BJA Education, 22(1): 33e37 (2022)
doi: 10.1016/j.bjae.2021.09.001
Matrix codes: 1H02,
2E03, 3B00, 3E00
Persistent pain after childbirth
H.S. Tan1 and B.L. Sng1,2,*
1
KK Women’s and Children’s Hospital, Singapore, Singapore and 2DukeeNUS Medical School, Singapore,
Singapore
*Corresponding author: sng.ban.leong@singhealth.com.sg
Keywords: chronic pain; vaginal delivery; Caesarean section
Learning objectives
By reading this article, you should be able to:
 Identify factors contributing to the large varia-
tions in the estimated incidence of persistent
pain after childbirth (PPAC).
 Describe the significant impact of PPAC on
maternal outcomes and quality of life.
 Explain the proposed pathophysiology of PPAC
and that the aetiology is still unclear.
 Recall the biological, psychosocial, and peri-
partum factors associated with PPAC.
Introduction
Persistent pain after childbirth (PPAC) occurs in a significant
proportion of postpartum women, and is an important soci-
etal and healthcare issue. Given that more than 140 million
births occur annually, a large number of women are placed at
risk of PPAC-related morbidity such as interference with ac-
tivities of daily living and care of their newborn infant. In
addition, PPAC may be associated with the development of
postpartum depressive symptoms and increased healthcare
Hon Sen Tan MD MMed (Anaesthesiology) MHSc is an associated
consultant at KK Women’s and Children’s Hospital. His major clin-
ical and research interests include persistent pain, and the use of
medical devices to improve pain and haemodynamic management.
Ban Leong Sng MMed (Anaesthesiology), FANZCA, FFPMANZCA,
MCI, FAMS is a senior consultant and head of the Department of
Women’s Anaesthesia at KK Women’s and Children’s Hospital. He is
also an associate professor at DukeeNUS Medical School. His major
clinical and research interests include persistent pain, and the impact
of maternal pain and psychological risk factors on acute and
persistent pain.
Accepted: 14 September 2021
© 2021 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
For Permissions, please email: permissions@elsevier.com
Advance Access Publication Date: 8 November 2021
Key points
 Lack of consensus definition results in wide
variation in the reported incidence of persistent
pain after childbirth (PPAC).
 PPAC has significant impact on maternal
outcomes.
 The pathophysiology of PPAC is uncertain
because the available evidence is limited.
 Biological, psychosocial, and peripartum factors
have been associated with PPAC.
utilisation. Until recently, PPAC has been an unrecognised
morbidity of childbirth. One of the top research priorities in
obstetric anaesthesia and perioperative medicine is to identify
the risk factors contributing to PPAC to improve risk-
stratification and pre-emptive interventions.
This review aims to provide a pragmatic overview of the
difficulties in estimating the incidence, impact on maternal
quality of life, proposed pathophysiological mechanisms un-
derlying the transition from acute to persistent pain, and po-
tential risk factors associated with PPAC. Furthermore, the
association between severe acute postpartum pain and sub-
sequent PPAC suggests that improving peri- and postpartum
analgesia could potentially reduce the risk of PPAC. Clinical
strategies to optimise analgesia after Caesarean section are
discussed. It should be noted that a multitude of obstetric and
non-obstetric pain conditions may be present after delivery
and are beyond the scope of this review, which is limited to
persistent postpartum pain associated with Caesarean and
vaginal deliveries only.
