1 / 18

Total Knee Arthroplasty and Parkinson Disease: Enhancing Outcomes and Avoiding Complications

Total Knee Arthroplasty and Parkinson Disease: Enhancing Outcomes and Avoiding Complications. Macaulay W, Geller JA, Brown AR, Cote LJ, Kiernan HA. Introduction I. PD is the second most common neurodegenerative disorder after Alzheimer disease USA Australia World 0.3% population

huyen
Download Presentation

Total Knee Arthroplasty and Parkinson Disease: Enhancing Outcomes and Avoiding Complications

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Total Knee Arthroplasty and Parkinson Disease: Enhancing Outcomes and Avoiding Complications Macaulay W, Geller JA, Brown AR, Cote LJ, Kiernan HA

  2. Introduction I PD is the second most common neurodegenerative disorder after Alzheimer disease USA AustraliaWorld 0.3% population 1-2% persons ≥ 65 yrs 3-6-4.9%1.8% 4-5% persons > 85 yrs 2.6% TKR outcome has proved a challenge in PD: • Musculoskeletal Rigidity • Tremor • Contracture • Gait Instability Chan DK, Dunne M, Wong A, Hu E, Hung WT & Beran RG 2001. Pilot study of prevalence of Parkinsons disease in Australia. Neuroepidemiology 20: 112-7 de Rijk MC et al (2000). Prevalence of Parkinsons disease in Europe: a collaborative study of population-based cohorts. Neurology 54(Suppl)

  3. Introduction II “integrative, systematic, multidisciplinary approach to patients with PD undergoing TKR” “the lack of evidence-based medicine and overall paucity of published studies severely limits review of this topic.”

  4. Parkinson Disease Pathophysiology Idiopathic Secondary medications, toxins, environmental factors herbicide/ pesticide/ chemical exposure, FHx, smoking, tea drinking, high cholesterol Disease optimisation can be difficult due to idiopathic nature. Loss of dopaminergic neurons in the substantianigra = no dopamine = no regulation of excitatory and inhibitory outflow from basal ganglia = disturbance of motor pathways

  5. Parkinson Disease Severity Rating Scales Unified Parkinson’s Disease Rating Scale mentation, behaviour, mood, motor ability, ADLs, therapy complications Schwab and England Scale Modified Hoehn and Yahr Scale

  6. TKA and Parkinson Disease TKR is less successful in PD than in typical patients with OA Oni & MacKenny(1985) 3 patients, 2 ruptured quadriceps tendons, all died within 24 weeks. Vince et al. (1989) 9 patients, 13 TKRs, 4.3 yr follow up, all HK 1-3. Duffy & Trousedale(1996) 24 patients, 33 TKRs, 33 month follow up, achieved pain relief but not functional status Erceg & Maricevic(2000) Case report, recurrent posterior dislocation requiring revision Shah et al. (2005) Case report, diabetic coma, UTI, recalcitrant flexion contracture, 2200 U botulinum toxin type A into biceps femoris and semitendinosis, and subsequently gastrocnaemius, with greatly increased ROM

  7. TKA and Parkinson Disease Recurring Themes • Extensor mechanism problems • Wound necrosis • Post-operative confusion • Limited functional improvement

  8. Avoiding Early Complications Difficult to conclude whether PD is a contraindication to TKR. Achieving pain relief while minimising perioperative complications, may be the target goal. Multimodal approach required Patients expectations and goals need to be clearly established

  9. Medical Management I Decreased function may be as a result of OA, or PD This may be more appropriately addressed with physical therapy and botox TKR should be considered only after failure of these measures, and presence of debilitating joint pain. Perioperative plan from patient’s neurologist regarding recommencement of PD medications

  10. Medical Management II Mehta et al report that neurological intervention preoperatively, or on day of surgery, was the key to a good clinical outcome after TKR. immediate rather than delayed consultation with neurologist perform better (LOS, KS Scores) Triggers required for repeat consultation change in mentation, deterioration in neurological status, pharmacological management Intraoperative anaesthesia and post-operative analgesia regional preferable to general anaesthesia (particularly in pts with ongoing levodopa/carbidopa therapy) general anaesthesia has been shown to mask myopotentials and PD symptoms Opiod drugs effect dopaminergic pathway, and hence mental state and Parkinsonian symptoms

  11. Medical Management III Ketorolac 15 to 30 mg Intramuscularly Q6H for 48 hrs Perioperative risks may outweigh benefits for pts no able to tolerate regional anaesthesia or non-opiod analgesics Interactions between analgesics and patient’s medications should be addressed. Almost no data available in the literature. PD patients have a high risk of falls, and hence nursing vigilance is recommended.

  12. Orthopaedic Management CR and PS prostheses: mild disease, normal quadriceps and hamstrings function Authors prefer CR, condylar-constrained, or hinged prostheses, due to the incidence of subluxation of PS components Hinged prostheses may be the safest option in patients with severe disease. Activity levels of these patients mitigate the concerns of using a fully constrained prosthesis Author’s recommendation based on severity of flexion deformity and rigidity

  13. Orthopaedic Management II No literature recommending particularly surgical approach Pt should be assessed regularly for: • Surgical site infection • Intact extensor mechanism • Flexion contracture – serial bracing, splinting, casting, (No evidence for CPM) • Patellar maltracking • Sialorrhea (PD patients higher risk for silent aspiration)

  14. Orthopaedic Management II Seyler et al described the use of botulinum toxin type A to improve flexion contractures following TKR improved and sustained ROM in 9/11 knees at 2 year follow up Orthopaedic/Neurology communication should continue post-discharge

  15. Summary I Limited data to aid and predict outcome following TKR in PD patients

  16. Summary II Recommendations for TKA • Only perform TKA after failure of nonsurgical measures and in the presence of debilitating joint pain • Use cruciate-retaining, condylar constrained kinetic, or hinged-knee devices in patients with severe PD • Do not use isolated femoral blockade, which may potentiate the early development of postoperative flexion contracture • Use sciatic blockade or hamstring botulinum toxin type A injection • Do not use CPM • Use extremely well-padded braces, splints, or casts in full extension Contraindications to TKA • Any level of preoperative delirium • Patient is not a candidate for regional anesthesia or it is not achievable (ie, due to body habitus) and general anesthesia is the only option • Opiates required postoperatively • Multidisciplinary team members are not available (ie, orthopaedic staff, neurologist, pain service staff, highly trained nursing staff, geriatrics specialists, physiatrist) • Hoehn and Yahr rating ≥3 • Preoperative knee flexion contracture >25° • No response to preoperative diagnostic bupivacaine hydrochloride injection

  17. Thank you

More Related