NON-OSSEOUS COMPLICATIONS FOLLOWING DISTAL RADIUS FRACTURES

Peter J. Stem, M.D.* Ron G. Derr, D.O. INTRODUCTION

Colles' fracturesareoftenconsideredlightlyand treated

inadequately6'12'13'24.

A poor outcome canresult in per-manentloss ofmobility, weakness,andpain12. Bacornand Kurtzke6 stated that Colles' fractures result in some residual impairment inhand andwristfunctionevenunder themostfavorablecircumstances, andonly3%ofpatients are free ofdisability followingthis fracture.

Complications following Colles'fracture may be classi-fiedasosteoarticular, softtissue, orboth'3.Inareview of 565 patients, Cooney et

al.13

reported a 31% overall complication rate. They noted a positive correlation be-tween fracture severity and the incidence of complica-tions. Zemel also correlatedanincreasedcomplicationrate withinadequate reduction61.

This paper reviews soft tissue complications following Colles' fractures. Complication categories include:

1. Nerve injury

2. Post-traumatic sympatheticdystrophy 3. Tendon injury

4. Compartment syndrome 5. DeQuervain's tenosynovitis

6. Dupuytren's disease/Palmar fasciitis 7. Shoulder-hand syndrome

8. Hand stiffness

NERVE INJURY Median Nerve

MediannerveinjuryiswellrecognizedfollowingColles' fractures and is the most frequent

complication'18.

Causes ofnervedysfunctioninclude hematoma within the carpal tunnel or beneath the deep forearm fascia at the fracture site, wrist hyperextension at the time of injury causingnervestretch, injectionof localanesthetic into the fracture hematoma, immobilization in wrist flexion, and excess callusfromhealing ormalunion20.

The incidence of median nerve injury is variably re-ported. In 1984, McCarroll34 reviewed the literature and reported an incidence from 0.2-3.2% depending on the

degree of symptoms and the duration of

follow-up.

Both

Wainapel et

al.57

and

Stewart55

noted a 12% incidence;

Aro et

al.2,

8%;

Cooney

et

al.13,

7%;

Lynch

and

*Departnent

ofOrthopaedic Surgery, Universityof Cincinnati Col-legeofMedicine, 213Bethesda, Cincinnati, Ohio45267-0212

Lipscomb30, 3%; and Stark53, 5%. Wainapel et al.57 suggested that electromyography (EMG) was not to be considered more sensitive than the history and physical examindetecting mediannervedysfunction. It should only be utilized to "confirm" the diagnosis.

Hematoma and swelling following Colles' fracture can causeacuteonsetofmediannervedysfunction1828. Com-pressioncanbelocated within the carpaltunnel or deep to the forearmfascia nearthe fracture site28. Hematoma in the carpal tunnel causing median nerve compression has been reported due toanticoagulant therapy7'18'28. Kong-sholm and Olerud25 stated that hematoma formation can berelatedtothedegree oftrauma atthetime offracture, and they related increased tunnelpressures to increased Frykman classification. Lewis28 drewattention to forma-tion of hematoma and subsequent fibrosis beneath the deep fascia atthe level of the fracture site. He presented four cases, stating that this can be anisolated finding or occur in association with compression within the carpal canal. Ifsymptoms of carpaltunnel syndrome are severe enough to warrant decompression and findings in the carpal tunnel are normal, the incision should be extended proximally to include division of the antebrachial fascia overthe fracture.

Clinically, it may be impossible to distinguish between direct median nerve contusion or stretch, and nerve compression due to increased carpal tunnelpressure7'19.

Directnerveinjuryis reported, but is felttobe raredueto soft tissue protection offered by the pronator quadratus and the flexor tendons34. Acute onset of symptoms can follow reduction maneuvers. To aid in the diagnosis, a good neurologic exam before and after reduction is

mandatory34.

The ability to directly measure increased pressure within the canal and to compare this to estab-lished pressure thresholds has increased our recognition ofnerve compression followingwrist

trauma18'

Post-reduction radiographsarealso neededtolookfora bonyfragment (spike)which may betentingthe nerve Wong and Pho59 and Kumar26 noted median nerve im-pingement at the fracture site due to displaced volar fragmentswithnoactual contactofboneandnerve. Goldie andPowell20reported the onlycaseoftransfixation of the mediannervebyavolarbonyspike.All resolvedfollowing

decompression.

