Adverse effects of neuraxial analgesia and anesthesia for obstetrics

INTRODUCTION — Neuraxial analgesia and anesthesia (ie, spinal, epidural, and combined spinal epidural) for labor and delivery are generally very safe, but all interventions are associated with adverse effects. The practice of obstetric anesthesia has evolved in large part to minimize such adverse effects. This topic will review the side effects and complications of neuraxial anesthetic techniques used for labor and delivery.

Serious neurologic complications of neuraxial anesthesia (eg, meningitis, spinal epidural abscess, arachnoiditis, spinal cord injury) are discussed separately. (See "Serious neurologic complications of neuraxial anesthesia procedures in obstetric patients".)

The relevant anatomy, techniques, indications, contraindications, and physiologic effects of neuraxial analgesia and anesthesia are discussed in detail separately. (See "Overview of neuraxial anesthesia" and "Neuraxial analgesia for labor and delivery (including instrumental delivery)".)

SIDE EFFECTS — The side effects of neuraxial analgesia and anesthesia result from the physiologic effects of neuraxial block or direct effects of the local anesthetics and/or opioids used for the techniques.

Hypotension — Neuraxial anesthesia-induced sympathetic blockade causes vasodilation and decrease in venous return to the heart, which can result in maternal hypotension (figure 1). A reduction in blood pressure can also occur with abrupt onset of pain relief, as may occur after intrathecal analgesic administration for combined spinal epidural (CSE) labor analgesia.

Hypotension is usually defined as either systolic blood pressure <100 mmHg or a reduction of >20 percent from baseline. Hypotension is considered clinically significant if it is associated with maternal symptoms such as lightheadedness and nausea and/or deterioration of the fetal heart rate, a sign of compromised uteroplacental perfusion. (See "Anesthesia for cesarean delivery", section on 'Goal blood pressure'.)

Patients are usually positioned with left uterine displacement during cesarean delivery, and after initiation of neuraxial labor analgesia, to avoid aortocaval compression and possible hypotension. The need for left uterine displacement in healthy parturients has been questioned. (See "Anesthesia for cesarean delivery", section on 'Intraoperative positioning'.)

●Incidence – Hypotension occurs more commonly after onset of neuraxial anesthesia for cesarean delivery than after initiation of labor analgesia. Spinal anesthesia may result in quicker and more profound hypotension when compared with epidural anesthesia (see "Anesthesia for cesarean delivery", section on 'Hemodynamic management'). The reported incidence of hypotension (systolic blood pressure <100 mmHg or <80 percent of baseline) after spinal anesthesia for cesarean delivery is as high as 70 percent [1], and can be reduced by fluid co-loading and prophylactic administration of vasopressors (eg, phenylephrine or ephedrine). (See "Anesthesia for cesarean delivery", section on 'Hemodynamic management'.)

Hypotension occurs much less commonly after initiation of low dose neuraxial labor analgesia, with a reported incidence between zero and approximately 14 percent [2-5].

●Fluid loading – A practical strategy for avoiding hypotension during initiation of neuraxial anesthesia for cesarean delivery includes a rapid bolus of intravenous crystalloid (500 to 1000 mL) at the time of induction/neuraxial placement (co-load), in conjunction with administration of vasopressors. (See "Anesthesia for cesarean delivery", section on 'Fluid management'.)

Intravenous fluid loading is unnecessary with the low dose epidural techniques that are usually used for labor analgesia. In one study, there was no difference in hypotension between parturients who were randomly assigned to receive a one liter IV crystalloid bolus or no preload before initiation of epidural labor analgesia (ELA; 6 and 10 percent, respectively) [6].

●Vasopressors – For prevention of neuraxial anesthesia-induced hypotension during cesarean delivery, for most patients we suggest prophylactic, titrated administration of low-dose phenylephrine infusion (ie, starting at 50 mcg/min) with phenylephrine rescue boluses, along with crystalloid co-loading, aiming for maternal blood pressure close to baseline. Phenylephrine is the preferred vasopressor rather than ephedrine for most patients in this setting in the absence of bradycardia. Limited data suggest that norepinephrine may be beneficial for prevention and treatment of spinal hypotension during cesarean delivery. (See "Anesthesia for cesarean delivery", section on 'Vasopressors'.)

Symptomatic hypotension during labor is usually easily treated with small IV doses of phenylephrine (eg, 40 to 80 mcg) or ephedrine (eg, 5 to 10 mg) and IV fluids. Repeated doses of phenylephrine and/or ephedrine should be administered as needed until the hypotension is corrected. An infusion of phenylephrine is rarely required during low-dose neuraxial labor analgesia.

Prophylactic administration of ephedrine or phenylephrine prior to labor analgesia is not indicated when low-dose techniques are used.

Pruritus — Pruritus is a common side effect of neuraxial opioid administration, and is more likely to occur in pregnant and postpartum women than in other patient populations [7,8]. Fentanyl and sufentanil are relatively lipid soluble and may cause pruritus in the legs, abdomen, and thorax. Morphine and hydromorphone, which are much more water-soluble, may cause pruritus in the neck and head as well.

●Pruritus occurs more commonly after intrathecal opioid administration than after epidural administration, with a reported incidence of close to 100 percent for fentanyl, which is often used for CSE labor analgesia [9-11]. In a meta-analysis of 11 trials involving 959 women, CSE was associated with more pruritus than low-dose epidural (average risk ratio [RR] 1.80; 95% CI 1.22-2.65) [4].

●The incidence of pruritus after neuraxial opioid administration is dose dependent [12-17].

●The duration of pruritus after intrathecal or epidural administration of the lipid soluble opioids fentanyl and sufentanil is relatively brief compared to the duration of pruritus associated with neuraxial morphine and hydromorphone.

●Coadministration of local anesthetics (LAs) with opioids may reduce the incidence of pruritus [10].

The etiology of neuraxial opioid-induced pruritus is unclear, but it is not caused by histamine release [18]. Thus, treatment with an antihistamine such as diphenhydramine is not indicated, as any benefit is due to sedation or perhaps placebo effect.

The most effective treatment for opioid-induced pruritus is administration of a small dose of an opioid antagonist such as naloxone (40 to 80 mcg intravenously [IV], or infusion at 0.25 to 1 mcg/kg/h IV [19]), naltrexone (6 mg orally), or the mixed opioid agonist-antagonist nalbuphine (2.5 to 5 mg IV) [20,21]. Higher doses or infusion of any opioid antagonist may reverse analgesia [22]. Limited literature suggests that nalbuphine may be more effective for relief of pruritus than naloxone, but is associated with increased sedation [21]. Practice for treatment of neuraxial opioid induced pruritus varies: one contributor on this topic administers nalbuphine 2.5 to 5 mg IV in this setting, whereas the other administers naloxone 40 to 80 mcg IV, repeated in five minutes if necessary, and patient controlled intravenous naloxone when indicated for prolonged pruritus.

