Carpal Tunnel Syndrome in Emergency Medicine

Conservative management

Reported prognosis is widely variable for patients managed conservatively.  A systematic review showed that at 3 years, between 1/4 and 2/3 of patients were shown to have a negative outcome (defined as ongoing symptoms, progression of symptoms, or requiring surgery)[17] .

Factors associated with failed nonsurgical management include[15] :

• Higher initial scores on the Boston Carpal Tunnel Questionnaire (CTQ)-symptom severity scale that do not improve
• Duration of symptoms greater than or equal to 1 year
• Positive Phalen test
• Greater intensity of nighttime symptoms
• Thenar atrophy
• More than 1 prior failed nonsurgical intervention. 

Surgical management

Regardless of severity, most patients will experience significant symptom improvement within three months of surgery[18] .

For patients with severe disease, based on pre-operative electrodiagnostic studies, time to resolution of symptoms is longer with up to 19% of patients reporting ongoing symptoms at one year[19] .

CTS during pregnancy seems to be less severe than idiopathic CTS and has milder course with fewer cases requiring surgical treatment.

Risks factors for poorer-than-average prognosis include the following[17] :

• Advanced disease

• Atypical symptoms (normal nerve conduction studies, symptoms in fifth digit)

• Longer symptom duration

• Older age

• Coexisting disease (diabetes, other peripheral neuropathy)

• Heavy manual occupation

• Thenar wasting

• Positive Phalen's test

Patients typically complain of an intermittent "pins-and-needles" paresthesia in the median nerve distribution of the hand. Pain is generally worse at night than during the day. Patients may awaken with a burning pain or tingling that may be relieved with shaking their hands. Classic carpal tunnel syndrome (CTS) is associated with symptoms that affect at least 2 of the first through third digits; symptoms affecting the fourth and fifth digits, wrist pain, and radiation of pain proximal to the wrist may also occur, but classic CTS is not associated with symptoms on the palm or dorsum of the hand.[13]

Symptoms of probable CTS are the same as classic CTS except palmar symptoms may be present, unless confined solely to the ulnar aspect. Possible CTS involves symptoms in at least one of the first 3 digits. The sensitivity of classic or probable CTS symptoms for diagnosing CTS is 80%. CTS is unlikely if no symptoms are present in any of the first 3 digits.[13]

Symptoms are most often bilateral, insidious in onset, and progressive in nature. With advanced nerve compression, an aching sensation is persistent and static and may radiate to the forearm and elbow. Enquire with regard to repetitive strain risk, such as waitperson, assembly packing, computer keyboard work, playing a musical instrument, or craftwork. Determine if any significant trauma has occurred. The presence of symptoms in the ring and small finger may be much more common than previously thought.[20]

Weakness of resisted thumb abduction (ie, movement of the thumb at right angles to the palm) is helpful in determining which patients will have an electrodiagnosis of CTS.[21]

Sensory hypalgesia as demonstrated by diminished ability to perceive painful stimuli applied along the palmar aspect of the index finger when compared with the ipsilateral little finger also is associated with the electrodiagnosis of CTS.[21]

Hyperflexion of the wrist for 60 seconds may elicit paresthesia in the median nerve distribution (ie, Phalen sign). A literature review showed the average sensitivity and specificity of the Phalen sign to be 68% and 73%, respectively.[3]

Tapping the volar wrist over the median nerve (ie, Tinel sign) may produce paresthesia in the median distribution of the hand. Pooled data show the sensitivity and specificity of the Tinel sign to be 50% and 77%, respectively.[3]

Shaking or flicking one's hands for relief during maximal symptoms (ie, Flick sign) has been shown to have a sensitivity of 47% and specificity of 62%.[3]

The loss of 2-point discrimination in the median nerve distribution or abductor pollicis brevis atrophy has a high specificity (>90%) but low sensitivity (< 25%).[3]

Causes of carpal tunnel syndrome include the following:

