Obstetric Pain

Introduction

Unrelenting dedication and hard work by clinicians, scientists, and professional organizations in the past 2 centuries have significantly increased our knowledge and improved the safety of obstetric anesthesia to make childbirth a more pleasant and memorable experience. However, the advance in obstetric analgesia and anesthesia is not without controversy and has been influenced significantly by social values and popular demands, as well as by scientific evidence.

The first use of an anesthetic for delivery can be credited to James Young Simpson, who administered diethyl ether to anesthetize a woman with a deformed pelvis for delivery on January 19, 1847 ( ). In search of a safer anesthetic than the dangerously flammable ether, Simpson pioneered the technique of chloroform anesthesia, which John Snow later refined. At that time the majority of physicians supported the view of Charles D. Meigs, who argued that labor pain was inseparable from contraction and should not be abolished ( ). In addition, the documented deaths of 123 non-obstetric patients that “could be positively assigned to the inhalation of chloroform” in a report from the Royal Medical and Chirurgical Society provided further support for non-intervention in labor and delivery (Committee Appointed by the Royal Medical and Chirurgical Society 1864). Even when John Snow administered anesthesia to Queen Victoria for delivery of Prince Leopold in 1953, strong public criticism against obstetric anesthesia prevailed, including Thomas Wakely, the founding editor of Lancet . It was not until after the birth of the Queen’s first grandchild in 1860 when she remarked, “What a blessing she [Victoria, her oldest daughter] had chloroform,” that obstetric anesthesia became a more acceptable medical practice ( ).

By the early 1900s, obstetric anesthesia had evolved to the use of morphine in combination with scopolamine, which was first introduced as Dammerschlaff or “twilight sleep” for labor analgesia by the Austrian physician Richard and later popularized by . With the side effects of amnesia and disorientation and even a report of the death of a prominent advocate of this technique during childbirth, the initial resistance by many physicians to twilight sleep resembled earlier objections to etherization but differed in that a more critical scientific examination of drug effects on the fetus and the mother was conducted.

With the introduction of regional cocaine anesthesia for eye surgery by Carl and the classic publication by Henry on the innervation of abdominal viscera, various publications on obstetric applications of regional techniques such as spinal, lumbar epidural, caudal, paravertebral, parasacral, and pudendal nerve blocks started to emerge between 1900 and 1930 ( ). However, inhalational and opioid forms of analgesia were still the preferred choices, probably because of limited availability of drugs and equipment for regional anesthesia and lack of knowledge on the advantages of regional over general anesthesia. Later, in 1933, John Cleland undertook a meticulous analysis of the nerve pathways mediating labor pain. A publication from Hingson and Edwards in 1941 described continuous caudal anesthesia with a malleable needle secured in place. Subsequently, with small flexible plastic catheters replacing malleable needles, continuous epidural anesthesia was made possible and resulted in continuous lumbar epidural analgesia and anesthesia, which remains the main effective technique for obstetric analgesia and anesthesia today.

Coincidentally, as regional analgesia and anesthesia started emerging, “natural childbirth,” originated by , was gaining popularity. Dick-Read attributed labor pain purely to fear and suggested that sympathetic nervous system activity results in uterine ischemia and therefore pain. Contemporary childbirth preparation does not erroneously attribute pain purely to fear but rather helps patients manage pain through education ( ). The goals of natural childbirth and obstetric anesthesia have converged many aspects: to have an awake, participating mother during delivery without maternal, fetal, or neonatal side effects or a negative impact on the course of delivery. Different professional organizations from various countries have been formed to promote and accelerate the understanding and advancement of safe obstetric anesthesia not only for research but also to provide better clinical guidelines and education. The Society of Obstetric Anesthesia and Perinatology and the Obstetric Anaesthetists’ Association are two examples with worldwide stature that continue to flourish and grow. The availability of in-house obstetric anesthesiologists has also gained much appreciation from colleagues not just for pain relief but also for the multidisciplinary approach to overall improvement in patient care from resuscitation to management of hemorrhage and other maternal and fetal co-morbid conditions. Strong clinical evidence supports the notion that properly administered analgesia/anesthesia for labor and delivery has a very low overall risk and improves maternal and perinatal mortality and morbidity ( ). More than a century ago, , after administering his first obstetric anesthetic, profoundly and insightfully stated, “It will be necessary to ascertain anesthesia’s precise effect, both upon the action of the uterus and on the assistant abdominal muscles; its influence, if any, upon the child; whether it has a tendency to hemorrhage or other complications.” With this, he identified the essential issues and provided a road map to guide many in the quest for better obstetric care. The surge of interest in obstetric pain relief in the past 50 years is attested to by many publications on the subject. Much of the research has been focused only on refinement of techniques or drugs to provide better analgesia with improvement in neonatal and maternal safety. Despite the many advances in understanding the neurobiology of pain, relatively little has emerged specifically regarding labor pain. Laboring patients mostly receive a local anesthetic with an opioid adjuvant aimed at blocking the spinal transmission of pain-related signals. Various clinical reports have suggested a relatively high incidence of inadequate or failed labor epidural analgesia that has resulted in patient dissatisfaction (Eappen et 1998, ). Many consider intrapartum pain relief an unmet medical need. Better understanding of the biological basis of labor pain will allow the development of target-directed therapy that may provide alternatives to achieve a better quality of intrapartum pain relief. In addition, recent research involving better modeling of labor pain, obstetric pharmacogenetics, prediction of the severity of acute and chronic obstetric pain, and its associated long-term public health concerns is likely to result in further improvement in the relief of labor pain.