Hematoma block anesthesia is also a potential causeof median nerve

compression25.

Kongsholm and

Olerud25

matched controls, measuring carpal tunnel pressures by the wick catheter technique. Measurements prior to manipulationwerecompared withthosefollowing injection of ten milliliters of 1% lidocaine. An average pressure increase of9.7 +/- 7.4 mmnHgwas recorded. Increased pressures correlated with fracture severity.

Positionof wrist immobilizationplays animportantrole in median nerve dysfunction. Specifically, the Cotton-Loder position (acute wrist flexion, ulnar deviation and forearmpronation)has beenimplicated byseveral authors and isstronglydiscouraged3034'35'4553. The carpaltunnel pressure is increased with the wrist in neutral position following Colles' fracture and strongly increased in posi-tionsofpalmarflexion or extension

18"9'25.

Kongsholmand Olerud25noted a 0.8 mmHglinear pressure increase for each degree ofvolar flexion.

Finally, radial malunion may be a contributing

factor28'45. Aroet al2observed that 85%ofpatientswith latemediannervecompression had radial collapse2. Wong and Pho59 suggested an above elbow cast to maintain radial length may be worthwhile in preventing carpal tunnel syndrome.

It is generally agreed that early recognition and

treat-mentof mediannervedysfunction is important in preven-tion oflongtermdisability6"7'28'34. Treatment varies with severity ofsymptoms. Mild symptoms canbemonitored, or the wristcan bebrought into a more neutralposition, andtight bandages loosened. When concerned,

electrodi-agnostic studies can be obtained to confirm the

diagnosis57.

Immediate decompression should be consid-eredinthe followingcircumstances:

1. Volar fracture spike fragments are noted on post-reductionfilms inassociationwith symptoms.

2. Acute unresolving symptoms occurfollowing reduc-tionmaneuvers.

3. Significant symptomspersistfollowing adjustment of wrist positionfromaflexed to a more neutral

position34.

4. Finally, ifan openreduction ofthe radial fracture is being carriedout, concomitant mediannerve

decompres-sion is

recommended34.

Ulnar Nerve

Ulnar nerve dysfunction is much less common than median nerve

dysfunction34.

Bacorn and

Kurtzke6

noted one caseof isolated ulnarnervepalsyoutofmorethantwo thousand workmen's compensation cases in New York State.

Frykman17

reporteda0.9%incidence.

Zoega62,

and Vance and

Gelbennan56

each reported three cases of acute isolated ulnar neuropathies. These were noted in younger patients with higher injury traumas and with significant displacement of the distal fracture fragment. Aroetal.2 reporteda 4%late ulnar nervepalsyassociated with either Colles' fracture or volar subluxation of the ulnar head.

Several factorsmake the ulnar nerveless vulnerableto injury. VanceandGelberman56noted that therelationship of the ulnar andmediannerves to the bonesoftheforearm areverynearlyidentical fromthemid-forearmtothe wrist area. Bothnerves areprotected from bone by the prona-tor quadratus muscle and the digital flexor tendons. In addition, the ulnar nerve has more excursion across the wrist than the median nerve34, this is because Guyon's canal is shorter in length and more removed from the fracture site. Also, the volar carpal ligament is less substantial than the transverse carpalligament.

Treatment for these injuries varies and depends on presentation. Acute neuropathies generally require moni-toring with good return of function anticipatedin four to five months. Robinson et al.46 recommended aggressive treatmentfor severedysfunctionand found that electrodi-agnostic testing was ahelpful predictor of the benefit of surgical decompression with profound changes havingthe worst results. We recommend decompression for those cases presenting or worsening with closed reduction, as wellas latepresentations.

Combined medianand ulnar nerve injury is exceedingly

rare'1747'51'61.

SiegelandWeiden51 reported three cases, bothin comminuted fractures with persistent edema. No fracture fragmentswerecompressing thenervesin either case. Recovery with conservative treatment was com-plete in two of the three cases with one patient lost to follow-up.