• Inflammation of the flexor tendon sheath caused by activities involving repetitive wrist flexion (eg, assembly packing, computer keyboard work, playing a musical instrument, craftwork)

• Edema from trauma of any type (eg, fractures), which can compress the median nerve

• Compression of the median nerve from pregnancy[22] or oral contraceptive–related edema

• Strong association between being overweight or obese and the presence of CTS

• Acromegaly

• Rheumatoid arthritis

• Gout or pseudogout

• Tuberculosis

• Renal failure and hemodialysis

• Hypothyroidism

• Amyloidosis

• Diabetes mellitus

• Chemotherapy for breast cancer (anastrozole)[23]

The diagnosis of carpal tunnel syndrome in the ED is made presumptively. The clinician who follows the patient after the acute presentation usually orders the imaging studies and other tests discussed below. Plain radiography is low-yield.[24]

Magnetic resonance imaging (MRI) is reasonably accurate in diagnosing CTS. This imaging modality is only recommended when the clinical picture is confusing or when nerve conduction studies are equivocal or contradictory. Dynamic MRI imaging may be useful in identifying dynamic CTS (CTS symptoms brought on only by repetitive wrist motion).[25] MRI may also identify causative lesions in carpal tunnel.[26]

(See the images below.)

Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with fat saturation. Note the increased T2-weighted signal within the median nerve (arrow). A slightly increased cross sectional area of the nerve is noted but the nerve architecture is preserved, consistent with early or mild inflammation.

Carpal tunnel syndrome. Fast spin-echo T2-weighted MRI illustrates more pronounced increased signal within the median nerve (arrow). Note the small amount of fluid within the carpal tunnel, a secondary sign of inflammation. Slightly less optimal fat saturation is noted than on other images, which is a common occurrence.

Carpal tunnel syndrome. Axial fast spin-echo T2-weighted MRI with greater increase in signal and loss of definition within the nerve (arrow). Inflammatory change is noted within the carpal tunnel, adjacent to the flexor digitorum superficialis tendons. The appearance is consistent with pronounced inflammatory change within the carpal tunnel.

Carpal tunnel syndrome. Normal findings of isointense-to-hypointense appearance of the median nerve on fast spin-echo T2-weighted MRI (arrow). Note the fairly well-defined nerve fascicles within the median nerve sheath.

Carpal tunnel syndrome. Normal findings on an axial spin-echo T1 MRI of the carpal tunnel showing the intermediate signal intensity of the median nerve (arrow).

High-resolution ultrasonography (US) has received increased attention in the evaluation of CTS. US as a modality is more widely available than electrodiagnostic studies and is noninvasive and has lower costs. Some studies have shown that patients with CTS have an increased cross-sectional area of the median nerve in the carpal tunnel. One study showed that both the cross-sectional area of the median nerve in the wrist (CSA-M) and of the ratio of the area of the median nerve between the wrist and the forearm (R-WF) were useful measures in the diagnosis of CTS, using electroneuromyography (ENG) as a reference test.[27]

Superb microvascular imaging (SMI) is a new imaging mode to detect blood flow. When compared with conventional color Doppler and power Doppler, the sensitivity and finer detail of the microvessels visualized with SMI appears significantly better.  In one series, SMI provided improved results for the evaluation of the blood flow in the MN compared to color Doppler ultrasonography (CDUS) and power Doppler ultrasonography (PDUS).[28]

There has been recent recognition of the diagnostic accuracy of ultrasound approaching that of nerve conduction studies[29] . Ultrasound has now been proposed as the initial diagnostic modality due to the added benefit of increased acceptability to patients, decreased cost, and the ability to assess carpal tunnel anatomy and guide corticosteroid injections.[30]

Electromyographic (EMG) and nerve conduction studies

EMG and nerve conduction studies help confirm the diagnosis of CTS. They are most helpful in the determination of the site and severity of nerve compression.

