotidine 20 mg orally the night before and on the morning of surgery. On arrival to the operating room, 30 mL of 0.3 M sodium citrate was given orally, and standard monitoring, including noninvasive arterial blood pressure, electrocardiography, and pulse oximetry, was attached. Fetal heart rate (HR) was monitored by external cardiotocography until the time of surgical preparation. Patients were allowed to rest undisturbed for several minutes, during which SAP was measured every 1–2 min. This was continued until measurements became consistent (3 successive measurements of SAP that had a difference of no more than 10%). Baseline SAP and HR were taken as the mean of the three recordings.
A 16-gauge IV catheter was then inserted under local anesthesia. No IV prehydration was given (4,7–10). IV infusion of lactated Ringer’s solution was started at 5 mL/min and was controlled with a peristaltic infusion pump (IVAC 531; IVAC Corp., San Diego, CA).
Spinal anesthesia was induced with patients in the right lateral position. After skin infiltration with lidocaine, a 25-gauge Whitacre needle was inserted at the L2-3 or L3-4 vertebral interspace, and hyperbaric 0.5% bupivacaine 2.0 mL and fentanyl 15 µg were injected intrathecally. Patients were then immediately turned supine with left uterine displacement. SAP was measured at 1-min intervals beginning 1 min after spinal injection. Hemodynamic data were downloaded to a computer from the anesthetic machine (Narkomed 4; North American Dräger, Telford, PA) by using software developed within our department.
Two identical syringes were prepared containing either phenylephrine 100 µg/mL or saline. According to computer-generated randomization codes contained in sealed, sequentially numbered envelopes, an investigator or anesthesiologist not involved with patient care or assessment then selected one of the syringes to be used for IV infusion and the other for IV boluses. The investigator administering the solutions (WDNK) and the patient were thus blinded to the contents of the syringes.
Immediately after the completion of intrathecal injection, infusion of study solution was started at 1 mL/min. Thus, patients in the infusion group had an IV infusion of phenylephrine started at 1 mL/min (100 µg/min), whereas patients in the control group had an IV infusion of saline started at 1 mL/min. Infusions were administered with a syringe pump (Terfusion STC-527; Terumo Corp., Tokyo, Japan) that was connected to the IV line via a three-way stopcock and were continued for a minimum of 3 min, after which the infusion was either stopped or continued according to a predefined protocol based on the SAP measurement each minute. After each 1-min measurement of SAP, the infusion was stopped if the SAP was more than baseline, and it was continued or restarted if the SAP was less than or equal to baseline. For the purposes of the study, we defined hypotension as a decrease in SAP to <80% of baseline. Each time there was a SAP measurement showing hypotension, patients received a 1-mL IV bolus of study solution. Thus, patients in the infusion group received a 1-mL IV bolus of saline, and patients in the control group received a 1-mL (100-µg) IV bolus of phenylephrine. The dosing regimens for phenylephrine were selected on the basis of initial experience after phenylephrine was recently introduced into clinical use in our unit.
Oxygen was not routinely given unless the arterial oxyhemoglobin saturation decreased to <95% when oxygen 5 L/min was given by clear face mask. Any incidences of nausea (reported by patients) or vomiting (observed by investigators) were recorded. We planned to treat nausea or vomiting that was not associated with hypotension with IV metoclopramide 10 mg and to treat bradycardia, defined by an HR <50 bpm that was associated with hypotension, with IV atropine.
Five minutes after intrathecal injection, the upper sensory level of anesthesia was measured by assessing loss of pinprick discrimination, and the surgeon was called. Further checks of the block height were made as required before the start of surgery, but these levels were not recorded as part of the study. The times of skin incision, uterine incision, and delivery were recorded. The infusion and bolus protocol was continued until the time of uterine incision, after which further management was at the discretion of the attending anesthesiologist, who was free to administer IV fluids and vasopressors as appropriate to replace surgical losses and maintain SAP. The total volumes of study solutions given by bolus and by infusion up to the time of uterine incision were recorded.