Other drugs that have been studied for the prevention and/or treatment of opioid induced pruritus include intravenous propofol, serotonin antagonists, and glucocorticoids [23]. A systematic review of randomized trials of treatment and/or prevention of opioid induced pruritus (neuraxial or systemic opioids) found that intravenous naloxone, naltrexone, nalbuphine, and droperidol were effective, based on overall low quality data [24].

Studies of the effect of serotonin (5-HT3) receptor antagonists on opioid induced pruritus have reported conflicting results. A meta-analysis of nine randomized trials involving patients who received intrathecal morphine for cesarean delivery reported that the incidence of pruritus was not reduced by prophylaxis with 5-HT3 receptor antagonists compared with placebo (81 percent versus 86 percent) [25]. However, 5-HT3 receptor antagonists reduced the severity and need for treatment of pruritus, were effective for treatment of established pruritus, and reduced the incidence of postoperative nausea and vomiting and the need for rescue antiemetic therapy. Practice varies regarding administration of 5-HT3 receptor antagonists; one contributor on this topic routinely administers ondansetron after cord clamping because of its benefits and low incidence of side effects, and the other does not.

For those laboring patients experiencing severe pruritus refractory to treatment, switching the epidural analgesic solution to one that is opioid-free is a reasonable option.

Nausea and vomiting — Nausea and vomiting occur commonly in the peripartum period, with or without neuraxial analgesia. Nausea may result from labor itself; nausea related to the pain of contractions tends to resolve after initiation of effective neuraxial analgesia. Nausea may also be a side effect of systemic opioid administration, or the result of one of several anesthesia-related causes, including the following:

●Hypotension – Nausea and vomiting may be caused by hypotension during neuraxial labor analgesia, or more commonly during neuraxial anesthesia for cesarean delivery. Nausea usually resolves with correction of blood pressure, and rarely requires further treatment.

●Neuraxial opioids – Nausea is an uncommon side effect of neuraxial administration of the lipophilic opioids (eg, fentanyl or sufentanil), which are often administered for labor analgesia, with a reported incidence <2.5 percent [26]. Nausea may be more likely with lipophilic opioids used for CSE compared with epidural labor analgesia [5].

Nausea and vomiting are more common after administration of neuraxial morphine, which is usually administered for post cesarean delivery pain. In a meta-analysis of studies of the effect of serotonin receptor antagonists for prevention of side effects of 0.1 to 0.2 mg intrathecal morphine, the reported incidence of postoperative nausea without prophylaxis was 30 to 37 percent, and the incidence of postoperative vomiting was 10 to 35 percent [25]. Prophylactic ondansetron reduced the incidence and severity of nausea and vomiting, and the need for postoperative rescue antiemetic.

Other drugs that are reported to reduce neuraxial opioid induced nausea and vomiting in various patient populations include metoclopramide [27,28], dexamethasone [29,30], and transdermal scopolamine [31]. An infusion of low dose naloxone was used in one reported case of intractable nausea and vomiting associated with intrathecal morphine [32]. (See "Postoperative nausea and vomiting", section on 'Antiemetics'.)

Neuraxial hydromorphone may be administered for postcesarean delivery pain when morphine is unavailable. Most studies have reported an incidence of nausea and vomiting with hydromorphone similar to neuraxial morphine [33-35].

Urinary retention — Urinary retention is a possible side effect of both neuraxial analgesia and anesthesia. Both neuraxial local anesthetics and neuraxial opioids can cause decreased ability to sense a full bladder and to void [36]. Small observational [37] and randomized trials [38] have reported an association between ELA and intrapartum or postpartum urinary retention, though a cause and effect relationship has not been proven, and postpartum bladder dysfunction is common in patients who have no anesthesia. (See "Overview of the postpartum period: Disorders and complications", section on 'Voiding difficulty and urinary retention'.)

Urinary retention may be less common with the low concentration epidural solutions that are commonly used, compared with the higher concentration solutions that were used in the past. In one trial, more patients randomly assigned to low dose labor analgesia (0.1% bupivacaine with fentanyl) were able to void spontaneously than those who received more concentrated epidural solutions (0.25% bupivacaine) (32 percent versus 11 percent) [39].

Bladder distention should be considered if patients complain of breakthrough pain during labor analgesia, and bladder catheterization should be performed as necessary.

Fever — Randomized trials and observational studies have consistently reported an association between the use of epidural analgesia and rise in maternal temperature. The etiology of the temperature increase associated with epidural analgesia is incompletely understood. This is discussed separately. (See "Intrapartum fever".)

Shivering — Postpartum shivering is a common event, even in the absence of analgesia/anesthesia for labor and childbirth. (See "Overview of the postpartum period: Normal physiology and routine maternal care".)

Shivering related to neuraxial anesthesia is not fully understood, but may be caused in part by sympathetic block-induced vasodilation, with redistribution of body heat from the core to the periphery [40]. Shivering can be bothersome and can interfere with blood pressure monitoring. Patients may be warmed with heated blankets or forced air warming systems. Further treatment with intravenous meperidine (12.5 to 25 mg IV) may be used when necessary.

Dexmedetomidine may be an alternative for treating shivering related to neuraxial anesthesia, including during childbirth. In a randomized trial of 80 patients who had shivering during cesarean delivery with spinal or epidural anesthesia, a single dose of dexmedetomidine 30 mcg IV after delivery of the infant reduced the duration of shivering without hemodynamic effects or sedation [41]. Shivering was eliminated within 15 minutes in 90 percent of patients who received dexmedetomidine, versus 22.5 percent of patients who received saline.

COMPLICATIONS

Local anesthetic systemic toxicity — Local anesthetic systemic toxicity (LAST) in obstetric anesthesia most commonly occurs after inadvertent injection of high volume of a high concentration of local anesthetic into an epidural vein. Pregnant patients, especially at term, are at increased risk for LAST because of the physiologic and hormonal changes of pregnancy. (See "Local anesthetic systemic toxicity", section on 'Patient risk factors'.)

LAST is uncommon during labor analgesia because of the low concentration of local anesthetics used for epidural labor analgesia (ELA).

