Measurement and Severity of Labor Pain

The recognition and acceptance of chronic pain, which frequently lacks an obvious outward cause, contrasts to the recurrent denial of labor pain, which is accompanied by visible tissue injury. Dick-Read suggested that labor is a natural process not considered painful by women in primitive cultures that should be handled with education and preparation rather than through pain medications. Lamaze popularized psychoprophylaxis as a method of birth preparation; this method now forms the basis for prepared childbirth training in the developed world. Although childbirth training acknowledges the existence of pain during labor, some scientific-thought leaders still consider labor pain to be minor.

The severity of labor pain has been recognized previously. Melzack, using a questionnaire developed to assess the intensity and emotional impact of pain, observed that nulliparous women with no prepared childbirth training rated labor pain to be as painful as a digit amputation without anesthesia ( Fig. 20.2 ). More than 30 years before Melzack’s quantification of pain, Javert and Hardy trained subjects to reproduce the intensity of labor pain with the sensation of noxious heat applied to the skin from a radiant heat source. In these experiments, several women achieved “ceiling pain”—resulting in second-degree burns to the skin—when they attempted to match the intensity of uterine contraction pain. Individual women also reported a close positive correlation between cervical dilation and pain intensity. Logistic regression analysis of the investigators’ original data indicates a high likelihood of severe pain as labor progresses, with a time course closely associated with cervical dilation ( Fig. 20.3 ). Other investigators have noted that uterine pressure during contractions accounts for more than 90% of the variability in labor pain intensity. These observations are consistent with the conclusion that cervical distention is the primary cause of pain during the first stage of labor.

A comparison of pain scores obtained through the McGill Pain Questionnaire. Scores were collected from women in labor, patients in a general hospital clinic, and patients in the emergency department after accidents involving traumatic injury. Note the modest difference in pain scores between nulliparous women with and without prepared childbirth training. PRI, Pain rating index, which represents the sum of the rank values of all the words chosen from 20 sets of pain descriptors.

(Modified from Melzack R. The myth of painless childbirth [The John J. Bonica Lecture]. Pain. 1984;19:321–337.)

Likelihood of severe pain during labor. A significant minority of women (approximately one-third) have severe pain in early labor, and the proportion of women with severe pain increases to nearly 90% later in labor, in close relationship with cervical dilation.

(Data from Hardy JD, Javert CT. Studies on pain: measurements of pain intensity in childbirth. J Clin Invest. 1949;28:153–162.)

In an effort to objectively measure pain in laboring women, Charier et al. studied the physiologic fluctuations of the iris, which is dependent on the input from the sympathetic and parasympathetic systems. By measuring the variation coefficient of the pupillary diameter (VCPD) as a mathematical extraction of pupil size fluctuation in 40 laboring women, researchers were able to demonstrate a stronger correlation ( r = .77 versus r = .42) with numerical pain scores in labor during a uterine contraction than pupillary diameter alone.

However, there is considerable variability in the rated intensity of pain during labor. Nulliparous women rate labor pain as more severe than do parous women; however, the differences are small and of questionable clinical relevance. There is a correlation between the intensity of menses and labor pain, especially back discomfort, although the reason for this relationship is unknown. It is possible that the rated intensity of labor pain reflects individual differences in the perception of all types of pain. In a study of factors affecting labor pain, 10 of 97 subjects reported that they had never experienced pain before childbirth; these women reported significantly less pain during labor and delivery compared with women who had previously experienced pain. In other studies, the variability of pain after cesarean delivery could be predicted with preoperative quantitative sensory testing (such as rating the intensity of pain with a standardized noxious thermal stimulus), psychological constructs, and their combinations.

The mechanism by which people perceive different levels of pain from the same stimulus remains unclear. A study involving brain imaging and a fixed acute noxious heat stimulus showed a strong correlation between verbal pain assessment and the level of activation of various cortical brain regions, especially the contralateral somatosensory cortex and anterior cingulate cortex. The investigators also found that the degree of activation of the thalamus was essentially identical in all subjects, suggesting that differences in perceived pain resulted from modulation at suprathalamic levels rather than in the peripheral nerves or spinal cord. The situation in labor may be more complex. For example, a large genetic polymorphism regulates cytokine production and function as well as pregnancy outcome. It is possible that interindividual differences in labor pain may partially reflect genetic differences in cytokine production or response.

