Introduction

The physiology of pregnancy is complex and poses several challenges to physicians who are caring for the musculoskeletal health of pregnant women. Fluid changes, hormonal fluctuations, and increased weight gain all stress the muscular system and predispose patients to a plethora of orthopedic issues. One of the most common pregnancy-related ailments is carpal tunnel syndrome (CTS).

In the general population, the prevalence of CTS ranges from 0.7% to 9.2% among women and 0.4% to 2.1% among men. These patients typically present with numbness in the median nerve distribution of the hand, wrist pain, nocturnal awakenings, decreased 2-point discrimination, and, in later stages, thenar muscle atrophy and weakness. In pregnant patients, CTS presents similarly. Most pregnant patients present with bilateral symptoms and most commonly in their third trimester, yet patients can present as early as the first few months of pregnancy and with unilateral symptoms. The incidence of CTS in pregnancy has been reported to be as high as 62%; however, it varies widely in the literature. For instance, the incidence of clinically diagnosed pregnancy-related CTS ranges from 31% to 62%, whereas the incidence of electrodiagnostically confirmed pregnancy-related CTS ranges from 7% to 43%. Variations in study designs, specifically diagnostic criteria and methods, account for this wide distribution of incidence in the literature, and thus, the true incidence of pregnancy-related CTS is still unknown.

Cause of pregnancy-related carpal tunnel syndrome

Term pregnancy consists of 37 to 42 weeks of hormonal fluctuations, intravascular and extravascular fluid shifts, and musculoskeletal changes. Maternal blood volume may increase as much as 30% to 50% with a single pregnancy and up to 100% with twins or triplets. The increased blood volume is a result of increases in both plasma and erythrocyte volume at a ratio of 2:1, yielding a dilutional anemia. Increased metabolism, increased heart rate, and increased stroke volume are coupled with a decrease in peripheral vascular resistance, and therefore the mean systemic blood pressure often is unchanged. Hormonal changes, such as increased levels of progesterone, rennin, and angiotensin, contribute to fluid retention, and this weight gain, coupled with the growth of the developing fetus, significantly taxes the musculoskeletal system. For instance, greater than 70% of pregnant women report back pain during the course of their pregnancy, making it the number one musculoskeletal condition in the peripartum period. The next most common musculoskeletal condition is CTS.

The true cause of pregnancy-related CTS is unknown. It is thought to be multifactorial, with median nerve compression resulting as a consequence of normal physiologic changes of pregnancy. Increased fluid volume, uterine pressure on the inferior vena cava, progesterone-mediated hyperemia, and fluid retention lead to generalized edema during pregnancy. Swelling in the carpal tunnel can cause compression of the median nerve. Specifically, pregnant patients with hand swelling that prevents them from wearing their rings have an increased incidence of carpal tunnel symptoms. In addition, patients who have gestational hypertension and preeclampsia have a higher incidence of CTS. Although there is a strong correlation of generalized increased volume load (generalized edema) and development of CTS, there is little evidence to support a direct correlation between weight gain during pregnancy and CTS.

It has also been shown that patients nursing their infants postpartum have increased development of CTS. These patients often have symptom relief with cessation of nursing. However, the cause of this phenomenon is unknown. CTS related to nursing may be secondary to new repetitive hand positions, but it could also be the result of residual fluid and hormonal changes associated with pregnancy. Lactating patients who develop CTS tend not to have preeclampsia or generalized edema during pregnancy. These patients also have a slower time course to symptom resolution, compared with resolution of carpal tunnel symptoms that begin during pregnancy. The literature has not addressed the causation between median nerve compression and lactation, yet a relationship has been well observed.

There is a known association between altered glucose metabolism, such as that in diabetes, and the development of CTS. Impaired fasting glucose levels and increased insulin resistance are independent risk factors for the development of CTS and, more specifically, for the development of bilateral disease. Pregnant women undergo alterations in glucose metabolism, including increased fasting insulin levels, increased hepatic glucose production, and decreased insulin sensitivity, to compensate for the increased metabolic demands of the mother and fetus. These endocrine adaptations of pregnancy would be expected to contribute to the development of CTS via a similar mechanism as that in diabetic patients. However, diabetes has not been proved to be a risk factor for the development of pregnancy-related CTS.

