Technique

Paracervical block is performed with the patient in a modified lithotomy position. The uterus should be displaced leftward during performance of the block; this displacement may be accomplished by placing a folded pillow beneath the patient’s right buttock. The physician uses a needle guide to define and limit the depth of the injection and to reduce the risk for vaginal or fetal injury. The physician introduces the needle and needle guide into the vagina with the left hand for the left side of the pelvis and with the right hand for the right side (Figure 24-2). The needle and needle guide are introduced into the left or right lateral vaginal fornix, near the cervix, at the 4-o’clock or the 8-o’clock position. The needle is advanced through the vaginal mucosa to a depth of 2 to 3 mm.⁸ The physician should aspirate before each injection of local anesthetic. A total of 5 to 10 mL of local anesthetic, without epinephrine, is injected on each side.⁹ Some obstetricians recommend giving incremental doses of local anesthetic on each side (e.g., 2.5 to 5 mL of local anesthetic between the 3-o’clock and 4-o’clock positions, followed by 2.5 to 5 mL between the 4-o’clock and 5-o’clock positions).^8,10,11

After injecting the local anesthetic in either the left or right lateral vaginal fornix, the physician should wait 5 to 10 minutes and observe the FHR before injecting the local anesthetic on the other side.¹¹ Some obstetricians do not endorse this recommendation. Van Dorsten et al.¹² randomly assigned 42 healthy parturients at term to either of two methods of paracervical block. The study group experienced a 10-minute interval between injections of local anesthetic on the left and right sides of the vagina. The control group had almost simultaneous injections on the left and right sides. No cases of fetal bradycardia occurred in either group. The investigators concluded that patient selection and lateral positioning after the block have a more important role in the prevention of post–paracervical block fetal bradycardia than spacing the injections of local anesthetic. However, because they studied only 42 patients and had no cases of fetal bradycardia in either group, they could not exclude the possibility that incremental injection might reduce the incidence of fetal bradycardia in a larger series of patients.

Choice of Local Anesthetic

The physician should administer small volumes of a dilute solution of local anesthetic. There is no reason to inject more than 10 mL of local anesthetic on each side. Further, there is no indication for the use of concentrated solutions, such as 2% lidocaine, 0.5% bupivacaine, or 3% 2-chloroprocaine. Nieminen and Puolakka¹³ observed that paracervical block with 10 mL of 0.125% bupivacaine (5 mL on each side) provided analgesia similar to that provided by 10 mL of 0.25% bupivacaine.

The choice of local anesthetic is controversial. The North American manufacturers of bupivacaine have stated that bupivacaine is contraindicated for the performance of paracervical block. In contrast, many European obstetricians—especially those in Finland—have expressed a preference for bupivacaine for this procedure. Bupivacaine has greater cardiotoxicity than other local anesthetic agents, and some investigators have suggested that its use leads to a higher incidence of fetal bradycardia or adverse outcome than use of other local anesthetics for paracervical block. In a review of 50 cases of perinatal death associated with paracervical block, Teramo¹⁴ found that the local anesthetic was bupivacaine in at least 29 of the 50 cases.

Palomäki et al.¹⁵ hypothesized that levobupivacaine might result in a lower incidence of post–paracervical block fetal bradycardia than racemic bupivacaine. In a randomized double-blind study of 397 laboring women, paracervical block was performed with 10 mL of either 0.25% levobupivacaine or 0.25% racemic bupivacaine. The incidence of transient FHR abnormalities was 10.4% in the levobupivacaine group and 12.8% in the racemic bupivacaine group, and that of fetal bradycardia was 2.6% in the levobupivacaine group and 3.8% in the racemic bupivacaine group (P = NS).

Some physicians have suggested that 2-chloroprocaine is the local anesthetic of choice for paracervical block. Published studies suggest but do not prove that post–paracervical block fetal bradycardia occurs less frequently with 2-chloroprocaine than with amide local anesthetics.^10,16–18 Weiss et al.¹⁶ performed a double-blind study in which 60 patients were randomly assigned to receive 20 mL of either 2% 2-chloroprocaine or 1% lidocaine for paracervical block. Bradycardia occurred in 1 of the 29 fetuses in the 2-chloroprocaine group, compared with 5 of 31 fetuses in the lidocaine group (P = .14). LeFevre¹⁸ retrospectively observed that fetal bradycardia occurred after 2 (6%) of 33 paracervical blocks performed with 2-chloroprocaine versus 44 (12%) of 361 paracervical blocks performed with mepivacaine (P = .29).

