Ankle and Foot Arthropathies

Contents

Description 

Arthropathy

An arthropathy is a disease which affects a joint. Although the terms arthropathy and arthritis have very similar meanings, the former is traditionally used to describe the following conditions:

  • Reactive arthropathy occurs as a reaction against an infection site elsewhere in the body.[1]
  • Enteropathic arthropathy is an arthropathy in association with, or as a reaction to, an enteric (usually colonic) inflammatory condition.[2]
  • Crystal arthropathy is characterised by accumulation of tiny crystals in one or more joints.[3]
  • Neuropathic arthropathy is gradual joint destruction when there is chronic damage of peripheral nerves and diminished proprioception. [4]
  • Diabetic arthropathy is a neuropathic arthropathy occurring in diabetic patients. [5]

An arthropathy can be degenerative, such as osteoarthritis, or associated with inflammation, e.g. rheumatoid arthritis. A joint disease can also occur following trauma.

Although arthropathy is less common in the ankle than the hip and knee, it can be just as disabling.[6]

Arthropathy is a blanket or global term for a wide range of joint presentations. Some specific arthropathies are detailed below:

OA ankle.jpg

Osteoarthritis

Osteoarthritis (OA) results when mechanical and biological factors destabilise the normal coupling of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix and subchondral bone. Destabilising factors include genetic, developmental, metabolic, and traumatic events. OA involves all the tissues of the diathrodial joint.
Ultimately, OA manifests as morphologic, biochemical, molecular and biomechanical change of tissues, cells and matrix, which soften and fibrillate articular cartilage. The sequelae then become ulceration and loss of articular cartilage, sclerosis and eburnation of subchondral bone, growth of osteophytes and development of subchondral cysts.[7]


 

RA ankle.jpg

Rheumatoid arthritis

Rheumatoid arthritis (RA) in the foot is categorised anatomically, i.e. forefoot, midfoot and hindfoot pathologies.[8]Most of the studies have focused on forefoot and hindfoot pathologies; there are fewer studies on midfoot RA.[9] Rheumatoid arthritis is a multi-system, chronic, progressive, inflammatory disease. Joints become swollen, tender and painful which can lead to severe deformity and disability. [9][10][11][12][13]


 

HA foot.jpg

Haemophilic arthropathy

In patients with severe haemophilia, arthropathy causes high levels of impairment. The degenerative changes caused by recurrent haemarthrosis are progressive. The ankle is frequently affected in haemophilic patients. [14]


Diabetic foot arthropathy.jpg

Diabetic foot arthropathy

Charcot neuropathic osteoarthropathy of the foot is a devastating neuropathic complication of diabetes and other metabolic illnesses. [15][16][17][18][19][20]

Charcot foot is a progressive and degenerative arthropathy of a single or multiple joints that ultimately leads to destruction of normal foot architecture and collapse of the arch. [17] It also frequently leads to foot ulceration, gangrene and foot amputation. [18][19][20]

The aetiology of Charcot neuropathic osteoarthropathy is thought to be unregulated inflammation that is triggered in people with peripheral neuropathy. The inflammatory process eventually stimulates the maturation of osteoclasts from osteoclast precursor cells. [18][20]


Gout foot.jpg

Gout

Gout is a crystal-induced arthritis, in which intro-articular monosodiumurate (MSU) crystals precipitate, causing reactive inflammation in local soft tissues. A susceptibility to MSU crystal formation occurs in people with excessive blood levels of soluble urate, which is a product of purine nucleotide metabolism. Hyperuricemia is when serum urate levels rise above a saturation point for MSU, i.e. >6.8 mg/dL [21]. When levels are over 6.8 the risk of crystallisation increases.

 

PsA ankle.png

Psoriatic arthritis

Psoriatic arthritis is a chronic inflammatory condition that affects the skin and musculoskeletal system. [22][23] If not diagnosed early and treated effectively Psoriatic Arthritis can result in joint deformity and disability. [22]

Psoriatic arthritis can cause considerable disability and pain, especially when not diagnosed and treated correctly. Approximately 15% of patients affected by psoriasis will develop associated joint disease. It was first recognised in 1964 and is now considered part of the spondyloarthropathy group of diseases. [22]


ReA ankle.jpg

Reactive arthritis

Reactive arthritis (ReA) is an infectious disease which may be initiated by several microbes in genetically susceptible hosts. [24] Reactive arthritis is one of the types known to primarily affect young men as it can be a complication of sexually transmitted infections.

