Carpal tunnel syndrome.
Carpal tunnel syndrome is a very common peripheral neuropathy; however, its symptoms are such that they are often overlooked by patients or misdiagnosed by their primary care physicians or nurse practitioners, leading to progression of the condition so severe that sometimes even surgical options will be of little benefit. This article reviews current literature on carpal tunnel syndrome and its signs and symptoms, diagnosis and differential diagnosis, and treatment options.
Carpal tunnel syndrome (CTS) is one of the most common peripheral neuropathies in the world (Andrews & Shpritz, 2004; Atroshi et al., 1999; Greenberg, 2006). Although not a common acute ailment that many neuroscience nurses (surgical or medical) would have to care for, its prevalence within the general population is such that general knowledge of the condition may be useful when considering acute patient care in context of associated comorbidities (with CTS as one of them). The following article reviews current literature on CTS and its related anatomy, signs and symptoms, assessment, diagnosis and differential diagnosis, and treatment options.
Research continues today into CTS in relation to its causes and most appropriate treatments. The risk factors and prevalence continue to be investigated among numerous and varied subgroups within the population considered being a risk. Potential factors that may contribute to CTS can be occupation, age, physical illness, and a number of factors that have been hypothesized (Bahrami, Rayegani, Fereidouni, & Baghbani, 2005; Bongers, Schellevis, van den Bosch, & van der Zee, 2007; Violante et al., 2007). How an appropriate diagnosis is determined (Bland, 2005, 2007; Longstaff, Milner, O'Sullivan, & Fawcett, 2001; Wainner et al., 2005) and its relevant treatment options (Akalin et al., 2002; Baysal et al., 2006; Crawford & Laiou, 2007; Gooch & Mitten, 2005; O'Connor, Marshall, & Massy-Westropp, 2007) also continues to be refined.
The carpal tunnel is a space located posteriorly between the carpal bones of the wrist (moving from fight to left: trapezium, trapezoid, capitate, and hamate), forming the hard "carpal floor," and anteriorly, where the transverse carpal ligament forms a fibrous sheath or the "carpal roof" (see Fig 1). The tunnel itself is filled with the flexor tendons of the hand and the median nerve. The median nerve originates from numerous spinal nerves from C5 to T1. It has both sensory and motor functions of the thumb and first, second, and the lateral aspect of the third digit. Consequently, it is vital for not only grip but also for sensory inputs related to hand function.
Any decrease in the space of carpal tunnel caused by flexion or extension of the wrist, increase in mass within the tunnel, or external forces compressing this space such as edema or inflammation will exert pressure onto the median nerve and potentially elicit CTS symptoms. This pressure can be caused by
1. repetitive use of the wrist through rotation, flexion (found in the automotive or building industries), or extension, particularly in the dominant hand (found in occupations like secretarial or computer work or musicians);
2. trauma to the wrist or hand area resulting in fracture and/or edema;
3. metabolic, inflammatory, and/or infectious processes which may change the associated and surrounding structures of tendons, nerves synovial spaces, or tissue (usually bilateral as a result of systemic condition); an example of metabolic/hormonal changes that may cause CTS is pregnancy;
4. medications that increase edema such as some hormone replacement therapies (estrogens);
5. congenital malformations associated with an abnormally small carpal tunnel space; and
6. idiopathic causes.
[FIGURE 1 OMITTED]
Carpal Tunnel Syndrome
The prevalence of CTS is approximately 3.8% of the general population; women are 3 to 4 times more likely to develop the condition (Burke, Ellis, McKenna, & Bradley, 2003), and it affects both wrists in 50% of cases (Greenberg, 2006). The syndrome itself is evident in patients' symptoms which are directly associated with the digits the median nerve innervates (see Fig 1). If this compression is prolonged, segmental demyelination of the median nerve will occur (Katz & Simmons, 2002), resulting in possible permanent damage to the nerve with a subsequent loss of sensory and motor function in the affected hand.
Signs and Symptoms
The affected individual usually first experiences sensory changes associated with CTS at night, and, if left untreated, the symptoms eventually become continuous. This altered sensation can be in the form of tingling, numbness, or pain (which can be described as sharp, electric shocks or even a burning sensation) affecting areas innervated by the median nerve and proximally as high as the elbow. Weakness in the affected hand is a late sign and is common for those with moderate to severe CTS. The patient usually complains of inability or frustration when it comes to gripping objects because of the related motor deficit.