In evaluating and studying labor pain and its treatment, most studies have tended to assess labor pain by using a set of discrete pain scores. However, labor pain is a complex, subjective, multidimensional, and dynamically changing experience with both sensory and affective components that are influenced by many factors. As a result, there are substantial individual differences in labor pain. Therefore, better identification of the covariates that affect labor progress and its associated pain is needed. Conell-Price et al. developed and validated a dynamic model to account for labor progress in the assessment of labor pain. Subsequently, Debiec et al., at the same institution, combined a biexponential model that describes labor progress with a sigmoidal labor pain model to assess the influence of patient covariates on labor pain. Both studies used retrospective patient data to develop and test their models. In the former study, the prediction error for the pain scores was large, but the purpose of the model was to identify and remove variability associated with labor progress so that other factors (e.g., genetic polymorphisms) can be quantitatively studied. In this study, cervical dilation accounted for only 16% to 20% of the variability in reported pain. In the latter study, the covariate of ethnicity was found to have a statistically significant but clinically trivial effect on labor progress. The modeling described by these investigators provides a useful quantitative tool for future studies to identify and assess the effect—or the lack of effect—of patient and/or environmental covariates on labor progress, labor pain, and therapeutic responses. Better understanding of underlying causes of interindividual variability in labor progress, labor pain, and therapeutic responses is likely to lead to more tailored therapy.

In summary, although significant variability exists in the rated intensity of pain during labor and delivery, the majority of women experience more than minimal pain. The close correlation between cervical dilation and the rated severity of pain implies the existence of a causal relationship and increases the likelihood that a parturient will request analgesia as labor progresses.

Personal Significance and Meaning

The International Association for the Study of Pain (IASP) has defined pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Recognition of an intensity-discriminatory component and an emotional-cognitive component, with powerful interactions between the two, has fostered current interventions heavily weighted toward the first component and assumes that labor pain is severe and in need of pharmacologic treatment. Largely ignored are coping strategies and the personal meaning of labor pain, which varies considerably among women. Williams and Craig suggested that the definition of pain should include the often overlooked cognitive and social elements, and Whitburn et al. suggested a further extension to etiologies that do not include tissue damage. These alterations would make the experience and study of pain more relevant to the labor experience; nociceptive pain intensity increases with cervical dilation, despite the absence of tissue damage.

Although many women rate the pain of labor and delivery as severe, the terms used to more fully describe this pain reflect an emotional meaning. In a pioneering study of the quantification of pain from experimental dilation of the cervix, Bajaj et al. compared pain descriptors in women who were in labor, had experimental cervical dilation, were undergoing spontaneous abortion, or who had dysmenorrhea ( Table 20.1 ). Women with dysmenorrhea used words that indicate suffering, such as “punishing” and “wretched,” whereas those in labor did not. Some researchers have drawn parallels between the pain derived from mountain climbing, which is associated with a sense of euphoria, and the pain of labor. As noted by one woman, “You mature and become a stronger personality when you’ve had a baby and have gone through the pain. I think that is the purpose of it, what the meaning of life is … to protect our children, to be stronger.” However, other women have found no deeper meaning to the pain of labor or reasons why it should not be treated. Many conditions that involve pain (e.g., trauma, severe dental disease, cancer) are considered a “normal” part of human life without a spiritual meaning, thereby making labor pain unique.

In summary, there are large interindividual differences in how women experience the personal significance or meaning of labor pain. These different perceptions can lead to a long-term sense of failure and guilt when pharmacologic pain relief is accepted or emotional trauma when it is withheld. The use of educational interventions and improved management of labor expectations may improve the birth experience by creating realistic pain expectations during labor and delivery.

Anatomic Basis

First Stage of Labor

Several lines of evidence suggest that the pain experienced during the first stage of labor is transduced by afferents with peripheral terminals in the cervix and lower uterine segment rather than the uterine body, as is often depicted ( Fig. 20.4 ). Uterine body afferents fire in response to distention, but in the absence of inflammation, uterine body distention has no or minimal effect on the behavior of laboratory animals. These observations suggest that uterine body afferents may be an important site of chronic inflammatory disease and chronic pelvic pain but are much less relevant to acute obstetric and uterine cervical pain. In addition, afferents to the uterine body regress during normal pregnancy, whereas those to the cervix and lower uterine segment do not. This denervation of the myometrium may protect against preterm labor by limiting α ₁ -adrenergic receptor stimulation by locally released norepinephrine. Javert and Hardy reproduced the pain of uterine contractions in women during labor by manual distention of the cervix. Bonica and Chadwick later confirmed that women undergoing cesarean delivery under a local anesthetic field block experience pain from cervical distention (which mimics that of labor pain) but do not experience pain from uterine distention.

