Painful arthroplasty with disproportionate pain: Recognition and management of complex regional pain syndrome

Abstract

Persistent pain following total hip arthroplasty and total knee arthroplasty is most commonly attributed to periprosthetic joint infection, aseptic loosening, instability, or other mechanical complications. However, complex regional pain syndrome (CRPS) represents an uncommon but important cause of disproportionate postoperative pain that is frequently underrecognized, highlighting the importance of timely and accurate diagnosis and management. This narrative review summarizes the current evidence regarding the epidemiology, pathophysiology, diagnosis, and management of CRPS following total joint arthroplasty, with particular emphasis on challenges unique to the arthroplasty population. The Budapest criteria remain the primary clinical framework for diagnosis after exclusion of infection and mechanical failure. Current management emphasizes early recognition, multidisciplinary rehabilitation, physical therapy, and multimodal pharmacologic treatment. Although sympathetic nerve blocks are commonly incorporated into treatment algorithms and may provide temporary diagnostic or therapeutic benefit in selected patients, contemporary systematic reviews demonstrate limited high-quality evidence supporting sustained clinical efficacy. Available arthroplasty-specific literature consists primarily of case reports and small observational studies. Orthopaedic surgeons should maintain a high index of suspicion for CRPS in patients with persistent pain that is disproportionate to expected recovery after total hip arthroplasty or total knee arthroplasty, particularly when standard diagnostic evaluation is unrevealing. Early recognition and appropriate evaluation may facilitate timely management of CRPS following arthroplasty. Further prospective studies are needed to define optimal diagnostic pathways and clarify the role of sympathetic nerve blocks in arthroplasty-associated CRPS.

Key Words: Complex regional pain syndrome; Total knee arthroplasty; Total hip arthroplasty; Arthroplasty; Persistent postoperative pain; Painful arthroplasty; Sympathetic nerve block

Core Tip: Complex regional pain syndrome is an underrecognized cause of persistent pain after total hip and knee arthroplasty, with features that overlap with normal recovery, infection, and mechanical complications. This review provides a systematic diagnostic approach and clarifies that sympathetic nerve blocks offer only limited, temporary benefit.

INTRODUCTION

Complex regional pain syndrome (CRPS) is a chronic pain condition characterized by persistent pain accompanied by sensory, vasomotor, sudomotor, and motor/trophic features that are disproportionate to the inciting injury[1,2]. Pain typically develops days to weeks after tissue injury and may extend beyond the affected region[1].

In the setting of total hip arthroplasty (THA) or total knee arthroplasty (TKA), CRPS represents a potential but underrecognized etiology of persistent postoperative pain when more common causes have been excluded, including periprosthetic joint infection, aseptic loosening, and mechanical complications such as instability or misalignment.

Diagnosis in this population remains challenging because of overlapping clinical features and the absence of a definitive diagnostic test. A high index of suspicion is therefore required, particularly in patients presenting with persistent pain exceeding the expected postoperative course accompanied by features of autonomic dysregulation.

Although several recent reviews have summarized the epidemiology, pathophysiology, and management of CRPS, few have focused specifically on the arthroplasty population. A recent systematic review examined CRPS following TKA, with an emphasis on incidence and functional outcomes[3]. Accordingly, this review aims to characterize the epidemiology and clinical presentation of CRPS following THA and TKA, outline a systematic diagnostic approach, and critically evaluate current management strategies, including the role of sympathetic nerve blocks.