During assessment, the examiner needs to bear in mind that CTS-like signs and symptoms may result from a number of other disorders including but not limited to
1. cervical radiculopathy,
2. thoracic outlet syndrome,
3. pronator syndrome,
4. direct injury of the median nerve,
5. entrapment of the deep palmar branch of ulnar nerve,
6. peripheral neuropathy, and
7. compartment syndrome of the forearm.
Because there are numerous possibilities for similar symptoms, it is best to perform a thorough upper limb assessment on any patient presenting with CTS-like symptoms.
Diagnosis of CTS requires thorough assessment of the patient. A detailed record of basic demographic data including a patient's age, gender, and occupation as well as a patient's medical past history is a good starting place. Clinical findings from a focused assessment are used in conjunction with neurodiagnostics to support a diagnosis of CTS. This assessment will also indicate the severity of CTS and the most effective treatment options.
Physical examination of the wrist and hand should include assessment of the presence of localized edema or bruising around the wrist, palm, or forearm. This visual assessment of the affected limb (or limbs) may indicate other pathology such as wrist fracture (and related compartment syndrome), localized infection, or any number of metabolic conditions. Atrophy of the muscles of the wrist and forearm should also be assessed, taking particular note of any thenar eminence atrophy (Burke et al., 2003), which is commonly found in severe causes of CTS along with an associated loss of function.
A description of how the altered sensation is perceived by the patient is critical. When assessing sensation, consider the normal dermatomes associated with the affected hand and arm as well as abnormal findings that may indicate other neurology (see Table 1). CTS should only affect the palmar aspect of the hand but can radiate up the arm as high as the elbow (D'Arcy & McGee, 2000). Ask the patient to describe these altered sensations: Does the patient experience pain, tingling, or numbness? Where is the altered sensation located? Does the altered sensation radiate or move elsewhere such as the shoulders or neck (the latter may indicate cervical cord problems)? What is the time of onset? What factors exacerbate or alleviate the symptoms? One common behavior patients may exhibit with CTS is the shaking of their affected hand in a downward "flick-like motion," which allows some relief of their symptoms; this is commonly referred to as the flick sign. The clinician must decide whether the clinical picture is indicative of CTS or some other neurological, neuromuscular, or vascular disorder.
Assessment of sensory perception of light touch and two-point discrimination in the affected fingertips and palmar aspects of the hand controlled by the median nerve as well as the forearm should be performed. This will not only allow the examiner to determine the severity of CTS but also identify whether it is purely a local condition or symptom that may be initiated more proximally such as cervical radiculopathy. Reproduction or exacerbation of symptoms can be elicited in any number of ways.
Compression of the median nerve also affects motor function of the hand. The examiner must evaluate hand motor function, appropriately grade it, and document his or her findings (Table 2). This should be done systematically from shoulder to finger tips (Table 3). First, asking the patient to grip the examiner's hands will assess generalized strength and function of flexion of the hand (C7-T1 nerve roots). The median nerve also serves the abductor pollicis brevis, the opponens pollicis, and the superficial head of the flexor pollicis brevis; involves the muscles to the thumb (Li, Harkness, & Goitz, 2005); and is the most specific motor assessment for CTS. Assessment of thumb strength is performed by instructing the patient to raise his or her thumb perpendicular to the palm as the examiner applies resistance to it; this isolates the strength of the abductor pollicis brevis, which is innervated only by the median (D'Arcy & McGee, 2000). Any decrease in power may be attributed to CTS (Eathorne, 2005).
To complete the clinical neurological assessment of the patient, reflexes should be tested (see Table 4), graded (Table 5), and documented. The significance of reflexes is not to specifically diagnose CTS, but rather it is to rule out other pathology which may present with CTS-like symptoms and complete a thorough upper limb neurological examination.
Interpretation of General Clinical Assessment Findings
Because any diagnosis may have a number of differential possibilities, an understanding of clinical assessment findings is vital for the practitioner to narrow down and sometimes determine the site of the nerve dysfunction. In relation to CTS, its symptoms can be associated with either the distal points of the peripheral nerve itself (radial, median, and ulnar) or those more centrally located in the origin of the nerve roots (C5-T1). These findings are usually described as lower motor neuron (LMN) when signs of peripheral nerve damage are evident or upper motor neuron (UMN) when signs indicate centrally located damage.
