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Acute Carpal Tunnel

Syndrome

Abstract

Carpal tunnel syndrome is considered the most common of the

chronic compressive neuropathies. Its cause is generally unknown.

Acute carpal tunnel syndrome, which is much less common, is

more often directly related to fractures and fracture-dislocations

about the wrist, hemorrhagic conditions, and vascular disorders

involving the wrist. Many rare and unusual causes have been de-

scribed, including chronic conditions that may be associated with

acute carpal tunnel syndrome, such as rheumatologic disorders and

anomalous anatomy. In contrast to the more common chronic idio-

pathic form, the acute form of carpal tunnel syndrome requires ur-

gent surgical intervention to avoid or diminish serious sequelae.

Carpal tunnel syndrome (CTS)is a median nerve impairmentsecondary to chronic use injuriesand systemic disorders (eg, diabetes,rheumatoid arthritis, amyloidosis).It is thought to be the most common

of the chronic compressive neurop-athies.1 Excellent reviews of CTSare available.2,3 Acute carpal tunnelsyndrome (ACTS), which is muchless common than CTS, is more of-ten related to trauma and requiresurgent surgical intervention toavoid serious sequelae. ACTS ischaracterized by unrelenting painand dysesthesias in the mediannerve distribution resulting from arapid rise in pressure within the car-pal tunnel. It can be differentiatedfrom chronic CTS by the rapid onsetof severe symptoms and by its pro-gressive course over hours, ratherthan weeks or months.

Although not a separate anatom-ic compartment, the carpal tunnelbehaves physiologically like a closedcompartment, and compartmentsyndrome can develop within it. Thecarpal tunnel is intolerant of space-occupying lesions, and symptoms

quickly ensue secondary to in-creased pressure within the tunnel.Etiologies of and predispositions toACTS include hand, wrist, and car-pal bone trauma; infection; rheuma-tologic, hemorrhagic, and vascular

disorders; burns and thermal injury;high-pressure injection injuries; andseveral other uncommon disordersand injuries (Table 1). A mass effectappears to be common to many ofthese diverse etiologies. In each case,an intracompartmental pressurethreshold is exceeded and epineuralblood flow is compromised, produc-ing pain and dysesthesias in the me-dian nerve distribution. Early recog-nition and management of ACTS isnecessary to preserve function ofthe median nerve. The distinctionamong chronic CTS, ACTS, andnerve contusion is significant. Al-though urgent surgical interventionin chronic CTS is seldom needed,rapid surgical management is re-quired to perform nerve-sparing de-compression in the patient withACTS.4,5 Nerve contusion can be ad-equately treated with rest and closeobservation.

Kent A. Schnetzler, MD

Dr. Schnetzler is Orthopaedic Surgeon,

Springfield, MO.

Neither Dr. Schnetzler nor a member of

his immediate family has received

anything of value from or owns stock in a

commercial company or institution

related directly or indirectly to the

subject of this article.

Reprint requests: Dr. Schnetzler, 5806

South Foxboro Trail, Springfield, MO

65804.

J Am Acad Orthop Surg2008;16:276-

282

Copyright 2008 by the American

Academy of Orthopaedic Surgeons.

276 Journal of the American Academy of Orthopaedic Surgeons

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Anatomy andPathophysiology

The carpal tunnel is a small, rela-tively fixed-volume space normallyoccupied by the four superficialistendons, the four profundus tendons,the flexor pollicis longus tendon,and the median nerve (Figure 1).Anomalous structures within thecarpal tunnel are associated withboth ACTS6 and chronic CTS. Someauthors have characterized the car-pal tunnel as a closed space.7 Thevolume of the carpal tunnel mea-sures approximately 5 mL, with across-sectional area of approximate-ly 185 mm2.8