Incidence and characteristics
The International Association for the Study of Pain (IASP) has
recently proposed a definition of chronic post-surgical pain
(CPSP) for inclusion in the International Classification of Dis-
eases, 11th Revision (ICD-11) as pain that develops or
33
Persistent pain after childbirth
increases in intensity after a surgical procedure or tissue
injury, persists beyond the healing process of 3 months and is
localised to the area of injury or referred to the innervation
territory of a nerve situated in this area, with other causes of
pain excluded.1 However, inconsistency and lack of
consensus in the definition of PPAC used in the literature have
contributed to the wide variation in estimated incidence; scar
pain after Caesarean section has been reported in 6.9e30.7%
of women at 3 months and 1.9e19% at 6 months, whereas
vaginal delivery was associated with perineal or vaginal pain
in 1.3e48% of women at 6e8 weeks, 4.4%e55.7% at 3 months,
and 2e6.4% at 6 months.2
The definition of PPAC used in previous studies varies in
three main aspects. First, there is significant variation in the
duration of postpartum pain that ranges from 2 months to
more than 6 months after childbirth. Given that the incidence
of PPAC generally decreases with time, it is vital to establish
the minimum duration at which pain after childbirth should
be considered PPAC.2 Second, pregnancy is associated with a
high prevalence of pain conditions such as pelvic pain, back
pain and headache that may continue into the postpartum
period,2 and it may be challenging to differentiate pre-existing
pain conditions from new onset pain. Based on a question-
naire administered between 6 and 18 months after Caesarean
section, Nikolajsen and colleagues reported that 18.6% of
women had abdominal wound pain lasting more than 3
months but did not differentiate pre-existing from new-onset
pain.3 This may be especially relevant in the 16.8% and 32.3%
of the study cohort who had previous abdominal surgery and
Caesarean section, respectively. In comparison, Eisenach and
colleagues reported a lower incidence of PPAC (9.8%) when
only new onset pain at 8 weeks after vaginal or Caesarean
section was considered.4 Third, it is important to specify
which postpartum pain conditions are attributable to tissue
injury during childbirth, and should therefore be considered
PPAC. A prospective cohort study found abdominal scar pain
in 9.2% of women at 3 months after Caesarean section, but
also noted that pain at other locations was present in 68.4% of
women not considered to have persistent pain.5 It is possible
that inclusion of these pain conditions may result in a higher
estimated incidence of PPAC. Furthermore, a significant pro-
portion of postpartum women develop neuropathic pain, but
there is no consensus on whether these cases should be
considered PPAC. In a multicentre study investigating surgical
site pain and neuropathic pain after Caesarean section at 3
months, only 6.6% of women had persistent surgical site pain
whereas 21.4% were positive for neuropathic pain based on a
modified Douleur Neuropathique-4 (DN4) questionnaire.6
Hence, whether neuropathic pain is included in the defini-
tion of PPAC will have a significant impact on its estimated
incidence.
In addition, the estimated incidence of PPAC may be
influenced by social and cultural barriers preventing women
from reporting persistent pelvic pain or pain during sexual
intercourse, or the belief that such conditions are normal after
birth.7 Also, retrospective studies often rely on the mother’s
recollection of pain and its associated characteristics, and are
therefore susceptible to recall bias. Therefore, to reduce con-
flicting information and improve comparability of data from
various studies, a consensus definition of PPAC that clearly
specifies the duration, onset and characteristics of persistent
pain is required.
34 BJA Education - Volume 22, Number 1, 2022
Clinical significance
Persistent pain after childbirth has a significant impact on
maternal outcomes. Nikolajsen and colleagues investigated
the effects of scar pain at 6e18 months after Caesarean section
on mood, sleep and common daily activities and reported that
78% of women had pain when carrying heavy objects, 37% had
pain with sports, 33% had significant mood changes and 30%
had pain with stair climbing.3 When defined as new onset pain
lasting at least 8 weeks after childbirth, pain adversely affected
walking, sleep and mood in 40%, 36% and 19% of women after
vaginal delivery, and 72%, 57% and 40% after Caesarean sec-
tion, respectively.4 Similarly, 88% of women reported inter-
ference with carrying heavy objects, 53% with rising from a
chair and 39% with standing and stair climbing because of scar
pain after Caesarean section.5 Another study evaluated the
impact of pain at 3, 6 and 12 months after Caesarean section
using the Brief Pain Inventory, and found moderate to severe
functional and quality of life impairment that were signifi-
cantly correlated to pain intensity at all time points.8 In addi-
tion to its pain-related effects, PPAC has been associated with
the development of symptoms of postpartum depression.4
PPAC is also likely to exert significant socioeconomic impacts
although the magnitude is unclear.7
Proposed pathophysiology
Few studies have focused on elucidating the pathophysiology
of PPAC, and high-quality evidence is lacking. It is also unclear
if the mechanisms underlying PPAC are similar to those of
other conditions causing CPSP, which are thought to involve
the transition from acute to persistent pain through a com-
plex and poorly understood process.9 In this paradigm, post-
surgical pain is related to the nociceptive input resulting
from tissue trauma, which is subsequently modified by pe-
ripheral and central sensitisation. It has been suggested that
failure of this hyperalgesic state to resolve despite tissue
healing and activation of antinociceptive mechanisms leads
to the development of CPSP.