LITERATURE SEARCH

An initial targeted literature search of PubMed/MEDLINE was conducted in April 2026 and subsequently updated on July 1, 2026 to identify relevant studies published within the previous ten years addressing CRPS following total joint arthroplasty. Search terms included “complex regional pain syndrome”, “CRPS”, “total knee arthroplasty”, “TKA”, “total hip arthroplasty”, and “THA”, used in multiple combinations. Articles addressing the epidemiology, diagnosis, risk factors, prevention, or management of CRPS following THA or TKA were considered for inclusion. Because arthroplasty-specific evidence was limited, systematic reviews, clinical guidelines, and other studies of general CRPS populations were also included when they provided clinically applicable evidence regarding diagnosis or management. Additional studies were identified through reference-list review, author recommendations, and consultation with a health science librarian. Only English-language full-text publications were considered. Preprints and conference abstracts without a corresponding full-text publication were not included. Duplicate publications were considered once. Because this was a narrative review rather than a systematic review, formal systematic screening, risk-of-bias assessment, and Preferred Reporting Items for Systematic reviews and Meta-Analyses-style study selection were not performed. A total of 42 papers were identified, of which 39 met inclusion criteria and were incorporated into this review.

For purposes of evidence interpretation, evidence discussed in this review is characterized as arthroplasty-specific when derived directly from patients following THA or TKA, lower-extremity CRPS-specific when derived from CRPS involving the lower extremity but not specifically arthroplasty, and general CRPS evidence when derived from broader CRPS populations. Where direct arthroplasty-specific evidence is unavailable, extrapolation from these indirect populations is explicitly acknowledged.

OVERVIEW OF CRPS

CRPS is broadly classified into two subtypes. Type I occurs in the absence of a confirmed nerve injury and has historically been referred to as reflex sympathetic dystrophy, whereas type II follows a defined nerve injury and has historically been termed causalgia or posttraumatic neuralgia when symptoms are more severe[4].

Although the precise pathophysiology remains incompletely understood, CRPS is considered multifactorial, involving inflammatory, neuropathic, and autonomic mechanisms[1,2]. Following peripheral tissue injury, there is an excess release of proinflammatory neuropeptides and cytokines, resulting in an exaggerated inflammatory response[2,5]. Mediators such as tumor necrosis factor-alpha and interleukin-1beta contribute to peripheral and central sensitization (the increased responsiveness of peripheral nociceptors and amplified pain signaling within the central nervous system, respectively), thereby sustaining chronic pain[5].

Clinical features often develop within four to six weeks of the inciting event and include disproportionate pain that can be described as burning, electric shock-like, stabbing, or tingling[6]. Sensory abnormalities, including allodynia, pain elicited by normally non-painful stimuli, or hyperalgesia, arise from peripheral nociceptor sensitization[1,2].

Autonomic dysfunction may manifest as temperature or color asymmetry. Warm CRPS often appears earlier, with erythema, warmth, and edema, whereas cold CRPS is more typical of chronic disease, presenting with a cool, dusky, or diaphoretic extremity[6]. Trophic changes may include alterations in hair and nail growth and skin texture[1,2]. Motor involvement is also common and may present as tremor, stiffness, or, in more severe cases, weakness[1,2].

INCIDENCE AND RISK AFTER ARTHROPLASTY

Reported incidence rates of CRPS following arthroplasty vary considerably across the literature. Recent registry data from more than 85000 surgical procedures reported CRPS incidences of approximately 0.13% following THA and 0.07% following TKA, with slightly higher rates after revision arthroplasty[7]. In contrast, a prospective longitudinal study of 110 patients undergoing primary TKA reported that 19.1% met the Budapest criteria for CRPS at 2 weeks, decreasing to 9.1% at 6 weeks and 1.8% at 12 weeks[8]. Conversely, a prospective study by Kosy et al[9] of 100 patients following TKA identified no cases of CRPS when the new diagnostic criteria were applied. These substantially different estimates likely reflect differences in study design, diagnostic approach, and timing of assessment. The registry study relied on claims-based diagnostic coding over 12 months, whereas the prospective studies used clinical assessment with standardized diagnostic criteria at defined postoperative time points[7-9]. The high proportion meeting criteria at 2 weeks in the 110-patient study, followed by a marked decline by 12 weeks, contrasts with the absence of cases reported by Kosy et al[9], and suggests that early postoperative findings may be susceptible to misclassification when pain, edema, warmth, and restricted motion overlap with expected recovery. Thus, early postoperative CRPS-like findings should be interpreted in the context of how CRPS was defined, when patients were assessed, and how diagnoses were ascertained.

