Hand and Wrist Surgery - part 3 pdf

If compressionproduces axonal interruption in some fibers, the EMG reveals changes in musclesfrom decreases in motor unit action potentials to fibrillation potentials of muscles.radiculo

Cervical Root Compression Bradley M Thomas, John M Olsewski, and Jerry G Kaplan

History and Clinical Presentation

A 49-year-old right hand dominant electrician presented with complaints of gressive weakness in his right arm He also described having pain in his neck ex-tending down the front of his arm to his hand He was having difficulty liftingobjects with his right hand and performing repetitive-type motions, with weakness

pro-of his right shoulder and biceps He reported occasional numbness in his thumband index finger while at work

He did not recall any trauma to his neck or arm He denied bowel or bladderdysfunction, and was not experiencing disturbances in his gait On further ques-tioning he denied any history of smoking, diabetes, or hypertension He also de-nied night pain

Physical Examination

Examination revealed a patient in no acute distress, with a full range of motion

of the cervical spine Reproduction of his right arm pain was elicited with tension of the neck and rotation of his head to the right (Spurling’s maneuver)

ex-He appeared to have mild deltoid wasting on his right with prominence of hisacromion Motor testing was symmetric with 5/5 strength in bilateral deltoids,biceps, triceps, wrist flexors, wrist extensors, finger flexors, finger extensors, andhand intrinsics His deep tendon reflexes were 2+ and symmetric, with the ex-ception of the biceps reflex, which was depressed on the right side comparedwith the left He had a negative Hoffman’s sign and his gait was within normallimits Tinel’s and Phalen’s testing of the median nerve at the wrist were notprovocative

Diagnostic Studies

Radiographs taken included an anteroposterior, lateral, obliques, and sion laterals of the cervical spine There is evidence of multilevel degenerativechanges, with principal changes at the C5-C6 level These changes include loss ofC5–6 disk height on the lateral and narrowing of the C6 neural foramen with en-croachment on the foramina by osteophyte on the oblique views (Fig 18–1) Mag-netic resonance imaging (MRI) of the cervical spine showed evidence of multilevelmild cord impingement with disk herniation at C3–4, C4–5, C5–6, and C6–7,along with focal increased signal intensity within the cord at the C5–6 level on theT2-weighted images consistent with cord edema (Fig 18–2) There is also bilateralforaminal narrowing on the axial images at the C5–6 level (not shown) A needleelectromyogram (EMG) was performed, which showed membrane instability of theC6 innervated muscles on the right side C5, C7, and C8 muscles were normal Thenerve conduction studies did not exhibit peripheral nerve slowing as evidence forperipheral nerve compression

flexion/exten-C O M P R E S S I O N N E U R O P A T H Y

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PEARLS

• Spurling’s maneuver

repro-duces a patient’s arm pain

and paresthesias by turning

the patient’s head toward

the symptomatic side and

ex-tending the neck This position

decreases the size of the

neu-roforamina.

• Use an EMG to differentiate

first-degree shoulder problems

from a C5 root problem

• Biceps weakness may be the

first sign of rotator cuff disease,

although a herniated C6 root

can give similar findings

PITFALLS

• Patients with sensory changes

in the thumb and index

fin-ger may have carpal tunnel

syndrome and not a C6

radiculopathy

• Check for a local Tinel’s and

Phalen’s sign

• An incomplete cervical spine

exam in a patient with upper

extremity problems often leads

to an incorrect diagnosis

• A full cervical spine x-ray series

should be used to see on

oblique films encroachment on

the foramina by osteophytes.

Differential Diagnosis

Carpal tunnel syndromeRotator cuff tear

C5 radiculopathyC6 radiculopathyBrachial neuritisThoracic outlet syndrome

Diagnosis

C6 Radiculopathy

Cervical radiculopathy represents impingement of an exiting cervical nerve rootgenerally caused by herniated disk material or from degenerative cervical spon-dylosis, or commonly a combination of the two In cases where the etiology is

a herniated disk, the symptoms are more acute in onset and may be bated by coughing or other Valsalva-type maneuvers Cervical spondylosis as acause for radiculopathy has an insidious onset, with degenerative changes oc-curring at the disk and the zygapophyseal and neurocentral joints (Fig 18–3).Other causes of cervical root irritation or compression include intraspinal tu-mors, infection, inflammatory arthritic changes, and chemical irritation fromneurohumeral factors

exacer-The presentation of cervical radiculopathy begins with varying degrees of pain,paresthesias, and motor weakness in the neck and upper extremity Significant neckpain is often associated with the radicular pain and sensory changes, which generallyfollow a dermatomal distribution Breast pain and angina-like symptoms should also

be considered as potential radicular complaints Weakness and reflex changes are alsoroot specific, but significant overlap exists in the muscular innervation of the upperextremity and may occasionally be confusing Table 18–1 outlines the clinical symp-toms and findings seen with individual root involvement, and other potential causesfor similar findings

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Cervical nerve root

Cord

Intervertebral foramina (neuroforamen)

Uncinate process (joint of Luschka) Disk

Vertebral body

Articular process (facet joint)

Figure 18–3 Axial anatomy

of the cervical spine at the level of the disk and exiting nerve root at the interverte- bral foramina Note the disk herniation on the left side impinging the nerve root.