LAST primarily affects the central nervous system and cardiovascular system, and may be fatal. The clinical presentation, prevention, and management of LAST are discussed separately. (See "Local anesthetic systemic toxicity" and "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'The epidural test dose in obstetrics'.)

Inadequate anesthesia — Failed neuraxial block may be defined as inadequate analgesia/anesthesia following an epidural, spinal, or combined spinal–epidural (CSE) technique. The reported incidence of failed block varies, and may be affected by patient factors (eg, obesity, anatomic or postsurgical spine abnormalities), stage of labor, skill of the anesthesia clinician, the specific neuraxial technique, and/or technical factors (eg, equipment used, depth of catheter insertion).

In one single institution review of anesthesia records and quality assurance data for approximately 12,500 neuraxial labor analgesia techniques, the overall failure rate was 12 percent, with a lower failure rate for CSE compared with epidural analgesia (10 versus 14 percent) [42]. In the same review, seven percent of labor epidurals failed when used for cesarean delivery, and spinal anesthesia planned for cesarean delivery failed in 2.7 percent of patients. In another single institution prospective study of 250 parturients who received epidural analgesia, inadequate analgesia at 30 minutes after block initiation occurred in 17 percent of patients. [43].

Management of inadequate analgesia during labor, and management of failed neuraxial anesthesia for cesarean delivery are discussed separately. (See "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Clinician epidural top-ups' and "Anesthesia for cesarean delivery", section on 'Failed or inadequate neuraxial block'.)

Motor block — Neuraxial administration of local anesthetics in high concentrations causes motor block, an undesirable side effect during labor. The drugs and administration techniques (eg, patient controlled epidural analgesia, programmed intermittent epidural bolus) for neuraxial analgesia are chosen in part to minimize motor block. (See "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Modes of drug administration' and "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Goals for neuraxial drug choice'.)

The drugs used for neuraxial labor analgesia techniques usually include a combination of dilute local anesthetic and a lipid soluble opioid. The combination allows the use of lower doses of each agent, thereby minimizing side effects, including motor block. Maintenance of motor function preserves the parturient's ability to push, may allow her to ambulate (if only to the bathroom), maintains maternal satisfaction, and may reduce the effects of neuraxial anesthesia on the incidence of instrumental delivery. (See "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Goals for neuraxial drug choice' and 'Effects on the progress and outcome of labor' below.)

High neuraxial block — Total spinal anesthesia can be a complication of either spinal or epidural anesthesia. It may result from the unrecognized and unintentional injection of medication intended for the epidural space into the subarachnoid or subdural space (via a malpositioned catheter or needle), transfer of medication from the epidural space into the subarachnoid space through a dural rent, or an overdose of medication injected into the subarachnoid space. The reported incidence in the obstetric population in the United States is 1 in 4336 blocks [44]. A study of data from 2011 to 2014 from the United Kingdom Obstetric Surveillance System reported 66 cardiac arrests during approximately 2,350,000 pregnancies [45]. The leading cause of cardiac arrest was a complication of obstetric anesthesia (nearly one in four pregnant patients who had cardiac arrest); 10 of the 17 arrests attributed to obstetric anesthesia resulted from total spinal anesthetic following de novo intrathecal block.

High or total spinal block is discussed separately. (See "Anesthesia for cesarean delivery", section on 'High neuraxial block' and "Overview of neuraxial anesthesia", section on 'High or total spinal anesthesia'.)

Post dural puncture headache — Post dural puncture headache (PDPH; also called spinal headache or post lumbar puncture headache) is a positional headache (ie, worse when the patient sits or stands) that occurs because of leakage of cerebrospinal fluid (CSF) through a dural puncture. PDPH may occur after spinal anesthesia (ie, intentional dural puncture) or after unintentional dural puncture (UDP) with an epidural needle. The mechanism of headache after CSF leak is unclear, but appears to involve cerebral vasodilation and/or traction on intracranial structures. (See "Post dural puncture headache", section on 'Pathophysiology' and "Post dural puncture headache", section on 'Clinical Features'.)

●Incidence – The rate of PDPH after dural puncture varies widely across patient populations; young pregnant women with a low body mass index (BMI) are at highest risk [46]. A meta-analysis of 51 randomized and observational studies of PDPH in over 300,000 obstetric patients reported a risk of UDP of 1.5 percent, with a risk of PDPH of approximately 52 percent after UDP [47]. The risk of PDPH after dural puncture with a spinal needle was 1.5 to 11.2 percent, and varied with the size and type of spinal needle. (See "Post dural puncture headache", section on 'Procedural risk factors'.)

●Treatment – Most PDPHs will resolve in 7 to 10 days if untreated. Conservative management with symptomatic therapy (eg, oral analgesics, caffeine) may be indicated if the patient does not desire epidural blood patch (EBP) or if the headache is not severe [48] (see "Post dural puncture headache", section on 'Treatment'). Intracranial hemorrhage should be suspected with a prolonged headache. (See "Post dural puncture headache", section on 'Differential diagnosis'.)

•Epidural blood patch – The recommended treatment for severe, debilitating PDPH is epidural blood patch (EBP). The initial blood patch gives complete or partial relief in 95 percent of obstetric patients with PDPH, but the headache may recur. In one series, headache recurred in 31 percent of parturients who had an EBP for PDPH, and 28 percent received more than one EBP [49]. EBP is performed by injecting the patient's blood into the epidural space to form a clot over the dural defect [50,51]. EBP is thought to work by two mechanisms, initially by increasing the subarachnoid CSF pressure, and later by forming a fibrin plug that seals the hole in the dura and prevents further CSF leak [52]. EBP is discussed in detail separately. (See "Post dural puncture headache", section on 'Epidural blood patch'.)

•Sphenopalatine ganglion block – A novel noninvasive approach to treating PDPH using an old technique, transnasal sphenopalatine ganglion block (SPGB), has been described [53-56]. (See "Post dural puncture headache", section on 'Alternative treatments for PDPH'.)

Literature on the efficacy of SPGB is limited, consisting of case series and a small randomized trial. SPGB for PDPH is discussed separately. (See "Post dural puncture headache", section on 'Transnasal sphenopalatine block'.)

As we await more robust prospective trials comparing SPGB with other treatments of PDPH, the author offers SPGB to all patients with PDPH because of its low risk. He suggests it particularly for patients who do not desire a blood patch, or for whom a blood patch is relatively or absolutely contraindicated.

Other therapies to treat or prevent PDPHs have not been consistently efficacious.

