Forearm fracture plates: To remove or not to remove Eighty dynamic compression plates used to fix fractures of the radius and/or ulna were removed from 51 of 98 adult patients.
Thirty-seven
patients had plates removed
electively. Fourteen
patients had plates removed for clinical reasons. The average time from insertion to removal was 13.6 months, with a range from 4.4 to 36 months. Only one refracture occurred through the unhealed both hone forearm fracture site in a patient whose plate was taken out 6 months after surgery. One refracture also occurred through the proximal screw hole of a still implanted
ulna plate that had been inserted 3 years earlier. Leaving a plate in for the remaining life of a young patient cannot be considered a benign decision considering the persisting chance for refracture and the potential complications from prolonged exposure to metal corrosion complexes and metal ions. (J HAND SURG 1990;15A:294-301.)
David A. Labosky, MD, Mary Beth Cermak, MD, and Carol A. Waggy, PT, Morgantown, W.Va.
Dynamic compression plate fixation has become a common method of treatment, if not the standard, for diaphyseal fractures of adult forearm bones. Once the bones have healed, however, the surgeon is presented with a dilemma. Should the plate be taken out or left in? In patients who complain of pain associated with the presence of a bone plate, the clinical decision to remove the plate can be justified even though it exposes the patient to a second operation and to the risk of refracture. But if the plate causes no symptoms, are the risks of removal, particularly the risk of refracture, still overridden by the potential benefit of removing the metallic implant from the body? To determine the level of risk encountered by patients who have had forearm plates removed for any reason, we retrospectively reviewed a series of patients at West Virginia University Hospital treated with plate fixation for fractures of diaphyseal segments of forearm bones. From the Hand and Microvascular Surgery Section, Department of Orthopedic Surgery, and the Department of Physical Therapy, West Virginia University. Morgantown, W.Va. Received for publication May 5, 1989.
March 9, 1989; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: David A. Labosky, MD, 3511 Health Sciences South, West Virginia University, Morgantown, WV 26.506. 311114326
294
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Materials and methods Ninety-eight patients treated with plate fixation for diaphyseal forearm fractures between June 1981 and June 1987 were followed for at least 1 year after initial surgery or plate removal. Patient ages ranged from 20 years to 55 years, with the average age of 3 1 years. One hundred fifty-five plates were implanted in 78 ulnae and 77 radii with 57 both bone fractures treated. From this group, 80 plates were removed from 51 patients. Eleven plates were removed from isolated ulna fractures, 11 from isolated radius fractures, and 58 from both bone forearm fractures. Patient ages in the plate removal group ranged from 20 to 55 years, with an average age of 30 years. Forty-three of the 51 patients had elective plate removal. Seven plates were removed from five patients because of tenderness or prominence of the plate under the skin. Three patients whose fractures had already healed had four plates removed because of late development of osteomyelitis. All responded to removal of hardware and 4 to 6 weeks of intravenous antibiotics. None experienced relapse of the infection in the followup period. The average time from plate insertion to plate removal in all patients was 13.6 months, with a range from 4.4 to 36.0 months. Cast or splint immobilization after plate removal was used for only 17 of the 51 patients and was used for an average of 2% weeks, with a range from 1 to 6 weeks.
Vol. 15A, No. 2 March 1990
Fig. 1. Case 1: Immediate postoperative fixation of both bone fracture.
Forearm fracture
x-ray film after plate
Results
Six complications occurred among the 51 patients who had plate removal surgery; one a refracture through the previous fracture site occurred in a patient who had her plates removed 6 months after insertion: Case reports Case 1. S. J., a 33-year-old woman, was treated the day of injury with plate fixation for a segmental fracture of the radius and a midshaft fracture of the ulna (Fig. 1). Immobilization was stopped after 6 weeks. In spite of physical therapy, restriction of forearm rotation persisted so her surgeon removed the plates 6 months after the original fixation surgery (Fig. 2). Within 2 weeks of plate removal and while in a long arm cast, the fracture angulated. Manipulation and long arm cast failed to maintain reduction so surgery was advised (Fig. 3). The patient refused to have plates put back in her forearm so the ulna was fixed with a Samson rod (Fig. 4). Both fractures subsequently healed and the patient is not interested in having the rod removed from her ulna. Eight other patients without refracture had 13 plates removed at times from 4.4 to 10 months after insertion. There were five other complications that occurred as a result of plate removal surgery. One patient had an exacerbation of a partial radial sensory nerve palsy after plate removal. This resolved over several months. In one patient a hematoma developed that had to be drained. He had had an extensive excision of a cross union at the time of plate removal. The wound was
plates
295
Fig. 2. Case 1: Six months after open reduction and internal fixation the plates have been removed and a long arm cast applied.
left open and allowed to heal secondarily. Three patients had minor wound problems requiring only local care. In the group of patients who retained their plates, one had an obvious complication secondary to the continued presence of the plate (Fig. 5). Case 2. D. S., a 24-year-old man, had plate fixation of a closed comminuted fracture of the right forearm in 1984. The fracture healed uneventfully and the patient was lost to followup. He returned to the emergency room in October 1987 after striking his right forearm on the dashboard during a low speed automobile accident. A nondisplaced fracture of the ulna through the most proximal screw hole was noted on x-ray films. He was treated with a long arm cast for 4 weeks and the fracture healed. He was again lost to follow-up. No other patients in the plate retention group demonstrated problems directly attributable to the presence of the plate during the study period.
Discussion Many authors advocate routine removal of the currently used internal fixation devices. I-‘* The A0 group recommends removal of all plates after healing has occurred except for hip fracture plates in elderly patients or plates on non-weight-bearing bones, particularly the humerusI Some authors suggest that removal of plates from upper extremity bones needs to be done only in cases with significant local symptoms associated with the plate or in athletes returning to contact
296
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Labosky, Cermak, and Waggy
Fig. 3. Case 1: Four weeks after plate removal the fracture
sites have angulated significantly.
Fig. 4. Case I: One year after repeat open reduction of the
ulna fracture and internal fixation with a Samson rod both fractures are healed. The patient is asymptomatic and refuses removal of the rod.
sports. 14-17Recently Hidaka and Gustilo” and DeLuca and associates” reported high refracture rates after removal of forearm plates, especially plates removed before 1 year after fixation. Both of these authors advised against routine removal of plates, with DeLuca noting refracture even after ceasing to use protective immobilization. Our single refracture after plate removal (case 1) occurred while a patient who had plates removed very early was in a long arm cast. X-ray films (Figs. 2 and 3), however, show that the fractures had not healed adequately and reangulation of the fracture was not surprising. No other refracture occurred in the plate removal group even though some plates were removed very early, and only 17 of the 51 patients had any type of protective immobilization after removal. Refractures after plate removal generally occur through an insufficiently healed fracture or at the site of a screw hole. A freshly drilled hole in a bone weakens it significantly, ‘O but after enough time for bone remodeling the screw holes should not unduly weaken the bone.21 The process of screw removal, however, produces microfractures in the wall of the screw hole. These create fresh stress concentrators that weaken the bonez2 making it more susceptible to refracture. Removing a plate also exposes the patient for a second time to the usual risks of an orthopaedic operation.