The physical exam should be focused on identifying a dermatomal distribution

of radicular complaints and sensory changes Specific muscle group weakness andreflex changes as compared with the opposite side should also be recorded Specialtests like the previously mentioned Spurling’s sign and the Valsalva maneuver canreproduce a patient’s radicular complaints by decreasing the size of the neuroforam-ina Davidson’s shoulder abduction relief sign functions to relieve a patient’s radicu-lar complaints with abduction of the shoulder and presumably decreased tension onthe cervical root

In this patient’s presentation a typical C6 radiculopathy is present with neck painradiating down the biceps region of the arm to the lateral aspect of the forearm intothe thumb and index fingers Although he did not exhibit weakness on testing, he didreport difficulty maintaining biceps strength with repetitive motion, and he had a de-pressed biceps reflex Spurling’s maneuver was provocative for reproducing his radic-ular pain The radiographs and MRI are significant for loss of C5–6 disk space, C6neural foramen narrowing, encroachment on the foramina by osteophyte, and focalcord edema at the C5–6 level The EMG confirmed denervation at the C6 level

Differential Diagnosis

Other conditions that may mimic C6 radiculopathy include other level thies, carpal tunnel syndrome, rotator cuff tendinopathies, brachial neuritis, andthoracic outlet syndrome

radiculopa-C E R V I radiculopa-C A L R O O T radiculopa-C O M P R E S S I O N

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Table 18–1 Clinical Symptoms and Physical Findings Seen in Individuals with Cervical Root Involvement and Other Potential Causes for Similar Findings Pain or

Root Level Sensory changes Motor Reflex Diagnosis with Similar Findings

Mastoid regionEar

Along the trapeziusAnterior neck

top of the shoulder Rotator cuffOver the deltoid

arm and forearm Wrist extensors Brachioradialis Upper trunk BPNThumb and index

fingers

to the middle finger Wrist flexors Pronator syndrome

Finger extensors Radial tunnel synd

Posterior cord BPNC8 C7–T1 Ulnar side of the Finger flexors X Ulnar nerve entrapment at Guyon’s

AIN, anterior interosseous nerve; BPN, brachial plexus neuropathy.

Clinical neurophysiologic testing is very important for differentiating thy from peripheral neuropathies Needle EMG has traditionally been the most use-ful electrophysiologic tool for diagnosing cervical radiculopathy If compressionproduces axonal interruption in some fibers, the EMG reveals changes in musclesfrom decreases in motor unit action potentials to fibrillation potentials of muscles.

radiculopa-In radiculopathy the nerve compression is proximal to the dorsal primary ramus,which should produce changes in the paraspinal muscles, differentiating this lesionfrom a brachial plexus injury or more distal nerve compression

The sensory changes involving the thumb and index finger seen in C6 lopathy are also present in carpal tunnel syndrome The differences can be seen inthe dorsal and volar distribution of sensory changes in the hand and the proximalfindings associated with radiculopathy

radicu-Coexisting distal nerve entrapment and cervical radiculopathy can occur, known

as the double crush phenomenon EMG is useful for differentiation of proximalversus distal nerve entrapment, with nerve conduction velocities identifying periph-eral neuropathy

Pain that originates in the neck and extends to the shoulder and arm is very typicalfor radiculopathy, but patients with rotator cuff disease often have associated neck paindue to shoulder weakness and trapezium muscle spasm In addition, biceps weaknessmay be a subjective complaint with rotator cuff disease due to an associated bicepstendinopathy causing pain and restricted motion Specific testing of the rotator muscu-lature and an MRI of the shoulder are helpful in diagnosing a rotator cuff tear

Proximal arm pain and weakness may be present in brachial neuritis In this dition of unknown etiology a patient might awaken with shoulder pain and armweakness without an inciting event The symptoms are usually self-limited andtreated symptomatically Again, electrodiagnostic testing along with a thorough his-tory and physical examination should differentiate this entity from radiculopathy.Thoracic outlet syndrome may involve nerves of the brachial plexus and may presentwith weakness and numbness of the hand Physical findings of asymmetric pulses, vas-cular bruits, and a positive Adson’s test are tips to suspect thoracic outlet syndrome

con-Nonsurgical Management

The majority of patients with first-time symptoms of radiculopathy may be aged nonoperatively Initial management should include immobilization in a softcollar with the neck slightly flexed, antiinflammatory medications, and physicaltherapy Narcotic medications may be used in conjunction with nonsteroidal anti-inflammatory drugs (NSAIDs) in the acute period in cases of severe pain Physicaltherapy consists of heat and ultrasound modalities to make the patient more com-fortable, cervical traction, and stretching exercises when tolerated Epidural or se-lective nerve root corticosteroid injections are also an option, but require accurateneedle placement around an irritated nerve root Improvement in symptoms should

man-be seen within 2 weeks; if symptoms worsen or marked neurologic deficits are ent, more aggressive management should be considered

upper extremity weakness, and nerve root compression that is proven diagnosticallyand correlates clinically.

Surgical choices include anterior cervical diskectomy and fusion as described byRobinson, or posterior diskectomy involving a hemilaminectomy or foraminotomy.The anterior approach is considered the best option for the acute disk herniation

to decompress the nerve root from impinging disk fragments in the intervertebralforamen, and for cases where the nerve root is compressed by osteophytes fromthe joints of Luschka (Fig 18–3) This anterolateral approach in the neck takes ad-vantage of the fascial plane between the carotid sheath laterally and the tracheaand esophagus medially, which affords visualization of the entire surgical spine Theposterior approach is useful for cases of chronic compression due to degenerativechanges at the facet joints, and for cases where several levels need to be addressed.Both approaches produce excellent results for relieving radiculopathy, but the an-terior approach is more consistent for relieving axial neck pain Postoperatively, thepatients are immobilized in a hard collar in cases of fusion and a soft collar if a sim-ple diskectomy is performed

Suggested Readings

An HS Cervical root entrapment Hand Clin 1996;12:719–730.

Bohlman HH, Emery SE, Goodfellow DB, et al Robinson anterior cervical

dis-cectomy and arthrodesis for cervical radiculopathy J Bone Joint Surg 1993;75A:

1298–1307

Dumitru D Electrodiagnostic Medicine Philadelphia: Hanley & Belfus; 1995.

Levine MJ, Albert TJ, Smith MD Cervical radiculopathy: diagnosis and

nonopera-tive management J Am Acad Orthop Surg 1996;4:305–316.

Lomen-Hoerth C, Aminoff MJ Clinical neurophysiologic studies: which test is

useful and when? Neurol Clin 1999;17:65–74.

Morgan G, Wilbourn AJ Cervical radiculopathy and coexisting distal entrapment

neuropathies: double-crush syndromes? Neurology 1998;50:78–83.

