IDIOPATHIC AVASCULAR NECROSIS OF THE SCAPHOID

T. J. HERBERT and M, LANZETTA

St Luke’s Hospital Hand Unit, Sydney, Australia

Idiopathic avascular necrosis of the scaphoid is a rare condition. A review of the literature showsa variety of conditions labelled as spontaneous avascular necrosis or Preiser’s disease. In thispaper we report on a study of eight patients with idiopathic avascular necrosis affecting only theproximal pole of the scaphoid. Seven of these patients had positive ulnar variance. The possibleaetiology is discussed and the natural history has been studied. A staging system is proposed, asthis helps to determine the prognosis and appropriate management. Two of our patients weremanaged conservatively; the others were treated successfully by partial silastic replacement of thescaphoid.Journal of Hand Surgery (British and European Volume, 1993) 19B: 174-182

Avascular necrosis of the carpal bones can affect thelunate (Kienb6ck, 1910), the pisiform (Olah, 1968), capitate (Urman et al, 1977; Rahme, 1983) and thescaphoid. When the whole scaphoid becomes avascular,following a fracture or an injury, this condition hasbeen called Preiser’s disease (Bray and McCarroll,1984), after Preiser’s original article in 1910. Althoughavascular necrosis may occur without any known historyof injury (Ekerot and Eiken, 1981), it may be difficultto exclude the possibility of mild or repetitive trauma(Allen, 1983).

Other known causes of avascular necrosis includesteroid therapy (Milgram and Riley, 1976), chemo-therapy (Harper et al, 1984) and connective tissuediseases such as systemic lupus erythematosus (Urmanet al, 1977) or progressive systemic sclerosis (Kawaiand al, 1983). In the latter, high doses of steroids aregenerally used, so that it is difficult to establish whetherthe primary cause of the scaphoid necrosis is the diseaseitself or the steroid therapy.

The literature contains reference to 14 cases of idio-pathic avascular necrosis of the scaphoid, (Guelpa et al,1980; Ekerot and Eiken, 1981; Allen, 1983; Ferlic andMorin, 1989; Alnot et al, 1990; Table 1).

We present our experience with eight cases of idio-pathic avascular necrosis of the scaphoid. In all cases

or=ly the proximal pole of the bone was affected(Table 2).

The history and physical signs were remarkably simi-lar in all cases. All patients complained of increasinglysevere radial-sided wrist pain of spontaneous onset,without any significant history of trauma. Physicalexamination showed marked synovial swelling and ten-derness around the dorso-radial aspect of the wrist.

Range of motion and function were severely impairedbecause of pain, a condition we recognize as an "irritablewrist". X-ray findings varied, depending on the durationof’ the disease. Since this is a progressive disorder, wehave attempted to classify our patients according to theX-ray appearance at the time of examination. Thefollowing staging system was used:

--- Stage I. Normal X-raysPositive bone scan

--- Stage 2. Increased density of proximal poleGeneralized osteoporosis

--- Stage 3. Fragmentation of proximal pole_+ pathological fracture

--- Stage 4. Carpal collapse pattern, osteoarthritis.

CASE REPORTS

Table 1--Literature review ofavascular necrosis ofthe scaphoid (numberof cases)

Author Post trauma or Idiopathicfracture

(Preiser’s disease)

Preiser (1910) 5Guetpa et al (1980) 2Ekerot and Eiken (198I) 2Allen (1983) 2*Bray and McCarroll (1984) 1Ferlic and Morin (1989) 5Alnot et al (1990) 3

Total . 6 14 20

*Borderline -- possible mild or repetitive trauma.

Case 1

A healthy 46-year-old male company director (LA)presented with a 14-month history of pain in his domi-nant right wrist. There was no history of injury. He hadtenderness and swelling over the anatomical snuff boxand the dorsum of the right wrist. The range of motionwas reduced by approximately 50%.

X-ray films showed complete avascular necrosis ofthe proximal half of the scaphoid with a pathologicalfracture and significant carpal collapse deformity (stage4; Fig 1). He had been treated previously with a singlecortisone injection, with significant pain relief. His symp-toms were not considered severe enough to warrantsurgery, and he was fitted with a wrist support andadvised to undergo regular review. Over a period of 29months the situation has remained unchanged.

