A 56-year-old right hand dominant woman presents with a chief complaint of numbness and tingling in the right thumb index and long finger. It is worse at night, worse with holding a book or newspaper, and she describes nocturnal awakenings. She describes a positive “Flick maneuver”, or needing to “shake the hand” to wake it up. She has tried splints at night with some but not complete benefit. Her symptoms have been bothersome to her for approximately 2 years, but have gotten worse, particularly over the past 6 months. She had a prior corticosteroid injection 5 months ago that gave her complete relief for 3 months, but her symptoms have recurred and she desires further treatment options.
Her medical history is remarkable for hypothyroidism for which she takes replacement. It is otherwise unremarkable. She is a homemaker and is a nonsmoker.
On examination, her cervical spine motion is full flexion, extension, lateral rotation and bending. She has a negative Spurling’s maneuver. Her wrist and elbow motion are symmetric and unrestricted. Her two-point discrimination is 4-5 mm in the median and ulnar nerve distributions, bilaterally. Semmes Weinstein testing is not performed, but vibratory sensibility is diminished in the right median nerve distribution relative to the left median and ulnar distributions and the right ulnar nerve distribution. She has a positive Tinels’ at the carpal tunnel on the right but not left, a positive median nerve compression test, and positive Phalen’s and reverse Phalen’s maneuvers. There is no intrinsic atrophy, specifically no thenar atrophy.
Should nonoperative treatments fail, surgical release may be considered, which consists of open or endoscopic division of the transverse carpal ligament.1
The patient is identified and side and site marked; a time-out is performed.
Typically this procedure is done under local anesthesia; sedation may be considered. Local anesthesia with epinephrine is very helpful for this procedure. The patient is anesthetized by the surgeon in the preoperative holding area with approximately 20 cc of 1% lidocaine with epinephrine 1:100,000 and then brought to the operating room. It is most helpful if at least 30 minutes can elapse between administration of the anesthesia and the surgical procedure to allow for the epinephrine effect to be optimized.2,3
Figure 1. A longitudinal incision is made in line with the radial aspect of the 4th ray over the carpal tunnel.
Figure 2. Dissection proceeds with the scissors to the palmar fascia
Figure 3: The palmar fascia is identified which is sharply incised with a # 15 blade.
A longitudinal incision is made in line with the radial aspect of the fourth ray parallel to the thenar crease or in line with the crease (figure 1). Dissection proceeds with the scissors to the palmar fascia (figure 2) which is sharply incised with a # 15 blade (figure 3). One or two small Heiss retractors are helpful at this point to retract the skin and soft tissue. The transverse fibers of the transverse carpal ligament are identified and sharply incised (figure 4). The distal forearm fascia is released under direct visualization (figure 5). The release is confirmed to be adequate proximally and distally and the carpal canal inspected for any masses, retained lubricals or other anomalies. The wound is then irrigated and closed with 4-0 nylon or 5-0 monocryl sutures. A sterile dressing is applied. There appears to be no value to use a splint postoperatively. Postoperatively, the patient is allowed gentle use of the hand as tolerated and works on digital motion.
Figure 4: The transverse fibers of the transverse carpal ligament are identified and sharply incised.
Figure 5: The distal forearm fascia is released under direct visualization.
Carpal tunnel syndrome (CTS) represents a clinical constellation of symptoms often including numbness or tingling in the median nerve distribution resulting from compressive neuropathy of the median nerve at the wrist. Patients often describe a “Flick maneuver” or needing to dangle or shake the hands to wake them up. Symptoms often are worse at night as patients may sleep in a fetal position with the wrist flexed. Digital flexion or gripping (driving, holding a book) may worsen symptoms. Although popular culture suggests typing as a causative factor, several series suggest this is not etiologically nor epidemiologically linked to this condition. CTS has been linked to age, use, genetic and hormonal factors. Factors that diminish the space available for the median nerve in the carpal canal such as tenosynovitis associated with thyroid disease, diabetes mellitus, renal failure, amyloidosis, gout, or the like; arthritis including basilar thumb arthritis; carpal malalignment or tumors or anomalous muscles.
The reader is suggested to familiarize himself with the American Academy of Orthopaedic Surgeons clinical practice guidelines for treatment recommendations of carpal tunnel syndrome. A course of nonsurgical treatment is an option; alternatively the patient may proceed with surgery when there is evidence of “median nerve denervation or when the patient so elects”. Nonoperative treatment options that are supported by the existing literature include splinting and corticosteroid injections.1
The role of and need for electrodiagnostic studies (EDS) remains a matter of discussion. Although EDS are particularly helpful in the setting of an unclear diagnosis or to determine severity of disease and provide prognostic information, in many cases they are avoided. Moreover, a discrepancy can exist between electrodiagnostic evidence of median neuropathy at the level of the wrist and the clinical syndrome of carpal tunnel syndrome. The two can exist simultaneously; however, it is also possible for EDS evidence of median neuropathy to exist without the syndrome of CTS, and rarely, for CTS to exist without EDS evidence of median neuropathy. In addition, EDS are subject to variability between examiners, and examinations, and can be influenced by temperature, obesity, and patient cooperation. Although the parameters at which one determines an abnormal result differ from lab to lab, most agree that a conduction velocity of < 50 m/s, a median motor latency at the wrist of > 4.5 ms or a sensory study of > 3.5 ms represent abnormalities in the median nerve.3,4,5,6,7
A variety of clinical examination tests are helpful. If wrist range of motion is not symmetric, one might wish to consider radiographs of the wrist. Two-point discrimination (an innervation density test) is often preserved until late in the course of the condition except in the setting of acute median nerve compression, however, it is useful as a gross marker of severity. Vibratory sensibility (which is a threshold test, as is Semmes Weinstein monofilament) is often altered earlier in the course of the condition. Provocative maneuvers include the median nerve compression test, Phalen’s or reverse Phalen’s maneuver. In addition, other conditions should be excluded by assessing for neck pain or altered cervical spine motion and Spurling’s maneuver as well as assessing the ulnar nerve at the elbow and ruling out the rarer pronator syndrome by assessing thumb FPL and index FDP strength and assessing for discomfort over the pronator.8,9,10,11,7
Julie E. Adams, M.D.
University of Minnesota
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