by Rafael Laguna, MD; Jesús Barrientos, MD
Poliomyelitis is an acute infection disease caused by a group of neurotrophic viruses, which has a special affinity by the anterior horns cells of the spinal cord and for certain motor nuclei of the brain stem. Paralysis is a flaccid type and characteristically paralysis is asymmertrical.1 It is said that the joints of the affected limb by poliomyelitis are protected from the development of osteoarthritis.1-3
This article presents a case of a patient with degenerative hip disease in paralytic dislocation by poliomyelitis.
Case Report
A 38-year-old woman was referred for evaluation of left groin and buttock pain and difficulty walking. Anti-inflammatory medications provided minimal pain relief. She had a history of poliomyelitis as an infant and had undergone 3 surgeries in her left hip; however, she had no medical records regarding the procedures. The patient also reported lumbar pain, and radiographs showed scoliosis and spondylolysis at the L5 level.
On physical examination, the patient experienced severe pain with left hip motion. Her range of motion was 90° of flexion, 25° of rotation, 15° of adduction, and a complete loss of abduction.
Her muscle strength was grade 3 of 5 below the knee. Her knee strength was grade 4 of 5 of extensors and 3 of 5 for flexors. Around the hip, she had grade 3 of 5 for flexors and extensors, and no function in her adductors and abductors.
Her right lower limb was a flail limb. She had recurvatum and valgus knee deformity, and both feet had equinus cavovarus deformity. She walked with a Trendelenburg lurch with the aid of crutches and a Thomas brace (ischial tuberosity support and locking of the knee in extension during the gait) on her right limb.
Her left lower limb presented a shortening of 3 cm. The incisions for the patient’s three previous hip surgeries were identified as being from anterior, lateral, and ilioinguinal approaches.
Radiographs (Figure 1) demonstrated the left hemipelvis was hypoplastic. The acetabulum had type III dysplasia as classified by Crowe et al.4 The femur had a high neck-shaft angle, which could have been related to the interpretation of an anteverted femoral neck5 and a narrow canal. The right femur also was hypoplastic.
Total hip arthroplasty on the left side was planned using a transtrochanteric approach with a chevron osteotomy. The false acetabulum was in anterosuperior position related to the true acetabulum. The latter was shallow and deficient superolaterally and anteriorly. In the femur, there was increased anteversion and the trochanter was placed posteriorly. The femoral head was used as a bulk autograft and was fixed to the false acetabulum with 1 screw. The true acetabulum and graft then were reamed close to the normal hip center.6
An uncemented porous-coated J-LOC 1200 acetabular component (DePuy, Leeds, England) with a diameter of 40 mm was impacted and augmented with 2 cancellous screws. An ultra high molecular weight polyethylene liner with a lip of 10° was implanted.
In the femur, a cementless Corail dysplastic femoral stem (DePuy, Annecy, France) 6 mm in diameter with hydroxyapatite coating and a short neck was implanted. The femoral head was 22 mm.
The femoral stem was implanted with neutral version, and the lip of the liner was situated anteriorly to decrease the risk of dislocation. The trochanter was reattached with wires. The limb was lengthened by 2 cm without neurovascular complication. Two suction drains were left in the surgical field for 48 hours.
Postoperatively, weight bearing was not permitted for 4 months, and the patient underwent isometric and muscle strengthening exercises. During this time, the patient required a wheelchair because of neurological disease. Four months postoperatively, the patient began ambulating with crutches and an orthosis on her right lower limb.
Forty-six months postoperatively, the patient had no pain in the hip. She walked 1 hour daily with the aid of 2 crutches; occasionally, she walked with only 1 crutch but her gait still exhibited a Trendelenburg lurch. Range of motion in her hip was enhanced, with external rotation of 40°, internal rotation of 50°, and abduction and adduction of 30°. There was no change in flexion or extension and or in her muscle strength.
Plain radiographs (Figure 2) showed a well-fixated implant with no signs of loosening. The cup was situated in the normal hip center, and no reabsortion of the graft was visualized. Migration and nonunion of the greater trochanter were evident.
Discussion
Hip dislocation in poliomyelitis is an acquired deformity caused by flaccid paralysis and the resulting muscular imbalance. In young children, when the gluteus maximus and medius muscles are paralyzed and the hip flexors and adductors are of normal strength, eventual luxation of the hip is almost inevitable.4 There is only 1 report in the literature regarding hip replacement in a patient who had postpoliomyelitis sequelae.5 In that case, the patient did not have bilateral compromise, the acetabulum dysplasia was less, and the hip was not dislocated.
Treatment options for a painful degenerative hip joint include resection arthroplasty, arthrodesis, and total hip arthroplasty. Resection arthroplasty was ruled out as it would have relegated the patient to a wheelchair permanently because of her bilateral compromise. Arthrodesis was contraindicated because of our patient’s lumbar and ipsilateral knee pathology. Therefore, we opted to perform a total hip replacement because it offered the highest probability of pain relief for our patient.
In the dysplastic hip, reconstruction of the acetabulum is crucial to the success of the hip arthroplasty. The socket is usually shallow and sloping, with superolateral and anterior deficiency, as well as a diminished anteroposterior dimension.6 In such cases, placement of the acetabular component is problematic. When the acetabulum is at an intermediate height and the femoral head articulates with a false acetabulum that partially overlaps the true acetabulum,7 a decision must be made regarding whether to place the acetabular component at the level of the false acetabulum or to bring it down to the true acetabulum.2 Despite the poor bone quality in our patient, we chose to reconstruct the true acetabulum with femoral head autograft and bring the cup down to the true acetabulum.