ReA is classified as a type of spondyloarthritis. This group of joint diseases features mono- or oligoarthritis, often associated with extra-articular inflammatory manifestations involving the musculoskeletal, ophthalmologic, dermatologic, and genitourinary systems. These were previously referred to as seronegative spondyloarthritides because the rheumatoid factor is usually negative. [25]


Clinically Relevant Anatomy

More information about the anatomy of the ankle and foot can be found here: Biomechanics of Foot and Ankle and Ankle Joint.

Epidemiology /Etiology

Osteoarthritis

Approximately 1% of the world’s adult population is affected by ankle OA, which results in pain, dysfunction, and impaired mobility. The mental and physical disability associated with end-stage ankle OA is at least as severe as that associated with end-stage hip OA. Numerous clinical and epidemiologic studies have identified previous trauma as the most common origin of ankle OA. 79.5% of patients with ankle OA had a verified history of 1 or more joint injuries. [14]

Rheumatoid arthritis

The prevalence of foot pain in patients with RA has been reported in varying numbers within the published literature. The prevalence of foot pain depends on the stage of the disease. Ranging from 60 to 94 % at some stage of the disease. [11][12] In the early stages of RA the prevalence is lower: only 16 % in one study and 32 in another study. [11]

Haemophilic arthropathy

Recurrent haemorrhages that occur with haemophilia result in severe joint destruction. Many authors have reported changes in the synovial membrane and cartilage in chronic haemarthrosis. Repeated episodes of intra-articular bleeding cause damage to the joint, leading to deformity.
Several joint disorders, degenerative ones, such as osteoarthritis, inflammation-mediated ones, such as rheumatoid arthritis, and blood-induced ones, such as haemophilic arthropathy, result in cartilage damage and changes in the synovial tissue. [26]

Diabetic foot arthropathy

Diabetes affects approximately 387 million people worldwide. Together with neuropathy, diabetes mellitus, is currently considered the main cause of Charcot neuropathic osteoarthropathy. The disease often goes undiagnosed amongst patients living with diabetes and its diagnosis greatly depends on the type of investigation: changes diagnosed by X-ray and corresponding to Charcot neuropathic osteoarthropathy are detected in up to 29% of diabetics, whereas under MRI the detection rate rises to 75%.[20]

Gout

The global prevalence of gout is substantial and seems to be increasing in many parts of the world over the past 50 years. The distribution of gout is uneven across the globe, with prevalence being highest in Pacific countries. Developed countries tend to have a higher prevalence of gout than that of developing countries and incidence of the disease appears to be on the increase. [27]

In various geographical regions, men are more likely to report gout than women [28]. Less than 10% of cases reported occur in women. Most women diagnosed with gout are reported to be 15 years or more beyond menopause. This type of arthropathy is rare in children. [29]

The results of several studies suggest that environmental, racial, and hereditary differences may influence the development of gout. For example, Tokelauan migrants to New Zealand have a greater prevalence of gout than non-migrants and certain populations, such as the Maori, have a greater frequency of gout than other New Zealand populations. [28]

Some ethnic groups are particularly susceptible to gout, supporting the importance of genetic predisposition. [27]

Hyperuricemia is the most important risk factor for gout [30] and is affected by both genetic factors and environmental factors [31]. Factors that increase serum urate levels include hypertension, thiazide diuretic intake, obesity, alcohol use, and a high animal protein diet [32].