UMNs are located within the central nervous system and run from the motor cortex via the corticospinal tract of the brain to the spinal cord. These signs are associated with voluntary movement and inhibitory impulses, which innovate muscle and thus affect tone and reflexes. If damaged, the UMN stops sending voluntary and inhibitory impulses to the peripheral nerves. This causes motor function to rely on LMN to function, and without the inhibitory action of the UMN impulses, dysfunction occurs, as described in Table 6. LMNs are part of peripheral nervous system which send sensory impulses to the UMN and can independently initiate primitive reflex mechanisms. If these are damaged, no nerve impulse can be sent to the UMN or to the muscle.
There are two main provocative tests generally used to isolate the median nerve: Phalen's sign is of use because it is considered a very good indicator for CTS (Katz & Simmons, 2002) with a high sensitivity and specificity (LaJoie et al., 2005; MacDermid & Wessel, 2004) because it localizes the median nerve at the carpal tunnel. This is performed by asking the patient to hold his or her wrist in a flexed position at approximately 90 degrees. The test is considered a positive Phelan's sign (and thus positive to CTS) if numbness or pain is felt by the patient within 30-60 s.
Tinel's sign isolates the median nerve at the carpal tunnel by percussing it at the distal palmar crease. This also should elicit numbness or pain (D'Arcy & McGee, 2000). This is not considered as clinically accurate as the Phalen's sign. Phalen's and Tinel's signs, although they may assist in the diagnosis of CTS (LaJoie et al., 2005), are not pathomnemonic for the disorder.
The vascular assessment consists of evaluating the color, temperature, pulse status, and capillary return of both upper limbs.
Color--adequacy of circulation and perfusion is assessed by pink-colored skin or the absence of pale white, mottled, or black appearance.
Temperature--adequacy of circulation and perfusion is indicated by warm tissue, not cool or cold. Consider the environmental temperature when performing this assessment because high or low ambient temperatures may cause an inaccurate interpretation of actual skin temperature.
Pulse status--adequacy of circulation is indicated by a radial pulse at the wrist.
Capillary refill--assess the limb at the level of the heart. Adequate capillary perfusion is indicated when refill of nail bed or tip of digit is rapid (less than 3 s). Abnormal capillary refill is rated as sluggish or absent.
Finally, the practitioner needs to assess the patient's pain at rest and with movement. Location, quality, and degree of pain need to be determined.
To complete the diagnostic picture, formal diagnostic testing should also be performed. CTS requires the clinician to order nerve conduction studies (NCSs) to rule out other differential or coexisting diagnosis such as cervical radiculopathy and ulnar or radial nerve entrapment. This type of study measures the transmission velocity of an impulse through nerves in response to an electrical stimulus initiated by stimulating and recording electrodes from one point to another (Lindsay, 2004). Any delay in the transmission of impulses when testing the median nerve can determine the severity of CTS. However, if normal velocities (see Table 7) are found and CTS persists despite conservative treatment, further investigations such as magnetic resonance imaging may need to be performed to rule out other diagnoses.
A variety of nonsurgical options are available to treat CTS, including splinting, steroid injection, work place modification, ultrasound, and oral medications. Nonsteroidal anti-inflammatory drugs, diuretics, steroids, and vitamin B12 have been used. A 2004 literature review of nonsurgical management of CTS found that conservative management has a place in mild to moderate CTS and may decrease the number of patients who ultimately undergo surgery (Goodyear-Smith & Arroll, 2004). Ideally, patients who are more likely to respond to conservative treatments are younger than 50 years and have had symptoms less than 6 months (Hayward, Bradley, & Burke, 2002).
Acetaminophen (paracetamol) for pain associated with CTS is usually first-line conservative management. An example of nonpharmaceutical conservative management for CTS is the use of nocturnal wrist splinting. Splints hold the wrist in neutral position, thus preventing compression related to extension or flexion of the wrist while the patient sleeps. It can be very helpful in controlling symptoms of mild to moderate CTS (Burke et al., 2003) and is particularly useful when the patient is awakened by painful paresthesias (Sailer, 1996). Debate continues whether work practices or environment causes CTS. However, its prevalence among certain workers, particularly those considered "blue collar" (roles involving manual labor), does demonstrate a causal link within certain populations (Atroshi et al., 1999; Davis, 2006).
In light of this, it is reasonable to consider that modification of workplace tasks can help alleviate symptoms. Work modifications may include avoidance of repetitive hand and wrist movements or regular breaks and ergonomic assessment of work areas and/or tools (Burke et al., 2003; Hayward et al., 2002).