Nerve conduction studies show a high specificity (95%) with a wide range of sensitivity depending on the choice of cutoff values (75-92%).  Due to this high specificity, nerve conduction studies are recommended prior to considering surgical intervention[14] .

Clinically symptomatic CTS may have normal nerve conduction findings.[31]

In the emergency department setting, the mainstay of treatment for carpal tunnel syndrome (CTS) is rest, wrist immobilization with a splint, and nonsteroidal anti-inflammatory drugs (NSAIDs). For some individuals with CTS, nonsurgical management is curative; however, more than 50% of patients undergoing nonsurgical management progress to surgery within 1 year.[15]

A volar splint should be placed in neutral position because flexion and extension of the wrist increases carpal intracanal pressure. Splinting has been shown to have a statistically significant decrease in symptoms compared with controls. Studies comparing nocturnal-only splinting to full-time splinting have not revealed a clear difference, although the studies may have been underpowered.[32, 33, 34]

No data support that NSAIDs are superior to placebo in the treatment of CTS.[33] However, in the absence of contraindications, a trial of NSAIDs may be appropriate.

Oral steroids have been shown to have an advantage in treating CTS over placebo. The benefit appears short-lived, and the studies do not assess the long-term effectiveness or complications of oral steroids used in treating CTS.[32, 33]

Although not typically performed in the emergency department, corticosteroid injections have been shown to have a statistically significant benefit in CTS at 1 month compared with placebo. The effects of corticosteroid injection appear to be time limited, and the benefit beyond 1 month is unclear. Two steroid injections do not appear to add significant clinical benefit to one injection.[35, 36] Local injections have been shown to be superior to systemic corticosteroids.[32] Steroid injection combined with splinting has been shown to be superior to splinting alone.[37]  Single corticosteroid injection has been shown to be superior to night splinting at 6 months.[38]  Ultrasound-guided injections have been shown to be more effective than blind injections.[39]

Diuretics have not been shown to be superior to placebo in the treatment of CTS.[33]

Ultrasound has been proposed as a treatment for carpal tunnel syndrome, though evidence is conflicting. A recent randomized controlled trial showed no benefit for therapeutic ultrasound, while a systematic review of extracorporeal shockwave therapy showed improvement in symptoms, function, and electrodiagnostic study results when to corticosteroid injection.[40, 41] Evidence is limited for newer modalities such as manual techniques, transcutaneous electrical nerve stimulation (TENS), and laser therapy[42] .

Surgery

Definitive therapy consists of surgical release of the transverse carpal ligament. Surgery for CTS has a long-term success rate of greater than 75%. The surgical approach may be open or endoscopic.[43]  A randomized, controlled trial showed that patients who underwent endoscopic surgery for carpal tunnel syndrome had less postoperative pain than patients who underwent open surgery; however, the difference was small.[44] The authors of this study extended the follow-up period to 5 years, and it demonstrated an equivalent improvement in CTS symptoms between an open and an endoscopic carpal tunnel release. An article in the Cochrane Database of Systematic Reviews states that endoscopic surgery allows an earlier return to work and fewer wound problems, but possible disadvantages may be higher complication rates and cost.[33, 34, 35, 45, 46]

American Academy of Orthopaedic Surgeons Guidelines

The AAOS has published guidelines on diagnosis and treatment of carpal tunnel syndrome, including the following[16] :