Given its multifactorial pathophysiology, several risk factors have been identified. Female sex has been associated with up to a fourfold increased risk, particularly during the perimenopausal period[10]. Pre-existing psychological comorbidities, including post-traumatic stress disorder, anxiety, and pain-related fear, have also been linked to increased risk and more severe disease courses[10]. Additionally, preoperative pain sensitization, elevated inflammatory markers, and a history of chronic pain are associated with an elevated postoperative risk[10]; higher levels of preoperative pain sensitization in particular have been associated with persistent postoperative pain and CRPS-related symptoms following TKA. Revision arthroplasty may further increase the risk through repeated surgical trauma, prolonged inflammation, and enhanced peripheral and central sensitization, although arthroplasty-specific evidence remains limited[11-13].

Perioperative strategies aimed at minimizing acute postoperative pain and nociceptive input have been proposed as potential preventive approaches, given the association between preoperative sensitization and CRPS-related symptoms. These include regional anesthesia techniques (e.g. peripheral nerve blocks or neuraxial anesthesia) to reduce perioperative nociceptive signaling, multimodal analgesic protocols that limit reliance on opioids while targeting multiple pain pathways, and early postoperative mobilization to reduce prolonged immobility-related sensitization and stiffness[11]. However, evidence specifically supporting these strategies for CRPS prevention after arthroplasty remains limited, and no perioperative protocol has been shown to reliably reduce CRPS incidence[11].

Vitamin C supplementation has demonstrated potential benefit for CRPS prevention following TKA, with both a prospective randomized study and a propensity score-matched observational study reporting significantly lower rates of CRPS with prophylaxis[14,15]. However, additional prospective validation is needed before routine prophylaxis can be recommended.

DIAGNOSTIC CHALLENGES IN THE PAINFUL ARTHROPLASTY PATIENT

A systematic evaluation is required in patients presenting with persistent pain that is atypical for the expected postoperative course following total joint arthroplasty. Diagnosis may be particularly difficult because postoperative stiffness, swelling, and pain overlap with more common arthroplasty complications[16]. Key distinguishing features between CRPS and other postoperative etiologies are summarized in Table 1.

Table 1 Clinical features distinguishing complex regional pain syndrome from other causes of persistent pain following total joint arthroplasty[1,6,20-22].

Feature	CRPS	PJI	Aseptic loosening	Arthrofibrosis	Peripheral nerve injury
Typical onset	Usually within weeks of surgery	Early postoperative or delayed presentation	Gradual over months to years postoperatively	Weeks to months postoperatively	Immediate or early postoperative period
Pain character	Disproportionate burning pain with allodynia or hyperalgesia	Deep aching pain with swelling	Mechanical pain worsened with activity	Painful stiffness with restricted motion	Neuropathic pain in a defined nerve distribution
Sensory findings	Diffuse hypersensitivity	Typically absent	Absent	Absent	Sensory deficits localized to affected nerve
Skin/trophic changes	Color/temperature changes, edema, sweating changes, trophic changes	Local inflammatory changes possible	Absent	Absent	Typically absent
Range of motion	Pain-limited motion	Limited secondary to pain or effusion	May be painful with instability	Markedly restricted with firm mechanical endpoint	May be limited by pain or weakness
Motor findings	Weakness, tremor, or guarding	Usually absent	Mechanical instability possible	Joint stiffness predominant	Weakness in affected nerve distribution
Laboratory findings	Typically normal inflammatory markers	Elevated ESR and CRP; abnormal synovial fluid analysis	Typically normal inflammatory markers	Normal inflammatory markers	Normal inflammatory markers
Imaging findings	Usually normal or nonspecific	Evidence of effusion or implant-related infection	Radiolucent lines, component migration, or loosening	No implant failure; postoperative fibrosis may be present	Usually normal prosthetic image
Diagnostic considerations	Budapest criteria, multisystem involvement	Joint aspiration and culture remain diagnostic standard	Radiographic evidence of implant failure	Clinical restriction in motion without autonomic findings	Electromyography or nerve conduction studies may assist diagnosis

Complex regional pain syndrome features derived primarily from the Budapest criteria and current diagnostic guidelines. CRPS: Complex regional pain syndrome; PJI: Periprosthetic joint infection; ESR: Erythrocyte sedimentation rate; CRP: C-reactive protein.