•Prophylactic epidural blood patch – An EBP may be performed prophylactically, before a headache occurs after an inadvertent dural puncture. Blood is injected into the epidural catheter prior to its removal after delivery. The efficacy of prophylactic EBP is unclear. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.)

•Spinal catheter – Threading an epidural catheter into the intrathecal space at the time of UDP has been advocated to reduce the incidence of PDPH. We do not routinely place an intrathecal catheter after UDP, but place intrathecal catheters selectively (eg, after a difficult epidural procedure). The efficacy of intrathecal catheter placement has not been established in randomized controlled trials, and most studies have reported no benefit of intrathecal catheter placement. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.)

Pneumocephalus — Injection of air into the subarachnoid space during placement of neuraxial block may result in acute onset of severe headache and other neurologic signs and symptoms [57]. This complication may occur with an unintentional dural puncture if air, rather than saline, is used for loss of resistance to identify the epidural space. (See "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique'.)

A pneumocephalus headache can occur within a few seconds if the epidural procedure is performed with the patient in the sitting position, but may be delayed until she sits up if the epidural procedure is performed in the lateral decubitus position. Treatment of pneumocephalus headache is symptomatic. An EBP is of no value for this type of headache.

Spinal epidural hematoma — Hemorrhage into the neuraxis, a rare complication of spinal and epidural techniques, may occur if a blood vessel is punctured by a needle and/or catheter. Spinal epidural hematoma (SEH) can occur in any patient and may occur spontaneously without neuraxial instrumentation, but is more likely in patients with disorders of coagulation and in those receiving anticoagulants. The incidence of SEH appears to be significantly lower in obstetric patients than in other populations. Retrospective studies have reported an incidence of spinal hematoma in obstetric patients between 0 and 0.6 per 100,000 epidural catheterizations [44,58-61]. As an example, an analysis of data from the Nationwide Inpatient Sample found 15 epidural hematomas among over 2,300,000 obstetric epidural catheterizations, for an incidence of 0.6 per 100,000 [61]. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Incidence and risk factors for SEH after neuraxial anesthesia'.)

SEH is less likely with a single-shot spinal technique due to the relatively small size of the spinal needle [62] and the lack of an indwelling catheter. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Spinal epidural hematoma (SEH)'.)

The diagnosis of SEH is complicated by the concealed nature of the bleeding; thus, a high index of suspicion must be maintained. The most common presenting symptoms of neurologically significant SEH are progressive motor and sensory block, and bowel or bladder dysfunction. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Typical presentation'.)

Back pain occurs in only 25 percent of cases. Low-dose neuraxial techniques for labor analgesia produce minimal motor block and facilitate continuous monitoring of lower extremity function in patients at risk for development of neuraxial hematoma. Evaluation and management of suspected SEH are discussed separately. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Evaluation, management, and prognosis'.)

Neuraxial analgesia and the anticoagulated patient — Pregnant women may be treated with anticoagulants for a variety of indications, including thrombophilia or history of venous thrombosis or thromboembolism. The risk of hemorrhage into the neuraxis is increased in anticoagulated patients; thus, one must consider the type of anticoagulant used, the dose, and the timing of its administration. (See "Use of anticoagulants during pregnancy and postpartum" and "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

Neuraxial analgesia and low platelets — A low platelet count or deficient platelet function predispose to SEH upon neuraxial instrumentation. The precise platelet count needed to safely perform neuraxial analgesia is unknown [63], because epidural hematoma is so rare in parturients. Estimates of risk are based on reported neuraxial techniques in parturients with thrombocytopenia. As examples:

●A review of 1525 reported neuraxial techniques performed in parturients with thrombocytopenia found no cases of epidural hematoma, as indicated by the need for decompressive laminectomy [64]. The upper bounds of the 95 percent confidence intervals for the incidence of epidural hematoma were 11 percent for a platelet count <49,000/microL, 3 percent for a platelet count of 50,000 to 69,000/microL, and 0.2 percent for a platelet count 70,000 to 100,000/microL, based solely on the number of patients in each group.

●In a subsequent single center review of 308 parturients who had neuraxial block with a platelet count <100,000/microL, there were no SEHs [65]. It is difficult to draw a conclusion for those parturients with platelet count below 70,000/microL, because neuraxial block was avoided in the majority of these parturients. When the authors analyzed this data along with the data from the study above, the upper bounds of the 95% confidence interval for the incidence of epidural hematoma with a platelet count 70,000 to 100,000 was 0.19 percent.

●In a meta-analysis of 131 case reports/series, retrospective and prospective observational studies involving various different populations of thrombocytopenic patients (7476 procedures) who underwent lumbar neuraxial procedures, there were four reported cases of SEH in obstetric patients with platelet counts between 76,000 and 91,000 x 10⁶/L [66]. These patients had risk factors other than thrombocytopenia, or had either preeclampsia or hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome.

The threshold platelet count for performing neuraxial techniques varies among clinicians, and should be individualized based on patient factors, including the specific patient's risks associated with general anesthesia should it become necessary. Our approach is consistent with a 2021 consensus statement from the Society for Obstetric Anesthesia and Perinatology (SOAP) [67], which is shown in an algorithm (algorithm 1). We typically avoid neuraxial anesthesia in thrombocytopenic patients with a history of bleeding associated with thrombocytopenia or current signs of coagulopathy (eg, bleeding from intravenous catheter sites or mucous membranes). We perform neuraxial anesthesia techniques in patients without a bleeding history with stable platelet counts above 70,000/microL. For patients with platelet counts 50,000 to 70,000/microL, we perform neuraxial anesthesia if there is compelling reason to do so after risk-benefit analysis [68], and prefer a spinal rather than an epidural technique (see "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)"). We avoid neuraxial techniques in patients with platelet counts below 50,000/microL.

The rate of decline of the platelet count should be considered when deciding when or whether to perform neuraxial techniques. The platelet count may decline precipitously in patients with HELLP syndrome. In these patients, the platelet count should be measured within six hours of performing a neuraxial block or removing a neuraxial catheter, and compared with previous counts.

It is not necessary to routinely obtain a platelet count before administration of regional anesthesia in parturients with no history or clinical evidence of a coagulation disorder (bleeding, bruising). (See "Preoperative assessment of bleeding risk".)

Respiratory depression — Respiratory depression is a risk when opioids are administered by any route, including neuraxial injection. Clinically significant respiratory depression after neuraxial opioids is rare at usual doses; risk is increased by prior or concomitant administration of systemic opioids. (See "Post-cesarean delivery analgesia", section on 'Side effects and complications'.)