The carpal tunnel is surroundedby unyielding margins. It is borderedradially by the scaphoid, the trapezi-um, and the fascial septum overlying

the flexor carpi radialis. Its ulnar bor-der consists of the hook of thehamate, the triquetrum, and thepisiform. The dorsal border isformed by the carpal bones, and the

volar border by the flexor retinacu-lum. This latter structure consists ofthe deep forearm fascia, the trans-verse carpal ligament, and the distalaponeurosis between the thenar andhypothenar musculature. The nar-rowest and most vulnerable part ofthis unyielding tunnel lies immedi-ately below the transverse carpal lig-ament. Variations in the diameter ofthe carpal tunnel do occur. In addi-tion to size variations, conditionsthat increase the contents of the car-pal tunnel (eg, proliferative tenosy-novium) can contribute to the etio-logic process.

The inability of the carpal tunnelto expand with mass-occupying le-sions or structures can lead to in-creased pressure within the tunnel.Analogous to a compartment syn-drome, the final result of this in-creasing pressure is the cessation ofblood flow caused by reduction in

the pressure differential through thecapillaries supplying the mediannerve, leading to median neuropa-thy. Rydevik et al9 used an experi-mental rabbit model to demonstrate

that acute compression of a nervemay cause persistent impairment ofintraneural microcirculation via me-chanical damage to blood vessels.Follow-up studies demonstrated theimportance of the duration of nervecompression.10 Szabo4 reported thatcarpal tunnel pressures within 30mm Hg of diastolic blood pressurecan cause significant motor and sen-sory dysfunction, which suggests is-chemia as a cause of conductionblock. Therefore, a hypertensive pa-tient may display symptoms of CTSonly after carpal tunnel pressureshave significantly exceeded those ofa normotensive patient. Conversely,a hypotensive patient may demon-strate symptoms at significantlylower tunnel pressures than a nor-motensive counterpart. Decreasedmicrovascular blood flow clearlyplays a role in acute nerve compres-sion.11 This hypothesis is supported

Table 1

Unusual Conditions and

Pathologies Associated With Acute

Carpal Tunnel Syndrome

Pyogenic infection

Septic arthritisFilarial infection

Calcifying tendinitis

Hydroxyapatite deposition

Pseudogout

Snake bite

Combined organ transplant

Soft-tissue infection

Metacarpal osteomyelitis

Respiratory tract infection

Peritendinitis calcarea

Periarthritis

Toxic shock syndrome

Hansen disease

Decompression illness

Intracarpal canal sepsis

Parvovirus infection

Tumoral calcinosis

Alendronic acid deposition

Tophaceous gout

Pigmented villonodular synovitis

Tumescent fluid administration

Interleukin-2 therapy

Figure 1

Transverse section through the carpal tunnel. The median nerve is the most

superficial structure. A = ulnar artery, C = capitate, CT = carpal tunnel, fpl = flexorpollicis longus tendon, H = hamate, M = median nerve, P = pisiform, PCL = palmarcarpal ligament, S = scaphoid, t = profundus and sublimis tendons, T = triquetrum,TCL = transverse carpal ligament, U = ulnar nerve, UT = ulnar tunnel. (Adapted fromSzabo RM, Steinberg DR: Nerve entrapment syndrome in the wrist. J Am AcadOrthop Surg1994;2:115-123.)


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by the correlation between nervefunction and blood pressure. Com-pression of the nerve affects micro-circulation, increases vascular per-meability (leading to edema), andimpairs axonal transport (all leading

to nerve dysfunction).12

Any increase in pressure withinthe carpal tunnel may adversely af-fect median nerve perfusion. Proxi-mal to the flexor retinaculum, themedian nerve receives its blood sup-ply from both the radial and ulnar ar-teries. If a median artery is present,it usually terminates in the distalforearm. Rarely, it accompanies themedian nerve through the carpaltunnel.13 Thrombosis of a persistentmedian artery has been implicated