After delivery, oxytocin 10 IU was given by slow IV injection. Apgar scores were assessed 1 and 5 min after delivery by the attending pediatrician, who was blinded to the patient’s group. Arterial and venous blood samples were taken from a double-clamped segment of umbilical cord by for immediate blood gas analysis with a Ciba-Corning 278 Blood Gas System blood gas analyzer (Ciba-Corning, Medfield, MA).
Prospective power analysis was based on the primary outcome, which was defined as the UA cord blood pH. Using data from previous studies, we calculated that a sample size of 22 patients per group would have 90% power at the 5% significance level to detect a difference in UA pH of 0.05 U between groups. To allow for potential dropouts, we decided to recruit 50 patients. Secondary outcomes included the incidence, frequency, and magnitude of hypotension, the incidence of reactive hypertension (defined by an increase in SAP to >120% of baseline), and the incidence of nausea or vomiting.
Univariate intergroup comparisons were made with the Mann-Whitney U-test. Nominal data were compared by using the 
2 test and Fisher’s exact test. Serial changes in SAP and HR were compared by using analysis of variance for repeated measures; for these analyses, because the time from induction to delivery varied among patients, we compared only data recorded up to the time of uterine incision of the patient with the smallest induction-to-uterine incision interval. The incidence and timing of hypotension were analyzed by using Kaplan-Meier survival analysis, and comparison between groups was performed with the log-rank test. Survival time was defined as the time from the induction of anesthesia to the first episode of hypotension. Patients who delivered without any incidence of hypotension were considered "censored." All analyses were performed with StatView for Windows 4.53 (Abacus Concepts Inc., Berkeley, CA). Values of P < 0.05 were considered statistically significant.
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Results |
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All patients completed the study. Patient characteristics and surgical times were similar between groups (Table 1). The median maximum block height at 5 min was one segment lower in the infusion group (T5; interquartile range, T4 to T6) compared with the control group (T4; range, T3 to T4.5; P = 0.02). Insufficient UA blood was obtained for analysis in one patient in the infusion group. No patient required supplemental oxygen.
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Neonatal outcome was similar between groups (Table 2). Umbilical cord blood gases were similar between groups, and only one patient in each group had a UA pH <7.2. This was despite a total consumption of phenylephrine that was considerably more in the infusion group (median, 1260 µg; interquartile range, 1010–1640) µg) compared with the control group (median, 450 µg; interquartile range, 300–750 µg; P < 0.0001). Two neonates in the infusion group had an Apgar score of 6 at 1 min, whereas no other Apgar score at 1 min was <8 and no Apgar score at 5 min was <9. For the first of these 2 cases, the total phenylephrine dose was 940 µg, the uterine incision-to-delivery time was 136 s, the UA pH was 7.36, and the Apgar score at 5 min was 10. Postnatal progress was uneventful, and no reason for the low Apgar score at 1 min could be ascertained. For the second case, the total phenylephrine dose was 1100 µg, the uterine incision-to-delivery time was 171 s, the UA pH was 7.31, and the Apgar score at 5 min was 10. In this case, the baby was subsequently found to have a dysplastic kidney, but neonatal progress was otherwise unremarkable.
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Serial analysis of hemodynamic changes showed that SAP was significantly greater over time in the infusion group compared with the control group (P < 0.0001; Fig. 1) and that HR was significantly slower over time in the infusion group compared with the control group (P < 0.0001; Fig. 2). Although some patients in the infusion group had relatively slow HRs and two patients had one or more episodes of bradycardia (HR <50 bpm), in each case this was associated with an increase in SAP to more than baseline. In all of these cases, HR increased after the phenylephrine infusion was stopped, and no patient required treatment with atropine.