Persson LC, Moritz U, Brandt L, Carlsson CA Cervical radiculopathy: pain, muscleweakness and sensory loss in patients with cervical radiculopathy treated with

surgery, physiotherapy, or cervical collar A prospective, controlled study Eur Spine J

1997;6:256–266

Saal JS, Saal JA, Yurth EF Nonoperative management of herniated cervical

inter-vertebral disc with radiculopathy Spine 1996;21:1877–1883.

Stewart JD Focal Peripheral Neuropathies 2nd ed New York: Raven Press; 1993.

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Complex Regional Pain Syndrome Type 1 (Reflex Sympathetic Dystrophy)

Carole W Agin

History and Clinical Presentation

A 50-year-old woman was undergoing magnetic resonance imaging (MRI) withcontrast Intravenous access was started in her right antecubital fossa As the infu-sion of gadolinium was started, the patient reported a burning pain in her arm fromthe antecubital fossa to her fingers Her forearm and hand swelled As the swellingincreased, she reported numbness and cyanosis Over the next few days the swellingresolved Slowly sensation returned to her arm; however, the patient reported a con-stant burning pain The patient also noted changes in the color of her hand andpain with movement of her wrist, elbow and shoulder

Diagnostic Studies

There are no radiologic findings that are pathognomonic for complex regional painsyndrome (CRPS) type 1, reflex sympathetic dystrophy (RSD) Radiologic findingsare often nonspecific, and many findings are a result of prolonged disuse, which

is attributable to the pain associated with the syndrome However, imaging studiescan support a diagnosis of CRPS (RSD)

Fine detail radiography may help to suggest the presence of CRPS Early radiologicchanges seen with sympathetic hyperdysfunction include patchy demineralization ofthe epiphyses and short bones of the hands and feet Periarticular osteoporosis in longbones and diffuse osteoporosis in small bones may be seen on plain radiographs Sub-periosteal resorption, striation, and tunneling of the cortex may occur Comparisonwith the unaffected limb is always required Unfortunately, these findings may be seenwhenever there is disuse of a limb As CRPS advances, patchy osteopenia may be seen.Triple-phase scintigraphy has also been used to help diagnosis CRPS (RSD).Three-phase bone scanning measures the uptake of a radionucleotide tracer at threedifferent times: arterial phase, measured seconds after the injection of tracer; softtissue phase, measured after several minutes have passed; and mineral phase, mea-sured hours after the tracer is given The triple-phase bone scan pattern most consis-tently seen in a patient with CRPS (RSD) is that of increased flow to the involvedextremity and delayed static images that show diffusely increased uptake activitythroughout the involved extremity, usually in a periarticular distribution

MRI studies may show skin thickening and tissue edema Nuclear bone densitymeasurements have been used to follow the progression of the syndrome

• When presented with a

ques-tionable case of CRPS early

after symptom development,

a three-phase bone scan may

be helpful.

• CRPS (RSD) is often a diagnosis

of exclusion

PITFALLS

• Radiologic studies performed

late in the disease process

may show changes secondary

to disuse atrophy, which may

be caused by other medical

conditions

• If the sympathetically

main-tained pain is the result of a

persistent but treatable

condi-tion, the condition needs to

be treated Treating only the

signs/symptoms of CRPS

with-out addressing the underlying

condition may prove futile

• If the patient has a diagnosed

psychiatric illness (i.e.,

post-traumatic stress disorder,

de-pression), this must be treated

or it can adversely affect any

potential improvements

ob-tained from other treatment

modalities

Infectious diseaseVascular diseaseConnective tissue disorderReflex sympathetic dystrophyCRPS (RSD) is often a diagnosis of exclusion Other causes of similar pain com-plaints include peripheral neuropathies, which may also present with neuropathicpain Traumatic injuries to nerves may present with dysesthesia and hyperpathia,but without the sympathetic component Inflammatory and infectious causes forpain needed to be ruled out when autonomic dysfunction is the primary presentingsymptom Examples of this would include tenosynovitis and bursitis Vasculitis andvascular disorders can also manifest with similar findings In many instances vascu-lar diseases present with bilateral symptoms Raynaud’s disease produces vasospasmthat will lead to findings of pallor, cold skin, and potentially cyanosis Connectivetissue disorders also have to be ruled out Myofascial pain may also present with anondermatologic distribution of pain These patients may report burning pain as asymptom and have tender trigger points in the affected muscles Malingering andpsychiatric disorders must also be ruled out as a cause of the patient’s unremittingpain, which presents out of proportion to the inciting event.

Diagnosis

Complex Regional Pain Syndrome, Type 1 (Reflex Sympathetic Dystrophy)

The Committee on Taxonomy of the International Association for the Study ofPain (IASP) recently renamed reflex sympathetic dystrophy as complex regionalpain syndrome type 1 This new taxonomy was promulgated in an attempt to estab-lish uniform diagnostic criteria This will aid in the development of treatment pro-tocols for the syndrome Previously many symptom constellations were includedwithin the category of RSD, making treatment pathways and outcome studies dif-ficult A study done to evaluate the validity of the IASP’s CRPS diagnostic criteria

to distinguish between CRPS and other neuropathies showed that the new cation did assist in improved accuracy of diagnosis

classifi-To meet criteria for CRPS type 1 a patient must present with regional pain side of the distribution of a single peripheral nerve and out of proportion to the in-citing event CRPS has been reported to develop after compression/crush injuries,lacerations, fractures, sprains, burns, or surgery Allodynia and hyperalgesia are typ-ically present Abnormalities in skin blood flow (causing changes in skin tempera-ture and color), abnormal sudomotor activity, and edema are also present Dystoniaand weakness, although not necessary for the diagnosis, may also be present.Trophic changes and personality changes may develop as the disease progresses.CRPS type 2 has all of the same signs and symptoms; however, it follows injury of

out-a mout-ajor peripherout-al nerve

Methods of Management

As the pathophysiology of CRPS type 1 (RSD) is not well understood, multipletreatment protocols have been described The consensus is that these patients dobest with a multidisciplinary treatment plan (Table 19–1) This includes regionalblockade (Fig 19–1), physical therapy, pharmacologic therapy, and psychological

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Table 19–1 Treatment Modalities Pharmacologic Interventional Technique Physical Modalities Psychological Interventions

Antidepressants, Sympathetic blockade Physical/occupational Psychiatric evaluation

Lumbar sympathetic

IV regionalMembrane stabilizers Spinal cord stimulator Contrast baths Cognitive behavior skillsAnticonvulsants

Local anesthesia

Antiarrhythmic

intervention The earlier the syndrome is diagnosed and treatment is started, thebetter the chances for complete recovery.