in ACTS.14,15 Obstruction of venousreturn within the perineural andepineural plexuses can lead to anox-ia and endoneural edema.16 Fluid canleak from disrupted endoneurial mi-crovessels into the endoneurium.With an intact perineurium, this flu-id leakage can increase endoneurialpressure and create a mini com-partment syndrome within the fasci-cle.13,17 The magnitude of conduc-tion blockage and edema are related

to the magnitude and duration of thecompressive force.18 Acute compres-sion of a nerve can cause impairedintra- and extrafascicular circulationfrom mechanical injury of a specificnerve segment.9 Lundborg et al19 pro-vided compelling evidence to sup-port the ischemia theory. Using anarm tourniquet, they showed that is-chemia is a greater determinant ofdysfunction than is mechanical de-formation. The authors also foundthat nerve fiber viability is acutelyaltered at critical pressure between60 and 90 mm Hg.

Swelling within the endoneuriumcan interfere with nerve function viaalteration in an axonal ionic environ-ment,19 and blockage of axonal trans-port can occur with pressures of 30mm Hg that last for at least 2hours.20 Time for recovery of normaltransport was correlated with themagnitude of compression.21 Higher

pressures resulted in changes innerve function and structure.22 Low-pressure balloons placed adjacent tonerves quickly produced endoneuraledema and persistent increase in in-traneural pressure, which reduced

function in a dose-dependent man-ner. The amount of endoneuraledema appeared to be important.23

Experimental studies indicate a dose-response curve, with a correlationbetween greater duration and pres-sure, and greater nerve dysfunction.A direct cause-and-effect relation-ship between carpal tunnel pressureand median nerve dysfunction wasdemonstrated in an animal model.24

The acuity and time-dependencyof pressure increase within the carpal

tunnel is another important determi-nant of median neuropathy. In a nor-mal hand, pressure within the carpaltunnel is approximately 2.5 mm Hg.With wrist flexion or extension, max-imum pressures remain well below32 mm Hg, the average capillary re-fill pressure.25 However, with maxi-mal flexion or extension, pressure in-creases to approximately 30 mm Hg.The earliest detectable manifestationof nerve compression occurs with re-

duction of epineural blood flow to be-tween 20 and 30 mm Hg. Axonaltransport is impaired, and the normo-tensive patient may experience par-esthesia.26 Lim et al27 demonstrateda dose-responsive reaction during de-velopment of acute pressure-inducedmedian neuropathy in a rabbit model.At higher compartmental pressures,progressively less time is required toproduce conduction blockage.28 In an-other study, graded compression ofthe median nerve in the carpal tun-nel affected grip force and tactile sen-sibility at various sensory nerve ac-tion potentials, but not in parallelwith reductions in the sensory poten-tials.29

Etiology

Potential etiologies of ACTS includewrist and carpal bone trauma, includ-ing fracture and fracture-dislocation;

hemorrhagic, vascular, and bleedingdisorders; chronic and acute rheuma-tologic conditions; and, less com-monly, infection; anomalous anato-my; burn and thermal injury; andhigh-pressure injection injury. A

patient with a chronic condition maydevelop ACTS, but as an associatedpathology rather than as a directresult of the chronic condition.

Traumatic

Distal radius fracture is likely themost frequent cause of traumaticACTS secondary to compression ofthe median nerve caused by hemor-rhage or edema.30 Volar displace-ment of fracture fragments or directcontact with the median nerve can

result in direct nerve contusion orACTS. Patients with contusion inju-ries typically had immediate senso-ry loss and nonprogressive symp-toms,31 a finding that aids indistinguishing between these twoconditions.

Graf and Dorn32 described attritionand rupture of the flexor pollicis lon-gus tendon secondary to a scaphoidpseudarthrosis that led to ACTS.ACTS caused by rupture of the pal-

maris longus has been reported.33Olerud and Lnnquist34 describedACTS associated with a nondisplaceddistal pole of the scaphoid fractureand a nondisplaced ipsilateral 5thmetacarpal base fracture. Prompt sur-gical decompression of a tense he-matoma resulted in immediate painrelief, with near normal sensation in12 hours and completely normal sen-sation in 3 weeks. Fracture healingwas uneventful. We have observedACTS in association with an isolatedscaphoid fracture.