Leaving the plate in, however, may not be a totally benign alternative. Once the plate has completed its job promoting fracture healing, its presence becomes superfluous to the function of the bone. The length of time it takes to do this is actually quite short according to current knowledge about the biology of fracture healing.23 Some authors have suggested that after this short time the plate may become a liability to the bone.24-26 A large volume of literature is devoted to the effects of a rigid plate on the cortical bone beneath it and in its immediate vicinity.7-‘1, 23,26-36Because the plate absorbs some of the normal loads, the bone following Wolff’s law, loses strength by cortical thinning and/or osteoporosis. The loss of strength may predispose the bone to fracture near the plate ends where stresses are concentrated. Since during the last 2 decades most of the emphasis in design has been to increase plate strength, (Muller believed that the stability of the bony fragments must be sufficient to prevent even microscopic movement at the site of fracture”) the potential for the stress shielding effects of modem stainless steel plates has increased. Even rigid external fixators have been shown to produce stress shielding and resultant osteoporosis .38 Most of the osteoporosis under fracture plates can be
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Forearm fracture plates
297
Fig. 5. Case 2: Three years after treatment of a both bones forearm fracture with plate fixation
this patient refractured the ulna through the most proximal screw hole.
attributed to vascular disturbances of the bone resulting from plate insertion. However, a number of authors ‘I. 29.39*4o42have shown that less rigid fixation not only weakens the bone less but also allows easier radiographic assessment of healing so the plate can be removed at the earliest possible date. Some authors have found that the longer plates are left in place the greater the effect on the bone and for this reason strongly recommend plate removal after fracture healing.‘-” Aside from the fact that stainless steel plates left in the forearm may cause mechanical problems for the bone, other considerations have to be kept in mind when contemplating permanent insertion of a metal implant in a young person. The most commonly used alloy employed in fracture plates is 316L stainless steel, which is composed mainly of iron, nickel, chromium, and molybdenum. It is considered to be a relatively corrosion-resistant material, but all metals implanted in the saline environment of the body have a finite corrosion rate. The in vivo environment constantly bathes the metal with a protein-rich electrolyte solution that contains a very low concentration of chemical complexes and ions of the material that make up the plate. Consequently the metal is constantly going into solution with release locally and systemically of constituent ions and corrosion complexes. 43-51These products of metal degradation range from fine metal particles to a wide spectrum of metallic salts. Implanted metal devices undergo corrosion by a variety of pathways.5” 53-56Uniform attack is a process of
ionization of the metallic surface in an area of active corrosion. In areas where the protective surface passivation coat remains, uniform attack produces slow dissolution of the passive film. Depassivation is the loss of the implanted metal’s surface protective layer. This can occur by mechanical damage such as scratching or bending with tools of implantation or from abrasion between the screw head and the plate. The protective layer normally reforms except when there is continued mechanical damage as with micro motion between the screw and plate. Fretting corrosion is a degradation process in which friction between the screw head and plate creates small pieces of metal at the site of abrasion5’ The generation of these fine particles greatly increases the surface area of the metal exposed to the saline environment of the body resulting in greater oxidation and ion release. Fretting products may even be small enough to be transported by bulk lymph flow or in phagocytic cells to remote sites where corrosion may continue.” Galvanic or bimetallic corrosion occurs between two different metals sharing the same elctrolyte environment .55.58-61A classic example of galvanic corrosion in vivo is when a plate and screws are made of two different metals. A less flagrant expression of this process can be set in motion when the tools used to implant the plate and screws are made of a different metal or even a different alloy of the metal from which the plate and screws are made.48. 58,62*63 Small deposits of the tool or screw driver metal contaminate the surface of the plate or screw thus setting up the galvanic cell effect.
298
Labosky,
Cermak.
The Journal of HAND SURGERY
and Waggy
This process can even occur between two areas of the same piece of metal when its properties are altered as through work hardening or plastic deformation while the plate is being bent for implantation. Crevice corrosion is a form of corrosion particularly common with fracture plates and screws. Whenever a crevice or crack is present in the metal or between two metal parts such as between the screw head and plate hole the process can occur.56’ 58*62.65 In addition all of the above processes can be affected by local chemical factors like pH and protein concentration. The ongoing process of corrosion and release of metallic substances into the patient’s system sets up the potential for pathologic effects. The major components of 3 16L stainless steel, iron, chromium, and nickel are all biologically essential trace elements, which are under precise physiologic regulation and function in the body.51 Even a small release of these substances is likely to have very high bioactivity. The physiologic consequences may be bacteriologic, metabolic, immunologic, or oncogenic.” The most common response is inflammation, an attempt of the body to isolate the foreign material with a fibrous sack.“. 65.66 Infection, although usually secondary to contamination at surgery, can occur late secondary to seeding of the implant. In vitro studies show that concentrations of stainless steel constituents in the immediate vicinity of an implant, inhibit both macrophage chemotaxis and phagocytosis thus making the implant area more susceptible to infection.52 Finally and most disturbing is the association of malignant disease with long-term retention of metal implantS.6’-‘0 Fine metal particles have been shown to be carcinogenic in mice. “. 72 A higher incidence of respiratory malignant diseases have been documented in industrial workers exposed to inhalation of nickel dust.“, 74 Metal salts have been proven to be carcinogenic even when the pure metals were not.“, 76Concern for the carcinogenic potential of retained fracture plates has been noted, most prominently in veterinary medicine.77-79Osteosarcoma in the presence of retained stainless steel plates has been found most commonly in the diaphyseal segments of long bones. Osteosarcoma is almost always confined to the metaphysis of canine long bones. Tumors in the proximity of retained metal implants in human patients have also been reported sporadically. 8o-86Longitudinal studies need to be done to evaluate the significance of these reported cases since the minimum latency period to be expected for this type of oncogenesis may be 5 to 10 years and may average 20 years. These reports describe only cases of tumor
in the implant area. Neoplastic transformation as a result of metal corrosion products is more likely in remote organs where tissues are capable of concentrating these chemicals. Organs such as the liver, pancreas, and lungs would be likely locations. These issues have yet to be addressed in epidemiologic studies.
Conclusions Removal of forearm fracture plates after healing is not a totally benign procedure. The patient is exposed to the risks of a surgical procedure, as well as the risk of refracture of the plated bone. Leaving the plate in, however, is not a benign decision. In our series as many refractures occurred in patients who had plates removed as ones who retained the plates. Since our population of patients was relatively young (average age, 30 years) the dangers of retained corroding metallic implants will continue to be borne by them for up to 40 to 50 years. The immediate complication rate for plate removal in this series was low, and a refracture rate of 2% is significantly less than has been previously reported. ~3,I9 We therefore believe that these risks are outweighed by the benefits of elimination of a potentially hazardous and no longer useful metallic implant. We do not recommend a cavalier attitude toward plate removal. When the fracture is solidly healed clinically and radiographically, we advise our patients to have their plates removed. Cast or splint protection of the affected extremity after plate removal made no statistical difference in our series, but it may help prevent refracture and should be considered in every patient, especially ones with both bone fractures. REFERENCES 1.
2.
3.
4. 5.
6.
Baggott DG, Goodship AE, Lanyon LE. A quantitative assessment of compression plate fixation in vivo: An experimental study using the sheep radius. J Biomech 1981;14:701-11. Harkess JW. Principles of fractures and dislocation. In: Rockwood CA, Green DP, eds. Fractures. Philadelphia: JB Lippincott, 1975:l. Hesketh KT. Rigid fixation of fractures by compression plating: A pilot study. Proc Roy Sot Med 1968;61: 983-6. Hicks JH, Cater WH. Minor reactions due to modem metal. J Bone Joint Surg 1962;44B:122-8. Radin EL, Simon SR, Rose RM, Paul IL. Practical biomechanics for the orthopaedic surgeon. New York: John Wiley & Sons, 1979:67. Scales JT, Winter GD, Shirley HT. Corrosion of orthopaedic implants, screws, plates, and femoral nail-plates. J Bone Joint Surg 1969;41B:810-20.