Initial evaluation should prioritize exclusion of periprosthetic joint infection, a critical and potentially treatable cause of persistent pain after arthroplasty. This workup includes serum inflammatory markers (erythrocyte sedimentation rate and serum C-reactive protein) and joint aspiration with synovial fluid analysis and culture when clinically indicated[17].

Mechanical complications, including dislocation, aseptic loosening, and component malalignment, should also be evaluated with appropriate imaging[17]. CRPS should be considered when pain is out of proportion to clinical findings and accompanied by multisystem features, including sensory abnormalities (e.g. allodynia, hyperalgesia), autonomic changes, and motor dysfunction. Allodynia is particularly characteristic of this presentation.

The Budapest criteria represent the most widely accepted diagnostic framework[18]. These require persistent, disproportionate pain; at least one symptom in three of the four categories (sensory, vasomotor, sudomotor/edema, and motor/trophic); at least one sign at the time of evaluation in two or more categories; and the absence of an alternative diagnosis explaining the presentation[18,19]. A summary of the Budapest clinical diagnostic criteria is provided in Supplementary Table 1.

The Budapest criteria have both clinical and research versions. Harden et al[20] demonstrated that the Budapest clinical criteria provide greater sensitivity than the earlier International Association for the Study of Pain criteria but have lower specificity than the more stringent Budapest research criteria. The clinical criteria are therefore appropriate for routine diagnosis, whereas the research criteria provide greater specificity for research classification[20]. In the arthroplasty setting, the clinical criteria should be applied cautiously during the early postoperative period because expected pain, edema, warmth, and restricted motion may mimic CRPS features[20].

Differentiating CRPS from other causes is essential. Periprosthetic joint infection typically presents with inflammatory findings, including elevated markers and abnormal synovial analysis[21]. Arthrofibrosis is characterized by progressive stiffness without prominent sensory or autonomic features[17]. Peripheral nerve injury may produce neuropathic pain in a defined distribution but lacks the multisystem involvement seen in CRPS[17]. Recent prospective data suggest that CRPS following TKA may be less common than previously reported when modern Budapest criteria are strictly applied, highlighting the importance of careful differentiation from neuropathic pain and other postoperative complications[9]. Recognition of these distinctions is critical to avoid diagnostic error and delayed treatment. The proposed diagnostic approach for evaluating CRPS in the painful arthroplasty patient is summarized in Figure 1.

Figure 1 Clinical algorithm for evaluation of suspected complex regional pain syndrome following total hip arthroplasty or total knee arthroplasty. The algorithm emphasizes sequential exclusion of periprosthetic joint infection, mechanical complications, arthrofibrosis, and peripheral nerve injury before application of the Budapest clinical diagnostic criteria. It has not been prospectively validated and should not replace individualized clinical assessment. THA: Total hip arthroplasty; TKA: Total knee arthroplasty; PJI: Periprosthetic joint infection; ESR: Erythrocyte sedimentation rate; CRP: C-reactive protein; WBC: White blood cell; CRPS: Complex regional pain syndrome; ROM: Range of motion.

Radiographic findings may provide supportive evidence for CRPS, although imaging is not required for diagnosis[22]. Plain radiographs obtained in later stages of the disease may demonstrate patchy periarticular osteopenia, demineralization, or regional bone loss[1,18,22].