The time course of neuraxial opioid induced respiratory depression depends on the lipid solubility of the drug.

●After neuraxial bolus administration of a lipophilic opioid (eg, fentanyl or sufentanil) respiratory depression, if it occurs, would be expected within approximately two hours [14].

●Respiratory depression after neuraxial administration of hydrophilic opioid (eg, morphine, hydromorphone) is delayed, and may not occur until 12 hours or more after injection, when a patient is usually on a postpartum floor without intensive monitoring. Thus, a protocol should be in place for postpartum care including respiratory monitoring for all patients who receive neuraxial opioids for postoperative pain control.

Respiratory depression after neuraxial hydrophilic opioids is much less common in parturients than in other patient populations. SOAP published a consensus statement on monitoring following administration of neuraxial morphine for cesarean delivery analgesia, stratified based on the dose of neuraxial opioid and patient risk factors [69]. (algorithm 2) These issues are discussed in detail separately. (See "Post-cesarean delivery analgesia", section on 'Side effects and complications'.)

Neuraxial opioid induced respiratory depression is treated with intravenous administration of an opioid antagonist (eg, naloxone). The dose should be titrated to effect (40 to 80 mcg IV increments), followed by an infusion at a dose sufficient to maintain an adequate respiratory rate until the effect of the opioid has dissipated (eg, 1 to 2 mcg/kg/minute) [70].

Backache — Localized back pain related to tissue trauma at the site of a neuraxial procedure may be present for several days, but prospective studies have consistently reported no correlation between neuraxial analgesia and long term back ache [71-77].

Postpartum neuropathy — Neurologic complications associated with neuraxial anesthesia are extremely rare. Neurologic injury can be the result of needle or catheter trauma, drug toxicity, SEH, or infection, and may involve injury to the spinal cord, nerve roots, or neuraxial vasculature. The incidence of most neurologic complications has not been determined because they are so rare. Neurologic complications of obstetric anesthesia are discussed in detail separately. (See "Serious neurologic complications of neuraxial anesthesia procedures in obstetric patients".)

Postpartum neuropathies usually have obstetric etiologies, and are often due to compression of nerves of the lumbosacral plexus by the descending fetal head, extrinsic neural compression (eg, by stirrup supports) or from ischemia due to prolonged stretching of nerves (eg, extreme hip flexion) during the second stage of labor. (See "Overview of the postpartum period: Disorders and complications", section on 'Neuropathy'.)

Severe infection — Epidural abscess and meningitis are uncommon but potentially catastrophic complications of neuraxial anesthesia procedures. Epidural abscess is more likely to occur after epidural techniques, particularly after prolonged epidural catheterization, whereas meningitis typically occurs after the dura has been punctured, either intentionally as part of a spinal anesthetic or unintentionally as a complication of an epidural procedure. Spinal epidural abscess is discussed separately. (See "Serious neurologic complications of neuraxial anesthesia procedures in obstetric patients", section on 'Meningitis' and "Serious neurologic complications of neuraxial anesthesia procedures in obstetric patients", section on 'Spinal epidural abscess'.)

FETAL EFFECTS — Neuraxial analgesia can affect the fetus directly by placental transfer of local anesthetic or opioids, or indirectly via maternal effects (ie, hypotension or uterine hypertonus). (See 'Effects on the neonate' below.)

Placental perfusion — The placental bed is not autoregulated and, therefore, its perfusion is entirely dependent upon maternal blood pressure. Hypotension caused by neuraxial block can result in decreased fetal oxygenation and a deterioration in the fetal heart rate pattern (eg, bradycardia, repetitive late decelerations). (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Physiologic significance of selected FHR characteristics'.)

However, in the absence of hypotension, epidural local anesthetics have been shown to improve intervillous blood flow [78], to have minimal effect on uterine or fetal umbilical vasculature as assessed by Doppler velocimetry [79,80], and to be associated with improved neonatal acid–base status [38,81].

Fetal bradycardia — Initiation of neuraxial analgesia may be followed by fetal heart rate abnormalities (eg, bradycardia, reduced variability, late decelerations) as a result of hypotension, uterine hyperactivity, or increased uterine tone. In the absence of hypotension, transient fetal heart rate abnormalities in this setting presumably relate to a reduction in maternal circulating epinephrine after rapid onset of analgesia, and loss of epinephrine's beta-sympathomimetic relaxant effects on the myometrium [82,83]. The resulting uterine hypertonus can compromise placental blood flow. Fetal bradycardia after rapid onset of analgesia usually occurs within the first 15 minutes, and when treated with usual measures, does not result in fetal acidemia, low Apgar scores, or the need for cesarean delivery [82].

If fetal bradycardia occurs after initiation of neuraxial analgesia, treatment should include the following:

●Discontinue intravenous oxytocin

●Place the parturient in the lateral decubitus position to relieve aortocaval compression

●Administer supplemental oxygen

●Correct hypotension

●Fetal scalp stimulation (if accessible)

●For persistent uterine hypertonus or tachysystole, administer tocolytic medication (eg, nitroglycerin 60 to 90 mcg intravenously repeated in two to three minutes, if necessary, followed by terbutaline 250 mcg subcutaneously if there is no response to nitroglycerin) (see "Induction of labor with oxytocin", section on 'Tachysystole')

Most studies have reported that fetal bradycardia is more common after intrathecal opioid administration, usually as part of combined spinal-epidural analgesia, than after initiation of epidural analgesia. A 2020 meta-analysis of randomized trials reported an increased risk of fetal bradycardia for combined spinal-epidural (CSE) compared with standard epidural labor analgesia (ELA) technique (RR 2.38, CI 1.57-3.62) [5]. Rates of cesarean delivery and apgar scores at 1 and 5 minutes were similar.

EFFECTS ON THE PROGRESS AND OUTCOME OF LABOR — Obstetric anesthesia practice has evolved with the goal of reducing or eliminating deleterious effects on the progress or outcome of labor and delivery.

●Timing of neuraxial analgesia – The timing of administration of neuraxial analgesia (early versus later in labor) has been shown to have no effect on the rate of cesarean delivery or other obstetric outcomes. A 2014 meta-analysis of nine studies including over 15,000 patients that compared early initiation (<4 cm cervical dilatation) with later initiation of neuraxial analgesia reported no difference in cesarean delivery rate, instrumental delivery, duration of second stage of labor, or fetal outcomes [84]. Thus, epidural analgesia should be administered on request for patients who are clearly in labor, without waiting for a specific degree of cervical dilation [85].