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7. Slatis P, Paavolainen P, Karaharju E, Holmstrom T. Structural and biomechanical changes in bone after rigid plate fixation. Can J Surg 1980;23:247-50. 8. Terjesen T. Plate fixation of tibial fractures in the rabbit. Acta Orthop Stand 1984;55:452-6. 9. Tonino AJ, Davidson CL, Klopper PJ, Linclau LA. Protection from stress in bone and its effects. Experiments with stainless steel and plastic plates in dogs. J Bone Joint Surg 1976;58B:107-113. 10. Uhthoff HK, Dubuc FL. Bone structure changes in the dog under rigid internal fixation. Clin Orthop 1971; 81:165-70. 11. Uhthoff HK, Finnegan M. The effects of metal plates on posttraumatic remodeling and bone mass. J Bone Joint Surg 1983;65B:66-71. 12. Walker RH. Biomechanics of fractures and of fracture fixation. Orthop Rev 1983;12:65-72. 13. Mtlller ME, Allgower M, Willenegger H, Schineider R. Manual of internal fixation techniques recommended by the A0 group. Berlin: Springer-Verlag, 1965:58. 14. Anderson LD, Sisk TD, Tooms RE. Compression-plate fixation in acute diaphyseal fractures of the radius and ulna. J Bone Joint Surg 1975;57A:287-97. 15. French GH, Cook SD, Haddad RJ Jr. Correlation of tissue reaction to corrosion in osteosynthetic devices. J Biomed Mater Res 1984;18:817-28. 16. Teipner WA, Mast JW. Internal fixation of forearm diaphyseal fractures: double plating versus single compression (tension band) plating: a comparative study. Clin Orthop 1980;1:381-91. 17. Thomas KA, Cook SD, Harding AF, Haddad RJ. Tissue reaction to implant corrosion in 38 internal fixation devices. Orthopedics 1988;11:441-51. 18. Hidaka S , Gustilo RB . Refracture of bones of the forearm after plate removal. J Bone Joint Surg 1984;66A: 1241-3. 19. DeLuca PA, Newington RWL, Ruwe PA. Refracture of bones of the forearm after removal of compresion plates. J Bone Joint Surg 1988;70A:1372-6. 20. Brooks DB, Burstein AH, Frankel VH. The biomechanits of torsional fractures: the stress concentration effect of a drill hole. J Bone Joint Surg 197&5219:507-14. 21. Burstein AH, Currey J, Frankel VH, Heiple KG, Lunseth P, Vassely JC. Bone strength: the effect of screw holes. J Bone Joint Surg 1972;54A:1143-56. 22. Malone CB, Heiple KG, Burstein AH. Bone strength: before and after removal of unthreaded and threaded pin and screws. Clin Orthop 1977;123:259-60. 23. Perren SM. Physical and biological aspects of fracture healing with special reference to internal fixation. Clin Orthop 1979;138;175-95. 24. Bennett JT, Dameron TB. Intramedullary migration of a plate and screws. Clin Orthop 1983;175:216-17, 25. Jaworski ZFG, Liskova-Kiar M, Uhthoff HK. Effect of long-term immobilization on the pattern of bone loss in older dogs. J Bone Joint Surg 1980;62B:104-10.
Forearm fracture plates
299
26. Stomberg L, Dalen N. Influence of a rigid plate for internal fixation on the maximum torque capacity of long bone. Acta Chir Stand 1976;142:115-22. 27. Cheal EJ, Hayes WC, White AA, Perren SM. Stress analysis of compression plate fixation and its effects on long bone remodeling. J Biomech 1985;18;14150. 28. Daum WJ, Chang SL, Simmons DJ, Webster D. Shoenecker PL. Healing of canine femoral osteotomies: effects of compression plates versus Eggers’ plates. Clin Orthop 1983;180:291-300. 29. Moyen BJ-L, Lahey PJ, Jr., Weinberg EH, Harris WH. Effects on intact femora of dogs of the application and removal of metal plates. A metabolic and structural study comparing stiffer and more flexible plates. J Bone Joint Surg 1978;6OA:940-6. 30. Moyen BJ-L, Comtet JJ, Roy JC, Basset R, deMourgues G. Refracture after removal of internal fixation devices: clinical study of 20 cases and physiologic hypothesis. Lyon Chir 1980;76: 153-7. 3 1. Olerud S, Danckwardt-Lilliestm G. Fracture healing in compression osteosynthesis in the dog. J Bone Joint Surg 1968;50B:844-5 1. 32. Pilliar RM, Cameron HV, Binnington AG, Szivck J, MacNab I. Bone ingrowtb and stress shielding with a porous surface coated fracture fixation plate. J Biomed Mater Res 1979;13:799-810. 33. Stomberg L, Dalen N. Atrophy of cortical bone caused by rigid internal fixation plates. An experimental study in the dog. Acta Orthop Stand 1978;49:448-56. 34. Terjesen T, Benum P. Mechanical effects of metal plate. fixation. In vitro investigation on intact and osteotomized human and rabbit tibiae. Acta Orthop Stand 1983; 54:256-62. 35. Terjesen T, Benum P. The stress-protecting effect of metal plates on the intact rabbit tibia. Acta Grthop Stand 1983;54:810-18. 36. Terjesen T, Nordby A, Arnulf V. The extent of stressprotection after plate osteosynthesis in the human tibia. Clin Orthop 1985;207:108-12. 37. Muller ME. Internal fixation for fresh fractures and for non-union. Proc Roy Sot Med 1963;56:455-60. 38. Akeson WH, Coutts RD, Woo SL-Y. Principles of less rigid internal fixation with plates. Can J Surg 1980; 23:235-9. 39. Tayton K, Johnson-Nurse C, McKibbin B, Bradley J, Hastings G. The use of semi-rigid carbon-fibre-reinforced plastic plates for fixation of human fractures. J Bone Joint Surg 1982;64B: 105- 11. 40. Woo SL-Y, Akeson WH, Levenetz B, Coutts RD, Matthews JV, Amiel D. Potential application of graphite fiber and methyl metbacrylate resin composites as internal fixation plates. J Biomed Mater Res 1974;8:321-38. 41. Woo SL-Y, Akeson WI-I, Coutts RD, Rutherford L, Doty D, Jemmott GF. A comparison of cortical bone atrophy secondary to fixation with plates with large differences
300
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52. 53. 54.
55.
56.
57.
58.
Labosky, Cermak, and Waggy
in bending stiffness. J Bone Joint Surg 1976;58A: 190-5. WOO SL-Y, Simon BR, Akeson WH, Gomes MA, Seguchi Y. A new approach to the design of internal fixation plates. J Biomed Mater Res 1983;17:427-39. Colangelo VJ, Greene ND, Kettelkamp DB, Alexander H, Campbell CH. Corrosion rate measurement in vivo. J Biomed Mater Res 1967;1:405-14. Ferguson AB, Laing PG. Corrosion and corrosion resistant metals in orthopaedic surgery. A.A.O.S. Instructional Course Lect 1958;15:96-103. Ferguson AB, Laing PG, Hodge ES. The ionization of metal implants in living tissues. J Bone Joint Surg 1960;42A:77-90. Ferguson AB, Akohoshi Y, Laing PG, Hodge ES. Characteristics of trace ions released from embedded metal implants in the rabbit. J Bone Joint Surg 1962;44A:32336. Lemons JE, Lucas LC. Corrosion and ion transfer from porous metallic alloys to tissue. A.A.O.S. Instructional Course Lect 1986;35:258-61. Mears DC. Electron-probe microanalysis of tissue and cells from implant areas. J Bone Joint Surg 1966; 48B:567-76. Oron U, Alter A. Corrosion in metal implants embedded in various locations of the body in rats. Clin Orthop 1984;185:295-300. Shirley HT. Corrosion of orthopaedic implants: screws, plates and femoral nail-plates. J Bone Joint Surg 1959; 41B:810-20. Smith GK, Black J. Estimation of in vivo type 316 L stainless steel corrosion rate from blood transport and organ accumulation data. In: Fraker AC, Griffin CD, eds. Corrosion and degradation of implant materials: second symposium, ASTM STP 859. Philadelphia: Am Sot Testing & Materials, 1985:223-47. Black J. Does corrosion matter? (Editorial). J Bone Joint Surg 1988;70B:517-20. Black J. Orthopaedic biomaterials in research and practice. New York: Churchill Livingston, 1988:235-66. Bundy KJ, Marek M, Ho&man RF. In vivo and in vitro studies of the stress-corrosion cracking behavior of surgical implant alloys. J Biomed Mater Res 1983;17:46788. Cahoon JR, Holte RN. Corrosion fatigue of surgical stainless steel in synthetic physiological solution. J Biomed Mater Res 1981;15:137-46. Clarke EGC, Hickman J. An investigation into the correlation between the electrical potentials of metals and their behaviour in biological fluids. J Bone Joint Surg 1953;35B:467-72. Brown SA, Simpson JP. Crevice and fretting corrosion of stainless-steel plates and screws. J Biomed Mater Res 1981;15:867-78. Griffin CD, Buchanan RA, Lemons JE. In vitro electrochemical corrosion study of coupled surgical implant materials. J Biomed Mater Res 1983;17:489-500.