174

ScAPHOID AVASCULAR NECROSIS

Table 2 --175

Case Name Sex Age Side Previous h~itial Stage Ulnar Trea,~ment Op. Last Fo)low-up Resultno. treatment X-rays rariance findings X-rays (mths)

1 LA M 46 R(D) Steroid AVN PP 4 + Conservative -- Unchanged 29 Satisfactoryinjection Path #-,-CCD

2 JM F 36 L(D) Arthroscopy Normal 1 + Silicone Segmental Satisfactory 16 Goodpos. partial necrosisbone .~ replacement No # seenscan. De Synovitis

AVP PP 3 Quervain’sPath # release

3 FS F 39 R(D) De AVN PP 3 0 Silicone Segmental RC OA 32 ,/" GoodQuervain’s partial necrosis //release replacement No # seen¯ synovitis4 PS M 39 R(D) Russe graft AVN PP 4 + Silicone Segmental Satisfactory 42 GoodRC OA partiN necrosis styloidectomy

replacementRadial

styloidectomy5 GC F 55 R(D) MU,~ & Sclerosis 2 + Silicone Segmental Satisfactory 84 Satisfactoryster6id pp partial necrosisinjection pos. replacement SL fig.bone Avulsion #scan

6 JR F 60 L(ND) -- AVN PP 2 + + Conservative -- Unchanged 24 FairPath # ~,3

7 IR F 66 R(D) -- AVN PP 2 + Silicone Segmental Satisfactory 8 Goodpartial necrosis

replacement8 BW F 51 R(D) Steroid AVN PP 3 + Silicone Synovitis Satisfactory 6 Goodinjection Path # partial Segmental( x 2) replacement necrosis

D: dominant; ND! non-dominant; MUA: manipulation under anaesthetic; AVN PP: avascular necrosis of the proximal pole; Path #: pathological fracture; CCD:carpal collapse deformity; RC OA: Radio-carpal osteoarthritis. ~

Case 2

A fit 36-year-old female cook (JM) presented with 5-month history of pain in her dominant left wrist. Nohistory of trauma could be elicited. On examination,swelling was noted in the anatomical snuff box and thedorsum of the wrist at the scapho-lunate junction. Thewrist joint was "irritable". Initially, X-ray films appearednorrnal, although a bone scan showed intense reactionadjacent to the scaphoid (stage 1; Figs 2a and b).Positive ulnar variance was noted. X-rays taken 2months later showed the development of cl~anges con-sistent with a diagnosis of avascular necrosis of theproximal pole of the scaphoid (stage 2; Fig 3a).

Arthroscopy showed marked synovitis on the radialside of the wrist, with an intact scapho-lunate ligament.The articular cartilage over the scaphoid was intactalthough soft to probing over the proximal pole.

Plans were made to admit the patient to hospital fora "revascularization" procedure, but these had to becancelled for social reasons. Her wrist remained painful,and 6 months later X-rays showed increased collapse ofthe proximal pole of the scaphoid, with the developmentof a fracture line at the junction between healthy and

unhealthy bone (stage 3; Fig 3b). By the time she wasadmitted to hospital for treatment (5 months later),X-rays showed a clear fracture line and complete avascu-lar necrosis of the proximal pole (Fig 3c).

At operation, the articular cartilage over the proximalpole was ’soft and unhealthy, but there was no externalsign of fracture or of scapho-lunate ligament damage.An osteotomy was carried out through the waist of thescaphoid, the proximal fragment was excised andreplaced with a stabilized silicone prothesis (Fig 3d).The patient’s symptoms were relieved although she didrequire treatment for an associated de Quervain’ssyndrome before she was able to return to work.Histological examination of the excised bone confirmeda diagnos:is of avascular necrosis with a pathologicalfracture through the trabeculae at the junction betweenhealthy and unhealthy bone.

