Injury Extra (2007) 38, 262—266

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CASE REPORT

Post-traumatic osteonecrosis of distal tibia

D. Chakravarty a,*, A. Khanna a,1, A. Kumar b,2

aDepartment of Orthopaedics, Peterborough and Stamford Hospitals NHS Trust,Edith Cavell Hospital, Bretton Gate, Peterborough PE3 9BR, United KingdombDepartment of Orthopaedics and Trauma, Peterborough Hospitals NHS Trust,Edith Cavell Hospital, Bretton Gate, Peterborough PE3 9BR, United Kingdom

Accepted 24 October 2006

Introduction

Post-traumatic osteonecrosis affecting the femoralhead, femoral condyles, humeral head, talus, tibialshaft, and proximal tibia has been commonlyreported, but it is very unusual in the distal tibiaalone.

* Corresponding author at: 27, Buckthorn Road, Peterborough PE7E-mail address: debasischakravarty@hotmail.com (D. Chakravarty

1 Tel.: +44 7894657349.2 Tel.: +44 1733332871.

1572-3461 # 2006 Elsevier Ltd.doi:10.1016/j.injury.2006.10.028

Open access under the Elsevier OA lic

We report a case of osteonecrosis of the distaltibia following fracture—dislocation of the ankle.Though the condition has been reported after ankleinjury in children,6 we believe this to be the firstclinical report in an adult. The patient respondedwell to conservative management and was reason-ably asymptomatic at the time of follow-up.

8EE, United Kingdom. Tel.: +44 7879452704/+44 1733 560069.).

ense.

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264 D. Chakravarty et al.

Post-traumatic osteonecrosis of distal tibia 265

Case report

A 25-year-old man sustained a fracture disloca-tion of his left ankle with a high fibular fracturewhen he was knocked down by a push-bike in June2002. He was taken to the local hospital where theankle was manipulated and a plaster backslab wasapplied. He was seen in our unit 4 days later and theankle was re-manipulated to correct mild talar shiftand immobilised in plaster. Surgery was delayed dueto gross swelling around the ankle. He was operatedon 5 days later. The medial malleolar fragment wasfixed with a single screw and a 2.0 mm K-wire. Thehigh fibular fracture with talar shift was treatedwith a single diastasis screw. Ten days later this wasrevised due to recurrent talar shift and the diastasis

was stabilised with two 3.5 mm fully threaded cor-tical screws. These were subsequently removed at 6weeks, the patient then started progressive weight-bearing over the next few weeks. Shortly afterremoval of plaster, the patient complained ofincreasing pain and swelling of his ankle. His gaitwas poor in the late stance phase due to pain, therewas significant limitation in activities of daily andsocial living due to pain and swelling. His AmericanOrthopaedic Foot and Ankle Society (AOFAS) score atthis stage was 60. Physiotherapy and orthotic sup-port failed to improve his symptoms. Check X-rayswere satisfactory. There was no rise in inflammatorymarkers and there were no systemic signs of infec-tion. An MRI scan was requested due the persistentnature of the problem and this revealed avascularnecrosis of the distal tibia laterally involving distal

266 D. Chakravarty et al.

tibiofibular syndesmosis. There was also a focaldefect in the distal tibial articular surface fromthe osteonecrosis. The fractures were completelyhealed. There was surrounding bone marrowoedema and oedema of the talar dome.

He was treated with a non-weight-bearing,below-knee plaster for 6 weeks, followed by grad-uated weight-bearing over the next 6 weeks in apatellar-tendon bearing cast. His symptoms settledand he was left out of the cast and allowed agraduated rehabilitation programme, avoidingundue stress to the joint. Although the stiffnesspersisted for some time, he was able to undertakeactivities of daily living reasonably well and hadreturned to office work. At annual follow-up for 3years following injury he had a normal gait cyclewith a good range of ankle movement (108 of dorsi-flexion to full plantarflexion). Apart from this mildstiffness, he had no other symptoms. His AmericanOrthopaedic Foot and Ankle Society score hadimproved to 77.

Discussion

The precise nature of the initiating event of osteo-necrosis still remains unknown. The most likelycauses are a primary vascular incident or a subchon-dral fracture from the traumatic insult with a sec-ondary intraosseous compartment syndrome andosteonecrosis.2,5 There seems to be a disturbanceof venous drainage from juxtachondral cancellousbone marrow causing intraosseous stasis and hyper-tension. Traumatically induced defects in the chon-dral surface may also might allow fluid from the jointto be expressed into the adjacent marrow space,producing an increase in marrow pressure and pain.3

The final common pathway of the bone infarctionis irreversible blockade of the microcirculatory bedby cellular aggregates and micro-thrombi leading to

alteration of capillary blood flow. The most wide-spread and consistent infarction occurs in embolisa-tion of the main nutrient artery.3

After a fracture there is usually a variable extentof bone death on either side of the fracture line.7

However, necrosis of a large segment of bone afterfracture is common to those sites that have a vul-nerable blood supply, mostly intra-articular in loca-tion and having a limited soft-tissue attachment.1 Itdepends on the site and type of fracture, the type oftreatment, the timing of surgery, and union of thefracture. Factors increasing the chances of osteo-necrosis are open or segmental fractures and frac-tures associated with dislocations. It is also morecommon in some bones, e.g. femoral head, talus,humeral head, scaphoid, and other bones.4,8

There is no account of osteonecrosis in the distaltibia alone.

References

1. Boss JH, Misselevich I. Experimental avascular osteonecrosis.Curr Orthop 2001;15:57—67.

2. Ficat P, Arlet J, Mazieres B. Osteochondritis dissecans andosteonecrosis of the lower end of the femur. Value of bonemarrow functional exploration. La Semaine des hopitaux1975;51(June (28)):1907—16.

3. Grigorovskii VV. The morphogenesis and pathogenesis of ametadiaphyseal infarct of the long bone in different typesof ischaemia. Klinichna Khirurhiia 1999;(12):46—8 [in Russian].

4. Hofmann S, Kramer J, Plenk Jr H, Leder K, Imhof H, Engel A.Osteonecrosis. Der Orthopade 1994;23(September (5)):331—41.

5. Hungerford DS. Pathogenetic consideration in ischemic necro-sis of bone. Can J Surg 1981;24:583—7.

6. Lagier R. Post-traumatic remodelling of the distal tibial epi-physis: a form of aseptic osteonecrosis. Skelet Radiol1989;18(4):331—3.

7. McLean FC, Urist MR. Bone. An introduction to the physiologyof skeletal tissue. Chicago: University of Chicago Press; 1955.

8. Simkin PA, Gardner GC. Osteonecrosis: pathogenesis and prac-ticalities. Hosp Pract (office edition) 1994;29. p. 73—8, 81—4.