The Journal of HAND SURGERY
59. Rostoker W, Galante JO, Lereim P. Evaluation of couple/crevice corrosion by prosthetic alloys under in vivo conditions. J Biomed Mater Res 1978;12:82330. 60. Thompson NG, Buchanan RA, Lemons JE. In vitro corrosion of Tl-6AL-4V and type 316L stainless steel when galvanically coupled with carbon. J Biomed Mater Res 1979;1:35-44. 61. Wright JK, Axon HJ. Electrolysis and stainless steels in bone. J Bone Joint Surg 1956;38B:745-53. 62. Bowden FP, Williamson JBP, Laing PG. The significance of metallic transfer in orthopaedic surgery. J Bone Joint Surg 1955;37B:676-90. 63. Laing PG. The significance of metallic transfer in the corrosion of orthopaedic screws. J Bone Joint Surg 1958;40A:853-69. 64. Homsy CA, Tulles HS, Anderson MS, King JW. Prevention of interfacial corrosion of SMO stainless steel appliances. Clin Orthop 1971;75:261-8. 65. Levine DL, Staehle RW. Crevice corrosion in orthopaedic implant metals. J Biomed Mater Res 1977;11:553-61. 66. Cook SD, Renz EA. Barrack RL, Thomas KA, Harding AF, Haddad RJ. Clinical and metallurgical analysis of retrieved internal fixation devices. Clin Orthop 1985; 194:236-47. 67. Black J. Biological performance of materials. New York: Marcel Dekker, 1981:128-47. 68. Black J. Orthopaedic biomaterials in research and practice. New York: Churchill Livingstone, 1988285-302. 69. Furst A, Horo RT. A survey of metal carcinogenesis. Prog Exp Tumor Res 1969;12:102-33. 70. Grogan CH. Experimental studies in metal cancerigenesis, VIII. On the etiological factor in chromate cancer. Cancer 1957;10:625-38. 71. Heath JC, Freeman MAR, Swanson SAV. Carcinogenic properties of wear particles from prostheses made in cobalt-chromium alloy. Lancet 1971; 1:564-6. 72. Roe FJE, Lancaster MC. Natural metallic and other substances as carcinogens. Br Med Bull 1964;20:127-33. 73. Doll R. Cancer of the lung and nose in nickel workers. Br J Ind Med 1958;15:217-23. 74. Morgan JG. Some observations on the incidence of respiratory cancer in nickel workers. Br J Ind Med 1958;15:224-34. 75. Dutra FR, Largent EJ. osteosarcoma induced by beryllium oxide. Am J Path01 1950;26:197-210. 76. Janes JM. The influences of splenectomy on the induction of osteogenic sarcoma in rabbits. J Bone Joint Surg 1969;51A:1432. 77. Banks WE, Morris E, Herron MR, Cerion RW. Osteogenic sarcoma associated with internal fracture fixation in two dogs. J Am Vet Med Assoc 1975;167: 166-7. 78. Harrison JW, Mclain DL, Hohn RB. Wilson GP III, Chalman JA, Macgowan KN. Osteosarcoma associated with metallic implants: report of two cases in dogs. Clin Orthop 1976;116:253-6. 79. Stevenson S, Hohn RB, Pohler OEM, Fetter AW, Olm-
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stead ML, Wind AP. Fracture-associated sarcoma in the dog. J Am Vet Med Assoc 1982;180:1189-96. 80. Bago-Granell J, Aguirre-Canyadell M, Nardi J, Tallada N. Malignant fibrous histiocytoma of bone at the site of a total hip arthroplasty. J Bone Joint Surg 1984;66B:3840. 81. Dodion P, Putz P, Amiri-Lamraski MH, Efira FM, Martelaere E, Heimann R. Immunoblastic lymphoma at the site of an infected vitallium bone plate. Histopath 1983;6:807-13. 82. McDonald I. Malignant lymphoma associated with internal fixation of a fractured femur tibia. Cancer 1981; 48:1009-11.
83. Penman HG, Ring PA. Osteosarcoma in association with total hip replacement. J Bone Joint Surg 1984;66B: 632-4. 84. Swarm M. Malignant soft-tissue tumor at the site of a total hip replacement. J Bone Joint Surg 1984;66B:62931. 85. Tayton K. Ewing’s sarcoma at the site of a metal plate. Cancer 1980;45:413-15. 86. Weber PC. Epithelioid sarcoma in association with total knee replacement: a case report. J Bone Joint Surg
1986;68B:824-6.
Irreducible palmar dislocation of the proximal interphalangeal joint of the finger Three patients with pahuar dislocations of the proximal interphalangeal The causes of irreducibility
joints are described.
were the interposition of one lateral band about the condyle of the
middle phalangeal head in two patients and the interposition of the central slip in one patient. (J
HAND
SURC 1990;15A:301-4.)
Goro Inoue, MD, and Noboru Maeda, MD, Nagoya, Japan
P
almar dislocations of proximal intcrphalangeal (PIP) joints are unusual injuries that sometimes cannot be reduced by manipulation, unlike the more common dorsal and lateral dislocations of PIP joints. Johnson and Greene’ reported the first such case in which a lateral band of the extensor mechanism was interposed within the joint. Mu&am? reported two similar cases in which a central slip of the extensor mechanism was interposed within the joint. Three From the Department of Orthopaedic Surgery, Division of Hand Surgery (Bun-in), Nagoya University School of Medicine, Nagoya, Japan. Received for publication March 8, 1989.
Dec. 3, 1987; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: Goro moue, MD, Instructor in Orthopaedics, Department of Orthopaedic Surgery, Division of Hand Surgery (Bunin), Nagoya University School of Medicine, l-l-20 Daiko-minami, Higashi-ku. Nagoya 461, Japan. 311112619
cases with similar pathologic conditions are described below. Case reports Case 1. A 23-year-old man sustained a twisting injury to the left index finger when his glove was caught by an electric drill machine. The diagnosis was an extensor tendon rupture and he was referred to our hospital 2 days later. Examination showed swelling and generalized tenderness of the PIP joint, that was held in 40 degrees of flexion, with 18 degrees of radial angulation and some rotation of the distal finger (Fig. 1, A). The finger could passively be extended to within 10 degrees of full extension. X-ray films showed radial angulation and palmar subluxation of the PIP joint with no fracture (Fig. 2, B). With the patient under digital block anesthesia closed reduction was unsuccessful. The following day open reduction was done through a curved dorsal incision. There was a total rupture of the ulnar collateral ligament and a longitudinal tear between the central slip and the ulnar lateral band which was shifted downward. The ulnar condyle was trapped between the tendinous noose (Fig, 1, C). Reduction was easily accomplished by using a hook to pull out the ulnar lateral band from the joint space. The ulnar collateral ligament and the rent in the extensor
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Thirty-seven
patients had plates removed
electively. Fourteen
patients had plates removed for clinical reasons. The average time from insertion to removal was 13.6 months, with a range from 4.4 to 36 months. Only one refracture occurred through the unhealed both hone forearm fracture site in a patient whose plate was taken out 6 months after surgery. One refracture also occurred through the proximal screw hole of a still implanted
ulna plate that had been inserted 3 years earlier. Leaving a plate in for the remaining life of a young patient cannot be considered a benign decision considering the persisting chance for refracture and the potential complications from prolonged exposure to metal corrosion complexes and metal ions. (J HAND SURG 1990;15A:294-301.)