●Cesarean delivery – Multiple randomized trials have shown that neuraxial analgesia does not increase the risk of cesarean delivery. A 2018 meta-analysis of 40 randomized trials that compared neuraxial analgesia with non-neuraxial analgesia or no analgesia reported that epidural analgesia did not significantly increase the risk of cesarean delivery (relative risk 1.07, 95% CI 0.96-1.08) [38].

●Instrumental delivery – Neuraxial analgesia using high concentrations of local anesthetic (LA) may increase the risk of instrumental delivery. However, standard obstetric anesthesia practice now involves the use of low concentration LA/opioid solutions for labor analgesia, partly to minimize the degree of motor block, and to preserve the ability to push during the second stage of labor. (See "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Goals for neuraxial drug choice'.)

A 2013 meta-analysis of randomized controlled trials that compared low concentration epidural LA for labor (eg, ≤0.1% bupivacaine or ≤0.17% ropivacaine) with higher concentration solutions found a reduced risk of instrumental delivery with the use of low concentration LAs (odds ratio [OR] = 0.70; 95% CI 0.56 to 0.86) [86]. Similarly, a 2017 meta-analysis of studies using only dilute epidural LA found no difference in the instrumental delivery rate between patients who had epidural analgesia, and those who did not [87]. A 2018 meta-analysis of randomized trials that compared epidural with non-epidural analgesia or no analgesia for labor reported no difference in instrumental delivery rate in trials conducted after 2005 [38].

●Emergency delivery for fetal compromise – In contrast with studies that have found no effect of neuraxial analgesia on the incidence of cesarean or instrumental delivery in contemporary practice, two studies [88,89] have found an association between neuraxial analgesia and emergency delivery for presumed fetal compromise. However, it is important to point out that association does not imply causation. Furthermore, the quality of the existing evidence is insufficient to recommend avoiding neuraxial analgesia for patients at high risk of cesarean delivery. In fact one of the indications for early labor epidural placement is to reduce the need for general anesthesia in the event of an unplanned cesarean delivery, particularly in high risk parturients. (See "Neuraxial analgesia for labor and delivery (including instrumental delivery)", section on 'Preparation for surgical anesthesia'.)

Examples of relevant studies include the following:

•In the meta-analysis of randomized trials described above, the incidence of cesarean delivery for fetal distress was similar in patients who had epidural analgesia, compared with those who had systemic opioid analgesia (13 trials, 6750 patients; 3.3 versus 2.3 percent, relative risk [RR] 1.32, 95% CI 0.97–1.79) [38].

•In a retrospective perinatal database study of approximately 630,000 singleton deliveries between 2014 and 2018 in the Netherlands, epidural labor analgesia was associated with increased risk of emergency delivery (cesarean or instrumental) compared with alternative analgesia (13.2 versus 7.0 percent, RR 1.72, 95% CI 1.67–1.77) [88]. Conclusions are limited by the very high rate of emergency delivery, the very low neuraxial analgesia rate (31 percent in nulliparous patients, 10 percent in parous patients), and higher incidence of comorbidities in patients who had epidural analgesia. In addition, there was lack of information on epidural or hemodynamic management or the indication for placing an epidural, which was potentially more likely in a patient with a poor fetal heart rate tracing.

•Another study was a post hoc analysis of per protocol data from a randomized trial that compared epidural analgesia with intravenous remifentanil patient controlled analgesia (PCA) for 619 singleton deliveries in the Netherlands from 2011 and 2012 [89]. The incidence of emergency delivery for presumed fetal compromise was higher in patients who received epidural analgesia (14.8 versus 8.3 percent, odds ratio 1.69, 95% CI 1.01–2.83). Conclusions are limited by the very high emergency delivery rate, and lack of information on the management of labor, or drugs used for epidural analgesia, and the incidence of hypotension after epidural analgesia. Epidural management is of particular concern because almost half of the patients originally randomized to epidural analgesia were excluded from this post hoc analysis because they had no pain relief.

●Duration of labor – Neuraxial analgesia may decrease the duration of the first stage of labor, and may prolong the second stage of labor to a variable degree.

•First stage of labor – A number of prospective randomized trials that compared epidural [90-92] or intrathecal [93] analgesia with systemic opioid analgesia for labor have reported shorter labor after early administration of neuraxial analgesia. As an example, in one trial, 750 nulliparous women were randomly assigned to receive intrathecal fentanyl or systemic hydromorphone at first request for analgesia [93]. The median time from initiation of analgesia to full cervical dilation was significantly shorter after neuraxial analgesia (295 minutes versus 385 minutes).

•Second stage of labor – The effect of neuraxial analgesia on the second stage of labor, and the clinical relevance of reported effects, are unclear, partly because the start of second stage (complete cervical dilation) is difficult to measure and depends on the timing of a cervical examination, rather than a defined obstetrical event. Retrospective reviews have reported an association between epidural analgesia and a longer second stage of labor. A multicenter retrospective study including approximately 62,400 nulliparous patients who delivered between 2002 and 2008 reported that the 95^th percentile in the duration of the second stage of labor was approximately 50 minutes longer in patients who had epidural analgesia than those who did not (3.6 versus 2.8 hours) [94]. In another retrospective review of labor in 22,370 nulliparous women between 1976 and 2008, epidural analgesia use prolonged 95^th percentile duration of the second stage of labor by 2 hours and 19 minutes (197 minutes without epidural versus 336 minutes with epidural) [95].

Randomized trials have reported a much smaller effect of epidural analgesia on the duration of the second stage of labor [87]. In addition, the use of low concentration epidural LA solutions (which is the current standard of care) may minimize prolongation of the second stage of labor, compared with higher concentrations. A 2011 meta-analysis of studies of neuraxial labor analgesia (with mixed low and higher concentration LAs) reported a mean increase of 13.66 minutes in the second stage of labor with the use of neuraxial analgesia [38], whereas a 2017 meta-analysis (exclusively low concentration LAs) reported a statistically insignificant mean increase of 5.7 minutes [87]. Similarly, meta-analysis of studies that compared higher concentration epidural LA with dilute LA solutions found a shorter second stage of labor (weighted mean difference -14 minutes) with the use of dilute solutions [86].

EFFECTS ON BREASTFEEDING — The effects of neuraxial analgesia on breastfeeding are controversial and difficult to study, and existing literature is insufficient to make recommendations on this issue. Studies of the effects of labor analgesia on breastfeeding have reported conflicting results, and have included heterogeneous patient populations and labor analgesia techniques, and differing methods for evaluating breastfeeding [85,96-101].