Case 3

A healthy 39-year-old right handed book-keeper (FS)presented with chronic right wrist pain, which waspreventing her from performing simple daily activities,

176

Fig 1 Case 1. Avascular necrosis of the proximal pole of thescaphoid. Fracture of the bone and carpal collapse are evident(Stage 4).

including driving. The patient was unable to recall anyhistory of injury. 9 years previously she had undergonesurgical release of the first extensor compartment for apossible de Quervain’s syndrome, without relief-of thesymptoms.

On examination she had a very irritable wrist, wi~hpain and swelli.n, g around the scaphoid. There were signsof mild mediah nerve compression at the wrist, but nothenar muscle wasting. X-ray films showed completeavascular necrosis of the proximalpole of the scaphoid(stage 3; Fig 4). The proximal pole of the scaphoid wasexcised and a partial silicone replacement performed;intra-operatively there was no sign of fracture or scapho-lunate ligament tear. 32 months after operation thepatient showed good function of the hand, with excellentrange of motion and grip strength, and no pain. X-raysshowed good function of the prosthesis, with no signsof silicone synovitis. However, early radio-carpal osteo-arthritis was noted, suggesting some increase in ~thecarpal collapse deformity.

Fig 2

THE JOURNAL OF HAND SURGERY VOL. 19B No. 2 APRIL 1994

Case 2. (a) Normal X-rays of both wrists at the time thepatient first presented with left wrist pain. Note posiuveulnar variance. (b) Bone scan showing dense uptake isotope adjacent to the proximal pole of the left scaphoid(Stage 1 ).

Case 4

A healthy 39-ye.a.r_-.old right-handed storeman (PS) pre-sented with a 10-year history of right wrist pain. 9 yearspreviously he had been diagnosed elsewhere as havingidiopathic avascular necrosis of the proximal pole of theright scaphoid. This was treated surgically by a Russetype bone graft to the scaphoid, with reasonable sympto-matic relief. However, there was no improvement in the

L 1994 SCAPHOID AVASCULAR NECROSIS ¯ 177

ne theositiveLke of~phoid

, pre-years~ving)fthe~usseapro-n the

Fig 3 (a-d) For legend please see page 178.

178

Fig 4 Case 3. Avascular necrosis of the proximal pole of the rightscaphoid (Stage 3).

radiological appearance, the proximal pole remainingcollapsed and deformed.

When first seen by us, he was found to have a stiffpainful wrist; X-rays showed the typical appearance ofavascular necrosis of the proximal pole of the scaphoidwith secondary radio-carpal osteoarthritis (stage 4).Review of his original films confirmed the diagnosis ofidiopathic avascular necrosis with no evidence of frac-ture, and positive ulnar variance. The proximal pole ofthe scaphold.was excised and partial slhcone replacementperformed 10 months after this operation he underwentradial styloidectomy for radio-carpal impingement pain.42 months later, the patient reported complete relief ofpain with very satisfactory function of the wrist.

THE JOURNAL OF HAND SURGERY VOL. 19B No. 2 APRIL t93,1

Case 5

A healthy 55-year old housewife (GC) presented with 7-month history of pain in her dominant right wrist.There was no specific history of trauma to the wrist,.although she did recall having sustained a severe electricshock to the arm a few days before the onset of hersymptoms. She had undergone manipulation of the wristunder anaesthesia with an intra-articular steroid injec-tion With no relief before presenting to us.

On examination she had a very painful wrist suggest.ing synovitis of the radio-carpal joint; the range ofmotion was severely restricted by pain and her gripstrength was markedly reduced. X-rays showed sclerosisand slight narrowing of the proximal pole of the scaph-old, consistent with avascular necrosis; there was noevidence of fracture (stage 2). Bone scan showed mark-edly increased uptake around the scaphoid. Positiveulnar variance was noted.

At operation, the avascular proximal scaphoid wasexcised and partial silicone replacement performed. Thescapho-lunate ligament was oedematous and loose, andthere appeared to be a small avulsion fracture at itsinsertion into the proximal pole of the scaphoid. 7 years

after operation, the patient is happy with the result,although she still has mild discomfort and weakness.