• Thenar atrophy is strongly associated with ruling in CTS but is poorly associated with ruling it out
• Do not use the Phalen test, Tinel sign, flick sign, or upper limb neurodynamic/nerve tension test (ULNT) criterion A/B as independent physical examination maneuvers to diagnose CTS, because alone, each has a poor or weak association with ruling in or ruling out the condition
• Do not use the following as independent physical examination maneuvers to diagnose CTS, because alone, each has a poor or weak association with ruling in or ruling out the condition: carpal compression test, reverse Phalen test, thenar weakness or thumb abduction weakness or abductor pollicis brevis manual muscle testing, two-point discrimination, Semmes-Weinstein monofilament test, CTS-relief maneuver, pin prick sensory deficit (thumb or index or middle finger), ULNT criterion C, tethered median nerve stress test, vibration perception (tuning fork), scratch collapse test, Luthy sign, and pinwheel
• Do not use the following as independent history interview topics to diagnose CTS, because alone, each has a poor or weak association with ruling in or ruling out the condition: sex/gender, ethnicity, bilateral symptoms, diabetes mellitus, worsening symptoms at night, duration of symptoms, patient localization of symptoms, hand dominance, symptomatic limb, age, and body mass index
• Do not routinely use magnetic resonance imaging (MRI) for the diagnosis of CTS
• Diagnostic questionnaires and/or electrodiagnostic studies can be used to aid the diagnosis of CTS
• The following factors are associated with an increased risk of developing CTS: peri-menopausal, wrist ratio/index, rheumatoid arthritis, psychosocial factors, distal upper extremity tendinopathies, gardening, American Conference of Governmental Industrial Hygienists (ACGIH) hand activity level at or above threshold, assembly line work, computer work, vibration, tendonitis, workplace forceful grip/exertion
• Physical activity/exercise is associated with a decreased risk of developing CTS
• The use of oral contraception and female hormone replacement therapy are not associated with increased or decreased risk of developing CTS
• The use of immobilization (brace/splint/orthosis) should improve patient reported outcomes
• The use of steroid (methylprednisolone) injection should improve patient reported outcomes
• Magnet therapy should not be used for the treatment of CTS
• There is no benefit to oral CTS treatments (diuretic, gabapentin, astaxanthin capsules, nonsteroidal anti-inflammatory drugs [NSAIDs], or pyridoxine) over placebo
• Oral steroids could improve patient reported outcomes in comparison with placebo
• Ketoprofen phonophoresis could provide reduction in pain in comparison with placebo
• The surgical release of the transverse carpal ligament should relieve CTS symptoms and improve function
• Surgical treatment of CTS should have a greater therapeutic benefit at 6 and 12 months in comparison with splinting, NSAIDs/therapy, and a single steroid injection
• There is no benefit to routine postoperative immobilization after carpal tunnel release
• There is no benefit to routine inclusion of the following adjunctive techniques: epineurotomy, neurolysis, flexor tenosynovectomy, and lengthening/reconstruction of the flexor retinaculum (transverse carpal ligament)
• Buffered lidocaine rather than plain lidocaine should be used for local anesthesia because buffered lidocaine could result in less injection pain
• There is no additional benefit to routine supervised therapy over home programs in the immediate postoperative period; no evidence meeting the inclusion criteria was found comparing the potential benefit of exercise versus no exercise after surgery

The goal of therapy is to reduce inflammation and prevent complications.

Class Summary

Most commonly are used for the relief of mild-to-moderate pain. Although the effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen usually is the DOC for the initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.

Flurbiprofen

May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Ketoprofen (Active-Ketoprofen)

For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.

Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Ibuprofen (I-prin, Advil, Motrin, Caldolor)

Usually the DOC for the treatment of mild-to-moderate pain if no contraindications exist.

Inhibits inflammatory reactions and pain, probably by decreasing the activity of cyclooxygenase enzyme, which results in the inhibition of prostaglandin synthesis.

Taking medication with at least 4 oz of water may minimize adverse effects.

Naproxen (Anaprox, Naprelan, Naprosyn, Aleve, Mediproxen)

Used for the relief of mild-to-moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase enzyme, which results in a decrease of prostaglandin synthesis. Inexpensive and effective.

Meloxicam (Mobic, Vivlodex)

Meloxicam decreases COX activity, and this, in turn, inhibits prostaglandin synthesis. These effects decrease the formation of inflammatory mediators.