Radial Nerve

Injury to the superficial branch of the radial nerve followingColles'fractures isextremelyrareand isusually of iatrogenic origin. Cooney et

al.13

noted five of 565 Colles' patients with radial nerve injuries, all acute pre-sentations following treatment. Three were caused by improper immobilization, and two byexternal pin fixation of the fracture. All resolved with removal of theoffending compressing or irritating agent. No late radial nerve injuries were noted. McCarroll34 noted that the radial nerve is uncommonly injured, unless via a direct lacera-tion.

POST-TRAUMATIC SYMPATHETIC DYSTROPHY Post-traumaticsympathetic dystrophy(PTSD)orreflex sympathetic dystrophy (RSD) is an ill defined syn-drome35. It is characterized by tenderness and pain,

burning or aching in nature, and disproportionate to the underlyinginjury854. Inadditionthereisvasomotor insta-bility, swelling, and

stiffness5'8'43.

Itsetiology isunknown, butit is commonly triggered byminor

injury5'8'27'54.

The incidence ofPTSDfollowing Colles'fractures in the literature is controversial, ranging from 2 to

37%4'5.

Retrospective

serieS6,17,2129,43.44

report a lower

inci-dence, while prospective studies3-5'55 which follow the patientsoonerafterinjurystate a higher incidence.

Atkins and co-workers3-5, suspecting a more common occurrence than realized, studied this extensively. In a prospective study following patients from the time of fracture, they notedPTSDin twenty-sevenof109(25%)5

patients atnine weeks after fracture. A secondfollow-up at six months noted a decreased incidence to 17% with eight patients lost to follow-up. A repeat study utilizing

dolorimetry4, an objective instrument that quantitates tenderness, noted an incidence of tenderness in twenty-three ofsixty(37%) patientsat two tosix weeksafter cast removal.Thereappears tobe nocorrelation ofoccurrence ofPTSDwithpatient'sage, severity of fracture,numberof

reductions,

or

adequacy

ofreduction4.

Plewes43 noted the plain radiographic appearance of PTSDtobe aspottyrarefaction (Sudeck's atrophy). This is notedmostlyinthephalanges, metacarpals, carpus,and distal radius and ulna. The shafts of the bones are only slightly affected. These changes develop six to eight weeksfollowing injury. This incontrast tothegeneralized ground glass appearance seen with disuse osteoporosis whichrequires longer todevelop.

Tests available to substantiate this syndrome include bone scan, thermography, and sympathetic blockade18. Bone scans will show diffusely increased uptake on the delayed

phase31.

Thermographywilldisplayabnormal heat patterns not conforming to typical neurological topogra-phy. Sympathetic blockade is useful as both a diagnostic andtreatment adjunct.

Thekey to treatmentisearlyrecognition.

Plewes43

felt thatif thediagnosiswas madewithin six weeks ofonset, thehandresponded welltoconservativemeasures. These can include heat (105-110°), elevation, graded function,

sympathetic blockade, or vigorous desensitization. Stein reportedfive cases of Sudeck's Syndrome following Col-les' fracture, all respondingto median nerve decompres-sion at the wrist54. Surgical sympathectomy is indicated only when all other modalities have failed and there has beena positive response to sympathetic blocks. Chronic disability is often relatedto treatment delay8.

TENDON INJURY Extensor Tendons

Extensor tendon ruptures as a complication of Colles' fractures occur three times more commonly thanflexor tendons9. The extensor pollicis longus (EPL)is the most

conu1on1 61.

The site of EPL rupture following Colles'

fractures is proximal to the extensor hood. The time interval between fracture and rupture is usually one to twelve

months32.

Engknist and

Lundborg16

did

microan-giographic

studiesincadavers whichshowed that the EPL intheregion of Lister's tubercle waspoorly vascularized.

Theypostulated that a hematoma within the third dorsal compartment could interfere with tendon nutrition and result in delayed rupture. McMaster36 concluded that a partial severance of the tendon at the time of fracture resulted in incomplete healing and ultimate rupture. He placed less emphasis on the theory of disruptive tendon blood supply leading to local tendon necrosis. Sadr49

attributed EPLrupture tocrushischemia, attritionover a bonyspur orcallus,oradherencetocallus. Helal etal.23in sixteen cases noted a higher incidence of EPL ruptures with undisplacedColles' fractures. Atsurgicalexploration, the extensor retinaculum was still intact and held the tendons tightly against the dorsal radius. Disruption was felttobe attritionaland occurred atthe distal edge ofthe retinaculum. In displaced fractures the extensor retinacu-lum was torn loose from the radius, which allowed the tendons tobe separated from thefracture site.