Chronic post-surgical pain results from a combination of
nociceptive, inflammatory and neuropathic sources. Tissue
injury stimulates nociceptor signalling and is exacerbated by
the release of inflammatory factors and increase in nociceptor
sensitivity. This phenomenon is known as primary hyper-
algesia, and disproportionately increases nociceptive input
transmitted to the CNS for a given level of stimulus.9 In
addition, nerve injury may result in neuropathic pain that
often clinically manifests as allodynia, hyperalgesia, hypaes-
thesia or dysaesthesia. Neuropathic pain may occur after
Caesarean section as a result of the increased risk of
ilioinguinal and iliohypogastric nerve entrapment associated
with the Pfannenstiel incision.10
Sustained nociceptive input from nociceptive, inflamma-
tory or neuropathic sources can invoke neuroplastic changes
in primary afferent neurones within the dorsal root ganglia,
termed peripheral sensitisation. This process involves
changes in gene expression and long-lasting alteration of
nociceptor sensitivity, tissue healing, remodelling and rein-
nervation. In turn, excessive peripheral nociceptive input may
lead to neuroplastic changes in the CNS and development of
central sensitisation; a form of spinal cord neuroplasticity
that results in abnormal nociceptive responses which are
 Persistent pain after childbirth

decoupled from the presence or intensity of peripheral noci- and access to medical care.5 However, an accurate and reliable
ceptive stimuli.9 risk-prediction model incorporating these factors has yet to be
The transition from acute to persistent pain is also influ- developed, and it is unclear if pre-emptive intervention tar-
enced by biological, psychosocial and peripartum factors via geting these risk factors will have significant effect on fore-
their effects on pain sensitivity and modulation.9 It was stalling the development of PPAC or improving maternal
postulated that the presence of these factors may increase an outcomes.
individual’s susceptibility to developing PPAC, and when
incorporated into a risk-stratification model, may aid in the
Genetic factors
identification of patients at elevated risk of PPAC. Prior
research has identified several risk factors associated with the Limited data are available on the association between
development of PPAC (Table 1). maternal genetics and PPAC risk, although a few gene poly-
morphisms have been investigated regarding their impact on
acute pain after Caesarean section. For instance, a single
Associated factors nucleotide polymorphism (SNP) at position 118 of the mu
Pre-existing pain conditions opioid receptor gene-1 (OPRM-1), A118G, is associated with
decreased opioid binding affinity and increased opioid re-
Pre-existing pain is an established risk factor for PPAC.2
quirements after surgery. A study in Asian patients showed
Nikolajsen and colleagues reported that pre-existing pain
increased 24 h systemic opioid requirements in women with
was present in 63% of women who developed persistent pain
the G118 allele after Caesarean section under spinal anaes-
after Caesarean section, compared with 19% in women
thesia compared with those with AA118 homozygosity.14
without PPAC.3 Pre-existing pain was independently associ-
The catechol-O-methyltransferase (COMT) enzyme is
ated with persistent pain after vaginal and Caesarean de-
involved in catecholamine and oestrogen metabolism, and an
liveries at 12 months.11 Pre-existing pain also predicted the
amino acid substitution Val158Met is associated with reduced
development of persistent pain after Caesarean section at 3
COMT enzyme activity and increased pain sensitivity. How-
months, with back pain and migraine being the most common
ever, the Val158Met polymorphism did not significantly alter
locations of pre-existing pain.5 Conversely, Eisenach and
acute analgesic requirements after Caesarean section and the
colleagues found no association between pre-existing pain
incidence of PPAC at 3 months.15
and PPAC, although further analysis was precluded by the low
incidence of PPAC in the study cohort.4
Factors related to surgery or tissue injury
Psychosocial factors Emergency Caesarean section has been postulated to increase
Psychological and pain vulnerability factors may influence the risk of PPAC, possibly because of the greater chance of
pain modulation and alter the risk of developing PPAC. Two iatrogenic nerve and tissue trauma, and the use of general
systematic reviews on psychological predictors of CPSP re- anaesthesia, which may be less effective in blocking noci-
ported that depression, psychological vulnerability, stress, ceptive input and central sensitisation compared with spinal
pain catastrophising and anxiety were associated with anaesthesia. However, in some studies the urgency of
CPSP.12,13 Social factors such as the lack of private insurance Caesarean section has not been found to be a significant risk
and social deprivation were also reported to be significantly factor.11,16 Furthermore, Nikolajsen and colleagues reported
associated with PPAC, attributable to the lack of social support that a greater proportion of women with PPAC had received
general anaesthesia (37%) compared with spinal anaesthesia
(17%).3 However, a subsequent prospective study by Liu and
colleagues showed no significant difference in PPAC risk
Table 1 Risk factors associated with persistent pain after associated with the use of either anaesthetic technique16.