Femoral reconstruction in the dysplastic hip also may be complicated by a small medullary canal, femoral hypoplasia, severe developmental distortion of femoral shape and version, and the effects of previous intertochanteric and subtrochanteric osteotomies.2 In our patient, we selected a small, straight, short femoral component that was implanted using uncemented fixation with no version to balance the excessive anteversion.
We did not observe any complications related to the surgery. There was no nerve palsy despite limb lengthening. The implantation of the stem without anteversion and the lip of the liner anteriorly ensured good stability of the prostheses. Weight bearing was not permitted postoperatively for 4 months to ensure biological fixation of the prosthesis.
Another point of interest in this case is the genesis of the arthritis. The patient’s postpoliomyelitis sequelae that affected the limb during growth and resulted in reduced muscular function eventually evolved into pelvic hypoplasia.5 In conjunction with this, the muscular imbalance led to paralytic dislocation. Although poliomyelitis may protect a joint from degenerative disease because the forces across the joints in these patients generally are decreased substantially,8 in our patient, the pelvis hypoplasia, luxation, and increased weight bearing about her hip because the contralateral hip was not subject to load resulted in degenerative arthritis.
One of the most important considerations in such cases is the stability of the prosthesis. In a patient with flaccid paralysis, it is necessary to obtain a stable articulation with tensioning of the soft tissues, correct position of the prosthetic components, and a stable approach to decrease the risk for trochanteric migration. In our patient, despite nonunion of the greater trochanter (Figure 2), the prosthesis did not dislocate. The risk of nonunion and migration of the greater trochanter should be less with trochanteric slide, in which the vastus lateralis is not released from the greater trochanter.
In our patient, we did not consider reattaching the greater trochanter because it did not produce pain and it would not have improved her gait due to her abductor paralysis. Although some authors believe zero abductor strength is a contraindication to this procedure, others do not. Cameron replaced the hip of a patient with no functioning abductors and minimal power of hip flexors.5
In some cases, a constrained cup should be considered. In our patient, the stability of the implant was excellent, and we did not feel a constrained cup was necessary because the incidence of aseptic loosening is higher with a constrained cup than with a conventional cup. Perhaps the previous surgeries our patient underwent, particularly if they involved muscle transfers, may have helped stabilize the hip, making total hip replacement more feasible.
Hip osteoarthrosis in a limb with poliomyelitis is an unusual entity because these limbs do not support excessive loads. In patients who present with the residual effects of poliomyelitis including degenerative disease and hip dysplastic, surgery is one of the most difficult challenges faced by reconstructive surgeons. In such cases, surgeons should attempt to optimize the component position and choice, surgical approach, and soft-tissue tensioning because stability of the prosthesis can be problematic.
Although follow-up in our patient is short term and complications may appear in the future, we believe this is the only procedure can be carried out to return our patient to her initial functional level. If gait is possible, there is no satisfactory alternative to total hip arthroplasty.9 However, there is concern in our patient regarding the longevity of the implant because of her young age, the forces across the joint, the incidence of osteolysis, and the possibility of femoral component breakage from fatigue.
References
- Tachdjian MO. Poliomyelitis. In: Tachdjian MO, ed. Pediatric Orthopedics. Philadelphia, PA: WB Saunders Co; 1990:1910-1978.
- Cameron HU. Total hip replacement in a limb severely affected by paralytic poliomyelitis. Can J Surg. 1995; 38(4):386.
- Cabanela ME. Total hip arthroplasty for developmental dysplasia of the hip. Orthopedics. 2001; 24(9):865-866.
- Crowe JF, Mani VJ, Ranawat CS. Total hip replacement in congenital dislocation and dysplasia of the hip. J Bone Joint Surg Am. 1979; 61(1):15-23.
- Haddad FS, Masri BA, Garbuz DS, Duncan CP. Primary total hip replacement of the dysplastic hip. Instr Course Lect. 2000; 49:23-39.
- Spangehl MJ, Berry DJ, Trousdale RT, Cabanela ME. Uncemented acetabular components with bulk femoral head autograft for acetabular reconstruction in developmental dysplasia of the hip: results at five to twelve years. J Bone Joint Surg Am. 2001; 83(10):1484-1489.
- Hartofilakidis G, Stamos K, Karachalios T, Ioannidis TT, Zacharakis N. Congenital hip disease in adults: classification of acetabular deficiencies and operative treatment with acetabuloplasty combined with total hip arthroplasty. J Bone Joint Surg Am. 1996; 78(1):683-692.
- Cabanela ME, Weber M. Total hip arthroplasty in patients with neuromuscular disease. Instr Course Lect. 2000; 49:163-168.
- Wicart P, Barthas J, Guillaumat M. Replacement arthoplasty of paralytic hip: apropos of 18 cases. Rev Chir Orthop Reparatrice Appar Mot. 1999; 85(6):581-590.
Authors
Drs Laguna and Barrientos are from the Department of Orthopedic Surgery, Gregorio Marañon University Hospital, Madrid, Spain.
Drs Laguna and Barrientos have no relevant financial relationships to disclose.
Correspondence should be addressed to: Rafael Laguna, MD, C/ Vía de las Dos Castillas, n° 5, portal 13; 1° 2, 28224 Pozuelo de Alarcon, Madrid, Spain.