FlexorTendons

Ruptures of flexortendons occurmuch less oftenthan ruptures of extensor

tendons9'10485260

. Etiologies

in-clude rheumatoid arthritis, forearm fracture, wrist dislo-cation, contusion, athletic injury, carpal bone anomaly, or

tenosynovitis41.

Anatomically, the flexortendons are sep-arated from the distal radius by the pronator quadratus, which tends to protect the tendons from insult and subsequent

rupture52660.

The high tensile strength and flexibility of these tendons also protects them. Normal tendons have abuilt-inreserve of strength and excessive force will not cause rupture, the bony insertion or the musculo-tendonousjunction will givewayinstead. For the tendontobecome the"weak link"atleast50% ofitsfibers mustbe

cut22.

Profundusruptures occurfive times more frequentlythansublimisruptures,with theringandmiddle fingers being mostcommon.

Boyes

et

al.9

in a review of

eighty

flexor tendon

ruptures documented only two (3%) flexor tendon

rup-tures following a wrist fracture. Southmayd et al.52 re-ported one case of immediate flexordigitorum profundus

(FDP) andflexor digitorumsuperficialis (FDS) rupture to the index finger. This was thoughtto be secondary to a volar bony spike which had penetrated the pronator quadratus muscle. Younger and

DeFiore6o

in 1977 noted that only threecases offlexor tendon ruptureassociated with Colles' fracture had been reported in the literature

priortotheirreportofonecase.Theynoted ruptureof the FDP and FDS to the small finger along with FDS of the ring finger secondary to attrition over the ulnar head. Diamond and

Newman14

in 1987 reported a case of multiple flexor tendon ruptures thought to be due to

compromised tendon blood supply and eventual rupture due to prolonged pressure over a malunited fracture.

Rymaszewski and Walker48 also reported a case of attri-tional rupture associated with incomplete healing of a partialtendon laceration.

Treatmentofthese injuries is beyond the scope of this paper. Secondary tenorrhaphy is usually not feasible, making tendontransferorintercalatedgraftthepreferred treatment.

COMPARTMENT SYNDROME

An acute compartmentsyndrome alongwith itspossible sequelaeofVolkmann's ischemiccontractureis uncommon following Colles'

fracture'

133,40,50. Cooney etal.13 noted that three of their four patients with an established Volkmann's contracture following a Colles' fracture had constrictingcastsretaineddespite persistent complaintsof pain. Continuous useofanalgesics had masked thepain in twoof thepatients. Patients shouldbe monitoredclosely, with frequent neurovascular checks and cautious use of analgesic medication. Compartment pressures should be measured and treatedpromptly with fasciotomy.

DEQUERVAIN'S TENOSYNOVITIS

Stenosing tenosynovitis following a Colles' fracture is extremely rare. Only one study mentioned this as a possible

complication61.

Due to the proximity ofthe first dorsal compartmentpulleytothefracturesite, edema and hematoma can lead tothickeningof the pulley, synovitis, and scar. The tendonsofthe abductorpollicislongus and extensor pollicis brevis can become constricted by sur-rounding synovitis andscar.As withDeQuervain'sdisease due tootheretiologies, cortisoneinjection and/orsplinting arefirst-linetreatments. Ifresults areless thanadequate, divisionof the thickenedpulley is suggested.

DUPUYTREN'S DISEASE/PALMAR FASCIITIS The literature regarding Dupuytren's disease in associ-ation withColles'fracture is sparse. Bacornand Kurtzke6 noted a 0.2% incidence. Stewart et al.55 reported an incidenceof4%atthreemonthsafter fracture and11% at six months. All cases were mild and mostly nodular in variety, with little progression as late as twenty-seven months following fracture. This association was noted

mostfrequentlyamongolder female patients. There was

no correlation with fracture severity. The nodules are

usually

painful in contrast topalmarfibromatosis unasso-ciated with Colles' fractures. Treatment is decidedly

nonoperative, as the nodules usually resolve or become asymptomatic overtime.

