Hypotension following central neural blockade in the obstetric patient occurs probably in more than 50 % of our patients [6, 7]. It may be due to several causes, chief of which is vasodilatation below the site of the block and hence pooling of blood in the lower limbs [21]. When the venous return to the heart is decreased, the cardiac output will naturally fall. With the parturient placed in the supine position, venous pooling is made worse by the presence of the term fetus obstructing the venous return following the blockade.

The extent of the obstruction and the decreased venous return is rarely appreciated. I once had a provider who was advised to place the parturient in the left lateral tilt position following a supervised spinal done in the sitting position. The provider failed to follow the instruction. Help was requested when the blood pressure dropped to near 45 mmHg systolic after the spinal blockade. In spite of the administration of fluids and vasopressor agents to improve the situation, the blood pressure continued to be low. It only improved when the patient was properly positioned as initially advised.

Most patients who need central blockade for vaginal delivery or cesarean section are required to fast and not eat solids or liquids. While a short fast may be well tolerated, longer fasting periods in an active parturient or a parturient moving around in pain, often leads to dehydration that may not be recognized and this can have significant impact on the cardiovascular system.

There are strategies to overcome this problem. Coloading with crystalloids [6] during the insertion of the central neural blockade is now the preferred technique as opposed to preloading which was previously used. Crystalloids are frequently used although colloids are often thought to be a better option. McDonald et al. found in a randomized controlled trial that there was no significant difference in the maternal cardiac output when these fluid management strategies were compared [22]. The cardiac output in the colloid group was, however, more sustained.

Vasopressors are often administered when coloading of fluids and positioning fail to sustain the blood pressure. There are providers who also administer vasopressors prophylactically in an attempt to prevent hypotension from occurring so as to reduce its impact on the parturient and the fetus [23, 24]. Previously ephedrine in small boluses of 5–6 mg per dose was favored as it has both direct (alpha and beta agonist) and indirect (release of norepinephrine from presynaptic terminals) effects and the beta agonist property was thought to better maintain uterine blood flow [25]. Ngan Kee et al. showed that placental transfer of ephedrine causes a slightly lower pH value of the umbilical blood of the newborn at the time of birth, in those whose mothers received ephedrine compared to phenylephrine [26]. A systematic analysis of the data of several studies confirmed the consistent finding of a slightly higher pH in those patients who were treated with phenylephrine for hypotension but there was definitely no fetal acidosis even in those who were given ephedrine [27]. The jury may be out as to the significance of this but there is now a definite shift to the use of phenylephrine to manage hypotension as it appears to be more effective [28].

Phenylephrine is more expensive than ephedrine and is not so readily available [27]. It has a rapid onset but is short acting and causes reflex bradycardia when the blood pressure improves. Ngan Kee et al. are now looking at the use of norepinephrine which with its weak beta agonist property may have less effect on the heart rate and cardiac output [29]. We are unlikely to start using this vasopressor in obstetrics any time soon. There are still many unknowns in the causation of hypotension following spinal blockade in many of the parturients we see everyday [30].

Local anesthetic agents are administered in greater quantities during an epidural blockade compared to a spinal blockade. This is because significant quantities of the local anesthetic agents have to diffuse from the epidural space to the intrathecal space to block the nerve roots concerned. Large quantities of local anesthetic drugs are required to achieve an adequate level of epidural blockade in obstetric patients. These patients are at risk for systemic toxicity if the epidural catheter is inadvertently inserted into a vascular structure. Subsequent injections of local anesthetic through the catheter result in a rapid increase in blood concentration of the local anesthetic thereby causing systemic toxicity.

Systemic toxicity primarily targets the CNS and cardiovascular systems [31]. The initial symptoms usually involve the CNS and include dizziness, tinnitus, or convulsions but with bupivacaine where the neurological/cardiovascular risk ratio is narrowed [32, 33], toxic manifestations in the form of life-threatening cardiac arrhythmias, cardiac collapse, or even cardiac arrest may occur in the early phase of toxicity. Local anesthetic toxicity is of particular concern for the obstetric patient as convulsions or arrhythmias can be life threatening not only to the parturient but the fetus too.

In order to avoid local anesthetic toxicity , there are many strategies that can be used. Slowly aspirating the contents of the catheter before injection is part of the process to exclude the possibility of intravascular placement after the initial insertion of the epidural. Test dosing is used before the administration of the larger epidural doses. These include the administration of at least 15 μg of adrenaline with the local anesthetic [34], but parturients in labor may manifest false positive values especially if the labor pain coincides with the administration [35]. The best advice is to treat every epidural injection, whether it is the initial dose or the subsequent top-up doses, as a test dose. This essentially requires the provider to administer small aliquots of the local anesthetic agent and to refrain from the administration of a large bolus dose at any time.

While the use of adrenaline-containing local anesthesia agents may allow the safe administration of more local anesthetic agents in the nonpregnant situation, in the obstetric setting, there are concerns about the effects of systemic absorption of adrenaline on the fetus and the parturient, especially those in the high-risk category with either cardiac disease or those with severe preeclampsia [36].

When there are signs of a local anesthetic systemic toxicity (LAST) occurring, additional injection of local anesthetics should stop [31]. Airway management and cardiovascular support are important considerations in the event of the occurrence of LAST. These measures to reduce the accompanying risk of hypoxia and acidosis complicating and prolonging the often difficult resuscitation of these patients [37]. Seizures should also be terminated with judicious use of benzodiazepines.