Three-phase bone scintigraphy has historically been investigated as an adjunctive imaging modality for CRPS, although its diagnostic utility remains controversial[23,24]. A systematic review concluded that bone scintigraphy alone is insufficient to either confirm or exclude the diagnosis because of inconsistent diagnostic accuracy[24]. In the arthroplasty population, radiographic findings must be interpreted cautiously because postoperative changes, aseptic loosening, and other periprosthetic pathology may produce overlapping imaging features[1,18,22]. Bone scintigraphy may have greater utility beyond one year after arthroplasty, whereas false-positive findings related to normal postoperative remodeling or implant-related pathology may persist for up to two years postoperatively[23].

Accordingly, formal assessment using the Budapest criteria should be considered when postoperative findings are persistent, disproportionate, progressive, or accompanied by characteristic multisystem abnormalities beyond the expected early postoperative course[18]. Particular attention should be given at approximately 6 weeks and thereafter, when persistent multisystem findings are less likely to represent routine postoperative recovery[8].

Overdiagnosis is an equally important concern; because several CRPS features overlap with expected postoperative recovery, premature attribution of persistent pain to CRPS may lead to inappropriate diagnostic closure and delay evaluation of treatable causes, including periprosthetic joint infection, aseptic loosening, instability, malalignment, arthrofibrosis, and peripheral nerve injury. The Budapest criteria should therefore be applied only after these alternatives have been reasonably excluded.

OVERVIEW OF MANAGEMENT

Management of CRPS requires a multimodal approach addressing both physical and psychological components (Figure 2)[2,18]. Physical therapy is a cornerstone of treatment, aiming to reduce pain, restore mobility, and improve function[1,18]. A recent analysis demonstrated that physical therapy and nonopioid analgesics remain the most commonly utilized treatments for postoperative CRPS, although real-world management often differs from established guideline recommendations[7].

Figure 2 Clinical algorithm for management of complex regional pain syndrome following total hip arthroplasty or total knee arthroplasty. Multidisciplinary management forms the foundation of treatment, with sympathetic nerve blocks considered selectively for diagnostic and temporary therapeutic benefit. Repeat blocks may be considered when meaningful benefit is demonstrated, while persistent or refractory symptoms may warrant additional pain-management interventions. The algorithm has not been prospectively validated, and treatment should be individualized according to clinical response and available evidence. CRPS: Complex regional pain syndrome; ROM: Range of motion; TCA: Tricyclic antidepressant; SNRI: Serotonin-norepinephrine reuptake inhibitor; CBT: Cognitive behavioral therapy; ADL: Activities of daily living; DRG: Dorsal root ganglion.

Pharmacological treatment is commonly incorporated into multimodal CRPS management, although the strength of evidence varies substantially among agents. Bisphosphonates have the strongest evidence among pharmacologic therapies[25]. A systematic review and meta-analysis concluded that bisphosphonates had sufficient evidence to support a treatment recommendation for CRPS[25]. Their potential benefit may be related to inhibition of osteoclast activity and modulation of inflammatory pathways, particularly when treatment is initiated earlier in the disease course[1,6,7]. A more recent publication found that bisphosphonates may reduce pain in the short term, while evidence for immediate and longer-term benefit remains limited or uncertain and adverse events may be increased[26]. Their role in arthroplasty-associated CRPS has not been specifically established.

Other agents are commonly used for symptom-directed treatment, although evidence supporting CRPS-specific efficacy is limited or of low certainty. Neuropathic agents such as tricyclic antidepressants (e.g., amitriptyline, nortriptyline) and serotonin-norepinephrine reuptake inhibitors (e.g., duloxetine, venlafaxine) may address neuropathic pain through enhanced descending inhibitory pain pathways[1,5,27]. Anticonvulsants such as gabapentin and pregabalin may also reduce pain and sensory disturbances through modulation of voltage-gated calcium channels[1,5,27]. Nonsteroidal anti-inflammatory drugs, which reduce prostaglandin-mediated inflammation, may be used to address inflammatory pain, while corticosteroids, which suppress inflammatory cytokine activity, may be beneficial during the early inflammatory phase of CRPS[1,6]. Calcium channel blockers have also been used to address vasomotor dysfunction, although evidence supporting their use remains limited[1,6,7].