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Cumulative survival (the proportion of patients who did not become hypotensive) over time until delivery was greater in the infusion group compared with the control group (P < 0.0001; Fig. 3). Overall, 6 (23%) of 26 patients in the infusion group had one or more episode of hypotension, compared with 21 (88%) of 24 in the control group (P < 0.0001), and the number of episodes of hypotension was smaller in the infusion group (median, 0; range, range 0–4) compared with the control group (median, 4.5; range, 0–12; P < 0.0001; Table 3). Of the six patients in the infusion group who had one or more episodes of hypotension, three had only a single episode, and in five of the six cases the hypotension was delayed and occurred after the initial infusion was stopped. In comparison, all of the 21 patients in the control group who had hypotension had
3 episodes, and half had 5 episodes. The minimum SAP recorded was lower in the control group compared with the infusion group.
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In the first few minutes after intrathecal injection, SAP increased slightly more than baseline in some patients in the infusion group, whereas SAP decreased in all patients in the control group (Fig. 1). The incidence of reactive hypertension was more frequent in the infusion group compared with the control group, but no patient complained of symptoms. The maximum SAP recorded was greater in the infusion group compared with the control group (Table 3).
There was a nonsignificant trend toward a less frequent incidence of nausea and vomiting in the infusion group compared with the control group (1 [4%] of 26 vs 5 [21%] of 24; P = 0.09). All episodes of nausea or vomiting were transient, and all were related to decreases in SAP. No patient received treatment with metoclopramide.
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Discussion |
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This study confirmed our clinical impression that starting a prophylactic infusion of phenylephrine immediately after the induction of spinal anesthesia for cesarean delivery would be effective at reducing the incidence, frequency, and severity of hypotension. It is noteworthy that in the infusion group, despite the administration of a large total dose of phenylephrine, the fetal acid-base status and clinical condition of infants were excellent and similar to those in the control group. This is in contrast to a previous study which investigated prophylactic ephedrine (11). In that study, we found that ephedrine 30 mg given by IV bolus reduced the incidence of hypotension to 35%, compared with 95% in a control group, but was associated with a 22% incidence of fetal acidosis.
A number of other studies have recently reported on the use of agonists in obstetrics (3–5,12–14). Despite early reports suggesting that use of agonists was associated with adverse fetal effects (15,16), more recently performed comparative studies have shown that agonists are associated with better fetal acid-base status compared with ephedrine (3,13,14). The results of this study are further support of the use of phenylephrine as a first-line vasopressor in obstetrics.
Although we found that a prophylactic infusion of phenylephrine was effective, and was not associated with a detrimental effect on fetal acid-base status, it did not eliminate hypotension completely. This is partly explained by the limitations of our standardized study protocol. We designed our infusion protocol to be as simple as possible, with one criterion for starting and stopping the infusion and one set infusion rate. Of note, in 5 of the 6 patients in the infusion group who had one or more episodes of hypotension, the hypotension occurred after the initial infusion was stopped. In these cases, although the infusion was restarted when SAP decreased to less than baseline again, because phenylephrine has a latency for effect (17), transient hypotension occurred. It is possible that a more flexible protocol that did not completely stop the infusion or that allowed small boluses to be given when the infusion was restarted may have further reduced or totally eliminated hypotension.
Most other strategies for decreasing the incidence of hypotension during spinal anesthesia for cesarean delivery have not proved to be reliable. Although early work suggested that IV prehydration with crystalloid solutions was effective (18), this has been questioned in more recent articles (4,7–10). Use of colloid solutions may be more effective than crystalloids (5,19), but the benefits are still limited, and infusion of large volumes of colloid may have other risks, including fluid overload, decreased oncotic pressure, and anaphylactoid reactions (20). Compression of the lower limbs has been described as an alternative technique but is not convenient and is not popular (21). Therefore, in accordance with our clinical practice, we elected not to give any IV prehydration in this study and relied solely on the vasopressor infusion to maintain maternal SAP. This practice is supported by previous work in which we used an infusion of the agonist metaraminol to maintain maternal SAP and found that maternal hemodynamic changes, neonatal acid-base status, and Apgar scores were similar between patients given crystalloid prehydration 20 mL/kg and patients given no prehydration (4). However, this remains a controversial issue among anesthesiologists, some of whom continue to advocate prehydration (22).