David A. Labosky, MD, Mary Beth Cermak, MD, and Carol A. Waggy, PT, Morgantown, W.Va.
Dynamic compression plate fixation has become a common method of treatment, if not the standard, for diaphyseal fractures of adult forearm bones. Once the bones have healed, however, the surgeon is presented with a dilemma. Should the plate be taken out or left in? In patients who complain of pain associated with the presence of a bone plate, the clinical decision to remove the plate can be justified even though it exposes the patient to a second operation and to the risk of refracture. But if the plate causes no symptoms, are the risks of removal, particularly the risk of refracture, still overridden by the potential benefit of removing the metallic implant from the body? To determine the level of risk encountered by patients who have had forearm plates removed for any reason, we retrospectively reviewed a series of patients at West Virginia University Hospital treated with plate fixation for fractures of diaphyseal segments of forearm bones. From the Hand and Microvascular Surgery Section, Department of Orthopedic Surgery, and the Department of Physical Therapy, West Virginia University. Morgantown, W.Va. Received for publication May 5, 1989.
March 9, 1989; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: David A. Labosky, MD, 3511 Health Sciences South, West Virginia University, Morgantown, WV 26.506. 311114326
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Materials and methods Ninety-eight patients treated with plate fixation for diaphyseal forearm fractures between June 1981 and June 1987 were followed for at least 1 year after initial surgery or plate removal. Patient ages ranged from 20 years to 55 years, with the average age of 3 1 years. One hundred fifty-five plates were implanted in 78 ulnae and 77 radii with 57 both bone fractures treated. From this group, 80 plates were removed from 51 patients. Eleven plates were removed from isolated ulna fractures, 11 from isolated radius fractures, and 58 from both bone forearm fractures. Patient ages in the plate removal group ranged from 20 to 55 years, with an average age of 30 years. Forty-three of the 51 patients had elective plate removal. Seven plates were removed from five patients because of tenderness or prominence of the plate under the skin. Three patients whose fractures had already healed had four plates removed because of late development of osteomyelitis. All responded to removal of hardware and 4 to 6 weeks of intravenous antibiotics. None experienced relapse of the infection in the followup period. The average time from plate insertion to plate removal in all patients was 13.6 months, with a range from 4.4 to 36.0 months. Cast or splint immobilization after plate removal was used for only 17 of the 51 patients and was used for an average of 2% weeks, with a range from 1 to 6 weeks.
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Fig. 1. Case 1: Immediate postoperative fixation of both bone fracture.
Forearm fracture
x-ray film after plate
Results
Six complications occurred among the 51 patients who had plate removal surgery; one a refracture through the previous fracture site occurred in a patient who had her plates removed 6 months after insertion: Case reports Case 1. S. J., a 33-year-old woman, was treated the day of injury with plate fixation for a segmental fracture of the radius and a midshaft fracture of the ulna (Fig. 1). Immobilization was stopped after 6 weeks. In spite of physical therapy, restriction of forearm rotation persisted so her surgeon removed the plates 6 months after the original fixation surgery (Fig. 2). Within 2 weeks of plate removal and while in a long arm cast, the fracture angulated. Manipulation and long arm cast failed to maintain reduction so surgery was advised (Fig. 3). The patient refused to have plates put back in her forearm so the ulna was fixed with a Samson rod (Fig. 4). Both fractures subsequently healed and the patient is not interested in having the rod removed from her ulna. Eight other patients without refracture had 13 plates removed at times from 4.4 to 10 months after insertion. There were five other complications that occurred as a result of plate removal surgery. One patient had an exacerbation of a partial radial sensory nerve palsy after plate removal. This resolved over several months. In one patient a hematoma developed that had to be drained. He had had an extensive excision of a cross union at the time of plate removal. The wound was
plates
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Fig. 2. Case 1: Six months after open reduction and internal fixation the plates have been removed and a long arm cast applied.
left open and allowed to heal secondarily. Three patients had minor wound problems requiring only local care. In the group of patients who retained their plates, one had an obvious complication secondary to the continued presence of the plate (Fig. 5). Case 2. D. S., a 24-year-old man, had plate fixation of a closed comminuted fracture of the right forearm in 1984. The fracture healed uneventfully and the patient was lost to followup. He returned to the emergency room in October 1987 after striking his right forearm on the dashboard during a low speed automobile accident. A nondisplaced fracture of the ulna through the most proximal screw hole was noted on x-ray films. He was treated with a long arm cast for 4 weeks and the fracture healed. He was again lost to follow-up. No other patients in the plate retention group demonstrated problems directly attributable to the presence of the plate during the study period.
Discussion Many authors advocate routine removal of the currently used internal fixation devices. I-‘* The A0 group recommends removal of all plates after healing has occurred except for hip fracture plates in elderly patients or plates on non-weight-bearing bones, particularly the humerusI Some authors suggest that removal of plates from upper extremity bones needs to be done only in cases with significant local symptoms associated with the plate or in athletes returning to contact
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Labosky, Cermak, and Waggy
Fig. 3. Case 1: Four weeks after plate removal the fracture
sites have angulated significantly.
Fig. 4. Case I: One year after repeat open reduction of the
ulna fracture and internal fixation with a Samson rod both fractures are healed. The patient is asymptomatic and refuses removal of the rod.
sports. 14-17Recently Hidaka and Gustilo” and DeLuca and associates” reported high refracture rates after removal of forearm plates, especially plates removed before 1 year after fixation. Both of these authors advised against routine removal of plates, with DeLuca noting refracture even after ceasing to use protective immobilization. Our single refracture after plate removal (case 1) occurred while a patient who had plates removed very early was in a long arm cast. X-ray films (Figs. 2 and 3), however, show that the fractures had not healed adequately and reangulation of the fracture was not surprising. No other refracture occurred in the plate removal group even though some plates were removed very early, and only 17 of the 51 patients had any type of protective immobilization after removal. Refractures after plate removal generally occur through an insufficiently healed fracture or at the site of a screw hole. A freshly drilled hole in a bone weakens it significantly, ‘O but after enough time for bone remodeling the screw holes should not unduly weaken the bone.21 The process of screw removal, however, produces microfractures in the wall of the screw hole. These create fresh stress concentrators that weaken the bonez2 making it more susceptible to refracture. Removing a plate also exposes the patient for a second time to the usual risks of an orthopaedic operation.