Socioeconomic and dietary factors, as well as comorbidities and medications that can influence uric acid levels and/or facilitate MSU crystal formation are also important in determining the risk of developing clinically evident gout. [27]

The risk of gout is lower in men who are more physically active, who maintain ideal body weight and who consume diets which are rich in fruit and limited in meat and alcohol. [33]

Psoriatic arthritis

In comparison to most other rheumatic disorders genetic predisposition plays a major role in the development of Psoriatic arthritis. [34] Psoriasis is known to affect approximately 2% to 3% of the general population, and the prevalence of Psoriatic arthritis in psoriasis patients is between 6% and 39%. It is possible that the condition remains generally underdiagnosed, related to lack of awareness by both the patient and physician. [35]

It is still not clear what exact mechanism lies behind the development of psoriatic arthritis. It is thought to be multifactorial and secondary to environmental, genetic, and immunological factors. When compared with other inflammatory rheumatic conditions, psoriasis and psoriatic arthritis are strongly heritable. [22]

Reactive arthritis

Data indicates that approximately 50% of reactive arthritis and undifferentiated oligoarthritis cases can be attributed to a specific pathogen by a combination of culture and serology. The predominant organisms are Chlamydia, Salmonella, Shigella, Yersinia and Campylobactor species. The annual incidence of ReA was found to be 28/100.000 individuals in one study. This may exceed that of rheumatoid arthritis. [36]

Characteristics/Clinical Presentation

The characteristics and clinical presentation of ankle arthropathies such as different forms of arthritis can be described as followed:

  • Ankle pain
  • Stiffness
  • Swelling
  • Limited range of motion (ROM)

Pain usually increases on activities such as standing, walking or running.

“Start-up pain” is also a common complaint, where the patient experiences pain and stiffness in the ankle on moving after being asleep or sitting for a long period, which takes a few minutes of motion to settle. The ankle will tend to increasingly swell, however, as the day progresses, particularly with a higher level of activity.

Pain is mostly felt in the entire ankle, although it may be more noticeable anteriorly if large boney spurs have formed. Arthritis often develops in an injured ankle joint. Degeneration of the overlying cartilage results in ankle arthropathy.

Osteoarthritis

There are four degrees of severity with osteoarthritis:

  1. Degree I: normal joint with a minimal osteophyte.
  2. Degree II: osteophytose on two points with minimal subchondral sclerosis, normal joint space and no deformity.
  3. Degree III: moderate osteophytose, early deformity of the bone ends and a narrowing joint space.
  4. Degree IV: large osteophytes, deformity of bone ends, narrowing joint space, sclerosis and cysts [37]

Rheumatoid arthritis

Hallux valgus, splaying of the forefoot and pes planus are the most typically seen foot deformities in RA. [9][12] The foot problems caused by RA can lead to mobility problems [13][38], slower gait speed and a decrease in toe strength. [11]

A systematic review and meta-analysis by Carroll et al. [39] showed that the majority of the evaluated studies reported gait adaptations in patients with RA and that as a consequence they also have a greater risk of falling than other elderly individuals. [12]

Fatigue is a frequent symptom in RA, even among patients who display low and moderate levels of the disease with approximately 40% of RA patients with RA reporting severe levels of fatigue. [40]

Haemophilic arthropathy

Haemophilic arthropathy refers to permanent joint disease occurring in patients with haemophilia as a long-term consequence of repeated haemarthrosis. In an acute joint bleed, patients may report sensations of tingling and warmth, followed by pain, swelling and decreased motion. The pathogenesis of the progression from recurrent haemarthrosis to arthropathy is not fully understood, but it is characterised by inflammatory synovitis and cartilage destruction. [41]

Haemophilic arthropathy, which shares some clinical and biological injury characteristics with rheumatoid arthritis, is characterised by 2 main features: chronic proliferative synovitis and cartilage destruction. It is the consequence of repeated extravasation of blood into joint cavities, but its exact pathogenesis, particularly with regard to early changes in the joint, is still not completely understood. [42]

Over the long term, repeated episodes of haemarthrosis may cause irreversible damage to the joint, leading to haemophilic arthropathy, a polyarticular disease characterised by joint stiffness, chronic pain and a severely limited range of motion. In the most severe cases, the bones become fused, resulting in a completely disabled and misshapen joint. [42]

Diabetic foot arthropathy

The Eichenholz classification describes the evolution of the condition over time. [20][43]