Measurement and Severity of Obstetric Pain

Many early descriptions of labor pain were inaccurate and confusing but influenced perceptions of the magnitude of pain endured by laboring parturients. Although most modern child-birth preparations, such as Lamaze’s psychoprophylaxis, acknowledge the existence of pain during labor, some may still consider labor pain to be minor or unimportant ( ). The early work of Bonica from personal observation and interviews indicated that 65% of laboring parturients had moderate to severe pain ( ). Melzack subsequently confirmed Bonica’s findings through systematic use of the McGill Pain Questionnaire and showed that women experiencing their first childbirth without training rated their labor pain to be as painful as digit amputation. More than 65% of women of mixed parity rated labor pain as being severe or very severe ( ) ( Fig. 55-1 ). Nulliparous women tend to have a higher total mean pain rating than parous women do. Twenty-five percent of primiparas and 11% of multiparas rated labor pain as “horrible.” However, there is considerable interindividual variability in rating the intensity of labor pain. Javert and Hardy reported that some laboring women equated labor pain to the “ceiling pain” generated by a second-degree burn from a radiant heat source applied to the skin ( ). Linear regression of the same data suggested that cervical dilation resulted in severe pain. Others have reported the intensity of labor pain to be associated with the magnitude of uterine contraction pressure ( ), menstrual pain intensity, age, parity ( ), maternal fatigue ( ), and even a history of a previous pain experience before childbirth ( ). It is possible that interindividual variation in labor pain may be partially due to genetic differences, including genetic polymorphisms regulating drug responses, cytokine production, functions, and responses ( ; also see Chapter 10 ). In evaluating and studying labor pain and treatment, most previous reports tended to compare labor pain by using one of two discrete pain scores. However, because labor itself and its associated pain are both dynamic processes that are affected by many factors and thus result in significant interindividual differences, better identification of the covariates affecting labor progress and pain is needed.

Recently, reported the development and validation of a dynamic model to account for labor progress in assessment of labor pain. Subsequently, , at the same institution, combined a bi-exponential model describing labor progress with the sigmoidal labor pain model to test the influence of patient covariates on labor pain. Both studies used retrospective patient data to develop and test their models. The prediction error for the pain score in the former study was large, but the purpose of the model was to remove the variability associated with labor progress so that other factors, such as genetic polymorphisms, can be quantitatively studied. In their study population, cervical dilation accounted for only 16–20% of the variability in reported pain ( ). In the latter study, covariates such as ethnicity were found to have statistically significant but clinically trivial effects on labor progress ( ). The technique suggested by these authors may provide a useful quantitative tool for future studies to identify and assess effect or lack of effect of patient or environmental covariates on labor progress, labor pain, and therapeutic responses. Better understanding of the underlying causes of interindividual variability in labor progress, pain, and response to therapy is likely to lead to better tailored therapy ( ).

Meaning, Significance, and Impact of Obstetric Pain

Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damages” by the International Association for the Study of Pain ( ). Fear, anxiety, and apprehension stimulate the sympathetic nervous system and also affect pain perception and behavior during labor. Unplanned pregnancy results in higher reported labor pain scores ( ), whereas the presence of a partner in the labor room leads to lower pain scores ( ). Other emotional factors, such as motivation, cultural influences, and cognitive intervention with preparatory classes, can affect modulation of sensory transmission and increase confidence in handling labor, which in turn is a strong predictor of a less painful labor experience ( ). Even when the pain level is the same, the meaning of labor pain may be different from that of non-labor pain. compared pain descriptors in laboring women and those with dysmenorrhea or spontaneous abortion. Those with non-labor pain used words implying suffering such as punishing and wretched, whereas laboring women generally did not. Some have associated labor pain with a sense of euphoria, as in pain derived from mountain climbing ( ) or a process making them more mature and resulting in a stronger personality ( ), but others find no deeper meaning in labor pain and expect complete pain relief. Some parturients planning natural childbirth but ending up receiving analgesia when the pain becomes intolerable may experience guilt, anger, and failure ( ). By contrast, unrelieved severe labor pain can also result in long-term emotional and even physical consequences that negatively affect the parturient’s emotion and bonding with her newborn, relationship with her partner, and postpartum depression ( ).