SHOULDER-HAND-FINGER SYNDROME

This condition ishighly complexandaconcise definition is difficult to find.

Moberg38

describes it as

having

two

components, a shoulder component and a hand-finger component. The shoulderis affected primarilybyeithera traumatic event to the upper extremity or by a visceral disease such as a heart condition21. Hand and finger involvementfollowstheshoulder symptoms and the elbow is never affected. Some feel it is a clinical form of RSD; however, the possible visceral etiology, less hand pain, and fingers stiff in extension rather than flexion help distinguish thissyndromefromRSD. Others attribute itto a decrease in the venous and lymphatic pumping mecha-nism ofthe upper extremity brought on by limitation of active shouldermotion1738. Causesfollowing Colles' frac-ture include excessive wrist flexion with median nerve dysfunction, radial nerve irritation due to pin irritation, severelydisplacedandunreduced fractures, orprolonged shoulderimmobilization'3.

The incidence ranges from 0.1 to

10%6,13,17.

Frykman'7

had the bestcontrolledstudy and noted a 2.1% incidence. He noted that the conditionnever occurredin patientsless thanfortyyearsand was mostcommonafter age fifty. He also noted a higher incidence (50%) in patients requiring repeated fracture reduction compared with only 4% in those requiring a single reduction. Emotional instability may also play an important role. Along with inactivity, Frykman included this as one of the two components necessaryfor development ofthissyndrome. One-thirdof the patients with this complication were emotionally un-stable.

The clinicalcourse is in three

stages'7.

The first stage begins less than twenty daysfollowingtrauma. It involves burning shoulderpain followed ashort timelater by hand and finger pain. There is also a loss of passive finger motion and flattening of the digital flexorcreases. Stage two is characterized by the absence of shoulder pain, decreasedhand and finger pain, and changes in the hand similartopalmar fibromatosis.Stagethree has nopainbut "frozen" hand and finger motion due to fibrosis and contractures. Each ofthefirsttwostages canlast three to sixmonths, with the last stage possibly leaving irrevers-ible changes. Resolutioncanalso occur spontaneously or withtreatment in each stage.

Treatment isdifficult and depends onwhat one consid-ersthecause'7. If it is felt that theetiology is mechanical, treatmentismainly preventative. Frykmanstated thathe kept the incidence very low "simply by instituting mea-sures topromotethecirculationrightfrom thestart". Use ofaslingisstronglydiscouragedbecauseitlimitsshoulder

motion38'58.

Earlyactive motionof the shoulder and hand are

encouraged'5.

Fingersshouldremainfreefrom immo-bilizationin the castorsplint58. Ifpatientsarereluctant to begin early motion, monitored physical therapy sessions are

initiated'7.

Afteronsetof the syndrome, treatmentis generally geared toward vigorous, progressive functional

motion of theinvolvedupperextremity58. Ifonefeels that this is a variant of RSD, treatment should be directed toward decreasing the sympathetic output to the upper extremity via chemical sympathetic blockadesor sympath-ectomy.

HAND STIFFNESS

Hand stiffness following Colles' fracture, although not considered a major complication, can cause

significant

morbidity6"13'21'39

Itmaybe due toedema, immobility, or pain39. The incidenceis unclear. Greenand

Gray2'

noted "finger stiffness" in only three of seventy-five private practice patients.

Morey39,

ontheotherhand, stated that handstiffness following distalupperextremityfractures is a common problem. Bacorn and Kurtzke6 noted a 48% incidence in more thantwo thousand Worker's Compen-sation casesof "restricted" motion ofdigits, although they did not suggest a cause for the stiffness. Flexion defects were noted twice as often as extension. The distal interphalangeal joints were the most commonly affected with the indexfinger beingthemostandthe thumbbeing the least common.

Digital immobility maybe due to fracture pain orpoor casting

techniques'3

39. Pain usually resolves fairly soon withproperfracture immobilization andearly digitmotion.

Casts which block metacarpophalangeal (MP) flexion or pushthe thumbmetacarpal into anadducted positionmay result inanMP extension contracture or athumb adduc-tion contracture respectively. Most patients tolerate the blocked motionand do notcomplainto theirphysician.

