Knee osteoarthritis
Patients often ask me ‘how do you know its knee osteoarthritis?’ (KOA), ‘what has caused my knee osteoarthritis?’, ‘how do steroid injections work?’, ‘do I need a steroid injection?’, ‘how do they work and for how long?’, ’What else can I do to help?’, this case will help you with the finer details and provide supporting evidence.
If we take the case of a sixty-two-year-old retired accountant who had had recently been told by his wife to go to his local Physiotherapist (MSK practitioner) about his persistent knee pain, the gentleman who shall be named Mr P, experienced pain on descending stairs and sometimes his left knee would giveway, this made him anxious. There was no locking but from time to time his knee would flare up in pain and mild swelling. To manage his pain he used paracetamol which was not helping as much as he would like. He was keen to avoid surgery, as he had learnt from his past medical history of right knee pain and locking which was successfully but painfully treated with arthroscopic meniscectomy in 2008. He has recently recovered from a string of painful kidney stones in 2014, but there were no red flags, allergies, intolerances or family history of inflammatory disease, he was otherwise fit and well.
How do you know its knee osteoarthritis? (KOA)
MSK practitioner assessment follows a well-established process of deductive reasoning (Petty and Moore, 2001). Mr P is a large gentleman with a high BMI (>35), he has visible muscle atrophy above his left knee, particularly the vastus medialis muscle group. He had no back pain, and presented a normal neurological assessment which leads the diagnosis away from a spinal neurogenic component causing the muscle wasting (Butler, 1991; Petty and Ryder, 2017). There was no knee joint redness or heat which would have implied an infection (Atkins et al., 2010), but there was some mild joint effusion. His passive movements were stiff and limited in a capsular pattern of discomfort, suggestive of degenerative changes or an acute inflammatory component (Petty and Moore, 2001). Stress testing the knee was unremarkable, implying intact ligamentous structures (Craft and Kurzweil, 2015). A McMurrays test was also unremarkable, providing a sensitivity and specificity of 70% and 71% for the absence of a cartilage lesion (Hegedus et al., 2007). Muscle testing showed quadriceps achieving full range actively against some resistance (Oxford scale rating 4/5) but in comparison to Mr P own body weight this muscle group was considered deficient (Porter, 2003). Palpation over the medial femoral condyle was moderately painful and reproduced Mr P’s symptoms, this offers a site for pathology (Maitland et al., 2005).
In a patient of this age the differential diagnoses could be fracture, perhaps from excessive forces, paying toll on osteoporotic bones. Insufficiency fractures of the Tibial plateau in patients with negative radiographs or showing only osteoarthritis have been documented and described as an often missed diagnosis (Prasad et al., 2006). Another diagnosis albeit very rare is described in the literature whereby a metastatic cancer patient suffers osteonecrosis of the distal femur (Rossi et al., 2015). Mr P case is different to those referenced with cancer who present with ‘red flags’; rapid unexpected weight loss (10lbs in 3 weeks), night pain unrelenting and not responsive to change in position, previous history of cancer. As there was no history of trauma and there was no immediate pain on weightbearing which is typical of fracture (Atkinson et al., 2005) this diagnosis was unlikely.
What clinical signs are present?
The presence of vastus medialis muscle atrophy is commonly seen in KOA, Fink et al (2007) histopathologically reviewed these muscles in 78 pre-operative knee replacement patients with late stage osteoarthritis. All patients exhibited atrophy of type 2 muscle fibres, and 68% of these were attributed to pain associated disuse. Changes such as neurogenic muscular atrophy and muscle fibre degeneration were seen and contribute as cofactors in the development or progression of KOA. This finding and the mild joint effusion, with reduced joint movement in a capsular pattern, provide support for the clinical diagnosis of primary osteoarthritis, and in this case confirmation was requested radiographically. The xray report supported the clinical presentation of KOA, interestingly clinicians often find this is the case and some question the benefit of exposing patient to radiation and associated delays before delivering treatment.
How common is my knee osteoarthritis?
The prevalence of symptomatic KOA in Malmo, Sweden were reported as 15% (Turkiewicz et al., 2015), but in Dorset, the retirement capital of the UK, this figure is higher at 17.8% and of these over 21,600 are cases known to be severe (ARC, 2018a). KOA is one of the most common chronic health conditions and a leading cause of pain and disability among adults (Allen and Golightly, 2015). Estimates place the total economic burden of arthritic diseases between 1 and 2.5% of gross national product in developed countries (Buckwalter and Martin, 2006).
What is knee osteoarthritis?
The knee joint is the meeting point of the Patella on the Femur and the Tibia, here these bony surfaces articulate with a layer of hyaline cartilage, this helps to reduce friction and distributes the force exerted evenly onto the underlying bone. Structures known as Proteoglycan aggrecans bind with lots of water and give hyaline cartilage a plentiful and hydrated matrix, that is stiff and resistant to loading (Adatia et al., 2012). In early KOA there is a reduction of proteoglycan concentration, this weakens the structure and results in fibrillation, which worsens to form clefts that erode and reveal the subchondral bone (Atkinson et al., 2005). Subchondral bone is frequently tender, especially in the knee, probably as a result of microfracture (Adatia et al., 2012). The inflammatory mediators produced by synovium and chondrocytes can lower the threshold of the Ad and C fibres, resulting in an increase in their firing rate in response to painful stimuli. These mediators include bradykinin, prostaglandins and leukotrienes (Dieppe and Lohmander, 2005).
Anatomy of knee pain video
Australian commission on safety and quality in healthcare
What metabolic factors result in knee osteoarthritis?
A recent systematic review and meta-analysis with 8 studies and a total of 3202 cases looked to identify what metabolic factors might contribute substantially to KOA, five components namely abdominal obesity, hypertriglyceridemia, low high density lipoprotein cholesterol, high blood pressure or diabetes were considered. The study found that metabolic factors contribute substantially and was prevalent in 59% of patients with KOA (Wang et al., 2016). It was acknowledged that these two conditions share the same mechanisms of inflammation, oxidative stress, common metabolites, and endothelial dysfunction (Sellam and Berenbaum, 2013). Genetic research has identified a variant, (rs4140564) on chromosome 1, coding for the prostaglandin endoperoxide synthase-2 gene (COX-2), as being associated with knee OA (Valdes et al., 2008). This is of particular significance in view of prostaglandins being central to pain and inflammation in KOA (Adatia et al., 2012).
What else can I do to help my knee osteoarthritis?
An updated literary summary from 2010 was recently compiled and included the highest quality of evidence, including systematic reviews and meta-analyses of randomised controlled trials ((RCTs (McAlindon et al., 2014)). An expert panel (n=13) was used to provide votes on the appropriateness of each treatment modality for KOA, they considered the benefit and risks. Several non-pharmacological modalities had good quality evidence. Weight management, trying to achieve 5% loss within 20 weeks, use of a walking stick, water based and land-based exercise namely, strength training programs primarily incorporate resistance-based lower limb and quadriceps exercises and are endorsed in physiotherapy practice (CSP and RDSPT, 2018). The pharmacological recommendations for paracetamol and non-steroidal anti-inflammatory drugs (Naproxen) were reserved for those without comorbidities, whereas those with comorbidities i.e. cardiovascular disease and hypertension could access topical NSAID gel with an equal benefit (RPS, 2017). Importantly there was a recommendation for intra-articular steroid injections which had demonstrated clinically significant short-term benefits for patients with and without comorbidities. This conclusion reinforced research by others (Bannuru et al., 2009), but stressed that for longer duration of pain relief, clinicians should consider other treatment options.
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