2-Chloroprocaine undergoes rapid enzymatic hydrolysis. Thus it has the shortest intravascular half-life among the local anesthetics used clinically. This rapid metabolism seems advantageous in the event of unintentional intravascular or fetal injection. Philipson et al.¹⁷ performed paracervical block with 10 mL of 1% 2-chloroprocaine in 16 healthy parturients. At delivery, only trace concentrations of 2-chloroprocaine were detected in one (6%) of the maternal blood samples and four (25%) of the umbilical cord venous blood samples. The investigators concluded¹⁷:

Some obstetricians dislike 2-chloroprocaine because of its relatively short duration of action. However, in one study the mean duration of analgesia was 40 minutes after paracervical administration of either 2-chloroprocaine or lidocaine.¹⁶ A 2012 Cochrane Review concluded that the choice of local anesthetic agent did not affect maternal satisfaction with pain relief after paracervical block.⁶

Maternal Complications

Maternal complications of paracervical block are uncommon but may be serious (Box 24-1).^19–22 Systemic local anesthetic toxicity may result from direct intravascular injection or rapid systemic absorption of the local anesthetic. Postpartum neuropathy may follow direct sacral plexus trauma, or it may result from hematoma formation. Retropsoal and subgluteal abscesses are rare but may result in maternal morbidity or mortality.^21,22

In some cases, fetal injury results from direct injection of local anesthetic into the fetal scalp during paracervical block.²³ Fetal scalp injection of 10 or 20 mL of local anesthetic undoubtedly causes systemic local anesthetic toxicity, which may result in fetal death. Fetal scalp injection seems more likely to occur when the obstetrician performs paracervical block in the presence of advanced (i.e., > 8 cm) cervical dilation.

Bradycardia is the most common fetal complication. Fetal bradycardia typically develops within 2 to 10 minutes after the injection of local anesthetic. Most cases resolve within 5 to 10 minutes, but some cases of bradycardia persist for as long as 30 minutes. Published studies have noted an incidence of bradycardia that varies between 0% and 70%.^{4,11,18,24–31} These figures represent extremes on either side of the true incidence of this complication. Some studies have overstated the problem by defining bradycardia as a baseline FHR of less than 120 bpm. (A baseline FHR of 110 bpm does not necessarily indicate fetal compromise.) Experienced obstetricians clearly do not encounter clinically significant fetal bradycardia after 70% of their paracervical blocks. It is equally clear that the incidence of clinically significant fetal bradycardia is not zero, and it is difficult to teach this technique without placing some fetuses at risk.

Shnider et al.²⁶ reported that fetal bradycardia occurred after 24% of 845 paracervical blocks administered to 705 patients with either 1% mepivacaine, 1% lidocaine, or 1% propitocaine (prilocaine). Neonatal depression occurred significantly more often in infants who had FHR changes after paracervical block than in a control group or in a group of infants with no FHR changes after paracervical block. In contrast, Carlsson et al.²⁷ performed 523 paracervical blocks with 0.125% or 0.25% bupivacaine in 469 women. Of the total, nine (1.9%) fetuses had bradycardia, but at delivery all nine of the newborns had a 5-minute Apgar score of 9 or 10.

Goins²⁸ observed fetal bradycardia in 24 (13%) of 182 patients who received paracervical block with 20 mL of 1% mepivacaine. He compared neonatal outcome for these patients with neonatal outcome for 343 patients who received other analgesic/anesthetic techniques. There was a slightly higher incidence of low Apgar scores at 1 minute and 5 minutes in the paracervical block group, but the difference was not statistically significant. LeFevre¹⁸ observed fetal bradycardia after 46 (11%) of 408 paracervical blocks. Fetal bradycardia was more common in those patients with a nonreassuring FHR tracing before the performance of paracervical block.