childbirth Data regarding surgical technique and PPAC are limited. A
systematic review found that the Pfannenstiel incision could
Maternal factors Surgical factors Anaesthetic result in ilioinguinal and iliohypogastric nerve injury and
factors neuropathic pain.10 However, two studies comparing Pfan-
nenstiel to vertical incisions found no significant difference in
Pre-existing pain Recurrent Severity of the risk of PPAC with either technique, although they were not
conditions Pfannenstiel postpartum pain
primarily designed and powered to evaluate incision type as a
incision
Depression Parietal General risk factor.3,11 Recurrent Pfannenstiel incision has been iden-
peritoneum anaesthesia tified as a risk factor for PPAC, possibly because of the greater
closure area of fibrosis that increases the risk of nerve entrapment.17
Psychological However, closure of the parietal peritoneum was reported to
vulnerability significantly increase the risk of both severe acute postpartum
Stress
pain and PPAC at 8 months, compared with non-closure.18
Pain
catastrophising In the context of vaginal delivery, increasing extent of peri-
Anxiety neal tissue injury is associated with severe acute postpartum
Lack of private pain, but not with PPAC. Macarthur and colleagues reported
health insurance increased pain intensity and analgesia requirement within the
Social deprivation first 7 days postpartum after perineal trauma or episiotomy, but
Genetic
found no significant difference in the incidence of PPAC at 6
susceptibility
weeks after first- or second-degree perineal injury, episiotomy,
and third- or fourth-degree perineal injury.19

BJA Education - Volume 22, Number 1, 2022 35

Persistent pain after childbirth
Acute postpartum pain
Severe acute pain in the postpartum period has been identi-
fied as a strong risk factor for PPAC.3 Severe acute postpartum
pain was associated with 2.5-fold increased risk of PPAC at 8
weeks independent of the mode of delivery.4 Sng and col-
leagues reported that higher acute pain intensity after
Caesarean section independently predicts PPAC at 3 months
(odds ratio 1.3; 95% confidence interval 1.2e1.5).5 The mech-
anism underlying this association between severe post-
partum pain and PPAC is unclear, and may be related to an
individual’s susceptibility to developing both acute and
persistent pain, or that suboptimal analgesic management
increases the risk of developing PPAC. Nonetheless, it should
be noted that the association between severe acute post-
partum pain and PPAC does not necessarily imply a causal
relationship; it is possible that similar risk factors exist for
both acute pain and PPAC, hence women possessing these risk
factors may be susceptible to both conditions.
Oxytocin
Experimental studies in animals that induced pain hyper-
sensitivity by spinal nerve ligation suggest that increasing
concentrations of oxytocin during labour and lactation may
protect against PPAC. The evidence for this is: (1) spinal
oxytocin concentrations were increased in postpartum rats
compared with non-pregnant controls; (2) weaning of the
pups and reduction in oxytocin concentrations led to
increased hypersensitivity; and (3) intrathecal oxytocin
reduced hypersensitivity, and this was attenuated by atosiban
(an oxytocin receptor antagonist).20 Nonetheless, human
studies are limited and further investigations into the physi-
ological mechanisms and therapeutic application of oxytocin
in the context of PPAC are warranted.
Prevention
Theoretically, identifying women at greater risk of developing
PPAC will facilitate individualised and preventive clinical
management. Yet, despite the recognition of several factors
associated with PPAC, the development of a robust risk-
stratification model remains elusive, and there is scarce evi-
dence that pre-emptive treatment targeting known risk fac-
tors significantly reduces its risk and incidence of adverse
outcomes.
