Case Report - (2023) Volume 13, Issue 1
Acute Osteomyelitis (AO) caused by haematogenous spread, accounts for 20% of osteomyelitis in adults. There are no reports of AO in renal transplant recipients. We describe AO in a 42-year-old renal allograft recipient, 7 years after the second transplant on triple immunosuppression with prednisolone, cyclosporine, and azathioprine. He presented to us with high-grade fever and weight loss for a month and was being treated for malaria and urinary tract infection. He complained of severe pain and swelling in his right leg, raising the clinical suspicion of osteomyelitis. This was confirmed by a radiological finding of a lytic lesion on the upper end of the right tibia, with cultures of E.coli both from pus aspirate from the bone and blood. We have reviewed the clinical features and radiological manifestations of AO with an emphasis on immunocompromised patients.
Acute Osteomyelitis • Post-renal transplantation • E.coli
A 42-year-old male - renal allograft recipient having had his first transplant 17 years ago (1990) and re-transplant, 7 years ago (2000) was on triple immunosuppression (prednisolone, cyclosporine, azathioprine) when he was admitted with a history of high-grade fever for a month. He had received anti-malarial therapy, empirical antibiotics for a week, and two units of packed red cells before referral. The graft function was normal. He had a history of recurrent urinary tract infections and was diagnosed with grade-4 vesicoureteral reflux into the renal allograft and was on long-term antibiotic prophylaxis. He was planned for ureteric re-implantation to prevent recurrent UTI.
On admission, there was severe tenderness and inflammation over the upper end of the right Tibia. He was afebrile, pulse was 80/min, and blood pressure was 140/90 mm Hg.
linically, AO of the right tibia was considered. Radiology of the right leg showed multiple lytic lesions in the right tibia tuberosity. Bone scan showed a hot spot over the same region. Pus aspirated from the lesion grew E.coli and he was treated with imipenem, according to the sensitivity report. The urine culture was sterile. CMV quantitative PCR was negative. Cultures for Nocardia, crytococcus and other fungi were negative. There was no feature of sickling. After starting antibiotics he became afebrile in 2 weeks and antibiotics were continued for total of 6 weeks. During this period his graft function remained stable. He received packed red cell transfusion and Erythropoietin . Patient developed leucopenia while on imipenem, requiring temporary cessation of azathioprine and use of GM-CSF. His wound healed with the treatment and he was started on active physiotherapy, for quick mobilization. Repeat cultures from the wound were sterile after a full course of antibiotics. C-reactive protein levels declined to 4.0 from 9.36. The patient was discharged with a healing wound and stable graft function.
AO is an inflammation is classified of the bone caused by an infecting organism. Incidence in the adult healthy population is 0.1%- 1.8%. It as of hematogenous and exogenous [1].Hematogenous osteomyelitis accounts for approximately 20% of cases of osteomyelitis in adults. It is more common in males. Long bones are some of the major sites for hematogenous osteomyelitis. Immunocompromised state (e.g. due to HIV or immunosuppressive drugs) and recurrent urinary tract infections are common predisposing factors [2].
Infections of long bones develop within the metaphysis and then spread laterally through the Haversian and Volkmann canals to the periosteum. The Periosteum is lifted or stripped from the surface of the bone by the pressure of accumulating purulence. When this occurs, the periosteal and endostea circulations are compromised, capillaries are lost, and large segments of the cortical and trabecular bone die. In adults, infection of the long bones usually begins in the diaphysis but may spread to involve the medullary canal.
Hematogenous osteomyelitis usually occurs after an occult bacteremic event, with a single pathogen. S. aureus remains the most commonly isolated organism in the normal host, but aerobic gram-negative organisms (rods) are found in 30% of the cases [3].
The diagnosis of hematogenous osteomyelitis relies importantly on clinical suspicion [4]. Routine laboratory tests are usually non-specific and include, increased TC (35%), increased ESR>20 mm/hr (92%), increased C-reactive proteins (98%), and blood culture positivity (41%-67%).
The earliest radiographic changes are swelling of the soft tissue, periosteal thickening and/or elevation, and focal osteopenia [5]. A bone biopsy or subperiosteally abscess aspirate for culture is necessary unless the patient has positive blood cultures along with radiographic findings consistent with osteomyelitis [6].
There have been reports of involvement of bone in immunosuppressed patients with Nocardia, Cryptococcus, Salmonella and mycobacteria. Invasive Candida infections tend to occur in selected patients, including those who are immunocompromised (e.g. neutropenia, steroid therapy). C. Albicans is the most common pathogen. Candida osteoarticular infections are most often due to hematogenous seeding of the joint or bone in patients who have been candidemic [7]. The area’s most often seeded are the intervertebral disc and knee joint. Clinical features include insidious onset of monoarthritis, immunocompromise, failure to identify the causative pathogen on synovial fluid cultures, and failure to respond to courses of antibiotic therapy. It is more easily confirmed than osteomyelitis since synovial fluid can be readily obtained for cultures [8].
Salmonella primarily affects the gastrointestinal tract, peripheral or visceral arteries or lumbar spine in immunocompromised patients [9].
Nocardia can disseminate hematogenously from a pulmonary or cutaneous focus to bones. Among other organs involved are the heart, joints, and kidneys [9]. Septic arthritis caused by Nocardia has been reported in a renal transplant recipient. Recently, mycophenolate mofetil has been recognized as a factor implicated in Nocardia infections [10].
Tuberculous osteomyelitis has been reported in immunocompromised individuals. In the early stages, CT and MRI may help to localize the lesions when plain radiographs are normal. On plain radiographs, the more advanced lesions may mimic chronic pyogenic osteomyelitis, Brodie's abscess, tumors, or granulomatous lesions [10].
Hematogenous osteomyelitis in adults is more refractory to therapy. Patients have been traditionally treated for 4 weeks with appropriate parenteral antibiotics, dating from the initiation of therapy or after the last major debridement surgery.
The relative rarity of bacterial AO in renal transplant recipients is surprising. It is likely that the initial bacteremic event is clinically apparent in a transplant recipient and is treated with antibiotics. If such an episode escapes clinical attention, an immunocompromised patient is unlikely to survive to have AO. However, bone tenderness and pain in afebrile transplant patients should raise the suspicion of acute osteomyelitis.
In summary, we report a rare case of post-renal transplant acute osteomyelitis. This condition should be considered in renal transplant recipients when there is a strong clinical suspicion. Early recognition and prompt treatment of the condition avoid fatal complications.
Citation: Tripathi, M. Acute Osteomyelitis in Post Renal Transplant. Prim Health Care. 2023, 13(1), 482
Received: 13-Jan-2023, Manuscript No. jphc-23-87039; Editor assigned: 16-Jan-2023, Pre QC No. jphc-23-87039 (PQ); Reviewed: 24-Jan-2023, QC No. jphc-23-87039 (Q); Revised: 26-Jan-2023, Manuscript No. jphc-23-87039 (R); Published: 29-Jan-2023, DOI: 10.35248/2376-0389.22.13.1.482
Copyright: ©2023 Tripathi, M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