Pharmacologic Therapy

Kingery reviewed the literature with respect to controlled clinical trials for CRPS

He found great disagreement as to the effectiveness of many of the medications rently being used in the treatment of CRPS He concluded that further double-blind controlled studies are needed

cur-Tricyclic antidepressants (TCAs) have been well studied in neuropathic pain.TCAs (amitriptyline, nortriptyline, desipramine) inhibit monoaminergic transmit-ters by blocking reuptake of serotonin and norepinephrine The dose used for treat-ment of neuropathic pain is typically much less than antidepressant doses Theselective serotonin reuptake inhibitors (paroxetine, sertraline), although used anec-dotally in chronic CRPS, have not been formally studied for this purpose

The mechanism of action of nonsteroidal antiinflammatory drugs (NSAIDs) isthe inhibition of cyclooxygenase This leads to a reduction in the production of painmediators and a reduction in inflammation NSAIDs may be helpful in the earlystages of CRPS type 1; however, the potential for gastrointestinal complications andrenal failure must be considered if continued use is to be recommended

Membrane stabilizing medications are also used This category includes convulsants, local anesthetics, and antiarrhythmic agents Gabapentin, a selectivevoltage-gated Ca2+channel blocker, has shown some efficacy in managing pain inCRPS Gabapentin has reduced side effects and an improved efficacy-to-toxicityratio when compared with phenytoin and carbamazepine Lidocaine, mexiletine,and tocainide effect sodium channels Lidocaine has been used intravenously in themanagement of neuropathic pain Intravenous lidocaine therapy is often followed

anti-by oral treatment with mexiletine

Topical medications have been tried for the hyperpathia and allodynia associatedwith CRPS Topical application of local anesthetics, lidocaine, and prilocaine (eutec-tic mixture of local anesthetics, EMLA) has been tried recently in the treatment

of neuropathic pain in patients with CRPS type 1 (RSD) Topical capsaicin causes

a reversible depletion in substance P and calcitonin gene-related peptide from theC-fiber nerve terminals There are anecdotal reports of its use for localized hyper-algesia; therefore, it can be tried for patients with CRPS with local areas of pain Pa-tients need to be informed that initially its application may cause increased pain.This is secondary to the release of substance P that occurs

The use of opioids in the treatment of neuropathic pain, and specifically inCRPS, has not been studied Opioids are useful in nociceptive pain, and their effect

is related to interaction at the level of the spinal cord with the opioid receptors though their use may be considered controversial in chronic, nonmalignant pain, apatient with unremitting pain should be tried on opioid therapy This should occurearly on in the treatment It is important to control the patient’s pain utilizing allavailable means so that active physical therapy can be pursued and disuse atrophyavoided As is true whenever using opioids, constipation should be expected andtreated prophylactically

Al-There have been anecdotal reports of the use of other medications for CRPS.Medications that inhibit ␥-aminobutyric acid (GABA), such as baclofen, have beenreported to be useful in neuropathic pain Controlled studies of their use in CRPShave not yet been done Clonidine has been shown to be useful when topically applied

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to areas of hyperalgesia It acts by blocking release of catecholamines presynaptically.Clonidine has also been administered epidurally and intrathecally in patients withCRPS These patients are at a much greater risk for hemodynamic complications whenthe drug is used transdermally Subcutaneous calcitonin has been shown to be effective

in treatment of spontaneous pain Its use in CRPS has not yet been documented In theearly stages of CRPS a patient may benefit from a trial of corticosteroids This is partic-ularly true for patients who present with edema or other signs of inflammation

Regional Blockade

Regional blockade, specifically sympathetic nerve blocks, are useful in both lishing the diagnosis as well as in the treatment of CRPS (RSD) Patients withCRPS report relief of pain with sympathetic blocks, which is very useful in givingpatients the analgesia that they require to participate in a physical therapy regimen

estab-If a patient responds positively to a trial of sympathetic block, these blocks should

be repeated as long as the patient continues to be afforded increasing duration ofpain relief and symptom improvement with subsequent blocks

In addition to assessing the level of pain relief reported by the patient, patientsshould be assessed for signs of a sympathetic block Blocks of the sympathetic nervoussystem interrupt nociceptor visceral and somatic afferents and vasomotor, sudomotor,and visceromotor fibers One would therefore look for signs of increased blood flow

to the limb(s) involved As cutaneous blood flow affects skin temperature and this iscontrolled by the sympathetic nervous system, an increase in skin temperature shouldoccur This can be measured using surface temperature monitors or plethysmography.The limb should be examined for visual signs of increased vasculature Blocking ofsudomotor functions can be measured using Ninhydrin, cobalt blue, or starch-iodide

A quantitative sudomotor axon reflex test (QSART) can also be used

For CRPS affecting the upper limb a stellate ganglion block is usually performed.Many patients develop Horner’s syndrome (enophthalmos, miosis, anhidrosis, andptosis) after a stellate (cervicothoracic) ganglion block Block of the thoracic sym-pathetic chain is technically difficult, requiring radiologic guidance, and is notcommonly done For CRPS affecting the lower extremities, sympathetic blockade isdone either by performing a lumbar sympathetic block or by an epidural injection

If required, continuous blocks can be done

Intravenous Regional Blocks (Bier Blocks)

Intravenous regional blocks allow for prolonged exposure of the affected limb to theganglionic blocking agent In the United States this technique is typically per-formed with bretylium Bretylium accumulates in adrenergic nerves and blocksnorepinephrine release These blocks have also been performed with guanethidineand reserpine

Spinal Cord Stimulation

Spinal cord stimulation is hypothesized to affect pain based on the gate control theorywhereby stimulation of large myelinated fibers blocks pain transmissions throughsmaller pain fibers (Fig 19–2)

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Figure 19–2 Patient with spinal stimulation of large myelinated fibers that in theory blocks pain transmis- sions through smaller pain fibers.

