Chronic pain, like other medical comorbidities such as cardiovascular disease and diabetes, is more prevalent in obese patients than in the overall population. One recent study showed close to 40% of obese people suffer from chronic pain, with an increased incidence as body mass index (BMI) increases.¹ A survey of more than 1 million people showed that overweight individuals had approximately 20% more pain compared to normal weight individuals, increasing to 254% more pain in individuals with BMIs greater than 40.²

Acute and chronic pain that develops during pregnancy as well as chronic pain related to gynecologic disorders or within pelvic structures can be challenging to manage in the obese population. As is the case with many other comorbid conditions related to obesity, weight reduction first and foremost can at least help correct some of the metabolic and physical derangements that contribute to pain, if not provide relief of pain symptoms in and of itself.³

Given the high prevalence of chronic pain disorders in obese patients plus the overall increased incidence of new musculoskeletal pain in pregnancy, addressing acute or chronic pain during pregnancy can be challenging in the obese woman. Although there are numerous texts and publications discussing pain and pain management during pregnancy, the focus here is on specific aspects as they relate to the obese pregnant patient.

The interplay between increased mechanical loading, increased inflammation, and a negative psychological state mediates some of the relationships between pain and obesity.⁴ Adipose tissue itself as well as high loading pressures on bones, joints, and muscles, can cause an increase in inflammatory markers that results in pain. Depression can also cause increases in systemic inflammation as well as unhealthy lifestyle choices that can lead to further weight gain. Obesity is associated not only with depression and anxiety but also with pain catastrophizing that can amplify the pain experience and hinder the physical activity required for weight loss due to a fear of causing more pain. As these factors are already an issue in the obese patient, the extent to which they affect the obese pregnant patient, for whom further weight gain, systemic inflammation and labile psychological states are generally inevitable, can be more extreme.

Medication Considerations

In general, it is always better to exhaust all nonpharmacologic means of treatment before prescribing any new medication to the pregnant patient. As polypharmacy may already be an issue given the comorbidities associated with obesity (e.g., hypertension, diabetes, and depression), avoiding additional medications that may have adverse side effect profiles for the mother or that may cross the placenta is always best if possible.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are relatively contraindicated during the third trimester of pregnancy due to their association with decreased fetal urine production, resulting in low amniotic fluid levels and constriction of the ductus arteriosus, both via inhibition of prostaglandin synthesis. This unfortunately removes one of the most effective classes of medications to treat musculoskeletal pain from a clinician’s armamentarium at a stage of pregnancy when pain complaints can be most severe. Indomethacin and ibuprofen are associated with a higher incidence of ductal closure than aspirin.⁵ However, aspirin has platelet-inhibiting properties along with its physiologic effects on the fetus as an NSAID. On top of an increased risk of bleeding in the parturient, aspirin at doses above 80 mg is associated with an increased risk of intracranial hemorrhage in the premature infant and should be avoided if possible.⁶ NSAID use after 34 weeks’ gestation has also been associated with pulmonary hypertension of the newborn.⁷

As a general rule based on the risks mentioned, it is prudent to discontinue any NSAID use at the start of the third trimester and encourage limited use during earlier stages of pregnancy. The use of low-dose aspirin in other obstetric or chronic medical conditions unrelated to musculoskeletal pain poses the least risk of any type of NSAID. However, it should probably still be avoided in the treatment of pain given the overall relative risk of bleeding from platelet dysfunction. Figure 14-1 outlines some of the pharmacokinetics and dosing recommendations for the most commonly prescribed NSAIDs. Although short-term use of NSAIDs may not pose an imminent risk to the fetus, in the absence of liver disease the clinician should consider acetaminophen first as it lacks any of the neonatal side effects of NSAIDs while providing similar analgesia for the mother.

Generally, NSAIDs are the first line of treatment for pain associated with uterine fibroids. Obesity is associated with an increased incidence of uterine fibroids, likely from increased circulating estrogen. Existing fibroids tend to increase in size during pregnancy due to even higher levels of circulating estrogen, leading to a concomitant increase in pelvic pain. However, aside from short courses (24–48 hours) before the third trimester, NSAIDs should again be avoided to address this pain syndrome during pregnancy if possible.