There have been previous reports of the use of phenylephrine infusions in which the incidence of hypotension was significantly more than in our study (23,24). This can be explained in part by the use of much smaller doses of phenylephrine in previous studies compared with our study. We used particularly large total doses of phenylephrine in the infusion group, and in this group SAP increased transiently to values more than baseline in some patients. This may cause concern about potential adverse effects on uteroplacental blood flow. However, although we did not directly assess uteroplacental flow or resistance, the high values for UA and venous pH in our study are indirect evidence that there was no significant adverse effect. However, it should be noted that we studied only healthy patients undergoing elective cesarean deliveries. It may not be valid to extrapolate our findings to patients with nonreassuring fetal HR patterns or impaired uteroplacental blood flow, to preeclamptic patients, or to patients with a very prolonged induction-to-delivery time.
We found that maternal HR was statistically significantly slower in the infusion group compared with the control group, and two patients in the infusion group had episodes of bradycardia (HR <50 bpm). However, because these cases were not associated with hypotension, the likely mechanism was a baroreceptor reflex. There were no associated adverse clinical sequelae, and in both cases the HR increased soon after the phenylephrine infusion was stopped. Of note, no patient received anticholinergic drugs that may have caused an exaggerated increase in SAP. An alternative approach that might decrease the risk of bradycardia is to combine phenylephrine with ephedrine, as described by Mercier et al. (12) and Cooper et al. (14). However, Mercier et al. reported a frequent incidence of fetal acidosis (31%) in patients who received combined phenylephrine (10 µg/min) and ephedrine (2 mg/min). Cooper et al. reported a smaller incidence of fetal acidosis (4%) when a larger dose of phenylephrine (up to 33 µg/min) was combined with ephedrine (up to 1 mg/min). However, they concluded that there was no advantage to combining phenylephrine with ephedrine because the incidence of nausea (55%) and vomiting (18%) was more frequent than in patients who received phenylephrine alone (17% and 0%, respectively). These findings, taken together with our results, suggest that phenylephrine administered alone via infusion may be the optimal vasopressor regimen.
Despite a more frequent incidence of hypotension in the control group, we found that fetal acid-base status was not worse compared with that in the infusion group. This likely reflects the fact that when hypotension occurred, it was treated promptly with boluses of phenylephrine. In our study, we defined hypotension as a decrease in SAP by more than 20% less than baseline. However, the exact degree of hypotension that should be treated is undetermined.
Although the difference in the incidence of nausea and vomiting between groups was not statistically significant, our sample size was small, and the study was not powered for determining differences in this outcome. Retrospective power analysis showed that a sample size of 52 patients per group would have been required to have 80% power to show a significant difference in the incidence of nausea and vomiting given the observed difference. Moreover, in our study protocol, we relied on observation by the investigators to detect nausea and vomiting. Had we specifically requested patients to report symptoms of nausea, the incidence and the power of the study in this respect may have been greater.
By chance, the level of block measured at 5 min was one segment higher in the control group compared with the infusion group. Unfortunately, our protocol did not include consistent measurement of block height at subsequent times. Although the clinical significance of a one-segment difference in block height is uncertain, because a higher block level might result in a greater degree of sympathetic block, this may have predisposed to a more frequent incidence of hypotension in the control group compared with the infusion group. This is a potential confounding factor in our analysis. Spinal anesthesia was successful in all cases, and the doses of bupivacaine and fentanyl used reflect our usual clinical practice, in which we use a uniform dose of bupivacaine and fentanyl without adjustment for the patient’s weight or height.
In conclusion, these data suggest that a prophylactic phenylephrine infusion is an effective and simple method of reducing the incidence and magnitude of hypotension during spinal anesthesia for cesarean delivery, with no adverse effect on neonatal outcome. Further work investigating more flexible regimens would be of interest and might result in the complete elimination of hypotension.
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Acknowledgments |
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We thank the midwives of the Labor Ward, Prince of Wales Hospital, Shatin, Hong Kong, China, for their assistance and cooperation.
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Footnotes |
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Presented at the annual meeting of the American Society of Anesthesiologists, San Francisco, CA, October 11–15, 2003.
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References |
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