In a review of four randomized controlled trials published between 1975 and 2000, Rosen³⁰ estimated that the incidence of post–paracervical block fetal bradycardia is 15%. More recently, Volmanen et al.³¹ reviewed four studies of paracervical block that had adequate sample size (n > 200), used the superficial injection technique, and administered 0.125% or 0.25% bupivacaine. Among the 1361 patients in these four studies, the incidence of fetal bradycardia was 2.2%. The observed episodes of fetal bradycardia were transient and did not require emergency cesarean delivery.³¹

Etiology of Fetal Bradycardia

The etiology of fetal bradycardia after paracervical block is unclear. Investigators have offered at least four theories that might explain the etiology of fetal bradycardia, as discussed here.

Reflex Bradycardia.

Manipulation of the fetal head, the uterus, or the uterine blood vessels during performance of the block may cause reflex fetal bradycardia.²⁵

Direct Fetal Central Nervous System and Myocardial Depression.

The performance of paracervical block results in the injection of large volumes of local anesthetic close to the uteroplacental circulation. Local anesthetic rapidly crosses the placenta³² and may cause fetal central nervous system (CNS) depression, myocardial depression, and/or umbilical vasoconstriction. Puolakka et al.³³ observed that the most common abnormality after paracervical block was the disappearance of FHR accelerations. They speculated that FHR changes result from rapid transplacental passage of local anesthetic into the fetal circulation, followed by a direct toxic effect of the local anesthetic on the FHR regulatory centers.

Some investigators have suggested that fetal bradycardia results from a direct toxic effect of the local anesthetic on the fetal heart.^34,35 Shnider et al.³⁴ reported that in four cases of fetal bradycardia, mepivacaine concentrations in fetal scalp blood were higher than peak concentrations in maternal arterial blood. Asling et al.³⁵ made similar observations in six of seven cases of fetal bradycardia. They suggested that local anesthetic reaches the fetus by a more direct route than maternal systemic absorption, and they speculated that high fetal concentrations of local anesthetic result from local anesthetic diffusion across the uterine arteries. This would lead to local anesthetic concentrations in intervillous blood that are higher than concentrations in maternal brachial arterial blood. High fetal concentrations would then occur from the passive diffusion of local anesthetic across the placenta.

High fetal concentrations of local anesthetic also may result from fetal acidosis and ion trapping.^36,37 Local anesthetics are weak bases, and if acidosis develops in a fetus, increasing amounts of local anesthetic will cross the placenta regardless of the site of maternal injection. It is also possible that the obstetrician may directly inject local anesthetic into uterine blood vessels.

Most studies have noted that local anesthetic concentrations in the fetus are consistently lower than those in the mother after paracervical block.⁹ Further, fetal bradycardia has not consistently occurred in documented cases of fetal local anesthetic toxicity. Freeman et al.³⁸ injected 300 mg of mepivacaine directly into the scalp of two anencephalic fetuses. The QRS complex widened, the PR interval lengthened, and both fetuses died, but fetal bradycardia did not occur before fetal death. In contrast, the investigators observed no widening of the QRS complex or lengthening of the PR interval in normal fetuses demonstrating bradycardia after paracervical block. Rather, the fetal electrocardiogram (ECG) changes were consistent with sinoatrial node suppression with a wandering atrial pacemaker. The investigators concluded that a mechanism other than direct fetal myocardial depression is responsible for fetal bradycardia after paracervical block.

Increased Uterine Activity.

Increased uterine activity results in decreased uteroplacental perfusion. Fishburne et al.³⁹ noted that direct uterine arterial injection of bupivacaine consistently caused a significant increase in uterine tone in gravid ewes. Uterine arterial injection of 2-chloroprocaine did not affect myometrial tone, whereas injection of lidocaine had an intermediate effect.

Myometrial injection of a local anesthetic also may cause greater uterine activity. Morishima et al.⁴⁰

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Fetal Physiology
2. Medicolegal Issues in Obstetric Anesthesia
3. Neurologic and Neuromuscular Disease
4. Endocrine Disorders

Stay updated, free articles. Join our Telegram channel

Join