In a study by Brske et al,35 ACTSdeveloped in 11 of 128 distal radiusfractures. Prompt recognition andsurgical decompression combinedwith external fixation decreased thepersistence of symptoms. In anotherstudy, ACTS developed in 2 of 109displaced distal radius physeal frac-tures treated with manipulation un-der anesthesia.36 Marked initial mal-

Acute Carpal Tunnel Syndrome


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position was a primary risk factorfor development of complications.In patients with displaced distal ra-dius fractures, carpal tunnel pres-sures measured before, during, andafter closed reduction demonstrated

acutely increased pressures and anovert compartment syndrome.37

Injection of local anesthetic into afracture hematoma increases pres-sure within the carpal tunnel, asdoes volar flexion of the wrist.38

Other wrist and hand trauma re-sulting in ACTS has been noted, in-cluding fracture-dislocation of thewrist. Gong and Lu39 described sev-eral cases of metacarpal fracturescomplicated by ACTS. Weiland et al40

described volar fracture-dislocations

of the second and third carpometa-carpal joints associated with ACTS.Martinet et al41 reported on carpalbone fractures (other than thescaphoid) that resulted in ACTS.McClain and Wissinger42 describednine cases of ACTS related to a vari-ety of causes, including transscaphoidperilunate dislocation, Colles frac-ture, and distal radius epiphyseal frac-ture. An unusual traumatic volar dis-location of the trapezoid previously

unreported in association with ACTSwas recently discussed.43 Three of 13patients with distal row carpal frac-ture developed ACTS.44

Immobilization of the injuredwrist and hand in positions ofmarked flexion also can cause ACTSby decreasing the volume of the car-pal tunnel. Finger flexion and fore-arm supination, as well as wrist ex-tension and flexion, can dramaticallyincrease pressures within the carpaltunnel.13 As early as the 1930s, thecommon practice of immobilizingwrist fractures in marked flexion (ie,Cotton-loader position) was recog-nized as deleterious.2 In a study byKuo et al,45 healthy volunteers withtheir wrists splinted in neutral expe-rienced the least compression of themedian nerve.

Gelberman et al46 reported that in-tracarpal canal fluid pressures in-creased with flexion of the wrist

following immobilization of Collesfracture; 45% of wrists had pressures>40 mmHg with 40 of flexion. A de-crease in carpal tunnel cross-sectionalarea with wrist flexion has been notedon magnetic resonance imaging

scans.47

Trauma may result in contu-sion of the median nerve. It must bedifferentiated from injury secondaryto nerve compression because treat-ment of these two distinct patholo-gies differs.4 A volarly displaced dis-tal radius fragment may compress themedian nerve against the proximaledge of the flexor retinaculum.48

ACTS is differentiated from nervecontusion by characteristic progres-sion of symptoms resulting from el-evated pressure caused by swelling

and edema. A patient with nervecompression may need rest andobser-vation, whereas one with ACTS re-quires urgent surgical intervention.4

Use of external fixation for thetreatment of distal radius fractureswith excessive wrist distraction mayhave important implications in thedevelopment of ACTS. In one study,the position of the distracted wristhad a considerable effect on carpaltunnel pressure. Extended wrist po-

sitions were associated with greaterincreases in carpal tunnel pressures,and flexed positions were associatedwith lesser increases in carpal tun-nel pressures.49 In a cadaveric study,a relationship was found betweenwrist distraction and increased car-pal tunnel pressures upon simula-tion of the distraction forces experi-enced with distal radius externalfixation.50