Case 6

A healthy 60-year-old secretary (JR) presented with history of chronic pain in her non-dominant left wrist.Although there was no history of acute trauma, sherecalled that the onset of pain and swelling in the wristfollowed an intense ~ession of typing. On examination,:she was found to have marked swelling over the tendonof abductor pollicis Iongus at the base ~)f the thumb,tenderness in the anatomical snuff box and over thedorsum of the wrist, which was irritable. X-ray filmsshowed avascular necrosis of the proximal pole of thescaphoid (stage 2) and ;marked positive ulnar variance(Fig 5a). The patient was fitted with a wrist supportand advised to rest the wrist. Her symptoms haveremained controlled with conservative treatment.Follow-up X-ray films show the development of a patho-logical fracture through the proximal pole of the scaph-old (Stage 3; Fig 5b). She remains under review andshows no further progression of the disease.

Case 7

A fit 66-year-old doctor (IR) presented with a 6-monthhistory of increasing pain and weakness in his dominant

Fig 3 Case 2. (a) X-ray of the same patient 2 months later, showing early signs of avascular necrosis of the proximal pole of the scaphoid; fracture is evident (Stage 2) (b) X-ray of the same patient’s left wrist taken 6 months later. This now shows the development pathological fracture through the scaphoid; the bone in the proximal fragment is starting to develop a "ground-glass" appearance (Stage3). (c) Appearance 5 months later. The fracture is more visible and the proximal fragment now shows the classical signs of avascularnecrosis. At :operation, the articular cartilage was intact and there was no demonstrable instability. (d) Post-operative X-ray showingpartial silicone replacement of the scaphoid.

1994

vith awrist.wrist,ectricff lnerwrist

in jet-

ggest-ee of- gri.p:roslszaph-tSnark-sitive

WaSThe

, and~t itsgears;SUlt,SS,

ith avrist.

sheecristtion,~donlrnb,thefilms’ theanceport3avelent.tho-~ph-and

of a;tag~:utar,ring {

Fig 5

sCAPHOID AVASCULAR NECROSIS179

Case 6. (a) X-ray showing radiological signs of idiopathic avascular necrosis of the proximal pole. A marked positive ulnar variance noted. (b) Pathological fracture is evident on X-ray taken 2 months later (Stage

right wrist, preventing him from lifting heavy objects orplaying croquet. There was no history of significantinjury.

f n examination, he had swelling and tenderness overthe anatomical snuff box and the dorsum of thescaphoid. X-ray films showed changes consistent withavascular necrosis of the proximal pole of the scaph~id(stage 2; Fig 6). The patient underwent a period conservative treatment of splinting and rest, but thisfailed to relieve hisx;}mptoms. At surgery, the proximalpole of the scaph6id was found to be completely avascu-lar and necrotic; a silicone prosthesis was used to replaceit. The removed bone was sent for histological examin-ation, which confirmed the diagnosis of avascularnec: ~sis. He reports marked improvement followingsurgery and has been able to resume playing croquet.

Case 8

A 51-year-old shop assistant (BW) presented with ’l-month history of pain in her dominant right wristfollowing a bump on the radial side of the wrist. She

had signs of a mild de Quervain’s syndrome treatedconservatively. 3 years earlier she had received twosteroid injections for a painfnl sterno-clavicular joint.Clinically, she had classical signs of avascular necrosisof the scaphoid with an "irritable wrist", and she hadsigns of mild carpal tunnel syndrome. X-rays showedavascular necrosis of the scaphoid with fragmentationof the proximal pole and signs of a pathological fracture(stage 3). Positive ulnar variance was noted. Surgicaltreatment was carried out, with replacement of theproximal pole with a silicone implant. 6 months post-operatively the patient’s wrist was stable and she hadregained virtually full range of motion. She reportedexcellent pain relief to the extent that she had been ableto resurae normal work and household duties.

DISCUSSION

The aetiology and pathogenesis of avascular necrosis ofthe carpal bones remains uncertain. A carpal bone, ora fragment thereof, may be completely devascularized(i.e. con~tpletely stripped of all its soft tissue attachments)

180

Fig 6 Case 7. Early avascular necrosis of the proximal pole (Stage 2).

and survive if is repositioned or if the fragment isreattached, yet avascular necrosis may occur followingsimple fractures of the scaphoid, lunate and capitate.Idiopathic avascular necrosis, by definition, occurs inthe absence of major trauma or pre-existing fracture,although a patient may have a scaphoid fracture withoutbeing aware of it, and the fracture may not always beobvious on X-ray. Our review of the literature suggeststhat a number of cases labelled as idiopathic avascularnecrosis of the scaphoid may well have been due to apre-existing undiagnosed fracture. We have reviewedcarefully all available X-ray films in the patients reportedin this series, and are confident that in none of thesewas there a pre-existing fracture.