Many women undergo delivery without negative sequelae, but some may experience significant persistent postpartum pain and even depression. Recent investigations of acute and chronic postpartum pain have shown a 7% incidence of perineal pain 8 weeks after vaginal delivery ( ), a 48% incidence of punctate hyperalgesia at 48 hours, and a 23% incidence of residual pain 6 months after cesarean delivery ( ). , in a multicenter, prospective, longitudinal cohort study of 1288 parturients delivering by either cesarean or vaginal delivery, tested whether the mode of delivery had an independent role in persistent pain and depression at 8 weeks postpartum. The impact of mode of delivery on acute postpartum pain, persistent pain, depressive symptoms, and their interrelationships was assessed by regression analysis and propensity adjustment. They reported a 10.9% prevalence of severe acute pain within 36 hours postpartum and a 9.8 and 11.2% prevalence of persistent pain and depression at 8 weeks postpartum, respectively. The severity of acute postpartum pain, but not the mode of delivery, was independently related to the risk for persistent pain and depression, both of which also resulted in negative effects on activities of daily living and on sleep ( ). Those with severe acute postpartum pain had a 2.5- and 3.0-fold increased risk for persistent pain and depression, respectively, when compared with those with mild acute postpartum pain ( ). These findings suggest that this morbidity may not be related to the degree of trauma to physical tissues but rather to an individual’s pain response to that injury. Furthermore, long-term follow-up of the postpartum patients showed that incidence of chronic pain at 6 months and 1 year later was remarkably low at 0.3% and 0.1%, respectively, as compared to surgery with similar tissue injury. Whether pregnancy, the process of labor and bonding with the newborn have a protective effect against chronic pain, or whether the severity of pain during labor and delivery would show the same correlation to postpartum morbidity as acute postpartum pain does has not been well studied. Studies in animals suggest that acute intervention at the time of tissue injury reduces the likelihood of chronic pain developing ( ). It is likely that the severity of the acute pain is not just a marker of chronic pain but rather an active participatory component in the pathophysiology of transitioning from acute to chronic pain ( ). More careful attention to pain treatment and follow-up in the days following childbirth may potentially reduce long-term morbidity and improve overall outcomes. Further research is needed to define predictive factors to identify those at risk for severe acute and chronic postpartum pain.

Mechanism and Pathways of Pain of Childbirth

First Stage of Labor

Pain experienced during the first stage of labor predominantly originates from afferents with peripheral terminals in the lower uterine segment and the cervix rather than the uterine body. In the absence of inflammation, uterine body afferents may be much less important in labor pain during uterine distention, as shown in laboratory animals ( ), whereas manual cervical distention reproduces labor pain in humans ( ). Furthermore, showed that patients undergoing cesarean section under a local anesthetic block did not experience pain from uterine distention but did from cervical distention, which resembled labor pain. Afferents innervating the lower uterine segment and endocervix have cell bodies in the thoracolumbar dorsal root ganglia and are different from those innervating the vaginal surface of the cervix and the vagina, which have cell bodies in the sacral dorsal root ganglia ( ). Dilation of the endocervix in rats, resembling first-stage labor, leads to activation of afferents from the endocervix and lower uterine segment, thus suggesting significant roles for these afferents in first-stage labor pain ( ) ( Fig. 55-2 ). However, afferents from the vaginal surface of the cervix and vagina are activated only during delivery, not during labor, and stimulation may result in antinociception or mating behavior in rats ( ). From , , and other investigators’ work we now know that first-stage labor pain is transmitted via visceral afferents with peripheral terminals in the lower uterine segment and cervix. They pass through the paracervical ganglion and the hypogastric nerve and plexus together with the lumbar sympathetic chain and enter the spinal cord in the T10–L1 region ( Fig. 55-3 ). From the spinal cord, second-order cells send axons to supraspinal sites as discussed in Chapter 51 . Visceral stimulation activates similar areas in the brain as somatic stimulation does ( ). Interestingly, visceral stimulation is perceived to be more unpleasant than somatic stimulation of similar intensity. The diffuse localization of visceral pain in first-stage labor versus the precise location of somatic pain in second-stage labor helps clinicians determine the appropriate type of regional analgesia needed at these times ( ).

Neurobiological Basis of Labor Pain

Role of Inhibitory Receptors

Endogenous inhibitory receptors modulating pain responses are expressed in the peripheral afferent terminals, spinal cord, and supraspinal central nervous system to provide analgesia. Opioid receptor agonists, in particular, mu (μ) and kappa (κ) receptors, have been more commonly studied and used for analgesia. μ-Opioid receptor agonists produce antinociception in response to uterine cervical distention (UCD) through actions in the supraspinal central nervous system and the spinal cord but not in the peripheral afferent terminals ( ) ( Fig. 55-4 ). With somatic stimulation, tonic estrogen exposure reduces the supraspinal but not the spinal (intrathecal) analgesic effect of μ-opioid receptor agonists ( ). κ-Opioid receptor agonists, which are unaffected by tonic estrogen exposure and have greater analgesic efficacy in women than in men, produce their antinociceptive effect through actions on visceral peripheral afferents and the supraspinal central nervous system ( ) (see Fig. 55-4 ).