Although ketamine and other agents have been investigated for CRPS, evidence remains insufficient to establish their routine use[1,28]. Pharmacologic therapy should therefore be individualized according to disease stage and symptom profile and used in conjunction with physical therapy and functional restoration strategies rather than as a standalone treatment[1,6].

Behavioral and rehabilitative strategies serve an important adjunctive role. Mirror therapy and desensitization techniques have been associated with improvements in pain and function[18,29]. Mental health screening and psychological support are also important components, as patients with CRPS have demonstrated higher rates of anxiety, mood disorders, insomnia, and substance use disorders compared with control populations[1,30]. In refractory cases, interventional strategies such as sympathetic nerve blocks may be considered.

Treatments that demonstrate efficacy in upper-extremity CRPS do not consistently produce comparable relief in lower-extremity disease, potentially reflecting the unique weight-bearing and functional demands placed on the lower extremities[18]. Despite widespread clinical use, few high-quality trials have quantified the effectiveness of these interventions[18,31].

SYMPATHETIC NERVE BLOCKS

Block types

Peripheral nerve blocks and sympathetic nerve blocks serve different purposes in the treatment of pain. Peripheral nerve blocks target specific somatic nerves to provide perioperative analgesia, reduce opioid consumption, and potentially decrease postoperative sensitization[11,13]. In contrast, sympathetic nerve blocks target the sympathetic nervous system and are generally reserved for patients with established CRPS who continue to experience pain and functional impairment despite conservative management (Table 2)[1,18]. These procedures are performed under fluoroscopic or ultrasound guidance and involve injection of local anesthetic near the paravertebral sympathetic chain ganglion[18,32].

Table 2 Summary of available evidence evaluating sympathetic nerve blocks in complex regional pain syndrome[12,18,31,33,35-37].

Ref.	Study type	Population	Arthroplasty specific	Block type	Take-home message	Duration of relief	Key limitations
Ferraro et al[31]	Overview of systematic reviews	Adults with CRPS	General CRPS	Multiple interventions including sympathetic blockade	Evidence remains low certainty; definitive benefit unclear	Variable	Limited high-quality trials
Lee et al[33]	Retrospective cohort	Lower-extremity CRPS	General CRPS	Lumbar sympathetic block with botulinum toxin A/B	Type B toxin produced longer pain relief	Approximately 15 days (type A) vs approximately 69 days (type B)	Small sample size; non-arthroplasty population
Hartrick et al[35]	Prospective observational study	CRPS patients	General CRPS	Sympathetic block	Early response associated with better outcomes	Variable	No standardized protocol; heterogenous population
Adam et al[12]	Case report	Multiple revision THA	THA	Sympathetic block	Marked pain reduction after failed treatments	Pain free at 6 months	Single case report
Zanotti et al[36]	Case report	Elective THA patients	THA	Sympathetic block	Progressive symptom resolution	Resolution by 8 months, symptom free at 6-year follow-up	Very small sample size
Royeca et al[37]	Case report	Post-TKA CRPS	TKA	Multimodal management (limited block data)	Highlights diagnostic difficulty and variable outcomes	Variable	Limited evidence; primarily descriptive
Harden et al[18]	Evidence-based review	CRPS patients	General CRPS	Sympathetic blockade	May provide temporary pain relief and facilitate rehabilitation	Variable	Limited high-quality evidence; variable response

Evidence types and methodological limitations are presented descriptively because this narrative review did not perform a formal systematic risk-of-bias or certainty-of-evidence assessment. CRPS: Complex regional pain syndrome; THA: Total hip arthroplasty; TKA: Total knee arthroplasty.