Multiple patient factors affect the likelihood that a patient will breast feed in the postpartum period and long term. Compared with systemic opioids for labor analgesia, neuraxial techniques result in lower or negligible fetal opioid levels, and would therefore be expected to interfere less with neonatal feeding behaviors.

A randomized trial including approximately 950 parturients reported no difference in the breastfeeding rate at six weeks or three months among those who received labor analgesia with epidural bupivacaine with or without fentanyl 1 mcg/mL or 2 mcg/mL [99]. The patients in this trial were multiparous, had previously breastfed an infant, and planned to breastfeed for more than three months; results may not apply to other patient populations.

EFFECTS ON THE NEONATE — In the absence of maternal hypotension prior to delivery, neuraxial analgesia and anesthesia do not negatively affect the neonate. (See 'Hypotension' above and 'Placental perfusion' above.)

Opioids administered systemically or epidurally rapidly enter the maternal circulation, cross the placenta, and equilibrate with fetal circulation [102]. However, with the low concentrations of lipophilic opioids (eg, fentanyl and sufentanil) used for labor analgesia, even prolonged epidural opioid infusion rarely causes fetal accumulation, neonatal respiratory depression, or reduced neonatal behavioral scores [102-105]. Similarly, with the dilute concentrations of local anesthetics used for labor, minimal placental drug transfer and neonatal accumulation occur [102]. Neurobehavioral studies in neonates whose mothers received epidural analgesia or systemic opioids have shown either no difference [106] or improved scores in neonates of mothers receiving epidurals [107].

A meta-analysis of 10 randomized trials reported that neonates of mothers who received epidural analgesia had fewer Apgar scores below seven and required naloxone less often than those whose mothers received systemic opioids [108]. In contrast, in a retrospective study of over 2200 neonates whose mothers received neuraxial labor analgesia with fentanyl, there was a dose dependent increase in positive neonatal toxicology testing for fentanyl [109]. Over 90 percent of infants whose mothers received >200 mcg neuraxial fentanyl tested positive. Five minute Apgar scores <7 were more likely in infants who tested positive, though other neonatal outcomes (eg, need for resuscitation, neonatal ICU admission) were similar in neonates who tested positive compared with those who tested negative.

Epidural fentanyl is routinely administered as an adjunct to local anesthetics during epidural anesthesia for cesarean delivery, to improve intraoperative analgesia (see "Anesthesia for cesarean delivery", section on 'Epidural drugs for CD'). Many clinicians wait until the umbilical cord is clamped to administer fentanyl, to avoid any risk of fetal transfer. However, many studies have reported no effects on neonatal outcomes (eg, Apgar scores, umbilical blood gases, neonatal behavioral tests) with administration of 50 to 100 mcg of epidural fentanyl during initiation of epidural anesthesia, prior to cord clamp [110-112]. Epidural morphine is routinely administered for postoperative pain relief, after the umbilical cord is clamped, and therefore has no effect on the neonate.

The doses of opioid used for intrathecal administration are considerably lower than epidural doses, and maternal systemic uptake is negligible, such that direct fetal or neonatal effects are unlikely to occur.

EPIDURAL ANALGESIA AND CHILDHOOD AUTISM — After review of available data, we believe that there is no convincing evidence that labor epidurals cause autism spectrum disorder (ASD) or other types of behavioral or learning disabilities in the parturient's infant, and no evidence that choosing another form of pain relief for labor, or no pain relief, reduces the risk of autism or other disabilities.

Relevant evidence consists of retrospective observational or database studies, and results are mixed. Given the retrospective nature of the data, confounding is possible and causation cannot be determined. In studies that have shown an association between epidural analgesia and offspring risk of ASD, that association usually disappears or becomes weak when adjusting for confounders [113-123]. In a meta-analysis of six observational studies including over 3.3 million parturients, neuraxial labor analgesia was associated with a small increase in the risk of ASD in offspring (adjusted hazard ratio 1.07, 95% CI 1.04 -1.10) [124]. The association was very weak, and the evidence was judged to be of very low quality, primarily due to high risk of bias and inconsistency. This association disappeared when studies with a high risk of bias and studies that accounted for unmeasured familial factors such as socioeconomic and genetic factors were excluded.

Examples of studies of the association between neuraxial analgesia and childhood ASD are as follows:

●In a United States insurance database cohort study including >1.6 million patients who had vaginal deliveries, exposure to maternal neuraxial labor analgesia was associated with a slightly increased risk of ASD by age 10 years in offspring, compared with unexposed offspring (adjusted hazard ratio 1.07, 95% CI 1.00-1.14) [120]. A meta-analysis of data from this study and three others (>2,470,000 patients) found a pooled adjusted hazard ratio of 1.10, 95% CI 1.06-1.13 [120].

●In a retrospective case control study of 465 children with ASD, 481 siblings of those children, and 1313 controls, the rate of epidural use during labor was higher in mothers who delivered children who were later diagnosed with ASD [113]. However, the rate of obstetric complications was also higher in mothers of children with ASD, and the reasons for epidural placement (eg, obstetric complications, pain relief) were not available, raising the possibility that the association between epidural use and ASD was due to complications for which the epidural was placed. The rate of epidural use during delivery of siblings without ASD was similar to the rate of epidural use in for delivery of children with ASD, supporting a lack of a causative relationship between epidurals and ASD.

●A large retrospective longitudinal birth cohort database study published in 2020 reported an association between labor epidural analgesia (LEA) in parturients and the diagnosis of autism in their children [114]. Among approximately 148,000 women who delivered vaginally, ASD was diagnosed in 1.9 percent of children of mothers who received LEA, compared with 1.3 percent of children in the non-LEA group (adjusted hazard ratio 1.37, 95% CI 1.23-1.53). However, like all observational studies, a causal relationship between LEA and autism was not established. There were significant methodologic problems with this study; there were numerous demographic differences between the cohort of patients who received LEA and those who did not, including factors that have been associated with an increased risk of autism. In addition, potentially important details about the course of labor and delivery and other possible causes of autism were not provided. Since the etiology of autism is unknown, even after controlling for known risk factors, there remains the possibility that the association between LEA and autism was due to unknown confounders.

In response to publication of this study, five major obstetric and anesthesia societies (Society for Obstetric Anesthesia and Perinatology, American Society of Anesthesiologists, Society for Pediatric Anesthesia, American College of Obstetrics and Gynecology, and the Society for Maternal-Fetal Medicine) issued a joint statement that this study does not provide credible evidence that LEA causes autism. Other anesthesia and obstetric professional societies in Canada [115] and the United Kingdom have also issued statements on the methodologic problems of the study and lack of evidence that labor epidurals cause autism.