Another option for relief of CTS is local steroid injection. This is performed just proximal to the carpal tunnel. Although it is considered the most effective nonsurgical treatment, it may possibly lead to complications such as nerve injury, scar, infection, allergic dermatitis, soft tissue atrophy, and tendon rupture (Gooch & Mitten, 2005). Systematic reviews of selected research into conservative measures for CTS (Hayward et al., 2002) and one clinical trial (O'Gradaigh & Merry, 2000) found that local steroid injection for CTS significantly improved symptoms for a period of up to 1 month after treatment. Whether or not injection is the ideal long-term treatment for those patients who have CTS is questionable, and it has been recommended that patients should eventually have decompression surgery (Wilson & Sevier, 2003).
Oral medications such as steroids, diuretics, and nonsteroidal anti-inflammatory drugs have been advocated, but most trials evaluating the effectiveness of these drugs have been small, and outcomes have been restricted to short-term symptomatic improvement and not permanent relief of CTS (Hui et al., 2001; Piazzini et al., 2007). Evidence to support the use of ultrasound treatment of CTS is limited at best and still requires further investigation (O'Connor et al., 2007).
Carpal tunnel release (CTR) surgery is a commonly performed procedure. It should be considered only for those patients with persisting symptoms considered moderate to severe (both on physical assessment and/or with NCS) or once conservative measures have been exhausted. It is a relatively straightforward outpatient procedure, taking only minutes on the operating table, and is essentially a neurolysis of the median nerve. Usually performed under local anesthetic or conscious sedation, the procedure itself involves a transverse incision of about 6 cm (2 inches) on the ulnar side of the interthenar crease (in line with middle finger; Lindsay, 2004) just below the transverse palmar crease and just proximal to the distal wrist flexion crease. Division of the transverse carpal ligament allows for visualization and provides more space for the median nerve, thus alleviating pressure-related symptoms. Another surgical option is endoscopic CTR which does not require an open incision to free up the median nerve; however, there is little evidence to support endoscopic over open CTR (Scholten et al., 2006; Zyluk & Strychar, 2006).
As with any surgical procedure, CTR carries the risk of complications; these are, however, rare and depend on the combined skill and input of all clinicians involved as well as patient adherence with postoperative orders. Intraoperative complications include not only those associated with anesthetic use, such as stroke and death, but also those associated with surgical technique, such as the laceration or complete severing of the superficial palmar arterial arch, flexor tendons, or the median nerve itself if the incision is made too deep and distal to the palmar arch (Russell & Kline, 2006).
Postoperatively, as with any surgery, a risk of infection, hematoma scarring, and/or adhesion exists. There is also a risk of failure to improve immediately postoperatively as a result of causes other than CTS such as cervical radiculopathy of the C5-C7 (double crush syndrome) or incomplete release of the transverse carpal ligament (Greenberg, 2006). Return to normal activities is anywhere from 14 to 56 days depending on nondominant versus dominant hand in open or endoscopic CTR (Work Loss Data Institute, 2006).
Postoperatively, the patient may be assessed again anywhere between 5 and 14 days depending on the surgical technique and procedure used (including method of closure). During this time, the patient is asked to perform passive excises of the hand to lessen scarring which may compromise healing. Any further assessment can be made at this time, as well as planning for other CTR.
Implications for Nursing Care
So how does understanding CTS affect neuroscience nursing practice? The answer depends on the level of understanding required of neuroscience nurses related to their individual scope of practice. A general registered nurse or clinical nurse specialist in an acute care setting, for example, may only require a limited understanding of CTS. CTS most likely would not be the primary diagnosis for admission. More likely, CTS would be a comorbidity of note and should be understood in relation to how it may influence optimal functional outcomes of the patients after their acute care stay.
On the other hand, CTS in the context of nurse practitioners or advanced practice nurses with credentialed extensions of practice may be required to provide not only patient education but also extensive and focused assessment, diagnosis with responsibilities of referral for conservative and invasive treatment options, and in some cases possibly even performance of the operation itself (Newey, Clarke, Green, Kershaw, & Pathak, 2006).
Although a relatively common peripheral entrapment syndrome, the diagnosis, treatment, and considerations of ongoing care for CTS can be complicated by any number of factors. When deciding on treatment or referral options for patients presenting with CTS, their age, length of time and severity of symptoms, NCSs, impact on lifestyle, and work and environment should all be taken into account to determine the most cost effective treatment for each individual patient.