Because they lack the physiologic side effects of NSAIDs, opioid analgesics can be a good alternative to address acute pain exacerbations during pregnancy. They should always be utilized sparingly as chronic use can lead to maternal as well as neonatal dependence, with abrupt stoppage precipitating withdrawal-type symptoms, such as fetal tachycardia, which can be life threatening in the later stages of pregnancy.

Aside from these risks, the choice to address acute pain with opioids in the obese patient should be carefully weighed against the risks posed by the inherent sedating side effects, especially given the increased incidence of obstructive sleep apnea (OSA) in these patients. The transient hypoxic episodes that accompany this condition can result in decreased placental blood flow and over time affect fetal growth and development. Opioids can further depress the respiratory drive that forces obese patients with OSA to breathe during apneic episodes and therefore worsen the amount and duration of hypoxia.

Given the fact that there is an increased incidence of type 2 diabetes mellitus in obese women compared to the general population, any preexisting diabetic neuropathy in an obese woman can potentially be worsened by the increased insulin resistance that occurs during pregnancy itself. In a prospective multicenter study of more than 16,000 patients, a BMI of 30–39.9 was associated with an increased risk of gestational diabetes mellitus and fetal macrosomia when compared with a BMI of less than 30.⁸ Patients with diabetic neuropathy are often treated with a combination of medications, which may include anticonvulsants or, more recently, antidepressants. The use of selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors has increased overall not only in the treatment of depression but also in the management of chronic migraine headaches and as adjuvant therapy in the management of chronic pain, including painful diabetic neuropathy. With the incidence of depression and chronic pain higher in the obese population overall, one can expect the use of these medications to be increased as well.

Most anticonvulsants and antidepressants fall under Food and Drug Administration categories C and D, meaning their use needs to be critically evaluated to address the risks of teratogenicity versus therapeutic benefit. Despite these medications being profoundly beneficial in certain chronic pain conditions, it is probably best to address pain syndromes and symptoms with therapies that pose less theoretical risk to the fetus. In conditions where the medications are being used to primarily treat seizure disorders or depression, discussion concerning discontinuation is best left to a patient’s treating neurologist or psychiatrist.

Musculoskeletal Pain Considerations

Musculoskeletal changes during pregnancy that can lead to chronic pain conditions include an increase in lumbar lordosis and neck flexion with decreased shoulder height, all to compensate for the gradually enlarging gravid uterus. These are all changes that occur to some extent in the obese woman depending on the amount of abdominal adiposity present prior to pregnancy. The twofold (or more) increase in force that presses down on joints and muscles in the obese woman can be amplified many times during pregnancy in this context.⁹

Although the hormone relaxin is known to contribute to myometrial relaxation and pubic diastasis (which can itself be a source of pain), increased levels do not correlate with laxity in other joints. However, joint pain and laxity are associated with increased levels of estradiol and progesterone.¹⁰

Obesity is not a purported risk factor for pubic diastasis in pregnancy. However, fetal macrosomia is a risk factor, which itself is associated with obesity.¹¹ Weight bearing alone can exacerbate pain from pubic diastasis in the postpartum period, and although the pelvis usually returns to normal in 4–12 weeks, the inactivity that it promotes can further contribute to weight gain in the obese postpartum patient.

Obesity itself has been shown to be an independent risk factor for osteoarthritis of the knee.¹² The joint laxity that occurs during pregnancy can affect the ligaments of the knee, which, already under stress from chronic loading pressures, experiences larger loading pressures as pregnancy progresses at the same time joint support decreases. Any underlying arthritis will inevitably worsen in this context.

The increased risk of osteoporosis due to elevated circulating estrogen levels in the obese woman can contribute to chronic hip and knee pain that can worsen during pregnancy. More worrisome is the risk of developing osteonecrosis of the hip as glucocorticoid levels and loading pressures further increase during pregnancy.¹³ Although this is rare, the risk is greater in the obese pregnant patient and can manifest as a progressive worsening of hip pain radiating to the groin that may be associated with dislocation or fracture of the femoral head.