Patients who either do not respond to regional blocks, medications, or physicaltherapy, or are unable to pursue those treatment options secondary to unacceptableside effects, may be candidates for spinal cord stimulation All patients must meetstrict selection criteria and have a successful trial with a temporary lead A trial isdeemed successful if the patient reports a decrease in pain, a reduction in medica-tion requirements, and an improvement in function

Physical Therapy

Physical therapy should be done concurrently with medications and sympatheticblocks in the treatment of severe CRPS It can be the main treatment modality forchildren with CRPS Multiple physical therapy modalities have been used to treatCRPS These include range-of-motion exercises, muscle strengthening and condi-tioning, massage, paraffin wax, contrast baths, ultrasound, and transcutaneous elec-trical nerve stimulation (TENS)

Psychiatric/Psychological Intervention

Secondary to the potential chronic pain and disability associated with CRPS, tients should be sent for psychological evaluation early on in their treatment Pa-tients often benefit from cognitive-behavioral skills training Some patients mayrequire ongoing psychiatric intervention

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Early diagnosis of CRPS is essential for pain relief and restoration of function Theincidence of poor outcomes is significantly higher in patients who present with aduration of CRPS greater than 12 months, in the second and third stages of disease,and in cases with coexisting nerve injuries or compression as a consequence of ini-tial trauma Studies have shown a correlation between CRPS and psychosocial dis-orders This may complicate treatment

Suggested Readings

Aprile AE Complex regional pain syndrome AANA J 1997;65:557–560.

Galer BS, Bruehl S, Harden RN IASP diagnostic criteria for complex regional painsyndrome: a preliminary empirical validation study International Association for

the Study of Pain Clin J Pain 1998;14:48–54.

Geertzen JH, Dijkstra PU, Groothoff JW, ten Duis HJ, Eisma WH Reflex thetic dystrophy of the upper extremity–a 5.5-year follow-up Part II Social life

sympa-events, general health and changes in occupation Acta Orthop Scand Suppl 1998;

279:19–23

Kingery WS A critical review of controlled clinical trials for peripheral neuropathic

pain and complex regional pain syndromes Pain 1997;73:123–139.

Raj PP Reflex sympathetic dystrophy In: Raj PP, ed Pain Medicine St Louis:

Mosby-Year Book; 1996:466–481

Sandroni P, Low PA, Ferrer T, Opfer-Gehrking TL, Willner CL, Wilson PR Complex

regional pain syndrome I (CRPS I): prospective study and laboratory evaluation Clin

J Pain 1998;14:282–289.

Schiepers C, Bormans I, De Roo M Three-phase bone scan and dynamic vascular

scintigraphy in algoneurodystrophy of the upper extremity Acta Orthop Belg 1998;

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Stanton-Hicks M, Baron R, Boas R, et al Complex regional pain syndromes:

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Walker SM, Cousins MJ Complex regional pain syndromes: including “reflex

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syn-physiologic mechanisms and therapy Neurol Clin 1998;16:851–868.

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Section IV

Nerve Injuries/ Palsies

Acute Nerve Laceration

Acute Nerve Laceration

Kevin D Plancher

History and Clinical Presentation

A 20-year-old right hand dominant male laborer caught his left hand in a circularsaw with the “guard” off He has a laceration to his left index finger and can’t feelthe tip of his finger, and has an open bleeding wound

Physical Examination

On physical examination, the patient has an acute open laceration involving the dial side of the right index finger A careful motor examination was performed Thefunctioning level of specific muscles is determined to assist with identifying periph-eral nerve injuries A two-point sensory discrimination test (Fig 20–1), as deter-mined by the Weber two-point discrimination test, using a dull pointed eye caliperapplied in the longitudinal axis of the digit without blanching the skin, and a two-point discrimination (2-PD) (both moving and static), Semmes-Weinstein monofil-aments, and vibrometer tests were used to assess the status of the nerves Denervatedskin responds differently to stimuli; when the injured hand is placed in water, inner-vated skin wrinkles and denervated skin does not This test can be helpful in deter-mining the affected peripheral nerves in the hand in unconscious patients

ra-Diagnostic Studies

Radiographs were performed to rule out associated fractures

Differential Diagnosis

Vascular injuryMuscle lacerationNeurologic disorderNerve laceration

• Occupational therapy

post-operatively will successfully

complete a desensitization

program

• The area of injury must be

de-fined for successful functional

nerve repair

PITFALLS

• Clean ends of nerve must be

sewn together to avoid a

neu-roma in continuity

• Missed diagnosis with a

devas-cularized finger may lead to

amputation

• Range of motion must be

con-trolled with splinting

Figure 20–1 Weber static two-point sensory discrimina- tion test.

Acute Laceration, Radial Nerve, of the Index Finger

Neurapraxia is the mildest form of nerve injury This usually involves demyelinationwithout axon disruption and degeneration This type of injury has a relatively shortrecovery time, and full function is expected without intervention

Axonotmesis occurs when axons, myelin, and associated internal nerve structuresare disrupted These injuries often result from situations in which traction over-comes the inelastic internal structures but leaves the elastic epineurium intact.When axons are disrupted and the endoneurium and the rest of the nerve are intact,degeneration and regeneration occur This is the first stage of injury that shows anadvancing Tinel’s sign Because the endoneurium is intact, regeneration should befull with complete sensory and motor function regained

Another type of injury occurs when the axons and the endoneurium are damagedand the perineurium and epineurium are intact This leaves the blood–nerve barrierintact but provides a disorganized bed through which the axons can travel Nerveregeneration may be slowed due to infiltration of scar tissue or a smaller number ofaxons capable of survival and regeneration An advancing Tinel’s sign, though some-what slowed, should be present

The worst form of closed nerve damage is when all structures are damaged exceptthe epineurial covering This disables the intact axons and no conduction down thenerve is possible Surgical intervention is required to restore function A Tinel sign

is present at the level of injury and does not move distally because the regeneratingnerve is kept from advancing by large amounts of scar tissue or debris