Finally, pregnancy may predispose women to nerve hypersensitivity. A study in dogs from Japan has shown that pregnant dogs have abnormal nerve susceptibility to pressure. In humans, a recent study evaluated 2 groups of age-matched women (1 group of pregnant women and 1 group of nonpregnant women) with the use of electrodiagnostic testing. Neither group had any hand symptoms or any clinical indication of median nerve pathologic conditions. However, on electrodiagnostic testing, 11% of the asymptomatic pregnant women had median nerve impairment compared with the asymptomatic nonpregnant group, implying a subclinical median neuropathy associated with pregnancy. Of note, 4 of the asymptomatic pregnant patients with subclinical median nerve compression developed symptoms of CTS later in their pregnancy. Perhaps the hormonal changes and increased volume of pregnancy provide a double-hit phenomenon on an overly susceptible median nerve. Can an increase in the volume within the carpal tunnel that would otherwise be insignificant cause the compression of a hypersensitive nerve?

Evaluation of the pregnant patient

Evaluating the pregnant patient with CTS is no different than evaluating any new patient presenting with hand paraesthesias. A thorough history and physical examination are warranted. The history should elucidate the duration, quality, and consistency of symptoms. Specifically, it is necessary to understand the distribution of the numbness and whether the symptoms are constant or intermittent. For pregnant patients, it is imperative to also inquire about gestational age, weight gain, nulliparity, excessive edema, previous pregnancy-related CTS, and any current complications of pregnancy, such as preeclampsia and/or gestational (pregnancy-induced) hypertension.

The classic presentation of CTS is numbness and pain in the palmar thumb, index finger, long finger, and radial half of the ring finger. Patients may complain of aching in the thenar eminence, weakness in thumb opposition, and thenar atrophy. Difficulties with activities such as buttoning shirts, writing, combing hair, and driving a car are common complaints. Symptoms are frequently exacerbated by repetitive hand motion and/or sleep. Furthermore, greater than 50% of pregnant patients report symptom exacerbation during the night. Compared with patients with idiopathic CTS, pregnant patients with CTS report significantly more pain and numbness.

When obtaining the history, it is important to discern the onset of symptoms. Pregnant patients presenting in their first 2 trimesters characteristically have more acute, rapidly progressing symptoms for which conservative treatment often fails. Electrodiagnostic testing of these patients can confirm acute median nerve lesions with motor and/or sensory conduction blocks at the wrist that may ultimately require surgical intervention. Seror described one patient who developed the rapid onset of conduction delays only 5 days after the onset of her symptoms. In contrast, when CTS occurs during the third trimester, it often has a slower onset of symptoms that frequently responds well to conservative treatment and usually resolves postdelivery.

During the physical examination, detailed attention should focus on sensory deficits, 2-point discrimination, muscle strength, and thenar atrophy. Provocative examination maneuvers that are useful in the diagnosis of CTS include Phalen’s test, reverse Phalen’s test, Tinel’s test, and Durkin’s compression test. The onset of numbness and tingling in the distribution of the median nerve during any of these maneuvers is a positive test. These maneuvers aid in making a clinical diagnosis but none have 100% sensitivity. For example, the sensitivity for Tinel’s test ranges from 45% to 75%, and that for Phalen’s test ranges from 49% to 89%. More recently, Cheng and colleagues reported a new provocative test called the scratch collapse test. It involves the clinician lightly scratching over the median nerve while the patient performs resisted shoulder external rotation. The test is positive if the patient demonstrates momentary loss of external resistance after scratching over the median nerve. This test is unique in that it does not rely on subjective patient response, like the other provocative tests described. It has been found to have 64% sensitivity in diagnosing CTS and a higher negative predictive value compared with Tinel’s and Phalen’s tests.