Leaving the plate in, however, may not be a totally benign alternative. Once the plate has completed its job promoting fracture healing, its presence becomes superfluous to the function of the bone. The length of time it takes to do this is actually quite short according to current knowledge about the biology of fracture healing.23 Some authors have suggested that after this short time the plate may become a liability to the bone.24-26 A large volume of literature is devoted to the effects of a rigid plate on the cortical bone beneath it and in its immediate vicinity.7-‘1, 23,26-36Because the plate absorbs some of the normal loads, the bone following Wolff’s law, loses strength by cortical thinning and/or osteoporosis. The loss of strength may predispose the bone to fracture near the plate ends where stresses are concentrated. Since during the last 2 decades most of the emphasis in design has been to increase plate strength, (Muller believed that the stability of the bony fragments must be sufficient to prevent even microscopic movement at the site of fracture”) the potential for the stress shielding effects of modem stainless steel plates has increased. Even rigid external fixators have been shown to produce stress shielding and resultant osteoporosis .38 Most of the osteoporosis under fracture plates can be
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Fig. 5. Case 2: Three years after treatment of a both bones forearm fracture with plate fixation
this patient refractured the ulna through the most proximal screw hole.
attributed to vascular disturbances of the bone resulting from plate insertion. However, a number of authors ‘I. 29.39*4o42have shown that less rigid fixation not only weakens the bone less but also allows easier radiographic assessment of healing so the plate can be removed at the earliest possible date. Some authors have found that the longer plates are left in place the greater the effect on the bone and for this reason strongly recommend plate removal after fracture healing.‘-” Aside from the fact that stainless steel plates left in the forearm may cause mechanical problems for the bone, other considerations have to be kept in mind when contemplating permanent insertion of a metal implant in a young person. The most commonly used alloy employed in fracture plates is 316L stainless steel, which is composed mainly of iron, nickel, chromium, and molybdenum. It is considered to be a relatively corrosion-resistant material, but all metals implanted in the saline environment of the body have a finite corrosion rate. The in vivo environment constantly bathes the metal with a protein-rich electrolyte solution that contains a very low concentration of chemical complexes and ions of the material that make up the plate. Consequently the metal is constantly going into solution with release locally and systemically of constituent ions and corrosion complexes. 43-51These products of metal degradation range from fine metal particles to a wide spectrum of metallic salts. Implanted metal devices undergo corrosion by a variety of pathways.5” 53-56Uniform attack is a process of
ionization of the metallic surface in an area of active corrosion. In areas where the protective surface passivation coat remains, uniform attack produces slow dissolution of the passive film. Depassivation is the loss of the implanted metal’s surface protective layer. This can occur by mechanical damage such as scratching or bending with tools of implantation or from abrasion between the screw head and the plate. The protective layer normally reforms except when there is continued mechanical damage as with micro motion between the screw and plate. Fretting corrosion is a degradation process in which friction between the screw head and plate creates small pieces of metal at the site of abrasion5’ The generation of these fine particles greatly increases the surface area of the metal exposed to the saline environment of the body resulting in greater oxidation and ion release. Fretting products may even be small enough to be transported by bulk lymph flow or in phagocytic cells to remote sites where corrosion may continue.” Galvanic or bimetallic corrosion occurs between two different metals sharing the same elctrolyte environment .55.58-61A classic example of galvanic corrosion in vivo is when a plate and screws are made of two different metals. A less flagrant expression of this process can be set in motion when the tools used to implant the plate and screws are made of a different metal or even a different alloy of the metal from which the plate and screws are made.48. 58,62*63 Small deposits of the tool or screw driver metal contaminate the surface of the plate or screw thus setting up the galvanic cell effect.
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and Waggy
This process can even occur between two areas of the same piece of metal when its properties are altered as through work hardening or plastic deformation while the plate is being bent for implantation. Crevice corrosion is a form of corrosion particularly common with fracture plates and screws. Whenever a crevice or crack is present in the metal or between two metal parts such as between the screw head and plate hole the process can occur.56’ 58*62.65 In addition all of the above processes can be affected by local chemical factors like pH and protein concentration. The ongoing process of corrosion and release of metallic substances into the patient’s system sets up the potential for pathologic effects. The major components of 3 16L stainless steel, iron, chromium, and nickel are all biologically essential trace elements, which are under precise physiologic regulation and function in the body.51 Even a small release of these substances is likely to have very high bioactivity. The physiologic consequences may be bacteriologic, metabolic, immunologic, or oncogenic.” The most common response is inflammation, an attempt of the body to isolate the foreign material with a fibrous sack.“. 65.66 Infection, although usually secondary to contamination at surgery, can occur late secondary to seeding of the implant. In vitro studies show that concentrations of stainless steel constituents in the immediate vicinity of an implant, inhibit both macrophage chemotaxis and phagocytosis thus making the implant area more susceptible to infection.52 Finally and most disturbing is the association of malignant disease with long-term retention of metal implantS.6’-‘0 Fine metal particles have been shown to be carcinogenic in mice. “. 72 A higher incidence of respiratory malignant diseases have been documented in industrial workers exposed to inhalation of nickel dust.“, 74 Metal salts have been proven to be carcinogenic even when the pure metals were not.“, 76Concern for the carcinogenic potential of retained fracture plates has been noted, most prominently in veterinary medicine.77-79Osteosarcoma in the presence of retained stainless steel plates has been found most commonly in the diaphyseal segments of long bones. Osteosarcoma is almost always confined to the metaphysis of canine long bones. Tumors in the proximity of retained metal implants in human patients have also been reported sporadically. 8o-86Longitudinal studies need to be done to evaluate the significance of these reported cases since the minimum latency period to be expected for this type of oncogenesis may be 5 to 10 years and may average 20 years. These reports describe only cases of tumor
in the implant area. Neoplastic transformation as a result of metal corrosion products is more likely in remote organs where tissues are capable of concentrating these chemicals. Organs such as the liver, pancreas, and lungs would be likely locations. These issues have yet to be addressed in epidemiologic studies.
Conclusions Removal of forearm fracture plates after healing is not a totally benign procedure. The patient is exposed to the risks of a surgical procedure, as well as the risk of refracture of the plated bone. Leaving the plate in, however, is not a benign decision. In our series as many refractures occurred in patients who had plates removed as ones who retained the plates. Since our population of patients was relatively young (average age, 30 years) the dangers of retained corroding metallic implants will continue to be borne by them for up to 40 to 50 years. The immediate complication rate for plate removal in this series was low, and a refracture rate of 2% is significantly less than has been previously reported. ~3,I9 We therefore believe that these risks are outweighed by the benefits of elimination of a potentially hazardous and no longer useful metallic implant. We do not recommend a cavalier attitude toward plate removal. When the fracture is solidly healed clinically and radiographically, we advise our patients to have their plates removed. Cast or splint protection of the affected extremity after plate removal made no statistical difference in our series, but it may help prevent refracture and should be considered in every patient, especially ones with both bone fractures. REFERENCES 1.
2.
3.
4. 5.
6.
Baggott DG, Goodship AE, Lanyon LE. A quantitative assessment of compression plate fixation in vivo: An experimental study using the sheep radius. J Biomech 1981;14:701-11. Harkess JW. Principles of fractures and dislocation. In: Rockwood CA, Green DP, eds. Fractures. Philadelphia: JB Lippincott, 1975:l. Hesketh KT. Rigid fixation of fractures by compression plating: A pilot study. Proc Roy Sot Med 1968;61: 983-6. Hicks JH, Cater WH. Minor reactions due to modem metal. J Bone Joint Surg 1962;44B:122-8. Radin EL, Simon SR, Rose RM, Paul IL. Practical biomechanics for the orthopaedic surgeon. New York: John Wiley & Sons, 1979:67. Scales JT, Winter GD, Shirley HT. Corrosion of orthopaedic implants, screws, plates, and femoral nail-plates. J Bone Joint Surg 1969;41B:810-20.