Lipid rescue in local anesthetic toxicity has become the recommended strategy to provide a “lipid sink” for the rapid decrease of the blood levels of the local anesthetic. The ASRA practice advisory recommends the administration of 1.5 ml/kg of the 20 % lipid emulsion as a bolus, followed by 0.25 ml/kg per minute to be given until there is attainment of hemodynamic stability lasting for 10 min [37]. An upper limit of 10 ml/kg of lipid emulsion for the first 30 min is advised. Those who have recovered from LAST should also be observed closely for the subsequent 12 h in order to prevent an occurrence especially with the redistribution of the local anesthetics back to the circulation.

While propofol is prepared in lipid, the lipid concentration in propofol is 10 % and hence it is not recommended to be used for the “lipid rescue” of local anesthetic toxicity [37]. The dose required if propofol is used for the purpose of lipid rescue will also cause excessive hypotension.

For additional discussion on this topic, please refer to Chap. 3.

Local anesthetic agents readily cross the placental barrier. It is possible to get direct fetal toxic effects from these agents in the fetal circulation exemplified by fetal bradycardia without clinically obvious maternal systemic toxicity [38].

Fetal bradycardia is most typically associated with the paracervical block [39]. The localized effects of vasoconstriction and myometrial hypercontractility from the local anesthetic agent infiltration of the cervical milieu, can have an impact on placental perfusion, resulting in fetal bradycardia. Placental perfusion should be maximized by moving the parturient into the left lateral tilt position which will most effectively alleviate aortocaval compression [40]. Maternal oxygen supplementation is probably better avoided if the intention is to alleviate fetal distress [41]. Fetal bradycardia is usually transient but if persistent and judged to be due to excessive uterine tone, 0.25–0.5 mg subcutaneous bolus dose of terbutaline could be used to initiate tocolysis [42].

Paracervical blocks with infiltration of local anesthetic agents typically into the inferior cervical periphery between the 3 to 9 o’clock positions [43], have largely been superseded in routine obstetric practice due to its relative ineffectiveness for relief of labor pain [15] and major concerns about fetal safety [44]. Correct infiltration can be challenging as the cervix undergoes dynamic changes of effacement and dilation in labor, altering landmarks and the cervical milieu. Paracervical blockade can cause local vasoconstriction and increase myometrial contractility resulting in diminished placental function culminating in fetal bradycardia, hypoxia, and even death [39, 44]. The incidence of fetal bradycardia following cervical block is about 15 % [45]. Such effects can also occur with the inadvertent intrauterine injection of local anesthetics [46]. Given the reliability and availability of neuraxial anesthesia, paracervical blockade is unlikely to make a comeback into routine obstetric practice for labor analgesia, though it retains a role in gynecological procedures restricted to the cervix [47], and to a more limited extent, transcervical intrauterine minor surgery [48].

Complications due to local anesthetic agent systemic toxicity to the mother caused by hypersensitivity, overdose, or inadvertent intravascular injection, should be treated accordingly as previously described, specific to the agent. Fetal bradycardia can be managed as outlined previously but if the response is insufficient, expedited delivery by emergency cesarean section is indicated, as paracervical block has been associated with fetal and neonatal mortality.

Pudendal nerve blockade is still in fairly common use but its use for obstetric analgesia is definitely declining [49]. An effective bilateral pudendal block is the minimum analgesia required for operative delivery [50, 51], but this is insufficient for mid-cavity or rotational forceps for which central neuraxial anesthesia should be used [52]. The pudendal block may also be used to augment inadequate local infiltration in postdelivery perineal tear or episiotomy repair [49, 53]; in this context, the total dose of local anesthetic agent infiltrated must be carefully accounted for to avoid toxicity from overdose. As the pudendal nerve supplies only part of the sensory innervation of the perineum, the pudendal block is less effective to relieve pain during the late second stage of labor compared to subarachnoid anesthesia [54]. A successful pudendal block also inhibits maternal bearing down [55]. Recent data suggest that practicing obstetricians can misidentify the exact injection site for transvaginal pudendal nerve blockade in a mannequin pelvis setting and they typically overestimate the block’s speed of action [56].

Potential complications in pudendal block are uncommon but include inadvertent maternal intravascular injections or overdose of local anesthetic agent. Hematomas can arise from injury to the pudendal artery. Large hematomas can extend to the ischiorectal fossa or into the retroperitoneal space [57, 58]. Ongoing pudendal artery bleeding may best be managed with embolization if interventional radiology expertise is available, as it is difficult to access surgically, it being close to important nerve bundles. Infection (retro-psoas and subgluteal abscess) can also occur [59], and suspicion should be aroused if there is severe hip or back pain associated with fever after delivery aided by a pudendal block. If not responsive to antibiotics, drainage of these abscesses may be required. Neonatal toxicity [60], from absorbed or inadvertent direct fetal injection of local anesthetic agent is rare but may be suspected if unexplained neonatal hypotonia, papillary mydriasis fixed to light, apnea, or seizures [49], occur in the newborn after delivery.

Dysfunction can be the result of failed care by the obstetrician or the anesthesiologist. It is often difficult to differentiate among the many causes but what is useful to understand is that the earlier the dysfunction is recognized [61], and attended to by the correct care provider—usually the involvement of a neurologist under these circumstances, the lesser the damage in the long term.