Cause of pregnancy-related carpal tunnel syndrome

Term pregnancy consists of 37 to 42 weeks of hormonal fluctuations, intravascular and extravascular fluid shifts, and musculoskeletal changes. Maternal blood volume may increase as much as 30% to 50% with a single pregnancy and up to 100% with twins or triplets. The increased blood volume is a result of increases in both plasma and erythrocyte volume at a ratio of 2:1, yielding a dilutional anemia. Increased metabolism, increased heart rate, and increased stroke volume are coupled with a decrease in peripheral vascular resistance, and therefore the mean systemic blood pressure often is unchanged. Hormonal changes, such as increased levels of progesterone, rennin, and angiotensin, contribute to fluid retention, and this weight gain, coupled with the growth of the developing fetus, significantly taxes the musculoskeletal system. For instance, greater than 70% of pregnant women report back pain during the course of their pregnancy, making it the number one musculoskeletal condition in the peripartum period. The next most common musculoskeletal condition is CTS.

The true cause of pregnancy-related CTS is unknown. It is thought to be multifactorial, with median nerve compression resulting as a consequence of normal physiologic changes of pregnancy. Increased fluid volume, uterine pressure on the inferior vena cava, progesterone-mediated hyperemia, and fluid retention lead to generalized edema during pregnancy. Swelling in the carpal tunnel can cause compression of the median nerve. Specifically, pregnant patients with hand swelling that prevents them from wearing their rings have an increased incidence of carpal tunnel symptoms. In addition, patients who have gestational hypertension and preeclampsia have a higher incidence of CTS. Although there is a strong correlation of generalized increased volume load (generalized edema) and development of CTS, there is little evidence to support a direct correlation between weight gain during pregnancy and CTS.

It has also been shown that patients nursing their infants postpartum have increased development of CTS. These patients often have symptom relief with cessation of nursing. However, the cause of this phenomenon is unknown. CTS related to nursing may be secondary to new repetitive hand positions, but it could also be the result of residual fluid and hormonal changes associated with pregnancy. Lactating patients who develop CTS tend not to have preeclampsia or generalized edema during pregnancy. These patients also have a slower time course to symptom resolution, compared with resolution of carpal tunnel symptoms that begin during pregnancy. The literature has not addressed the causation between median nerve compression and lactation, yet a relationship has been well observed.

There is a known association between altered glucose metabolism, such as that in diabetes, and the development of CTS. Impaired fasting glucose levels and increased insulin resistance are independent risk factors for the development of CTS and, more specifically, for the development of bilateral disease. Pregnant women undergo alterations in glucose metabolism, including increased fasting insulin levels, increased hepatic glucose production, and decreased insulin sensitivity, to compensate for the increased metabolic demands of the mother and fetus. These endocrine adaptations of pregnancy would be expected to contribute to the development of CTS via a similar mechanism as that in diabetic patients. However, diabetes has not been proved to be a risk factor for the development of pregnancy-related CTS.

Finally, pregnancy may predispose women to nerve hypersensitivity. A study in dogs from Japan has shown that pregnant dogs have abnormal nerve susceptibility to pressure. In humans, a recent study evaluated 2 groups of age-matched women (1 group of pregnant women and 1 group of nonpregnant women) with the use of electrodiagnostic testing. Neither group had any hand symptoms or any clinical indication of median nerve pathologic conditions. However, on electrodiagnostic testing, 11% of the asymptomatic pregnant women had median nerve impairment compared with the asymptomatic nonpregnant group, implying a subclinical median neuropathy associated with pregnancy. Of note, 4 of the asymptomatic pregnant patients with subclinical median nerve compression developed symptoms of CTS later in their pregnancy. Perhaps the hormonal changes and increased volume of pregnancy provide a double-hit phenomenon on an overly susceptible median nerve. Can an increase in the volume within the carpal tunnel that would otherwise be insignificant cause the compression of a hypersensitive nerve?