Precision management of post‐COVID pain: An evidence and clinical‐based approach

Abstract

BackgroundPain after a SARS‐CoV‐2 acute infection (post‐COVID pain) is becoming a new healthcare emergency but remains underestimated and most likely undertreated due to a lack of recognition of the phenomenon and knowledge of the underlying pain mechanisms. Evidence supporting any particular treatment approach for the management of post‐COVID pain is lacking. Large variability in the patient response to any standard pain treatments is clinically observed, which has led to calls for a personalized, tailored approach to treating patients with chronic post‐COVID pain (i.e. ‘precision pain medicine’). Applying the global concerted action towards precision medicine to post‐COVID pain could help guide clinical decision‐making and aid in more effective treatments.MethodsThe current position paper discusses factors to be considered by clinicians for managing post‐COVID pain ranging from identification of the pain phenotype to genetic consideration.ResultsThe ability of clinicians to phenotype post‐COVID pain into nociceptive, neuropathic, nociplastic or mixed type is suggested as the first step to better planification of a treatment programme. Further, the consideration of other factors, such as gender, comorbidities, treatments received at the acute phase of infection for onset‐associated COVID‐19 symptoms, factors during hospitalization or the presence of emotional disturbances should be implemented into a treatment programme.ConclusionsAccordingly, considering these factors, management of post‐COVID pain should include multimodal pharmacological and non‐pharmacological modalities targeting emotional/cognitive aspects (i.e. psychological and/or coping strategies), central sensitization‐associated mechanisms (i.e. pain neuroscience education), exercise programmes as well as lifestyle interventions (e.g. nutritional support and sleep management).SignificanceThis position paper presents an evidence‐based clinical reasoning approach for precision management of post‐COVID pain.

Post-Acute COVID-19 Joint Pain and New Onset of Rheumatic Musculoskeletal Diseases: A Systematic Review

“…A symmetrical polyarthritis involving wrists and hands has been reported, with an RA-like pattern reminiscent of other prototypical viral arthritis, while in other patients a different pattern has been observed, with monoarthritis or oligoarthritis of large joints, more similar to reactive arthritis, or PMR-like clinical presentations. Since treatment with non-steroidal anti-inflammatory drugs (NSAIDs) and local steroids has been used for post-COVID-19 arthralgia, a potential explanation of the pain origin could be the activation of peripheral nociceptors, suggesting a nociceptive phenotype [78,79]. Nevertheless, it has also been hypothesized that the damage to connective tissue caused by SARS-CoV-2 leads to widespread pain with nociplastic features, in particular in patients with joint hypermobility [78,79].…”

“…Since treatment with non-steroidal anti-inflammatory drugs (NSAIDs) and local steroids has been used for post-COVID-19 arthralgia, a potential explanation of the pain origin could be the activation of peripheral nociceptors, suggesting a nociceptive phenotype [78,79]. Nevertheless, it has also been hypothesized that the damage to connective tissue caused by SARS-CoV-2 leads to widespread pain with nociplastic features, in particular in patients with joint hypermobility [78,79]. Although the precise underlying mechanisms remain to be fully elucidated, growing evidence suggests the association between COVID-19 and the development of autoimmune conditions [17,79].…”

“…Nevertheless, it has also been hypothesized that the damage to connective tissue caused by SARS-CoV-2 leads to widespread pain with nociplastic features, in particular in patients with joint hypermobility [78,79]. Although the precise underlying mechanisms remain to be fully elucidated, growing evidence suggests the association between COVID-19 and the development of autoimmune conditions [17,79]. The role of pathogens in the onset of autoimmune diseases has been demonstrated for different viruses, such as influenza, Ebola, Zika and Chikungunya [80].…”