Aggressive range of motion exercise and the use of elasticgannents tocontroledemaareimportantmeasures in preventing digital

stiffness39.

In the Bacom and

Kurtzke6

review, physicaltherapy averaged four months. It did notaffectthefinallossof function. Rather, they felt that the willingness of the patient to perform early, frequentwrist andfingerexercisesplayedagreaterrole in reducing finaldisability. Theyalso noted agreement from others onthis

opinion21.

In contrast, Morey39 felt thata

team approach ofphysicaland occupational therapy less-ened the timeneeded for

full

recovery.

BIBLIOGRAPHY

'Amadio,

P.C.: Current Concepts Review: Pain Dys-function

Syndromes. J.

Bone and Joint

Surg.,

70A:944-949, 1988.

2-

Aro, H.; Koivunen,

T.; Katevuo, K.;

Nieminen,

S. and Aho, A.J.: Late Compression Neuropathies After Colles' Fracture. Clin. Ortho., 233:217-225, 1988.

3- Atkins, R.M.; Duckworth, T. andKanis,J.A.: Algod-ystrophy

Following

Colles' Fracture. J. Hand Surg., 14B:161-164, 1989.

4. Atkins, R.M.; Duckworth, T. and Kanis, J.A.: Fea-turesofAlgodystrophy After Colles' Fracture. J. Bone and Joint Surg., 77B:105-110, 1990.

5-

Atkins, R.M. andKanis, J.A.: The Use of Dolorimetry inthe Assessment ofPost-Traumatic Algodstrophy of the Hand. Br. J. Rheu., 28:404-409,. 1989.

6- Bacorn, R.W. and Kurtzke, J.F.: Colles' Fracture: A

Study ofTwo Thousand Cases from the New York State Workmen'sCompensation Board. J. Bone and Joint Surg., 35A:643-658, 1953.

7-

Bauman, T.D.; Gelberman, R.H.; Mubarak, S.J. and

Garfin, S.R.: The Acute Carpal Tunnel Syndrome. Clin.

Orthop., 156:151-156, 1981.

8-

Berg, E.E.: Radiology Review. Secondary Reflex

Sympathetic Dystrophy. Orthop. Nurs., 7:36-37, 1988.

9 Boyes, J.H.; Wilson, J.N. and Smith, J.W.: Flexor-TendonRuptures in the Forearm and Hand. J. Bone and Joint Surg., 42A:637-646, 1960.

10- Broder, H.: Rupture of Flexor Tendons, Associated

with aMalunitedColles'Fracture.J. Bone andJointSurg.,

36A:404-405, 1954.

"- Cassebaum, W.H.: Colles' Fracture. A Study of End

Results. JAMA, 143:963-965, 1950.

12- Colles, A.:On the Fracture of theCarpalExtremity of theRadius. Edinburg Med. Surg., 10:182-186, 1814. 13. Cooney, W.P.; Dobyns, J.H. and Linscheid, R.L.:

Complications of Colles' Fractures. J. Bone and Joint

Surg., 62A:613-619, 1980.

14-

Diamond, J.P. and Newman, J.H.: Multiple Flexor Tendon Ruptures Following Colles' Fracture: A Case Report. J. Hand Surg., 12B:112-114, 1987.

15-

Dobyns, J.H. and Linscheid, R.L.: Fractures and Dislocations of the Wrist. In: Rockwood, C.A., Green, D.P. eds. Fractures InAdults, Volume 1, 2nd ed. Phila-delphia: J.B. Lippincott, 411-509, 1984.

16-

Engkuist, 0. and Lundborg, G.: Rupture of the Ex-tensor Pollicis Longus Tendon After Fracture of the Lower End of the Radius. The Hand, 11:76-86, 1979.

17-

Frykman, G.: Fracture of the Distal Radius Including SequelaShoulder-Hand-Finger Syndrome, Disturbance in the DistalRadio-UlnarJoint andImpairment of theNerve Function: AClinicalandExperimentalStudy.ActaOrthop.

Scand. [Suppl], 108:1-153, 1967.

18-

Gelberman,R.H.: AcuteCarpalTunnelSyndrome.In: OperativeNerveRepairandReconstruction. Philadelphia: J.B. Lippincott Co., 939-948, 1991.