  1. Stage 0: Hot foot, usually painful, normal radiographic findings; MRI will show bone oedema and stress fractures
  2. Stage 1: Fragmentation, bone resorption, dislocations, fractures
  3. Stage 2: Coalescence, sclerosis, fracture healing, debris resorption
  4. Stage 3: Bone remodelling

Gout

There are four phases of gout. They include asymptomatic hyperuricemia, acute gout arthritis, intercritical gout and chronic tophaceous gout. [44]

  1. Asymptomatic hyperuricemia: Serum urate of more than 7 mg/dl but no symptoms are present. [29]
  2. Acute gout arthritis: joint pain, occurring suddenly at night, commonly in the first metatarsophalangeal joint. Localised and acute onset of intense pain, erythema, warmth, extreme tenderness and hypersensitivity are typically present. Chills, fever and tachycardia may accompany the joint complains. [29]
  3. Intercritical gout: Asymptomatic phase. [29]
  4. Tophaceous gout: sudden return of gout with increasing frequency and often in different joints. Characteristics are joint damage, functional loss, disability, deposits of monosodium urate crystals in soft tissue and bone abnormalities. [29]

Psoriatic arthritis

Typical symptoms include; inflammation in the Achilles tendon or the plantar fascia, and dactylitis (sausage-like swelling of the fingers or toes). [45] Pain, swelling, or stiffness in one or more joints is also commonly present in psoriatic arthritis. [34] Two features which are hallmarks of psoriatic arthritis are the presence of dactylitis and enthesitis (inflammation at the sites of insertion of tendons and ligaments into bone) [22]

Reactive arthritis

Reactive arthritis characteristically involves the joints of the lower extremities in an asymmetric, oligoarticular pattern. A dactylitis (‘sausage digit’) pattern in the feet is typical of reactive arthritis. Enthesopathy is often found in reactive arthritis. [36]

Differential Diagnosis

Intra-articular pathologic lesions must be distinguished from surrounding joint tendinitis and bursitis. This can be achieved with diagnostic tests such as MRI or with injection of a local anesthetic.

Avascular necrosis must be considered in cases inwhich sclerosis of the talar dome is present. Patients may have a history of talar neck fracture, steroid or alcohol usage, or nonspecific injuries. Avascular necrosis of the talus can result in progressive segmental collapse and an increasing amount of matter into the joint.  

Osteoarthritis-Rheumatoid arthritis

Primary, osteoarthritis is a diagnosis of exclusion. 

Post traumatic osteoarthritisis is the most common form of ankle arthritis. Post traumatic disease can be present after intra-articular fractures or improper joint biomechanics after extra-articular fractures. Frequently, deformity is present in the joint. The extent of bone loss after trauma and joint space collapse can be assessed with weightbearing radiographs and CT scans.
Osteoarthritis is best differentiated from rheumatoid arthritis by a thorough history and examination. Three factors can distinguish the two disorders: the absence of systemic inflammatory signs and symptoms, onset in later life, and the pattern of joint involvement.  

Systematic inflammatory diseases such as rheumatoid arthritis should be excluded prior to considering operative intervention. Ankle arthritis can be effectively treated medically prior to considering surgical intervention, particularly during a flare up of the disease. The majority of patients with rheumatoid arthritis will test positive for rheumatoid factors and a rheumatoid arthritis diagnosis requires the presence of certain other symptoms: morning stiffness, multiple joint swelling, rheumatoid nodules, and evidence of joint erosion on radiographs.

Patients with an absence of rheumatoid factor in the serum, but who show signs of inflammatory arthritis are classified as having seronegative arthropathy. The four major disorders include ankylosis spondylitis, psoriatic arthritis, Reiter’s syndrome, and inflammatory bowel arthritides.

Metabolic and infectious causes of arthritis must also be considered. This can include gonococcal disease, Lyme disease, and gouty uricemia. A patient history should also include questions about any possible exposure to disease sources for sexually transmitted diseases and insect bites.

Haemophilic arthropathy

Haemophilic arthropathy occurs in individuals who have haemophilia. Bleeds within a joint can cause multiple defects to the joint, as the result of a number of mechanisms affecting the synovial lining which becomes progressively fibrotic and the hyaline cartilage which becomes degenerative and is eventually lost. Mechanical and chemical processes cause degeneration of cells, but enzymatic processes appear to be primarily responsible for the degradation of the matrix of the articular cartilage.