Stellate ganglion blocks are typically used for upper extremity CRPS, commonly at the C6 or C7 levels[32]. Lumbar sympathetic blocks, typically performed at the L2 or L3 levels, are used for lower extremity involvement and may provide symptomatic relief[33].

Block mechanisms

The mechanisms of sympathetic nerve blocks in CRPS are incompletely understood; however, local-anesthetic sympathetic blocks transiently interrupt sympathetic activity and have historically been used to identify sympathetically maintained pain, a proposed CRPS phenotype in which sympathetic activity contributes to nociceptive signaling through sympatho-afferent coupling[34]. These effects may reduce peripheral sensitization and improve pain, facilitating participation in rehabilitation and reducing reliance on systemic analgesics[1,18]. A technically successful blockade is often associated with vasodilation, increased blood flow, and a rise in skin temperature[10,18].

Diagnostic role

Sympathetic nerve blocks may have a diagnostic adjunct role in patients with suspected sympathetically maintained pain[18]. Diagnostic blocks are typically performed using a single injection of local anesthetic, often lidocaine or bupivacaine, under fluoroscopic or ultrasound guidance[18,32]. A technically successful block may produce objective vasomotor changes, such as increased limb temperature, while temporary pain reduction and improved function provide supportive evidence of sympathetically maintained pain[10,18]. However, validated sensitivity, specificity, and predictive values have not been established for this test[18,31]. Temperature-based thresholds have also been used as surrogate markers of successful sympathetic blockade, but their relationship to clinical pain relief remains uncertain[18]. Therefore, sympathetic blocks should be interpreted alongside the overall clinical picture rather than as a standalone diagnostic test, and a negative response does not exclude CRPS[18,22].

Therapeutic role

When sympathetically maintained pain is suspected, sympathetic nerve blocks may be used as an adjunctive therapeutic intervention in patients with persistent symptoms despite conservative treatment[18]. Local anesthetics remain the standard injectate, while adjunctive agents such as botulinum toxin have been investigated in selected studies to prolong analgesia[18,33].

Recent evidence has questioned the overall effectiveness of local anesthetic sympathetic blockade. A multinational narrative review concluded that moderate-certainty evidence suggests local anesthetic sympathetic blockade is probably ineffective for reducing pain intensity, while a Cochrane review similarly found that lidocaine sympathetic blockade probably does not reduce pain intensity compared with placebo[2,31]. Repeated blocks may be considered for patients who experience meaningful but temporary pain relief that facilitates participation in rehabilitation; however, no standardized treatment series or interval between injections has been established[18,31]. Although an initial response may correlate with symptom improvement, repeated blocks appear to provide limited incremental benefit, and the initial response is not reliably predictive of long-term outcomes[35,36].

One study evaluating lumbar sympathetic blockade with botulinum toxin reported a mean duration of analgesia of approximately 15 days with type A toxin and 69 days with type B toxin[33]. Although isolated case reports following THA have described more prolonged symptom improvement after sympathetic blockade, these findings represent very low-level evidence and should be interpreted cautiously[12,36]. In TKA, data remain sparse and outcomes inconsistent[37].

Sympathetic nerve blocks may therefore provide diagnostic adjunct information and temporary therapeutic benefit in selected patients, particularly when pain relief facilitates rehabilitation; however, their efficacy remains uncertain and they should not be considered disease-modifying therapy[1,18,31]. To our knowledge, no standardized definition of a successful sympathetic block has been established; therefore, response should be interpreted using both the magnitude and duration of pain relief and, importantly, whether temporary analgesia permits improved participation in rehabilitation and functional activity.

Alternative management options

In patients with refractory symptoms, escalation of care may be required. Spinal cord stimulation modulates dorsal column signaling and has demonstrated efficacy in CRPS, although data in post-THA patients remain limited[1,13,18]. Long-term follow-up suggests that analgesic benefit may decline after approximately 3 years despite continued device implantation[38].