19.

Gelberman,

R.H.; Szabo, R.M. and Mortensen,

W.W.: Carpal Tunnel Pressures and Wrist Position in Patients with Colles Fracture. J. Trauma, 24:247-249, 1984.

20-

Goldie, B.S. andPowell, J.M.: BonyTransfixion of the Median Nerve

Following

Colles'Fracture: ACaseReport. Chin.

Ortho.,

273:275-277, 1991.

21. Green, J.T.andGay,F.H.:

Colles'

Fracture-Residual

Disability. Am. J. Surg., 91:636-646, 1956.

22-

Hallett,

J.P. and Motta, G.R.: Tendon Rupturesinthe

Hand with Particular Reference to Attrition Ruptures in the Carpal Tunnel. Hand, 14:283-290. 1982.

23-

Helal, B.; Chen, S.C. and Iwegbu G.: Rupture ofthe Extensor Pollicis Longus Tendon in Undisplaced Colles' TypeofFracture. Hand, 14:41-47, 1982.

24. Jupiter, J.B.: Current Concepts Review: Fractures of the Distal End of the Radius. J. Bone and Joint Surg., 73:461-469, 1991.

25-

KongshoLn,

J.andOlerud, C.: Carpal TunnelPressure intheAcute Phase AfterColles' Fracture. Arch. Orthop. TraumaSurg., 105:183-186, 1986.

26-

Kumar, A.: Median and Ulnar Nerve InjurySecondary to aCommunicated Colles Fracture. J. Trauma, 30:118-119, 1990.

Lankford, L.L. and Thompson,J.E.: ReflexSympathetic Dystrophy, Upper and Lower Extremity: Diagnosis and Management. In: AmericanAcademy ofOrthopaedic Sur-geons Instructional Course Lectures. 26th ed. 163-178, 1977.

28.

Lewis, M.H.: Median Nerve Decompression after

Colles' Fracture. J. Bone andJoint Surg., 60B:195-196, 1978.

29-

Lidstrom, A.: Fractures of the Distal End of the Radius: A Clinical and Statistical Study of End Results. Acta Orthop. Scand. [Suppl], 41:1-118, 1959.

30- Lynch, A.C. and Lipscomb, P.R.: The CarpalTunnel Syndrome and Colles' Fractures. JAMA, 185:101-104, 1963.

31-

MacKinnon,

S.E. and Holder, L.E.: The Use of Three-phaseRadionucide BoneScanningintheDiagnosis of ReflexSympatheticDystrophy. J. HandSurg., 9A:556-563, 1984.

32- Mannerfelt, L.; Oetker, R.; Ostlund, B. and Elbert, B.:Rupture oftheExtensorPollicis Longus Tendon After

Colles Fracture and by Rheumatoid Arthritis. J. Hand

Surg.,

15B:49-50, 1990.

33- Matthews, L.S.: Acute VolarCompartmentSyndrome

SecondarytoDistal Radius FractureinanAthlete: ACase

Report. Amer. J. Sports Med., 11:6-7, 1983.

34-

McCarroll, H.R., Jr.: Nerve Injuries Associated with WristTrauma. Ortho.

Chin.

NorthAm., 15:279-287, 1984.

35-

McClain, E.J. andWissinger, H.A.: The Acute Carpal TunnelSyndrome: NineCase Reports. J. Trauma., 16:75-78, 1976.

36.

McMaster, P.E.: Late Ruptures of Extensor and Flexor Pollicis Longus Tendons Following Colles Frac-ture.J. Bone andJoint Surg., 14:93-101, 1932.

37 Melone, C.P.: Articular Fractures of the Distal

Ra-dius. Ortho. Clin. NorthAm., 15:217-236, 1984.

38- Moberg, E.: The Shoulder-Hand-Finger Syndrome. Surg. Clin. North Am., 40:367-373, 1960.

39 Morey, K.R. and Watson, A.H.: Team Approach to Treatment ofthe Posttraumatic StiffHand. Phys. Ther., 66:225-228, 1986.

40- Naito, M. and Ogata, K.: Acute Volar Compartment Syndrome During Skeletal TractioninDistal Radius Frac-ture: ACase Report. Clin. Ortho., 241:243-237, 1989.

