5/3/22, 17:30 Adverse effects of neuraxial analgesia and anesthesia for obstetrics - UpToDate

Author: Gilbert J Grant, MD

Section Editor: David L Hepner, MD
Deputy Editor: Marianna Crowley, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2022. | This topic last updated: May 27, 2021.

INTRODUCTION

Neuraxial analgesia and anesthesia (ie, spinal, epidural, combined spinal epidural, and dural
puncture 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 instrumented
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

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>20 percent from baseline. (See "Anesthesia for cesarean delivery", section on 'Goal blood
pressure'.)

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.

Patients are usually positioned with left uterine displacement during cesarean delivery, and
after initiation of neuraxial labor analgesia, to avoid aortocaval compression. 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
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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.

● Co-administration 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. Thus, treatment with an antihistamine such as diphenhydramine is not indicated, as

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any benefit is probably due to sedation or 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 [18]), naltrexone (6 mg orally), or the mixed opioid agonist-antagonist nalbuphine
(2.5 to 5 mg IV) [19,20]. Higher doses or infusion of any opioid antagonist may reverse
analgesia [21]. Limited literature suggests that nalbuphine may be more effective for relief of
pruritus than naloxone, but is associated with increased sedation [20]. 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. A
systematic review of randomized trials of treatment and/or prevention of pruritus found that
intravenous naloxone, naltrexone, nalbuphine, and droperidol were effective in the prevention
of opioid induced pruritus, based on overall low quality data [22].

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) [23]. 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.

Nausea and vomiting — Nausea and vomiting occur commonly in the peripartum period,
with or without neuraxial analgesia. Nausea may result from labor itself, as a side effect of
systemic opioid administration, or for 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.

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● 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 [24]. Nausea may be more likely after
CSE than after ELA [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 without prophylaxis of
postoperative nausea was 30 to 37 percent, and the incidence of postoperative vomiting
was 10 to 35 percent [23]. Prophylactic administration of 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 [25,26],
dexamethasone [27,28], and transdermal scopolamine [29]. An infusion of low dose
naloxone was used in one reported case of intractable nausea and vomiting associated
with intrathecal morphine [30]. (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 [31-33].

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 [34]. Small observational [35] and randomized trials
[36] 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) [37].

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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 [38]. 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.

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 instrumented 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

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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) [39]. 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. [40].

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 instrumented delivery)", section on 'Clinician 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 instrumented delivery)", section on 'Modes of drug
administration' and "Neuraxial analgesia for labor and delivery (including instrumented
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 instrumented 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

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subarachnoid space. The reported incidence in the obstetric population in the United States is
1 in 4336 blocks [41]. 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
[42]. 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 [43]. 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 [44]. 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
[45]. (See "Post dural puncture headache", section on 'Treatment'.)

• Epidural blood patch – The classic treatment for severe, debilitating PDPH is 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 [46]. EBP is performed by injecting the patient's blood into the epidural
space to form a clot over the dural defect [47,48]. EBP is thought to work by two

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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
[49]. 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 in case reports and case series [50-52]. Although there are no prospective
trials comparing this treatment with other treatments of PDPH, because it is low-risk,
the author offers SPGB to all patients with PDPH. He suggests it particularly for
patients who do not desire a blood patch, or for whom a blood patch is relatively or
absolutely contraindicated. Transnasal sphenopalatine block for PDPH is discussed
separately. (See "Post dural puncture headache", section on 'Transnasal
sphenopalatine block'.)

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 [53]. 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 is placed with the
patient in the sitting position, but may be delayed until she sits up if the epidural is placed in
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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 [41,54-57]. 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 [57]. (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 [58] 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 spinal epidural hematoma 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 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

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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 [59], because epidural hematoma is so rare in
parturients. Estimates of risk are based on reported neuraxial techniques in parturients with
thrombocytopenia. As an example, 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 [60]. 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. Similarly, in a subsequent single center review of 308 parturients who had
neuraxial block with a platelet count <100,000/microL, there were no SEHs [61]. 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.

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) [62], 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 [63], 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

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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 hemostasis".)

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. (See
"Management of acute perioperative pain", section on 'Delayed respiratory depression'.)

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 [64]. ( 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) [65].

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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 [66-72].

Postpartum neuropathy — Neurologic complications associated with neuraxial anesthesia

are extremely rare. Neurologic injury can be the result of needle or catheter trauma, drug
toxicity, spinal epidural hematoma, 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,

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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 [73], to have minimal effect on uterine or fetal umbilical
vasculature as assessed by Doppler velocimetry [74], and to be associated with improved
neonatal acid–base status [36,75].

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 [76,77]. 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 [76].

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
● 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.

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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 [78]. Thus,
epidural analgesia should be administered on request for patients who are clearly in
labor, without waiting for a specific degree of cervical dilation [79].

● 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) [36].

● 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 instrumented 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) [80]. 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 [81]. 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 [36].

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● 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 [82-84] or intrathecal [85] 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 [85].
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 95th 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) [86]. In another retrospective review of labor in
22,370 nulliparous women between 1976 and 2008, epidural analgesia use prolonged
95th percentile duration of the second stage of labor by 2 hours and 19 minutes (197
minutes without epidural versus 336 minutes with epidural) [87].

Randomized trials have reported a much smaller effect of epidural analgesia on the
duration of the second stage of labor [81]. 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 [36], whereas a 2017 meta-analysis
(exclusively low concentration LAs) reported a statistically insignificant mean increase
of 5.7 minutes [81]. 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 [80].

EFFECTS ON BREASTFEEDING
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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 [79,88-93].

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 [91]. 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 [94]. 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 [94-97]. Similarly, with the dilute concentrations of local
anesthetics used for labor, minimal placental drug transfer and neonatal accumulation occur
[94]. Neurobehavioral studies in neonates whose mothers received epidural analgesia or
systemic opioids have shown either no difference [98] or improved scores in neonates of
mothers receiving epidurals [99]. 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 [100].

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

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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 [101-103]. 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. In studies that have shown an association between epidural analgesia and offspring
risk of ASD, that association usually disappears when adjusting for confounders [104-110].
Examples of such studies are as follows:

● 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 [104]. 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 [105]. 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

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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 [106] 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 [107]. 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).

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".)
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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 5th to 6th
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 10th to 12th
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 delivery (The
Basics)")

SUMMARY AND RECOMMENDATIONS

● Neuraxial analgesic and anesthetic techniques for labor and delivery are associated with
side effects and complications. Some are more common than others.

● 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
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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 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.)
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• Postpartum neuropathies usually have obstetric causes. Very rarely, neurologic

complications can be the result of needle or catheter trauma, drug toxicity, spinal
epidural hematoma, 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.)

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