Uterocervical afferents activated during the first stage of labor. Uterine body afferents (A) partially regress during pregnancy and may contribute to the pain of the first stage of labor. However, the major input is from afferents in the lower uterine segment and endocervix (B). By contrast, at least in animals, the activation of afferents that innervate the vaginal surface of the cervix (C) results in analgesia, not pain, and they enter the spinal cord in sacral areas rather than at the site of referred pain in labor.

The uterine cervix has dual innervation; afferents innervating the endocervix and lower uterine segment have cell bodies in thoracolumbar dorsal root ganglia (DRG), whereas afferents innervating the vaginal surface of the cervix and upper vagina have cell bodies in sacral DRG. These two innervations result in different sensory input and referral of pain. Pelvic afferents that innervate the vaginal surface of the cervix are almost exclusively C fibers, with the majority containing the peptides substance P and calcitonin gene–related peptide (CGRP). These afferents express alpha and beta estrogen receptors and have an innervation pattern that is not affected by pregnancy. Stimulation of the vaginal surface of the cervix in rats results in antinociception, lordosis, ovulation, and a hormonal state of pseudopregnancy, all of which are related to mating behaviors in this species. In rats, these vaginal afferent terminals are activated only during delivery and not during labor, which suggests that they are not relevant to the pain of the first stage of labor. By contrast, dilation of the endocervix in rats results in the activation of afferents entering the lower thoracic spinal cord and nociception rather than antinociception. These afferents, which are mostly or exclusively C fibers, are activated during the first stage of labor, suggesting that they are relevant to pain during this period.

More than 80 years ago, experiments in dogs allowed Cleland to identify T11 to T12 as the segmental level of entry into the spinal cord of afferents that transmit the pain of the first stage of labor. Because dysmenorrhea could be treated through the destruction of the superior or inferior hypogastric plexus, Cleland reasoned that the sensory afferents and sympathetic efferents were likely intermingled; he subsequently demonstrated that the bilateral blockade of the lumbar paravertebral sympathetic chain could produce analgesia during the first stage of labor. First-stage labor pain is transmitted by afferents that have cell bodies in T10 to L1 DRG and pass through the paracervical region, the hypogastric nerve and plexus, and the lumbar sympathetic chain.

Classical teaching states that pain-transmitting C and A-delta nerve fibers enter the spinal cord through the dorsal roots and terminate in a dense network of synapses in the ipsilateral superficial laminae (I and II) of the dorsal horn, with minimal rostrocaudal extension of fibers. Whereas this characterization is true for somatic afferents, visceral C fiber afferents enter the cord primarily—but not exclusively—through the dorsal roots and terminate in a loose network of synapses in the superficial and deep dorsal horn and the ventral horn. These afferents also cross to the contralateral dorsal horn, with extensive rostrocaudal extension of fibers. This anatomic distinction underlies the precise localization of somatic pain and the diffuse localization of visceral pain, which may cross the midline; it may also determine the potency or efficacy of drugs that must reach afferent terminals, such as intrathecal opioids.

Pain-transmitting neurons in the spinal cord dorsal horn send axons to the contralateral ventral spinothalamic tract (stimulating thalamic neurons) with further projections to the somatosensory cortex, where pain is perceived. These spinal neurons also send axons through the spinoreticular and spinomesencephalic tracts to provide signals to the areas of vigilance (locus coeruleus, reticular formation), cardiorespiratory regulation (nucleus tractus solitarius, caudal medulla), and reflex descending inhibition (periaqueductal gray, locus coeruleus and subcoeruleus, nucleus raphe magnus, rostral medial medulla, cerebellum). Thalamic activation from painful stimuli results in the activation not only of the somatosensory cortex but also areas of memory (prefrontal cortex), motor response (M1 motor cortex), and emotional response (insular cortex, anterior cingulate cortex). Supraspinal pain pathways activated by pain of the first stage of labor can be briefly described sequentially, starting with the ascending pathways projecting to the pons and the medulla, thereby activating centers of cardiorespiratory control and descending pathways as well as the thalamus, which in turn sends projections to the anterior cingulate, motor, somatosensory, and limbic regions.

The anatomic basis for pain of the first stage of labor implies that amelioration of pain should occur after blockade of peripheral afferents (by paracervical, paravertebral, lumbar sympathetic, or epidural [T10 to L1 dermatome] block) or after blockade of spinal cord transmission (by intrathecal injection of local anesthetic and/or opioid) ( Fig. 20.5 ). In addition, the widespread distribution of visceral synapses in the spinal cord implies that intrathecally administered drugs (e.g., opioids) must have physicochemical properties that facilitate deep penetration into the cord to reach the terminals responsible for pain transmission.

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