41- Okuhara, T.; Matsui, T. andSugimoto, Y.: Spontane-ous Rupture of Flexor Tendons ofa Little Finger due to Projection of the Hook of the Hamate: A Case Report. Hand, 14:71-74, 1982.

42. Paley, D. and McMurtry, R.Y.: Median Nerve Com-pression by Volarly Displaced Fragments of the Distal Radius. Clin. Ortho., 215:139-147, 1987.

43- Plewes, L.W.: Sudeck's Atrophyinthe Hand.J. Bone andJoint Surg., 38B:195-203, 1956.

44- Pool, C.: Colles' Fracture: A Prospective Study of Treatment. J. Bone andJointSurg., 55B:540-544, 1973. 45- Robbins, H.:AnatomicalStudyofthe Median Nervein the Carpal Tunnel and Etiologies of the Carpal-Tunnel Syndrome. J. Bone andJoint Surg., 45A:953-966, 1963. 46- Robinson, W.S.; Stern, P.J. and Reilly, K.E.: Evalu-ation andTreatmentofNeurologic Compromise Following Fracture ofthe DistalRadius. 1990. ASSH Annual Meet-ing, Toronto, 9/27/90.

47- Rychak,J.S.andKalenak, A.:Injurytothe Median and Ulnar Nerves Secondary to Fracture of the Radius. J. BoneandJoint Surg., 59A:414-415, 1977.

48. Rymaszewski, L.A. and Walker, A.P.: Rupture of Flexor Digitorum Profundus to the Index Finger after a Distal Radial Fracture.J. HandSurg., 12B:115-116, 1987.

49 Sadr, B.: Sequential Rupture of Extensor Tendons afteraColles Fracture.J. HandSurg., 9A:144-145, 1984. 50- Shall, J.; Cohn, B.T. and Froimson, A.I.: Acute

Compartment Syndrome of the Forearm in Association withFracture of the Distal End of the Radius.J. Bone and Joint Surg., 68A:1451-1454, 1986.

51-

Siegel, R.S. and Weiden, I.: Combined Median and Ulnar NerveLesions ComplicatingFractures oftheDistal Radius andUlna. J. Trauma., 8:1114-1118, 1968. 52. Southmayd, W.W.;

Millender,

L.H. and Nalebuff, E.A.: Ruptureof the FlexorTendons of the IndexFinger afterColles' Fracture. J. Bone andJoint Surg., 57A:562-563, 1975.

53-

Stark, W.A.: Neural Involvement inFractures ofthe Distal Radius. Orthopaedics, 10:333-335, 1987.

54- Stein, A.H.,

Jr.: The Relation of the Median Nerve

Compression

toSudeck's

Syndrome.

Surg. Gynecol. Ob-stet., 713-720, 1962.

55-

Stewart, H.D.;

Innes,

A.R. and Burke, F.D.: The Hand Complications of Colles' Fractures. J. Hand Surg.,

56- Vance, R.M. and Gelberman,

R.H.:

Acute Ulnar Neuropathy with FracturesattheWrist. J. Bone and Joint

Surg., 60A:962-965, 1978.

57 Wainapel, S.F.; Davis, L. and Rogoff, J.B.:

Electrodi-agnostic Study of Carpal Tunnel Syndrome after Colles Fracture. Am. J. Phys. Med., 60:126-131, 1981.

58- Weber, E.R.: ARationalApproachfor theRecognition andTreatmentofColles' Fracture. HandClinics, 3:13-21, 1987.

59 Wong, F.Y.H. andPho, R.W.H.: Median Nerve

Com-pression, with TendonRuptures, after Colles' Fracture. J. HandSurg., 9B:139-141, 1984.

'- Younger, C.P. and DeFiore, J.C., Jr.: Rupture of FlexorTendons to theFingersaftera Colles Fracture. J. Bone andJoint Surg., 59A:828-829, 1977.

61- Zemel, N.P.: ThePreventionand Treatmentof Com-plications from Fractures to the Distal Radius and Ulna. Hand Clinics, 3:1-11, 1987.

62. Zoega, H.: Fracture of the LowerEnd of the Radius

with Ulnar NervePalsy.J. BoneandJointSurg., 48B:514-516, 1966.