By Palanisamy Vijayanand
Since the worst things that happen are apt to be the things one doesn’t see coming, is there a kind of magic whereby, if only one can see them coming, one would somehow prevent them from happening? Following an otherwise technically successful total knee arthroplasty (TKA), around 20% of patients with osteoarthritis (OA) have chronic post-operative pain. The patients often undergo revision surgery with unfavourable pain outcome. This leaves the surgeon either hamstrung, or develop blindness as sharp as his sight – learning not to see any trouble that doesn’t see him first. It is a commonplace in science that often the questions under scrutiny seem simple enough at first: ‘why do some patients have persistent pain after what seems to be a successful procedure?’ With their recent research, the team from Aalborg University Hospital, Denmark have attempted to answer this question in every orthopaedic surgeon’s mind. In their patient unraveling of the answers to this question, we are led into something much more complex.
The pathophysiology of OA pain remains poorly understood, and like low back pain and MRI scan, the radiographic severity of OA is only weakly associated with the clinical severity. Factors outside the joint such as periarticular structures and sensitization of the nervous system seem important for the maintenance of pain. Hyperalgesia to pressure stimulation, before and after TKA, has been previously demonstrated at the painful joint (reflecting peripheral and central sensitization), and at extra-segmental sites (reflecting spreading sensitization). Similarly, facilitated temporal summation, another centrally mediated indicator of sensitization, has been demonstrated in painful OA before and after TKA if the pain is still present. Furthermore, OA disease progression seems better associated with pain and sensitization than with the actual joint destruction assessed by radiological scorings. But, how important are clinical knee pain intensity and knee pain sensitization for the spreading sensitization and facilitated temporal summation is the question which the recent research attempts to provide an answer. Since sensitization across different stages of treatment and knee hyperalgesia is unknown, this study compared sensitization in pain patients with knee OA and after TKA.
Using standardised Quantitative Sensory Testing (QST) protocols, the Pressure Pain Threshold (PPT) of the most affected knee was used to subgroup the patients who had OA and those who have had TKA as follows: group 1: OA patients with PPTs higher than the median PPT; group 2: OA patients with PPTs equal to or lower than the median PPT; group 3: TKA with PPTs higher than the median PPT; group 4: TKA with PPTs lower than the median PPT. Spreading sensitization was assessed by handheld pressure algometry at the tibialis anterior (TA) muscle and the extensor carpi radialis longus muscle (forearm) while temporal summation to repeated pressure pain stimuli was assessed at the TA muscle and the knee using a computer-controlled pressure algometer and an electronic VAS. These procedures were performed bilaterally.
They found that the mean clinical pain intensity was not significantly different between groups. The PPTs from both lower leg and forearm were significantly lower in group 4 compared to groups 1, 2, and 3 and in groups 2 and 3 compared to group 1 (p < 0.05). Temporal summations from the knee and lower leg were significantly facilitated in groups 3 and 4 compared to groups 1 and 2 (p < 0.05). Including all patients, significant correlations were found between peak clinical pain intensity in the affected knee and PPTs from the knee, and between duration of knee pain and PPTs from the knee and the forearm (p < 0.05). Likewise, the duration of knee pain and VAS sum (reflecting temporal summation of pain) at the most sensitive site in the peripatellar region and at the TA muscle was significantly correlated (p < 0.001)
They conclude that spreading sensitization and facilitated temporal summation is more pronounced in chronic pain after TKA than in symptomatic knee OA despite similar clinical pain intensities, and patients with high local knee hyperalgesia show more prominent spreading sensitization. A previous study showed that knee OA patients with higher pain intensities and longer pain durations had relatively more facilitated temporal summation compared to patients having lower pain intensities and shorter pain durations. The clinical implications of this study are (1) repeated surgeries in OA patients should be considered very cautiously particularly in patients with pronounced local knee hyperalgesia, and (2) analgesics that may interact with sensitization, such as gabapentinoids and duloxetine, may be optimal for pain management strategies in OA patients with continued pain after knee surgery. This study also suggests that the ongoing nociception from knee-related structures is important for the chronification process and for the development of sensitization. For some pain patients, a localized pain could become regional and even develop into chronic widespread pain seriously affecting their activities of daily living and quality of life.