●A large population-based cohort study of over 123,000 vaginal singleton births in Manitoba, Canada from 2005 to 2016 used information from four statewide databases to evaluate the association between exposure to maternal epidural labor analgesia (ELA) and autism diagnosed after the age of 18 months in offspring [116]. After adjusting for maternal sociodemographic, pregnancy-related and preexisting factors, and birth-specific factors, there was no association between ELA exposure and increased risk of autism in offspring (adjusted hazard ratio 1.08 (95% CI 0.78-1.22).

●In another Canadian administrative database study of >650,000 vaginal births, there was a small increase in the risk of autism diagnosed in childhood in offspring of patients who had intrapartum epidural analgesia (adjusted HR 1.14 (95% CI 1.08–1.21) [122]. The authors acknowledged that these findings were insufficient to demonstrate causation and results must be interpreted with caution given the methodological limitations inherent in observational studies.

ALLERGIC REACTION TO LOCAL ANESTHETIC — Allergic reactions to local anesthetics (LAs) are very rare. Most allergic reactions are delayed-type, cell mediated reactions (delayed local swelling or contact dermatitis), which are rarely dangerous. They occur more commonly with ester LAs (eg, 2-choloroprocaine, tetracaine) than with amide LAs (eg, lidocaine, bupivacaine, ropivacaine). Serious IgE-mediated reactions can also occur, including life-threatening anaphylaxis. Patients who describe symptoms suggestive of this type of reaction should be referred to an allergist if possible (table 1). Skin testing and graded challenge can determine which specific drugs the patient can safely receive. Allergic reactions to LAs are discussed separately. (See "Allergic reactions to local anesthetics".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Post dural puncture headache" and "Society guideline links: Obstetric anesthesia" and "Society guideline links: Local and regional anesthesia".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Managing pain during labor and childbirth (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Side effects

•Hypotension may occur primarily as a result of the sympathetic blockade associated with neuraxial block, and is more common during anesthesia for cesarean delivery than during labor analgesia. For prevention of neuraxial anesthesia-induced hypotension during cesarean delivery, for most patients we suggest prophylactic administration of a vasopressor along with intravenous crystalloid coloading (Grade 2C). We administer a low-dose phenylephrine infusion (ie, starting at 50 mcg/min) with phenylephrine rescue boluses, along with a rapid bolus of intravenous crystalloid (500 to 1000 mL), at the time of induction or neuraxial anesthesia placement, aiming for maternal blood pressure close to baseline. The patient is typically positioned with left uterine displacement to prevent aortocaval compression. (See 'Hypotension' above.)

•Pruritus is a common side effect of neuraxial opioids, and is treated most effectively with administration of a small dose of opioid antagonist (eg, naloxone [40 to 80 mcg intravenously]), naltrexone (6 mg orally), or the mixed opioid agonist-antagonist nalbuphine (2.5 to 5 mg intravenously [IV]). (See 'Pruritus' above.)

•Intrapartum fever, nausea and vomiting, urinary retention, and shivering are other possible side effects of neuraxial analgesia or anesthesia. (See 'Side effects' above.)

●Complications

•Pregnant patients are at higher risk of post dural puncture headache (PDPH) than other patients. Severe PDPH is usually treated with an epidural blood patch (EBP). (See 'Post dural puncture headache' above.)

•Local anesthetic systemic toxicity (LAST) is a rare but potentially lethal complication of epidural administration of local anesthetics. Pregnant patients are at increased risk for LAST when high doses of a high concentration local anesthetic are administered. (See 'Local anesthetic systemic toxicity' above and "Local anesthetic systemic toxicity".)

•Inadequate analgesia, motor block, and high neuraxial block are complications that can be minimized by management techniques and choice of neuraxial drugs. (See 'Inadequate anesthesia' above and 'Motor block' above and 'Post dural puncture headache' above.)

•Spinal epidural hematoma (SEH) is a rare, potentially devastating complication of neuraxial anesthesia techniques, that is more common in patients who are coagulopathic, either because of anticoagulant medication, systemic disease, or thrombocytopenia. For patients with thrombocytopenia, we perform neuraxial anesthesia in patients without a bleeding history with stable platelet counts above 70,000/microL. For patients with platelet counts 50,000 to 70,000/microL, we perform neuraxial anesthesia if there is compelling reason to do so after risk-benefit analysis, and prefer a spinal rather than an epidural technique (algorithm 1). (See 'Spinal epidural hematoma' above.)

•Postpartum neuropathies usually have obstetric causes. Very rarely, neurologic complications can be the result of needle or catheter trauma, drug toxicity, SEH, or infection, related to neuraxial anesthesia techniques. (See 'Postpartum neuropathy' above.)

•Strict aseptic technique should be followed during neuraxial anesthesia techniques, to reduce the risk of meningitis and epidural abscess, which are rare, serious complications. (See 'Severe infection' above.)

●Fetal effects

•Neuraxial analgesia can affect the fetus directly by placental transfer of local anesthetic or opioids, or indirectly via maternal effects (ie, hypotension or uterine hypertonus). Placental transfer of drugs is rare with low-dose epidural or spinal drug administration. (See 'Placental perfusion' above.)

•In the absence of hypotension, fetal bradycardia may occur with abrupt onset of analgesia, and is more common after intrathecal opioid administration for labor analgesia than after initiation of epidural analgesia. Fetal bradycardia in this setting is typically transient, and when treated with usual measures, does not increase the risk of cesarean delivery or adverse neonatal outcomes. (See 'Fetal bradycardia' above.)

●Effects on the progress and outcome of labor – Low dose neuraxial labor analgesia techniques administered at any time during labor do not increase the risk of cesarean delivery or instrumental delivery. Neuraxial analgesia may shorten the first stage of labor, and may prolong the second stage of labor to a variable degree. (See 'Effects on the progress and outcome of labor' above.)

●Breastfeeding – Neuraxial labor analgesia is unlikely to affect breastfeeding, though existing literature is insufficient to confirm this conclusion. (See 'Effects on breastfeeding' above.)

●Neonatal effects

•In the absence of maternal hypotension prior to delivery, neuraxial analgesia and anesthesia do not negatively affect the neonate. (See 'Effects on the neonate' above.)

•There is no convincing evidence that epidural labor analgesia (ELA) causes autism, or that choosing another form of pain relief for labor or no pain relief reduces the risk of autism or other disabilities. (See 'Epidural analgesia and childhood autism' above.)