Neurotmesis is the most severe type of injury This class of injury is easy to nose because it usually involves an open wound with nerve deficits Surgical repair is

diag-a requirement for diag-any return in function to occur Results following the surgicdiag-al pair of digital nerves are inconsistent Among the factors that could impact on out-comes are the amount of direct trauma to the nerve, the length of nerve that hasbeen traumatized, and the age of the patient Increased tension on the repair hasalso been shown to effect the final results

re-Nerve repair never results in the return of full sensibility However, reasonableprotective sensibility to light touch and pin pricks can be obtained Two-point dis-crimination can approach normal in as many as one patient in three (33%)

Surgical Management

After usual draping and prepping of the patient, the skin is marked The patient issupine and a regional anesthetic is administered If multiple structures need to berepaired, then general anesthesia is used and the arm is exsanguinated using atourniquet on the forearm or arm

Incision use for this procedure is a midaxial incision because it offers the bestextensile exposure to the palm and finger Some surgeons use a Bruner zigzag to ex-pose the nerve, but we feel excessive scarring results with this type of incision Grossexploration is accomplished under loupe magnification using tenotomy or otherscissors

After initial exploration, using a microscope for high-power magnification, tify the nerve and trim any necrotic or bruised tissue until normal fascicles are

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found (Fig 20–2A) Then transect the nerves perpendicular to the main axis andcarefully examine them to ensure that they are healthy and uninjured fascicles arefound (Figs 20–2B,C) Several sequential transections may be indicated beforefinding appropriate endings for repair.

Use a systematic approach consisting of a simple suture first being placed oneither side of the nerve anteriorly and this is followed by another in the midlineposteriorly The intervening epineurium is then sutured (Fig 20–3)

Many surgeons suggest the use of 9-0 or 10-0 nylon or Prolene sutures If thenerve is under too much tension, the sutures will not hold If there is any questionabout increased tension on the digital nerve repair, grafting should be considered be-cause holding a digit in flexion to oppose nerve endings often leads to contracture.Closure of the wound is accomplished with simple sutures A bulky bandage iswound circumferentially around the digit to help diminish swelling A dorsal andpalmar splint may be applied

Figure 20–2 (A) Intraoperative exposed injured radial digital nerve to the index finger (B) Epineurial repair of a nerve (C) Fascicular repair of nerve.

B

A

C

Postoperative Management

Splinting is done for a period of 3 weeks (Fig 20–4), but one sequela can be ness in the interphalangeal joints Absent undue tension on the repair and full ex-tension, range-of-motion exercises can be started at the time of suture removal orearlier depending on the quality of the repair

stiff-Hand therapy following nerve repair is individualized, and many patients require

no specific therapy If stiffness does develop, supervised hand therapy and dynamictherapy are useful interventions

Regeneration of the nerve is followed by measuring the paresthesia radiating tally from the level of nerve repair when the nerve is percussed (Tinel’s sign) Asregeneration continues, the focus of the paresthesia migrates distally As migrationand healing continue, sensibility is noted proximal to Tinel’s sign

dur-Suggested Readings

Allan CH Functional results of primary nerve repair Hand Clin 2000;16:67–72 Birch R, Raji AR Repair of median and ulnar nerves Primary suture is best J Bone Joint Surg 1991;73B:154–157.

Cabaud HE, Rodkey WG, Nemeth TJ Progressive ultrastructural changes after

peripheral nerve transection and repair J Hand Surg 1982;7A:353–365.

Chow JA, Van Beek AL, Meyer DL, Johnson MC Surgical significance of the motor

fascicular group of the ulnar nerve in the forearm J Hand Surg 1985;10A:867–872.

de Medinaceli L, Prayon M, Merle M Percentage of nerve injuries in which mary repair can be achieved by end-to-end approximation: review of 2,181 nerve

Diao E, Vannuyen T Techniques for primary nerve repair Hand Clin 2000;16:53–66.

Fu SY, Gordon T Contributing factors to poor functional recovery after delayed

nerve repair: prolonged denervation J Neurosci 1995;15:3886–3895.

Hobbs RA, Magnussen PA, Tonkin MA Palmar cutaneous branch of the median

nerve J Hand Surg 1990;15A:38–43.

Jabaley ME Techniques in nerve repair In: Hunter JM, Schneider LH, eds Tendon and Nerve Surgery in the Hand: A Third Decade St Louis: Mosby; 1994:89–94 Jarvik JG, Kliot M, Maravilla KR MR nerve imaging of the wrist and hand Hand Clin 2000;16:13–24.

Lundborg G, Dahlin LB, Danielsen N, et al Nerve regeneration across an extendedgap: a neurobiological view of nerve repair and the possible involvement of neu-

ronotrophic factors J Hand Surg 1982;7A:580–587.

Millesi H Techniques for nerve grafting Hand Clin 2000;16:73–91.

Smith KL Anatomy of the peripheral nerve In: Hunter JM, Schneider LH, eds

Tendon and Nerve Surgery in the Hand: A Third Decade St Louis: Mosby; 1994:

11–18

Vanderhooft E Functional outcomes of nerve grafts for the upper and lower

ex-tremities Hand Clin 2000;16:93–104.

Wilgis EF, Brushart TM Nerve repair and grafting In: Green DP, ed Operative Hand Surgery Vol 2 New York: Churchill Livingstone; 1993:1315–1340.

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PEARLS

• The EIP muscle belly must be

freed from surrounding soft

tis-sue completely so that when

the tendon is transferred

dor-sally, the muscle fibers are not

angulated

• The use of the EIP in lieu of

the FDS spares the tendon for

use in an intrinsic transfer if

necessary.

• No pulley is required for the

Burkhalter transfer

PITFALLS

• The EIP may not be sectioned

distal to the sagittal band Loss

of independence of index MP

joint extension may then occur

with a small extension lag at

the MP joint

• If there is an injury to the ulna

distal forearm, scar may cause

adhesions as it is in the path of

the transfer.