For example, the association between severe acute post-
partum pain and PPAC suggests that optimising postpartum
analgesia could potentially reduce the risk of PPAC.4 However,
most studies investigated the efficacy of perioperative anal-
gesics on reducing acute pain after Caesarean section, and it is
uncertain if improving postpartum analgesia will have sig-
nificant impact on the risk of developing persistent pain after
Caesarean or vaginal delivery. Furthermore, the use of anal-
gesics should be balanced against concerns of drug transfer
via breast milk and the possibility of opioid-related morbidity.
Nonetheless, inadequate analgesia may result in delayed
functional recovery, impaired maternalefetal bonding and
increased risk of postpartum depressive symptoms, and
should therefore be a priority for peripartum anaesthetic
management.21
Neuraxial anaesthesia is the technique of choice for
Caesarean section as it reduces maternal and fetal morbidity
compared with general anaesthesia. Neuraxial anaesthesia
36 BJA Education - Volume 22, Number 1, 2022
often combines local anaesthetic with lipophilic opioids such
as fentanyl and longer-lasting hydrophilic opioids such as
morphine. Long-acting neuraxial opioids improve analgesia
and reduce sedation compared with systemic opioids.
Because of the analgesic ceiling effects and dose-dependent
increase in adverse effects, the optimal dose of intrathecal
morphine is 50e100 mg, or 2e4 mg when given via the epidural
route.21 Neuraxial anaesthesia is often supplemented with a
multimodal regimen to reduce opioid consumption, and
should consist of oral paracetamol and NSAIDs at scheduled
regular intervals. Because the analgesic effects of paracetamol
and NSAIDs are synergistic, they should be given on a
scheduled basis as this further improves analgesia and de-
creases opioid consumption, nausea and vomiting compared
with as-needed regimens. Pain not responding to this regimen
can be managed with oral opioids as needed, with intravenous
opioids reserved for women in extreme pain or intolerant of
oral medications.21
Other analgesic adjuncts have been evaluated in the context
of reducing acute pain after Caesarean section, but careful
consideration of risks and benefits are required given the con-
flicting evidence available on their analgesic benefits and
increased risk of adverse effects. For instance, gabapentinoids
reduced 24 h pain scores in one study but others found no
analgesic benefits compared with placebo.21 In another study
there was no significant difference in the incidence of PPAC
between a single perioperative gabapentin dose and placebo.22
Conversely, ketamine has been shown to reduce cumulative
morphine consumption and increase time to request for anal-
gesia request compared with placebo in women receiving
neuraxial anaesthesia for Caesarean section.23 Although keta-
mine was not found to reduce PPAC after Caesarean section, S-
ketamine may attenuate hyperalgesia at 12 and 24 h after
Caesarean section.24 Finally, the role of perioperative clonidine
in reducing PPAC is unclear; Lavand’homme and colleagues
reported that intrathecal clonidine reduced incisional hyper-
algesia at 48 h after Caesarean section, but without change in
the incidence of PPAC at 6 months.25
Summary
Persistent pain after childbirth occurs in 0.3e55% of post-
partum women, with this wide incidence attributable to the
lack of a consensus definition. It has a significant impact on
maternal quality of life, is associated with postpartum
depressive symptoms and may increase healthcare uti-
lisation. Few studies have investigated the pathophysiology of
PPAC, and it is uncertain whether PPAC has a similar aetiology
to other forms of persistent pain. Increased peri- and post-
partum concentrations of oxytocin may have protective ef-
fects against PPAC, but it is yet unclear how this may be used
to reduce or treat PPAC. Conversely, pre-existing pain condi-
tions, severe postpartum pain, maternal genetics and psy-
chosocial factors such as depression, psychological
vulnerability, stress, pain catastrophising, anxiety and social
deprivation are potential risk factors for PPAC. In addition,
recurrent Pfannenstiel incision and closure of the parietal
peritoneum may be associated with increased incidence of
PPAC. Given that severe acute postpartum pain is a consistent
predictor of PPAC, it was hypothesised that providing appro-
priate analgesia may reduce PPAC, although this should be
verified in future research. In addition, a consensus definition
of PPAC that specifies the minimum duration, onset and
characteristics of persistent pain is required, and further

research is necessary to develop risk-stratification models to
identify patients at increased risk of developing PPAC as this
may facilitate early surveillance and intervention.
Declaration of interests
The authors declare that they have no conflicts of interest.
MCQs
The associated MCQs (to support CME/CPD activity) will be
accessible at www.bjaed.org/cme/home by subscribers to BJA
Education.
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