Gelbermarvand Menon (1980) have shown that thescaphoid ree~eives its blood supply through the areas ofsoft tissue attachment. The dorsal vasculature entersthrough numerous small foramina along the spiralgroove and dorsal ridge.

These feeding vessels arise from the dorsal scaphoidbranch of the radial artery and from the dorsal radialcarpal arch and account for approximately 80% of thetotal blood supply to the scaphoid; the remaining 20%is supplied by palmar vessels entering the tubercle anddistal pole. These authors failed to demonstrate anyintraosseous connection between these two areas ofblood supply and were unable to show any significant

THE JOURNAL OF HAND SURGERY VOL. 19B No. 2 APRIL 1994

blood supply entering the proximal pole through thearea of attachment of the scapho-lunate ligament.However, we have seen numerous cases in which a smallproximal pole fragment remains viable when the scapho-lunate ligament must be its main source of blood supply(Herbert, 1990). Similarly, we have seen patients whom avascular necrosis of the proximal pole of thescaphoid has occurred after traumatic avulsion injuriesof the scapho-lunate ligament (Herbert, 1990). It seems,therefore, that in a certain percentage of cases, theproximal pole must receive a blood supply through theattachments of the scapho-lunate ligament. If this is thecase, any interference with this blood supply could leadto the development of segmental avascular necrosis ofthe proximal pole of the scaphoid. This situation is, inmany ways, analogous to the hip joint, where damageto the ligamentum teres may lead to the developmentof segmental avascular necrosis of the femoral head insusceptible patients (Kamegaya et al, 1989).

Thus certain patients may be unusually susceptible tomild or repetitive trauma which may be sufficient todisrupt the blood supply entering the proximal pole byway of the scapho-lunate ligament. This theory is sup-ported by the findings of Guelpa et al (1980) and Ferlicand Morin (1989), who each reported a case of bilateralidiopathic avascular necrosis of the scaphoid. Whilst wehave yet to encounter this problem, we do have anumber of patients with bilateral avascular necrosisassociated with proximal pole fractures following rela-tively minor trauma, highly suggestive of an underlyingpredisposing factor. Case 5 in this series would furtherappear to support this hypothesis: at operation, damageto the scapho-lunat6 ligament was apparent, which couldwell have occurred as a result of the forces associatedwith an electric shock.

It is well-known that repetitive stress on the wrist cancause damage to the scapho-lunate ligament and thiscould be sufficient to interfere with the blood supply tothe proximal pole of the scaphoid in susceptible patients.In seven of our eight p~tients, it was the dominant wristthat was affected. It is interesting to speculate whether:manipulation and/or steroid injection of the wrist (Cases1 and 5) could have affected the outcome in any way.

The reason for the preponderance of females in thisseries (75%) compared with scaphoid fracture (6%) uncertain. In all except one of our cases, plain X-rayssuggested a positive ulnar variance, although in none ofthese were specific views for ulnar variance taken, sothat some allowance should be made for radiologicalerror. Nevertheless in case 6 the positive variance wasstriking, and it is difficult not to conclude there may be ~some correlation between ulnar variance and differentialloading in th.e~radio-carpal joint. This certainly warrantsfurther investigation.

Clinically, the onset of idiopathic avascular necrosisc,f the proximal pole of the scaphoid is heralded byincreasing pain and stiffness of the wrist. Examinationslhows signs of an "irritable" wrist joint with tenderness

’,IL 1994

ih the.merit.smallapho-;upplynts in)f t~e~juri.:,s;eems,s, the;h theis the

:t lead,sis ofis, in

tmz~ge3mc~t~ad in

ble to:nt to:)le bys sup-Ferlicateral1st weave acr~ <,is; r,rl)artherimagecould:iated

st call:t thisply to

v~ ;Isl.ratherCases,ray.n this;%) is~-ravs~ne ~f~n, so)gical~ p,as

av bee~tM-rants

:rosisd byationrness

sCAPHOID AVASCULAR NECROSIS

and swelling over the dorsum of the wrist due to chronicsynovitis. Histological examination of the synovium hasshown chronic inflammatory changes only, with nodiagnostic features.