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Questions or comments about this article may be directed to Andrew Scanlon, BN RN, at firstname.lastname@example.org. He is a neurosurgery nurse practitioner (candidate) at the Department of Neurosurgery, Austin Health, and a lecturer in the Faculty of Health Sciences, La Trobe University/Austin Health Clinical School of Nursing, Victoria, Australia.
Jennifer Maffei, BN RN, is an associate nurse unit manager and clinical support nurse at Austin Health, Victoria, Australia.
TABLE 1. Sensory Assessment--Upper Limb Nerve Sensory Radicular Pain Root Distribution Distribution C4 Base of neck and Neck and upper scapula medial shoulder C5 Lateral upper arm Scapula border and lateral upper arm C6 Bicep area, lateral Lateral forearm, thumb, forearm, thumb, and first finger and first finger C7 Posterior forearm Scapula, posterior arm, and middle finger dorsum of forearm, and third finger C8 Ulnar forearm and Shoulder, ulnar forearm, fifth finger and fifth finger T1 Medial upper arm Medial aspect of upper arm TABLE 2. Motor Function Grading Grade Strength 0 No movement 1 Flicker of tendon unit only 2 Full range of movement only when gravity is eliminated 3 Full range of movement against gravity but marked weakness against resistance that cannot be overcome 4 Full range of movement against gravity but weakness with examiner resistance but can be overcome 5 Full range of movement against gravity and examiner resistance TABLE 3. Motor Assessment-Upper Limb Assessment (Against Resistance)# Muscle# Elevate shoulder Rhomboids Shoulder abduction (with elbows Deltoid flexed like chicken wings push up) Elbow flexion (flex elbow) Biceps brachii Elbow extension (extend flexed elbow) Triceps Extension of wrist Extensor carpi Radialis Ulnaris Finger extension (with palms facing Extensor digitorum downwards push up) Finger flexion (squeeze hands) Flexor digtorum Finger abduction First doral interosseuos Finger abduction Second palmar interosseous Thumb adduction push up Abductor pollicis brevis Assessment (Against Resistance)# Nerve# Root# Elevate shoulder Spinal accessory C4, C5# Shoulder abduction (with elbows Axillary C5, C6# flexed like chicken wings push up) Elbow flexion (flex elbow) Musculocutaneous C5#, C6 Elbow extension (extend flexed elbow) Radial C6#, C7, C8# Extension of wrist Medain C6, C7# Ulnar Finger extension (with palms facing Radial C7, C8# downwards push up) Finger flexion (squeeze hands) Median C8 Finger abduction Ulnar Finger abduction Ulnar T1# Thumb adduction push up Median C8#, T1 Note. Bold typeface indicates primary nerve root. Note: Bold typeface indicates primary nerve root is indicated with #. TABLE 4. Reflex Assessment--Upper limb Assessment# Nerve# (Relax Limb)# Reflex# Root# Place finger over bicep, Bicep C5#, C6 tap finger with tendon hammer, watch bicep contraction Place finger over radial Brachioradialus C6#, C5 tubersosity, tap finger or supinator watch brachioradialus Tap tendon hammer Triceps C7# directly on the triceps tendon, watch muscle Note. Bold typeface indicates primary nerve root. Note: Bold typeface indicates primary nerve root is indicated with #. TABLE 5. Reflex Grading Grade Response -- Absent + Depressed or minimal response ++ Normal or average +++ Increased or brisk ++++ Hyperactive or clonus (repetitive muscle contractions) TABLE 6. Interpretation of Motor and Reflex Assessment--Upper Limb Clinical Upper Motor Lower Motor Sign Neuron Neuron Tone Initially hypotonic Hypotonic then hypertonic Motor Extensor weakness > Flexor weakness > weak but flexor weakness extensor weakness Reflex Hyperactive Depressed or absent or clonus TABLE 7. Nerve Conduction Velocities for the Median Nerve Sensory Motor Normal -3.7 -4.5 Mild 3.7-4 (75%) 4.4-6.9 (150%) Moderate 4.1-5 (50% to 75%) 7.0-9.9 (150% to 200%) Severe >5 (less than 50%) >10 (over 200%) Note. Derived from Chang, Wang, and Chang (2008) and Greenberg (2006).
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|Author:||Scanlon, Andrew; Maffei, Jennifer|
|Publication:||Journal of Neuroscience Nursing|
|Article Type:||Disease/Disorder overview|
|Date:||Jun 1, 2009|
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