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7. Slatis P, Paavolainen P, Karaharju E, Holmstrom T. Structural and biomechanical changes in bone after rigid plate fixation. Can J Surg 1980;23:247-50. 8. Terjesen T. Plate fixation of tibial fractures in the rabbit. Acta Orthop Stand 1984;55:452-6. 9. Tonino AJ, Davidson CL, Klopper PJ, Linclau LA. Protection from stress in bone and its effects. Experiments with stainless steel and plastic plates in dogs. J Bone Joint Surg 1976;58B:107-113. 10. Uhthoff HK, Dubuc FL. Bone structure changes in the dog under rigid internal fixation. Clin Orthop 1971; 81:165-70. 11. Uhthoff HK, Finnegan M. The effects of metal plates on posttraumatic remodeling and bone mass. J Bone Joint Surg 1983;65B:66-71. 12. Walker RH. Biomechanics of fractures and of fracture fixation. Orthop Rev 1983;12:65-72. 13. Mtlller ME, Allgower M, Willenegger H, Schineider R. Manual of internal fixation techniques recommended by the A0 group. Berlin: Springer-Verlag, 1965:58. 14. Anderson LD, Sisk TD, Tooms RE. Compression-plate fixation in acute diaphyseal fractures of the radius and ulna. J Bone Joint Surg 1975;57A:287-97. 15. French GH, Cook SD, Haddad RJ Jr. Correlation of tissue reaction to corrosion in osteosynthetic devices. J Biomed Mater Res 1984;18:817-28. 16. Teipner WA, Mast JW. Internal fixation of forearm diaphyseal fractures: double plating versus single compression (tension band) plating: a comparative study. Clin Orthop 1980;1:381-91. 17. Thomas KA, Cook SD, Harding AF, Haddad RJ. Tissue reaction to implant corrosion in 38 internal fixation devices. Orthopedics 1988;11:441-51. 18. Hidaka S , Gustilo RB . Refracture of bones of the forearm after plate removal. J Bone Joint Surg 1984;66A: 1241-3. 19. DeLuca PA, Newington RWL, Ruwe PA. Refracture of bones of the forearm after removal of compresion plates. J Bone Joint Surg 1988;70A:1372-6. 20. Brooks DB, Burstein AH, Frankel VH. The biomechanits of torsional fractures: the stress concentration effect of a drill hole. J Bone Joint Surg 197&5219:507-14. 21. Burstein AH, Currey J, Frankel VH, Heiple KG, Lunseth P, Vassely JC. Bone strength: the effect of screw holes. J Bone Joint Surg 1972;54A:1143-56. 22. Malone CB, Heiple KG, Burstein AH. Bone strength: before and after removal of unthreaded and threaded pin and screws. Clin Orthop 1977;123:259-60. 23. Perren SM. Physical and biological aspects of fracture healing with special reference to internal fixation. Clin Orthop 1979;138;175-95. 24. Bennett JT, Dameron TB. Intramedullary migration of a plate and screws. Clin Orthop 1983;175:216-17, 25. Jaworski ZFG, Liskova-Kiar M, Uhthoff HK. Effect of long-term immobilization on the pattern of bone loss in older dogs. J Bone Joint Surg 1980;62B:104-10.
Forearm fracture plates
299
26. Stomberg L, Dalen N. Influence of a rigid plate for internal fixation on the maximum torque capacity of long bone. Acta Chir Stand 1976;142:115-22. 27. Cheal EJ, Hayes WC, White AA, Perren SM. Stress analysis of compression plate fixation and its effects on long bone remodeling. J Biomech 1985;18;14150. 28. Daum WJ, Chang SL, Simmons DJ, Webster D. Shoenecker PL. Healing of canine femoral osteotomies: effects of compression plates versus Eggers’ plates. Clin Orthop 1983;180:291-300. 29. Moyen BJ-L, Lahey PJ, Jr., Weinberg EH, Harris WH. Effects on intact femora of dogs of the application and removal of metal plates. A metabolic and structural study comparing stiffer and more flexible plates. J Bone Joint Surg 1978;6OA:940-6. 30. Moyen BJ-L, Comtet JJ, Roy JC, Basset R, deMourgues G. Refracture after removal of internal fixation devices: clinical study of 20 cases and physiologic hypothesis. Lyon Chir 1980;76: 153-7. 3 1. Olerud S, Danckwardt-Lilliestm G. Fracture healing in compression osteosynthesis in the dog. J Bone Joint Surg 1968;50B:844-5 1. 32. Pilliar RM, Cameron HV, Binnington AG, Szivck J, MacNab I. Bone ingrowtb and stress shielding with a porous surface coated fracture fixation plate. J Biomed Mater Res 1979;13:799-810. 33. Stomberg L, Dalen N. Atrophy of cortical bone caused by rigid internal fixation plates. An experimental study in the dog. Acta Orthop Stand 1978;49:448-56. 34. Terjesen T, Benum P. Mechanical effects of metal plate. fixation. In vitro investigation on intact and osteotomized human and rabbit tibiae. Acta Orthop Stand 1983; 54:256-62. 35. Terjesen T, Benum P. The stress-protecting effect of metal plates on the intact rabbit tibia. Acta Grthop Stand 1983;54:810-18. 36. Terjesen T, Nordby A, Arnulf V. The extent of stressprotection after plate osteosynthesis in the human tibia. Clin Orthop 1985;207:108-12. 37. Muller ME. Internal fixation for fresh fractures and for non-union. Proc Roy Sot Med 1963;56:455-60. 38. Akeson WH, Coutts RD, Woo SL-Y. Principles of less rigid internal fixation with plates. Can J Surg 1980; 23:235-9. 39. Tayton K, Johnson-Nurse C, McKibbin B, Bradley J, Hastings G. The use of semi-rigid carbon-fibre-reinforced plastic plates for fixation of human fractures. J Bone Joint Surg 1982;64B: 105- 11. 40. Woo SL-Y, Akeson WH, Levenetz B, Coutts RD, Matthews JV, Amiel D. Potential application of graphite fiber and methyl metbacrylate resin composites as internal fixation plates. J Biomed Mater Res 1974;8:321-38. 41. Woo SL-Y, Akeson WI-I, Coutts RD, Rutherford L, Doty D, Jemmott GF. A comparison of cortical bone atrophy secondary to fixation with plates with large differences
300
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52. 53. 54.
55.
56.
57.
58.
Labosky, Cermak, and Waggy
in bending stiffness. J Bone Joint Surg 1976;58A: 190-5. WOO SL-Y, Simon BR, Akeson WH, Gomes MA, Seguchi Y. A new approach to the design of internal fixation plates. J Biomed Mater Res 1983;17:427-39. Colangelo VJ, Greene ND, Kettelkamp DB, Alexander H, Campbell CH. Corrosion rate measurement in vivo. J Biomed Mater Res 1967;1:405-14. Ferguson AB, Laing PG. Corrosion and corrosion resistant metals in orthopaedic surgery. A.A.O.S. Instructional Course Lect 1958;15:96-103. Ferguson AB, Laing PG, Hodge ES. The ionization of metal implants in living tissues. J Bone Joint Surg 1960;42A:77-90. Ferguson AB, Akohoshi Y, Laing PG, Hodge ES. Characteristics of trace ions released from embedded metal implants in the rabbit. J Bone Joint Surg 1962;44A:32336. Lemons JE, Lucas LC. Corrosion and ion transfer from porous metallic alloys to tissue. A.A.O.S. Instructional Course Lect 1986;35:258-61. Mears DC. Electron-probe microanalysis of tissue and cells from implant areas. J Bone Joint Surg 1966; 48B:567-76. Oron U, Alter A. Corrosion in metal implants embedded in various locations of the body in rats. Clin Orthop 1984;185:295-300. Shirley HT. Corrosion of orthopaedic implants: screws, plates and femoral nail-plates. J Bone Joint Surg 1959; 41B:810-20. Smith GK, Black J. Estimation of in vivo type 316 L stainless steel corrosion rate from blood transport and organ accumulation data. In: Fraker AC, Griffin CD, eds. Corrosion and degradation of implant materials: second symposium, ASTM STP 859. Philadelphia: Am Sot Testing & Materials, 1985:223-47. Black J. Does corrosion matter? (Editorial). J Bone Joint Surg 1988;70B:517-20. Black J. Orthopaedic biomaterials in research and practice. New York: Churchill Livingston, 1988:235-66. Bundy KJ, Marek M, Ho&man RF. In vivo and in vitro studies of the stress-corrosion cracking behavior of surgical implant alloys. J Biomed Mater Res 1983;17:46788. Cahoon JR, Holte RN. Corrosion fatigue of surgical stainless steel in synthetic physiological solution. J Biomed Mater Res 1981;15:137-46. Clarke EGC, Hickman J. An investigation into the correlation between the electrical potentials of metals and their behaviour in biological fluids. J Bone Joint Surg 1953;35B:467-72. Brown SA, Simpson JP. Crevice and fretting corrosion of stainless-steel plates and screws. J Biomed Mater Res 1981;15:867-78. Griffin CD, Buchanan RA, Lemons JE. In vitro electrochemical corrosion study of coupled surgical implant materials. J Biomed Mater Res 1983;17:489-500.