Ketamine infusion, an N-methyl-D-aspartate receptor antagonist that may reduce central sensitization, may provide short-term pain relief, typically lasting less than three months, but evidence for sustained benefit is limited[1,28]. Within this framework, sympathetic nerve blocks may function as an intermediate step between conservative management and more invasive interventions.

LIMITATIONS AND FUTURE DIRECTIONS

The current literature is limited by small sample sizes, heterogeneity in study design, and a lack of high-quality randomized trials[1,18,29,31]. Standardized treatment protocols are needed to improve reproducibility and allow for more consistent evaluation of outcomes.

The literature search was narrative rather than systematic and was primarily limited to PubMed/MEDLINE; the Cochrane Library and other bibliographic databases were not independently searched. Accordingly, relevant studies may not have been identified, and the included literature should not be interpreted as an exhaustive systematic synthesis of available evidence.

Future prospective studies in arthroplasty populations should better define the natural history of CRPS, identify predictors of treatment response, and clarify the optimal timing and role of sympathetic nerve blocks[1,11,31].

PRACTICAL CLINICAL CONSIDERATIONS

When to suspect CRPS

Consider CRPS in patients with persistent or disproportionate pain following THA or TKA, particularly when pain is accompanied by sensory abnormalities, vasomotor or sudomotor changes, or motor/trophic dysfunction. Early postoperative pain, edema, warmth, and restricted motion should be interpreted cautiously because these findings may occur during normal recovery[1,8,18].

Initial evaluation

First exclude more common and potentially correctable causes of persistent arthroplasty pain, particularly periprosthetic joint infection and mechanical complications. Evaluation should include appropriate inflammatory markers, joint aspiration when infection is suspected, and imaging to assess component position, loosening, instability, or other mechanical pathology[16,21].

When to apply the Budapest criteria

Formal assessment using the Budapest criteria should be performed when postoperative symptoms are persistent, disproportionate, progressive, or accompanied by multisystem abnormalities beyond the expected early recovery period[18]. Findings during the first several weeks should be interpreted cautiously because of overlap between normal postoperative recovery and CRPS features[8].

When to initiate multidisciplinary care

Once CRPS is suspected or diagnosed and competing arthroplasty complications have been reasonably excluded, early multidisciplinary management should be initiated. Physical therapy and functional restoration should remain central, with pharmacologic, behavioral, and other supportive interventions tailored to the patient’s symptoms and functional limitations[1,18,29].

When to refer to pain medicine

Referral to a pain medicine specialist should be considered for patients with persistent severe pain or functional impairment despite initial conservative management, diagnostic uncertainty requiring specialized assessment, or consideration of interventional therapies such as sympathetic nerve blocks, neuromodulation, or ketamine infusion[1,18,31].

CONCLUSION

CRPS may be both an underrecognized and overdiagnosed cause of persistent pain following total hip and knee arthroplasty. Diagnosis remains challenging because CRPS features overlap with expected postoperative recovery and more common complications, particularly prosthetic joint infection and mechanical failure. The Budapest criteria remain the primary clinical diagnostic framework, although their application during the early postoperative period requires caution[1,18]. Recent arthroplasty-specific studies suggest that CRPS is uncommon when strict diagnostic criteria are applied beyond the early postoperative period, although transient CRPS-like features may occur during normal recovery[7-9].

Much of the evidence supporting the diagnosis and management of CRPS is derived from broader CRPS populations rather than patients undergoing THA or TKA[1,2,18], and arthroplasty-specific data remain particularly sparse for pharmacologic and interventional treatment. Among pharmacologic options, bisphosphonates currently carry the most robust supporting data, though whether this benefit extends to the arthroplasty population specifically has not yet been established[25,31]. Interventional approaches such as sympathetic nerve blocks may offer short-lived diagnostic or symptomatic value in select patients, but systematic reviews have generally failed to confirm meaningful benefit from local anesthetic blockade; these procedures are best regarded as a supportive option alongside, rather than a substitute for, comprehensive multimodal care[2,31,34].