Charcot osteoarthropathy or pedal neuropathic joint disease is a condition associated with peripheral neuropathy , it is a progressive deterioration of weight-bearing joints, usually in the foot or ankle, and is characterised in its early stages by acute inflammation that leads to bone and joint fracture, dislocation, instability and Gross deformaties and often seen in patients with longstanding diabetes,

In the early stages of Charcot osteoarthropathy, the patient presents with a warm, erythematous and oedematous foot with or without associated pain or reported previous injury and it can clinically mimic cellulitis or gout. This can lead to gross structural deformities of the foot and ankle, and subsequent skin ulceration and lower limb amputation from soft tissue or bony infection. The Charcot foot occurs most often in patients with diabetic neuropathy, but other predisposing conditions include alcoholic neuropathy, sensory loss caused by cerebral palsy or leprosy, and congenital insensitivity to pain. However, it is often goes unrecognised, with deleterious consequences..

Differentiating between osteomyelitis and diabetic foot arthropathy is crucial, but can be difficult when both acute inflammation and bony changes are present. [16][20]

Gout

Gout may masquerade as septic arthritis, rheumatoid arthritis or neoplasm. [29]

Pseudogout often resembles gout and, like gout, is caused by the formation of crystals in the joints. Instead of being composed of uric acid, as true gout crystals are, the crystals in pseudogout are composed of a salt called calcium pyrophosophate dehydrate (CPPD). The condition is also called CPPD disease. [46]

Diagnostic Procedures

Osteoarthritis

Diagnosing an osteoarthritic ankle joint starts with a clinical assessment and includes assessing alignment, stability and range of motion. Different radiographic modalities may help to recognise and analyse the underlying reasons for ankle OA. Radiographs of the foot and ankle should be taken on weight bearing only. Additional imaging modalities such as MRI and SPECT-CT may help to evaluate the extent of degenerative changes and their biological activities. [14]

Rheumatoid arthritis

Different imaging techniques, e.g. MRI, CT and ultrasonography (US), can help clinicians to detect early onset or subclinical foot problems as the clinical signs of foot disease in RA are often subtle. [9][47]

Ultrasonography and MRI have shown to be superior to clinical examination in detecting joint inflammation. [48] Sonography is increasingly being used and has been found to be effective for the detection of bony erosions in patients with RA. Ultrasonography detected 6.5 times more bony erosions in the early stages of the disease than radiography. [47] As US is more readily available and less expensive than an MRI it is recommended as the second diagnostic imaging method, after radiography. [48]

Haemophilic arthropathy

Radiography remains the go to method in the diagnosis and follow-up of haemophilic arthropathy. Radiographical results of arthropathy often show an expected sequence of events and are found to be similar in different joints. An MRI, however, has advantages over radiography due to its ability to display soft tissue and cartilage changes in haemophilic joints. The recent development and standardisation of MRI scoring systems for measuring soft tissue and cartilage abnormalities may enable the comparison of pathological joint findings in clinical trials conducted at different institutions across the world [49]

Diabetic foot arthropathy

Diagnosis is based on the patient’s history, clinical examination, and imaging results. Due a lowered perception of pain, patients are quite often not aware of any injury.[20] Localised inflammation is the main symptom for diagnosing diabetic foot arthopathy. [16]

In Charcot feet arthropathies it is very important that the disease is diagnosed quickly, because a delay can lead to worsening structural damage or even limb loss.[16][50][51][52] Unfortunately the diagnosis is often missed at first presentation. A possible reason for the missed diagnosis is that Charcot feet are not emphasized in medical training. The result is that it is difficult to advocate the right choice of approach due to low evidence based information. [16]

Acute Charcot activity can be diagnosed if the temperature of the affected foot is 2°C or more than the contralateral unaffected foot. [52][20]

Gout

Gout is ideally diagnosed through identification of characteristic negatively birefringent crystals under polarized light microscopy in fluid aspirated from end-organ deposits, typically from a joint [53]. However, fewer than 10% of patients with gout see a rheumatologist, and most cases of gout are diagnosed in the primary care setting based on signs, symptoms, and serum uric acid level [54].

