The polypeptide relaxin, which is secreted by the corpus luteum to promote joint laxity in late pregnancy, has been associated with low back pain and pelvic pain of pregnancy; it has also been suggested as a possible contributing cause of CES during pregnancy.8,9 Additionally, increased lumbar lordosis with positional and postural stress may cause direct pressure by the gravid uterus on nerve roots. The great vessels may also be compressed by the uterus, resulting in ischemia of the neural element and back pain that radiates to the legs.10 Many cases of lumbar disk prolapse occur during the first and second trimesters. The most clinically incapacitated patients have been found to have the highest levels of relaxin.9
The Diagnosis
Early diagnosis of CES, through proper physical examination and radiologic studies, is paramount. A rectal examination should be performed to assess for sphincter tone (which may be diminished in 80% of patients) and to assess for perineal sensation.5 Catheterization yielding a postvoid residual urine greater than 100/200 cc is reported to have a specificity and sensitivity of 90% or greater for CES. Small et al5 recommend a straight leg raise maneuver to assess for radiculopathy.
Various studies in the literature support the use of MRI in the gravid patient to confirm the diagnosis of CES and to identify the degree and level of disk protrusion.2-4,11
Treatment
CES requires urgent surgical decompression.11 Early recognition of CES attributable to lumbar disk prolapse, report O’Laoire et al,12 is essential to prevent irreversible sphincter paralysis. They liken the condition’s urgency to that of extradural hematoma in a head injury.
Disk surgery during pregnancy—preferably a team effort, with obstetrics performing perioperative fetal monitoring—has been deemed a safe management method.2,4 Spinal or general anesthesia during nonobstetric surgery is generally considered safe for both mother and fetus.13,14 Adequate oxygenation without risk for hyperventilation is considered essential.15
PATIENT OUTCOME
In the immediate postoperative period, the patient continued to complain of RLE pain, which abated significantly by the time she was discharged. When she was seen in follow-up four days later, she was able to heel- and toe-walk on the right side, and her strength had improved to 3 or 4 out of 5 at the RLE. She continued to experience diminished sensation to the plantar aspect of the right foot, which persisted at the one-month follow up. At that visit, the patient also reported occasional pain in the right buttock. Physical therapy was started to strengthen the RLE.
By three months postsurgery, the patient had undergone uneventful vaginal delivery. She had an entirely benign exam with 5 out of 5 strength at the RLE and no neurologic deficits. She was cleared to return to light weightlifting with good technique and lumbar support but was told to refrain from running until the sixth month postsurgery.
CONCLUSION
Although the case patient did not have a “true” (ie, typical) presentation of CES, her symptoms warranted a full workup and treatment to prevent possible long-term sequelae. Medical practitioners should be familiar with the triad presentation of CES. They must differentiate lower back pain of muscular origin from lumbar disk herniation and be able to appreciate the degree of symptom severity reported by the gravid patient. A thorough history and physical assessment must be performed in every such case. When in doubt, the clinician must err on the side of caution, referring the patient for MRI and consulting with a specialist.
REFERENCES
1. Johnston RA. The management of acute spinal cord compression. J Neurol Neurosurg Psychiatr. 1993;56(10):1046-1054.
2. Brown MD, Levi AD. Surgery for lumbar disc herniation during pregnancy. Spine (Phila PA 1976). 2001;26(5):440-443.
3. LaBan MM, Perrin JCS, Latimer FR. Pregnancy and the herniated lumbar disc. Arch Phys Med Rehabil. 1983;64(7):319-321.
4. LaBan MM, Rapp NS, Van Oeyen P, Meerschaert JR. The lumbar herniated disk of pregnancy: a report of six cases identified by magnetic resonance imaging. Arch Phys Med Rehabil. 1995;76(5):476-479.
5. Small SA, Perron AD, Brady WJ. Orthopedic pitfalls: cauda equina syndrome. Am J Emerg Med. 2005;23(2):159-163.
6. Tay EC, Chacha PB. Midline prolapse of a lumbar intervertebral disc with compression of the cauda equina. J Bone Joint Surg. 1979;61(1):43-46.
7. Kostuik JP, Harrington I, Alexander D, et al. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am. 1986;68(3):386-391.
8. Russell R, Reynolds F. Back pain, pregnancy, and childbirth. BMJ. 1997;314(7087):1062-1063.
9. MacLennan AH, Nicholson R, Green RC, Bath M. Serum relaxin and pelvic pain of pregnancy. Lancet. 1986;2(8501):243-245.
10. Ashkan K, Casey AT, Powell M, Crockard HA. Back pain during pregnancy and after childbirth: an unusual cause not to miss. J R Soc Med. 1998;91(2):88-90.