• This EIP transfer just reaches

the site of insertion with little or

no leftover tendon Beware,

and be prepared if the transfer

is short

21

Low Median Nerve Palsy

Kevin D Plancher

History and Clinical Presentation

A 17-year-old girl presents following operative repair of a tendon with ulnarand median nerve injuries to the distal forearm Her surgery was ~1 year ago She

is now unable to achieve thumb abduction or metacarpal flexion, and she hasnoticed severe clawing of her digits She has been in occupational therapy for

1 year She would like to be able to grip wide-mouthed objects, as she was onceable to do

Diagnosis

The thumb is key in providing strength for prehensile pinch and grasp Opposition

is a complex motion involving abduction, flexion, and rotation of the carpal (CMC) joint and flexion and rotations of the metacarpophalangeal (MP)joint Median nerve palsy deprives the thumb of its ability to oppose Restoration ofopposition requires the presence of transferable functioning tendons and a thumbthat has adequate mobility without contractures

carpometa-At the level of the wrist, the median nerve lies between the flexor carpi radialis(FCR) and the palmaris longus tendons The nerve lies volar to the flexor pollicislongus and the flexor digitorum profundus The nerve then enters the carpal tunnelbeneath the transverse carpal ligament In the carpal canal the nerve may begin tobranch to supply the median-innervated hand intrinsic muscles

Surgical Management (Burkhalter EIP Transfer)

This transfer of the extensor indicis proprius (EIP) to the abductor pollicis brevis(APB) was descried by Burkhalter in 1974 and is perfect for patients with an iso-lated thenar paralysis due to low or high median nerve injury The transfer achievesexcellent thumb abduction, pronation, and MP flexion

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Figure 21–1 Relationship of sor indicis proprius (EIP) on the ulnar side of the extensor digitorum communis (EDC), seen over the index metacarpal (right hand dorsal approach).

exten-With the patient under either general or regional anesthetic, a tourniquet is plied to exsanguinate the operative extremity The planned incisions are outlinedand a longitudinal incision is made over the index MP joint The EIP tendon is thenidentified ulnar to the extensor communis tendon (Fig 21–1)

ap-An incision is then made on the ulnar side of the EIP, through the sagittal band,and extended distally A similar incision is made on the radial side, separating itfrom the extensor digitorum communis, and then connecting it to the distal inci-sion on the ulnar side (Fig 21–2) The sagittal band is repaired at this point in theoperation to avoid an extensor lag

Once the distal attachment of the EIP is released, a linear incision is made overthe dorsal, ulnar aspect of the distal forearm and the deep fascia is divided longitu-dinally The EIP tendon and muscle are identified and delivered to the proximalwound If delivery is hampered by adhesions or connection of the EIP tendon in thedorsum of the hand, another incision may be required to free the tendon and mus-cle belly fully

Once the EIP and muscle belly are freed, a small longitudinal incision is madejust distal to the pisiform, and a subcutaneous tunnel is created across the forearmfrom the dorso-ulnar distal forearm incision to this second incision distal to thepisiform (Fig 21–3A) Care should be taken to ensure that the tunnel is largeenough to accept the muscle belly of the EIP or it may prevent full excursion of thedonor tendon The tendon can be passed through the tunnel using a tendon passer

or hemostat

B

Figure 21–3 (A) Clinical photo of the EIP tendon being

pulled subcutaneously from dorsal to volar to be distal to the

pisiform (B) The EIP is transferred from the distal ulna

volar forearm to the insertion of the abductor pollicis brevis

(APB) subcutaneously.

Figure 21–2 Distal EIP is sutured to the EDC tendon and

trans-ferred subcutaneously to the midforearm.

Figure 21–4 The EIP is sewn into place, weaved into the APB tendon.

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A second subcutaneous tunnel is made across the palm to the thumb MP joint.The line of pull is estimated by placing the donor tendon to the proposed insertionsite on the distal thumb metacarpal (Fig 21–3B)

Regardless of the method of attachment used, the transferred tendon needs to besecurely fixed in place This can be accomplished using a bone tunnel or weavingthe EIP through the abductor pollicis brevis (Fig 21–4)

The thumb is placed in full opposition to the small finger The EIP transfer istensioned and secured The tourniquet is then released, hemostasis is obtained, andthe wounds are closed (Fig 21–5) When the procedure is completed, a bulky hand

The Royle-Thompson method also splits the EIP tendon into two slips One ispassed through a drill hole in the metacarpal neck from radial to ulnar with themetacarpal pulled to the highest degree of opposition as possible The other half ispassed dorsally over the extensor hood at the MP joint and through a small tunnel

in the fascia and periosteum at the base of the proximal phalanx The two slips aretied together The proximal insertion into the head of the metacarpal serves to assist

in the rotation of the thumb while the distal insertion achieves slight rotation of the

MP joint without causing flexion

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Figure 21–7 An alternative transfer such as a Riordan or Sterling Bunnell seen in this clinical photo with the flexor digitorum superficialis (FDS) ring as the donor tendon.

Use of the flexor digitorum superficialis (FDS) ring as an alternative techniquewas popularized by Sterling Bunnell (Fig 21–7)

Postoperative Management

The bulky hand dressing with splints is maintained until the sutures are removed

at 10 to 14 days after surgery Hand therapy is initiated to maintain motion in thefingers An Orthoplast splint is custom fit to maintain wrist flexion and full thumbopposition for a total of 4 weeks Range of motion, tendon gliding, and retrainingexercises are begun at 4 weeks

Complications

Complications with poor results after the opposition tendon transfers often are due

to an adduction contracture of the first metacarpal This problem may be avoided

by release of the contracture prior to the tendon transfer, whether it is by a surgical

or conservative fashion

Flexion or extension contractures of the MP joint of the thumb often reflect theposition of the transfer relative to the MP joint axis The transfer should be suturedmore dorsally if there is a flexion contracture and reattached more volarly if there is

an extension contracture

Other common complications with any transfer are placing the donor tendonsunder inadequate tension, or placing a repair in a poorly vascularized soft tissuebed These complications, along with a web contracture, or inappropriate splintingcan often be avoided if precision handling of all tendons is done along with under-standing the important general principles of tendon transfers

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Conney WP Tendon transfer for median nerve palsy Hand Clin 1998;4:155–165 Hollister A Giurintano, DJ Thumb movements, motions and moments J Hand Ther 1995;8(2):106–114.