It is hardly surprising that two of our patients alsol~:d signs of carpal tunnel syndrome, which resolvedo:~ce the synovitis had settled. Cases 2 and 6 appearalso to have had a related De Quervain’s syndromewhich settled following treatment.

In the early stages radiological examination may benormal, though bone scan is likely to show intenseactivity around the scaphoid (Stage 1). Before long,osteoporosis occurs, sparing the ischaemic proximal polewhich thus appears relatively dense on X-ray (Stage 2).The dead bone is later replaced by scar tissue and thenormal trabecular bone structure disappears, producing:~ ground-glass" appearance. The bone tends to collapsea:...I deform, and cystic changes and areas of sclerosisare commonly seen. In the later stages, pathologicalfracture may occur at the junction of healthy bone withthe avascular fragment (cases 2, 6 and 8; Stage 3). the scaphoid deforms, progressive carpal collapse occursleading to the development of radio-carpal osteoarthritis(Stage 4). Thus, as with Kienb6ck’s disease, idiopathicavascular necrosis of the scaphoid is a progressivecondition so that treatment and prognosis depend onthe stage of the disease.

n the early stages one should consider the possibilityc. eversing the pathological process. In our only StageI patient, we had planned to carry out a vascularizedbone graft; unfortunately, by the time she came tosurgery she had progressed to Stage 3 and required asalvage procedure.

Similarly, in Stages 1 and 2 it is tempting to consider"unloading" the scaphoid in some way (e.g. radialosteotomy) in order to prevent progressive collapsedeformity. If positive ulnar variance could be proved tobe of significance, then presumably ulnar shorteningwould be indicated in selected cases. Once the bone hasun -’rgone complete avascular necrosis (Stage 3), thesechanges are almost certainly irreversible so that recon-struction is no longer indicated. .

If the symptoms are not severe enough to justify asurgical procedure, the patient may benefit from con-servative measures~,, as in cases 1 and 6. When surgeryis indicated, our.preferred treatment to date has been apartial silastic,replacement of the scaphoid combinedwith a local synovectomy. A perpendicular osteotomyis carried out through the waist of the scaphoid and theentire proximal fragment is removed in one piece; a

’Sw~:Ison silastic scaphoid prosthesis is then cut downin such a way that it has a square stem distally, whichcan be locked into a suitably prepared "peg hole" inthe distal fra~mnent. The implant is thus stabilized andprovides an effective spacer which appears to preventfurther carpal collapse. We always choose the smallestpossible prosthesis (size 0 or 1) as this prevents over-loading the implant and therefore reduces wear problem~

181

to the minimum. Using the technique we have describedprev:iously (Herbert, 1990), this procedure has providedlasting pain relief with improved range of motion andwrisl function. To date, none of these patients hasdeveloped any signs of silicone synovitis.

The use of a silicone prosthesis does not preclude thepossibility of carrying out partial or total fusion at alater date, should wear become a problem. Similarly, ifscaphoid shortening results in symptomatic radio-carpalimpingement, the symptoms may be relieved by carryingout a limited radial styloidectomy.

In conclusion, we consider that idiopathic avascularnecrosis of the scaphoid is a distinct entity, similar inmany ways to Kienb6ck’s disease of the lunate. It isincorrect to call it Preiser’s disease since the conditionthat Preiser described occurred following definitetrauma, and was almost certainly avascular necrosis dueto fracture. Whilst most previous reports in the literaturerefer to idiopathic avascular necrosis affecting the wholeof the scaphoid, we believe that the problem alwaysstarts in the proximal pole of the bone.