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59. Rostoker W, Galante JO, Lereim P. Evaluation of couple/crevice corrosion by prosthetic alloys under in vivo conditions. J Biomed Mater Res 1978;12:82330. 60. Thompson NG, Buchanan RA, Lemons JE. In vitro corrosion of Tl-6AL-4V and type 316L stainless steel when galvanically coupled with carbon. J Biomed Mater Res 1979;1:35-44. 61. Wright JK, Axon HJ. Electrolysis and stainless steels in bone. J Bone Joint Surg 1956;38B:745-53. 62. Bowden FP, Williamson JBP, Laing PG. The significance of metallic transfer in orthopaedic surgery. J Bone Joint Surg 1955;37B:676-90. 63. Laing PG. The significance of metallic transfer in the corrosion of orthopaedic screws. J Bone Joint Surg 1958;40A:853-69. 64. Homsy CA, Tulles HS, Anderson MS, King JW. Prevention of interfacial corrosion of SMO stainless steel appliances. Clin Orthop 1971;75:261-8. 65. Levine DL, Staehle RW. Crevice corrosion in orthopaedic implant metals. J Biomed Mater Res 1977;11:553-61. 66. Cook SD, Renz EA. Barrack RL, Thomas KA, Harding AF, Haddad RJ. Clinical and metallurgical analysis of retrieved internal fixation devices. Clin Orthop 1985; 194:236-47. 67. Black J. Biological performance of materials. New York: Marcel Dekker, 1981:128-47. 68. Black J. Orthopaedic biomaterials in research and practice. New York: Churchill Livingstone, 1988285-302. 69. Furst A, Horo RT. A survey of metal carcinogenesis. Prog Exp Tumor Res 1969;12:102-33. 70. Grogan CH. Experimental studies in metal cancerigenesis, VIII. On the etiological factor in chromate cancer. Cancer 1957;10:625-38. 71. Heath JC, Freeman MAR, Swanson SAV. Carcinogenic properties of wear particles from prostheses made in cobalt-chromium alloy. Lancet 1971; 1:564-6. 72. Roe FJE, Lancaster MC. Natural metallic and other substances as carcinogens. Br Med Bull 1964;20:127-33. 73. Doll R. Cancer of the lung and nose in nickel workers. Br J Ind Med 1958;15:217-23. 74. Morgan JG. Some observations on the incidence of respiratory cancer in nickel workers. Br J Ind Med 1958;15:224-34. 75. Dutra FR, Largent EJ. osteosarcoma induced by beryllium oxide. Am J Path01 1950;26:197-210. 76. Janes JM. The influences of splenectomy on the induction of osteogenic sarcoma in rabbits. J Bone Joint Surg 1969;51A:1432. 77. Banks WE, Morris E, Herron MR, Cerion RW. Osteogenic sarcoma associated with internal fracture fixation in two dogs. J Am Vet Med Assoc 1975;167: 166-7. 78. Harrison JW, Mclain DL, Hohn RB. Wilson GP III, Chalman JA, Macgowan KN. Osteosarcoma associated with metallic implants: report of two cases in dogs. Clin Orthop 1976;116:253-6. 79. Stevenson S, Hohn RB, Pohler OEM, Fetter AW, Olm-
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stead ML, Wind AP. Fracture-associated sarcoma in the dog. J Am Vet Med Assoc 1982;180:1189-96. 80. Bago-Granell J, Aguirre-Canyadell M, Nardi J, Tallada N. Malignant fibrous histiocytoma of bone at the site of a total hip arthroplasty. J Bone Joint Surg 1984;66B:3840. 81. Dodion P, Putz P, Amiri-Lamraski MH, Efira FM, Martelaere E, Heimann R. Immunoblastic lymphoma at the site of an infected vitallium bone plate. Histopath 1983;6:807-13. 82. McDonald I. Malignant lymphoma associated with internal fixation of a fractured femur tibia. Cancer 1981; 48:1009-11.
83. Penman HG, Ring PA. Osteosarcoma in association with total hip replacement. J Bone Joint Surg 1984;66B: 632-4. 84. Swarm M. Malignant soft-tissue tumor at the site of a total hip replacement. J Bone Joint Surg 1984;66B:62931. 85. Tayton K. Ewing’s sarcoma at the site of a metal plate. Cancer 1980;45:413-15. 86. Weber PC. Epithelioid sarcoma in association with total knee replacement: a case report. J Bone Joint Surg
1986;68B:824-6.
Irreducible palmar dislocation of the proximal interphalangeal joint of the finger Three patients with pahuar dislocations of the proximal interphalangeal The causes of irreducibility
joints are described.
were the interposition of one lateral band about the condyle of the
middle phalangeal head in two patients and the interposition of the central slip in one patient. (J
HAND
SURC 1990;15A:301-4.)
Goro Inoue, MD, and Noboru Maeda, MD, Nagoya, Japan
P
almar dislocations of proximal intcrphalangeal (PIP) joints are unusual injuries that sometimes cannot be reduced by manipulation, unlike the more common dorsal and lateral dislocations of PIP joints. Johnson and Greene’ reported the first such case in which a lateral band of the extensor mechanism was interposed within the joint. Mu&am? reported two similar cases in which a central slip of the extensor mechanism was interposed within the joint. Three From the Department of Orthopaedic Surgery, Division of Hand Surgery (Bun-in), Nagoya University School of Medicine, Nagoya, Japan. Received for publication March 8, 1989.
Dec. 3, 1987; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: Goro moue, MD, Instructor in Orthopaedics, Department of Orthopaedic Surgery, Division of Hand Surgery (Bunin), Nagoya University School of Medicine, l-l-20 Daiko-minami, Higashi-ku. Nagoya 461, Japan. 311112619
cases with similar pathologic conditions are described below. Case reports Case 1. A 23-year-old man sustained a twisting injury to the left index finger when his glove was caught by an electric drill machine. The diagnosis was an extensor tendon rupture and he was referred to our hospital 2 days later. Examination showed swelling and generalized tenderness of the PIP joint, that was held in 40 degrees of flexion, with 18 degrees of radial angulation and some rotation of the distal finger (Fig. 1, A). The finger could passively be extended to within 10 degrees of full extension. X-ray films showed radial angulation and palmar subluxation of the PIP joint with no fracture (Fig. 2, B). With the patient under digital block anesthesia closed reduction was unsuccessful. The following day open reduction was done through a curved dorsal incision. There was a total rupture of the ulnar collateral ligament and a longitudinal tear between the central slip and the ulnar lateral band which was shifted downward. The ulnar condyle was trapped between the tendinous noose (Fig, 1, C). Reduction was easily accomplished by using a hook to pull out the ulnar lateral band from the joint space. The ulnar collateral ligament and the rent in the extensor
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