Atraumatic

Atraumatic causes of ACTS arerare, but several unusual etiologieshave been described (Table 1). Hem-orrhagic, vascular, and bleedingdisorders are the most commonatraumatic etiologies, including he-mophilia,51,52 von Willebrand dis-ease,53 oral anticoagulant use,54-57

rupture of the median artery,58

thrombosed aneurysm of an epineu-ral vessel,59 calcification,60 and aneu-

rysm61 or thrombosis14,15,62 of a per-sistent median artery. Bleeding canbe intraneural in the overly antico-agulated patient,63 can occur into thecarpal tunnel, or can be spontane-ous, with no apparent cause. A pa-

tient who presents with ACTS asso-ciated with bleeding tends to havemore severe pain, rapid onset ofswelling, and neurologic symptomsthat appear early and progress rapid-ly (ie, mass effect).2

Anomalous anatomy that crowdsthe carpal tunnel may predispose apatient to ACTS. Kono6 reported onACTS resulting from anomalousflexor digitorum superficialis musclebellies within the carpal tunnel.Symptoms occurred within 2 hours

of internal fixation of a scaphoid frac-ture associated with transscaphoidperilunate dislocation. Ametewee etal64 described an anomalous flexordigitorum superficialis muscle adher-ent to the median nerve as the causeof ACTS. Multiplicity and frequencyof anomalous structures within thecarpal tunnel may be higher than pre-viously anticipated.65

Diagnosis

Careful clinical examination leadingto prompt diagnosis and surgicaltreatment is critical to reducing oreliminating the sequelae of ACTS.Steadily progressive intense pain anddysesthesias or paresthesias in themedian nerve distribution are char-acteristic of ACTS. Surgery to re-lieve pressure within the carpal tun-nel performed up to 40 hours afterthe onset of symptoms has beenshown to hasten the return of nor-mal two-point discrimination to thehand. However, some patients withsimilar early return of function werereleased at just 4, 6, and 12 hours.5

Early release resulted in earlier andmore complete return of functioncompared with patients released lat-er and those with nerve contusion.In patients with delayed diagnosisand treatment, more adverse out-comes secondary to intraneural scar-



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ring have been reported,30,66 and re-turn of function is delayed and morevariable. Thus, early and accurate di-agnosis combined with early decom-pressive surgery is advantageous foroptimal results, including the avoid-ance of the undesirable long-term se-quelae of median neuropathy.

In some patients with acute trau-ma, the median nerve is contusedrather than compressed. The distinc-tion between chronic CTS andACTS has treatment implications;thus, it is also important to differen-

tiate between acute median nervecontusion and ACTS.4 Nerve dys-function with contusion appears ear-ly, whereas symptoms with nervecompression appear more graduallyand progress as edema increases.

With contusion injuries, sensoryloss appears immediately and typi-cally does not progress.31 Contusionrequires only rest and observation,while acute median nerve compres-sion requires surgical decompres-sion. The patient may have difficul-ty recalling onset of numbness in thesetting of acute trauma. When thepatient cannot be observed in acontrolled setting, specific instruc-tions regarding worrisome progres-sive symptoms must be given. The

physician should be alerted to a pos-sible diagnosis of ACTS when a pa-tient returns to the emergency de-partment with worsening symptomsand neurologic dysfunction afterwrist or hand trauma. Loss of two-point discrimination (normal, 6mm) with readings >15 mm general-ly indicate 100% sensory loss andcan easily be incorporated into theclinical examination.

Pressure measurement of the car-

pal tunnel with a wick catheter orthe STIC device (Stryker, Kalama-zoo, MI) can provide additional in-formation to help distinguish ACTSfrom contusion (Figure 2). Using apressure threshold of 40 mm Hg,Mack et al5 noted an average pres-sure of 52 mm Hg in four of fiveblunt wrist trauma patients withACTS; normal pressures were notedin two patients with nerve contu-sion only. However, not all physi-cians have such equipment avail-able, nor may all feel comfortablemeasuring pressures reliably in thecarpal tunnel. Some physicians mayadvocate a nonsurgical trial of strictelevation and observation in theemergency department to alleviatesymptoms. Others may forgo pres-sure measurements and elevation,and, when ACTS is suspected, mayproceed directly to decompressivecarpal tunnel release. Likewise,

some physicians may feel comfort-able casting patients who presentwith acute wrist trauma, while oth-ers never place a cast in the emer-gency department, instead advocat-ing splinting in all cases. No matter

the treatment algorithm chosen, thephysician must be aware of andmake a prompt diagnosis of ACTS.