As the disease progresses, the scaphoid collapses tothe extent that the distal pole becomes deformed andarthr!itic, mimicking the appearance of avascularnecrosis. The prognosis would appear to depend on thestage of the disease, and treatment should be plannedaccordingly.

It appears that the aetiology may be related to inter-ference in the extrinsic blood supply to the proximalpole of the scaphoid in susceptible patients, and itappears that positive ulnar variance may be significant.These: hypotheses warrant further investigation.

ReferencesALLEN, P. R, (1983). Idiopathic avascular necrosis of the scaphoid. Journal

of Bone and Joint Surgery, 65B: 3: 333-335.ALNOT, J. Y., FRAJMAN, J. M. and BOCQUET, L. (1990) Les ost4on4croses

aseptiques primitives totales du scaphoide. Annales de Chirurgie de la Main,9: 3: 221-225.

BRAY, T. J. and MCCARROLL, H. R.i1984). Preiser’s disease: A case report.Journal of Hand Surgery, 9A: 5: 730-732.

EKEROT, L. and EIKEN, O. ( 1981 ). Idiopathic avascular necrosis of the scaph-old: Case report. Scandinavian Journal of Plastic and ReconstructiveSurl.-,ery, 15: 69-72.

FERLIC, D. C. and MORIN P. (1989). Idiopathic avascular necrosis of thescaphoid: Preiser’s disease? Journal of Hand Surgery, 14A: l: 13-16.

GELBERMAN, R. H. and MENON, J. (1980). The vascularity of the scaphoidbone. Journal of Hand Surgery, 5: 5: 508-513.

GUELPA, G., CHAMAY, A., and LAGIER, R. (1980). Bilateral osteochon-dritis dissecans of the carpal scaphoid: A radiological and anatomical studyof one case. International Orthopaedics (SICOT), 4: 25-30.

HARPER, P. G., TRASK, C. and SOUHAML R. L. (1984). Avascular necrosisof hone caused by combination chemotherapy without corticosteroids.British Medical Journal, 288: 267-268.

HERBERT, T. J. The Fractured Scaphoid. St. Louis, Quality Medical, 1990.KAMEGAYA. M., MORIYA, H., TSUCHIYA, K., AKITA, T., OGATA, S.,

and SOMEYA, M., (1989). Arthrography of early Perthes’ disease: Swellingof the ligamentum teres_ as a cause of subluxation. Journal of Bone andJoint Surgery, 71B: 3, :’~13-417.

KAWAI, H., TSUYUGUCHI, Y., YONENOBU, K., INOUE, A. andTADA, K. (1983). Avascular necrosis of the carpal scaphoid associatedwith progressive systemic sclerosis. The Hand, 15: 3: 270-273.

KIENBOCK. R. (1910). Ober traumatische Malazie des Mondbeins und ihreFolgezustgnde: Entartungsformen und Kompressionsfrakturen. FortschritteGeb:iete Roentgenstrahlen. 16: 77-103.

MILGRAM, J. W. and RILEY. L. H. (1976). Steroid induced avascular necrosis

182

of bones in 18 sites: A case report. Bulletin of the Hospital for Joint Diseases37:11-23,

OLAH, J. (1968). BilateraIe aseptische Nekrose des Os pisiforme. Zeitschrift farOrthopedie und ihre Goenzgebiete 104: 590-59I.

PREISER, O. (1910). Eine typische posttraumatische und zur Spontanfrakturftihrende Ostitis des Naviculare carpi. Fortschritte GebieteRoentgenstrahlen, 15: 189-197.

RAHME, H. (1983). Idiopathic avascular necrosis of the c.apitate bone: Casereport. The Hand, 5: 274-275.

THE JOURNAL OF HAND SURGERY VOL. 19B No. 2 APRIL 1994

URMAN, J. D., ABELES, M., HOUGHTON, A. N. and ROTHFIELD, N. F.(1977}. Aseptic necrosis presenting as wrist pain in SLE. Arthritis andRheumatism, 20: 825-828.

Accepted after revision: 7 September 1993Timothy J. Herbert, St Luke’s Hospital Hand Unit, 18 Roslyn Street, Ports Point, SydneyNSW 2011, AustraIia. - ,

~ 1994 The British Society for Surgery of the Hand