Case: Osteomalacia Due to Malabsorption
Reported by Myles Clough, Orthopaedic Surgeon, Kamloops, BC, Canada
62 year old female. 25 years ago underwent partial gastrectomy for peptic ulcer disease. This was followed by severe dumping syndrome and malabsorption of such severity she had to have iron infusions. She presented on October 28 1991 with complaints of back and right hip pain of many months duration.
She had been investigated for hip pain including xrays and a bone scan by her family doctor in 1989 with no diagnostic findings. With the marked increase in hip pain a bone scan was repeated in 1991 showing increased uptake in the right hip.
Right hip, October 28, 1991. The xray shows a fracture of the base of the femoral neck with mild varus deformity.
"This patient appears to have a pathological fracture, in that there has been no event of trauma sufficiently severe to cause a fracture. In addition she has had progressive pain in the area . . . one must consider metabolic bone disease and Paget's or Vitamin D deficiency are reasonably good candidates for this type of aetiology . . . it is likely that a reduction of the deformity can be undertaken and that the femoral neck fracture can be treated operatively and result in healing. I have warned her that there is a risk of non-union requiring a total hip replacement."
Surgery was undertaken on 29th Oct 1991 and consisted of reduction by traction and internal rotation followed by fixation with a Dynamic Hip Screw. A bone biopsy was taken.
Right hip, November 1, 1991. Note persistent varus and high placement of the lag screw.
The bone biopsy was sent to a tertiary centre for un-decalcified examination. The report was as follows: "This biopsy consists entirely of cortical bone which has a normal dense lamellar structure. Normal osteons are present. There is no evidence of increased uncalcified osteoid and no evidence of either osteoblastic or osteaoclastic activity. Aluminum stains are negative. A small amount of fatty marrow is present and in several areas there are clusters of fibroblasts and mononuclear cells suggestive of a mild reactive process. There is no evidence either of ostoemalacia or Paget's disease."
At follow-up it was evident that the fracture was going into increasing varus and that the screw was cutting out. We waited for 2 months to see if the fracture would heal then undertook right total hip arthroplasty.
Right hip, January 23, 1992
The technique for hip joint replacement was discussed with the patient and we settled on hybrid technique with porous coated acetabulum and cemented femoral component. The argument for this was the incidence of persistent thigh pain with an uncemented femoral component in a proportion of patients. There was also the question of whether the abnormal bone had the capacity to in-grow. The operation was undertaken on 24 Jan 1992 and resulted in complete relief of symptoms.
She re-presented in May 1995 with sudden onset of severe right hip pain commencing in Dec 1994. Clinically and radiologically the femoral component had loosened.
She was found to have negative cultures and positive arthrogram and booked for revision to an uncemented femoral component. We chose AML fully coated. “If we can get an excellent fit and we have no fractures at the time of surgery the component should be well supported and should not sink down any further. However, if the bone is abnormal, there is a big question as to whether she will get bone ingrowth to totally stabilize the component. Without bone ingrowth a future of loosening and osteolysis is quite likely and would then present a very daunting problem for a second revision."
At surgery we noted that the femoral component was completely loose but still had most of the cement bonded to it, suggesting the loosening was at the bone cement interface. There was a substantial membrane. We inserted a 19.5 mm fully coated 8 inch AML component.
She has made a good recovery from this operation and showed signs of increased bone density on follow up 6 month later. The trochanteric osteotomy did not heal.
Right hip, May 25, 1995
Right hip, June 26, 1995
Right hip, December 12 1995
She re-presented on Oct. 20 1997 with right knee and left thigh pain. She had fallen in August 1997 and had a painful swollen knee with some valgus deformity since then; however, she was also unable to bear weight on the left because of thigh pain. Bone scan showed increased uptake in the left thigh and the right knee and xrays showed Looser's zone in the left thigh and fractures of the right distal femur and proximal tibia.
These injuries made no progress towards healing.
Bone scan, October 23, 1997. Note uptake in right knee and left femur. The right hip is cold.
Right knee, AP, January 6, 1998
Right knee, lateral, January 6, 1998
Left femur, January 5, 1998
On Jan 27 1998 she fractured the left femur with minimal trauma, completing the stress fracture. This injury was treated with IM rod fixation and she went on to heal.
Left femur, January 27, 1998
Left femur, February 2, 1998
Left femur, June 2, 1998
I was reluctant to treat the knee fractures operatively as previous experience had shown problems with holding fixation with screws and plates. I was also concerned that applying a cast would result in stress on the right femur and a periprosthetic fracture. The right leg was therefore treated in a hinged brace and also healed eventually.
Right knee, April 7, 1998
Medical treatment to this time included calcium, vitamin D and fosamax. Clearly this combination was insufficient and she was referred to a specialist in metabolic bone diseases. Before this could take place she sustained a new fracture of the right tibial shaft and a fracture of both bones of the forearm. The right tibia fracture was at the distal end of the brace she was wearing at the time.
Right tibial shaft fracture, left, and forearm fracture, right, July 22, 1998. Note multiple fractures of the radius and severe valgus deformities of the right limb. These were corrected by closed reduction and cast application.
She was started on clodronate infusions in October 1998 and this finally resulted in healing of her fractures.
Despite the normal bone biopsy of 1991 it is hard to believe that osteomalacia is not part of the problem with this patient. Prior to the introduction of clodronate infusions she was breaking bones much faster than she was healing them. Many of the fractures showed features typical of osteomalacia such as Looser's zones and gradual deformity without major trauma.
Orthopaedic operative treatment for her fractures only seemed effective if it was intramedullary. It remains to be seen whether she can maintain her bone mass and avoid further fractures with the present medical regime.