Surgical Treatment

When ACTS is to be treated concur-rently with surgical stabilization ofwrist trauma (most often a distal ra-dius fracture or fracture-dislocation),a careful preoperative plan address-ing proposed incisions must bemade. To decompress the carpal tun-

nel, a standard longitudinal or ser-pentine palmar incision can be madein line with the ring finger metacar-pal. The decision to cross the wristcrease is dictated by surgeon prefer-ence. Regardless of the incision cho-sen and incision length, the surgeonmust ensure that the carpal tunneland, in most cases, distal forearmfascia are adequately decompressed.A longer incision that crosses thewrist crease and extends proximally

may afford a better view of the con-tents of the carpal tunnel and allowfor easier decompression, such asevacuation of a tense hematoma orconstricting proximal structures (eg,antebrachial fascia).

Mack et al5 suggested the follow-ing treatment algorithm: (1) Consid-er ACTS in any patient with severe,progressive wrist pain and objectivesensory dysfunction even after frac-ture reduction. (2) Treat the patientwith nonsurgical measures (eg, ele-vation, cast or dressing release, ob-servation) for 2 hours. If these mea-sures fail to relieve symptoms, thesurgeon should consider measuringcarpal tunnel pressures directly witha wick catheter or other device todistinguish ACTS from nerve contu-sion. (3) When pressures exceed 40mm Hg, carpal tunnel release shouldbe done within 8 hours of onset ofsymptoms. To eliminate proximal

Figure 2

Carpal tunnel pressure measurementtechnique. The needle of the measuringdevice is inserted 1 cm proximal tothe proximal wrist crease and slightlyulnar from the palmaris longus tendon.If the palmaris longus is absent, the

needle can be inserted in-line with thelong axis of the ring finger metacarpal.The needle is directed distally at a45 angle and slightly radially, thenadvanced until it strikes the bony floorof the carpal tunnel. The needle iswithdrawn a few millimeters to avoiderroneous readings caused by tissueblocking the needle lumen.5,31



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constriction, the median nerve re-

lease should be extended proximally

under the antebrachial fascia and su-

perficialis muscles.

For wrist fractures treated with

closed reduction and stabilization

with percutaneously placed smoothwires, there is little difficulty in add-

ing an incision to release the carpal

tunnel. This is easily done concur-

rently with the originalsurgery. In the

patient in whom ACTS develops

later, carpal tunnel release can be per-

formed as a second surgery. If a volar

buttress plate is to be placed on the

distal radius via a flexor carpi radia-

lis incision, the incision can be ex-

tended in a sigmoid fashion to incor-

porate the carpal tunnel release, thusavoiding a narrow skin bridge and the

risk of skin necrosis. When two sep-

arate or multiple incisions are re-

quired, the surgeon must ensure ad-

equate skin bridges to avoid necrosis.

Summary

ACTS is often related to trauma, par-ticularly distal radius fracture andfracture-dislocation of the wrist.

However, nontraumatic etiologies ofACTS have also been reported. Ear-ly clinical recognition of ACTS isparamount because, unlike chronicCTS, the acute form requires promptrecognition and urgent decompres-sive surgery. It is important to differ-entiate between ACTS and nervecontusion because treatment is dif-ferent for each. Symptoms of ACTSare similar to those of compartmentsyndrome and include intense andprogressive pain with increasing dys-esthesia and dysfunction. Persistentsymptoms are likely related to acu-ity and duration of compression,leading to microvascular compro-mise and neural dysfunction.

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