Thompson CF Fusion of the metacarpals of the thumb and index finger to

main-tain functional positions of the thumb J Bone Joint Surg [Am] 1942;24:907 Thomson TC A modified operation for opponens paralysis J Bone Joint Surg [Am]

1942;24:632

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PEARLS

• Ulnar nerve dysfunction leads

to a claw deformity with

asyn-chronous motion, weakened

grip, and loss of lateral finger

mobility and sensation

• Various tendon transfers can

restore clawing and

asynchro-nous digital flexion To improve

weakness of grasp, the

trans-fer must utilize a wrist

muscle-tendon unit Using a digital

motor simply redistributes

balance within the hand

• Transfer selection is based

on patient age, requirements,

tendon availability, and

compliance

PITFALLS

• Claw deformity can result from

a variety of conditions

includ-ing lesions of the ulnar nerve,

lower cervical roots, inferior

brachial plexus, and more

gen-eralized neurologic conditions

(e.g., motor neuron disease)

• The diagnosis requires a

care-ful history, physical

examina-tion, and often

electrodiagnostic studies

• Contraindications to tendon

transfers include an

uncooper-ative patient, a lack of

ex-pendable donor tendons, and

stiff digits without full passive

mobility

22

Ulnar Nerve-Tendon Transfer

Mark S Cohen

History and Clinical Presentation

A 57-year-old man presents for evaluation of his dominant hand He complains of adeformity involving his small and ring fingers with loss of function, especially finemotor skills He relates his problem to a laceration he suffered at the wrist level sev-eral years prior He also reports numbness in his small and ring fingers He deniesany radicular symptoms or problems with his contralateral hand

Physical Examination

Obvious atrophy is visible in the hand involving the intrinsic musculature Thesmall and ring fingers are positioned in a claw deformity, although passive interpha-langeal joint extension is present and the joints are supple The patient has difficultyabducting and adducting his digits His flexor digitorum profundus function to thesmall and ring fingers is intact (he can actively flex his small and ring distal inter-phalangeal joints) Sensory examination reveals diminished two-point discrimina-tion in the small and ulnar half of the ring fingers

Diagnostic Studies

Roentgenograms were obtained of the hand including the wrist They were withinnormal limits Electrical studies were obtained and revealed a complete ulnar nervelesion at the wrist level with denervation present in all ulnar nerve innervated in-trinsic muscles tested (interossei and hypothenar muscles) No reinnervation po-tentials were present The thenar muscles were electrically normal and there was noevidence of a peripheral neuropathy or radiculopathy

Differential Diagnosis

Brachial plexus injuryUpper plexusLower plexusCervical root compressionPeripheral nerve dysfunctionCharcot-Marie-Tooth diseaseUlna nerve tunnel compressionCubital tunnel (source)

Pancoast tumorTendon lacerationsLaceration of the ulna nerve at the wristThe differential diagnosis of a claw deformity of the hand with loss of sensation inthe ulnar nerve distribution is somewhat limited One assumes a lesion of the ulnar

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nerve or possibly the lower cervical nerve roots (C8–T1) or inferior brachial plexus.Cervical nerve root compression typically results in neck pain with radicular symp-toms down the arm Weakness and atrophy would be expected in the thenar andhypothenar musculature, which are both innervated by the lower cervical and firstthoracic nerve roots A lesion of the lower brachial plexus (e.g., a Pancoast tumor ofthe lung apex) would result in similar findings The ulnar nerve is most commonlycompressed at the elbow (cubital tunnel syndrome) or at the wrist (ulnar tunnelsyndrome) Intact function of the two ulnar flexor digitorum profundus tendonswould point to a more distal lesion in the lower forearm or wrist

Lastly, one must rule out other causes of peripheral nerve dysfunction such as ageneralized peripheral neuropathy or hereditary motor-sensory neuropathy (Charcot-Marie-Tooth disease) Intrinsic atrophy with or without sensory loss may be seen insyringomyelia or motor neuron disease (amyotrophic lateral sclerosis, ALS) Thesetypically result in symmetric disease The history, physical findings, and corroborativeelectrical studies aid in localizing the nerve lesion and ruling out a more generalizeddisease process

Diagnosis

The diagnosis is a low complete ulnar nerve palsy The ulnar nerve innervates thefour dorsal interossei, the three volar interossei, the two ulnar lumbricals, the hypo-thenar muscles and typically the deep head of the flexor pollicis brevis It suppliessensation to the small finger and ulnar half of the ring finger

A claw deformity develops due to imbalance between absent intrinsic (interosseiand lumbricals) and intact extrinsic muscle function The claw deformity is morepronounced in the ring and small fingers due to the intact index and middle fingerlumbricals, which are innervated by the median nerve Clawing is more significant

in a low ulnar nerve palsy than a lesion at the elbow due to the intact flexor rum profundus tendons to the ring and small fingers These tend to accentuate theflexion posture of the interphalangeal joints

digito-Loss of ulnar nerve function can be quite disabling The intrinsic muscles are sponsible for simultaneous flexion of the metacarpophalangeal (MP) joints and ex-tension of the interphalangeal (IP) joints (the intrinsic-plus position) Although fullfinger flexion and extension is present, with intrinsic loss the fingers tend to roll upduring flexion due to asynchronous motion of the MP and IP joints (MP flexiondoes not begin until IP flexion has been completed) IP joint extension requirescontraction of the extrinsic extensor tendons (extensor digitorum communis) Thisleads to MP joint hyperextension and contributes to the claw posture

re-The ability to place the hand around objects such as a glass or doorknob is lost.These activities requires the intrinsic-plus posture All fine motor skills that requiresimultaneous MP flexion and IP extension, such as writing or threading a needle,are similarly impaired Lastly, pinch and grip strength are markedly diminished due

to loss of the interossei and hypothenar muscles

Nonsurgical Management

Conservative treatment of ulnar nerve dysfunction relies on the use of externalsplints to block clawing of the digits A lumbrical bar splint is commonly utilized forthis purpose (Fig 22–1) It is a static splint, usually made of Orthoplast by a hand