Psoriatic arthritis

A diagnostic test for psoriatic arthritis does not exist unlike in RA which is cyclic citrullinated peptide and rheumatoid factor positive. As in other inflammatory conditions, markers such as erythrocyte sedimentation rate and C-reactive protein can be raised in psoriatic arthritis. [22]

Scoring systems have been developed to try and identify psoriatic arthritis at an early stage and criteria have been developed to aid in classification of the disease from the other SPAs and inflammatory arthritides. Not only are they useful for identifying psoriatic arthritis earlier, they can also help identify cases of psoriatic arthritis which do not present in the typical manner. Some criteria include psoriatic arthritis with the SPA group. The classification for psoriatic arthritis (CASPAR) criteria was developed specifically for psoriatic arthritis. It has good sensitivity and specificity for those presenting with disease of <2 years’ duration. Although primarily used for classification, it can be used for diagnostic purposes. [22]

Further imaging such as MRI can help to identify soft tissue involvement in further detail, particularly when a patient is suffering from enthesitis. Ultrasound has also become a useful tool in the investigation of arthritis as it can help to identify bony erosions in those patients where synovitis or dactylitis is not always evident clinically. Studies have shown that ultrasound and MRI are more sensitive for detecting inflammation than plain radiographs in psoriatic arthritis. [22]

Outcome Measures

Osteoarthritis

The Ankle Osteoarthritis Scale (two subscales: pain and disability) [55] is a reliable and valid self-assessment instrument that specifically measures patient symptoms and disabilities related to ankle arthritis.[56]

More outcome measures of ankle osteoarthritis can be found on the page Ankle Osteoarthritis

Rheumatoid arthritis

American College of Rheumatology (ACR) response criteria for RA. [57] The ACR20 response criteria requires a 20% improvement in both tender and swollen joint counts and a 20% improvement in 3 of 5 items:

  • Patient global assessment (VAS),
  • Physician global assessment (VAS),
  • Patient pain score (VAS),
  • Health Assessment Questionnaire (HAQ),
  • Erythrocyte sedimentation rate or C-reactive protein (CRP). [57]

Haemophilic arthropathy

MRI images of bone or cartilage damage in the index joints can be used as an outcome measure. Tentative haemophilic arthropathy scales based on MRI findings have been developed in the last decade. In 2005, the International Prophylaxis Study Group (IPSG) presented a preliminary comprehensive scoring scheme that combined the Denver and European MRI scores. The use of such scales should result in a more consistent assessment of haemophilic joints and should facilitate the development of more targeted treatment to prevent or delay further destructive osteoarticular changes.[49]

Diabetic foot arthropathy

Gout

Numerous different instruments can be used to assess the acute gout core domains; VAS, 5 point Likert scales, 4 point Likert scales of index joint swelling and tenderness and 5 point PGART instruments meet the criteria for the Outcome Measures in Rheumatology (OMERACT) filter. [58]

Psoriatic arthritis

The Psoriatic Arthritis Response Criteria (PsARC) is recommended in the assessment and monitoring of PsA. It consists of four components: assessment of joint tenderness and swelling utilizing 68/66 joint counts respectively, the patient’s opinion of their global health and the physician’s global assessment. [57][59]

The ACR20 response criteria require a 20% improvement in both tender and swollen joint counts, and a 20% improvement in 3 of 5 items:

  • Patient global assessment (visual analog scale, VAS),
  • Physician global assessment (VAS),
  • Patient pain score (VAS),
  • Health Assessment Questionnaire (HAQ),
  • Erythrocyte sedimentation rate or C-reactive protein (CRP).

For some PsAstudies the joint count was increased to 78 to include distal interphalangeal (DIP) joints of the feet. To achieve an ACR50 or ACR70 response, the same guidelines apply but the level of response is 50% or 70% improvement, respectively. [57]

Reactive arthritis

The outcome measures of reactive arthritis can be found on the page Reactive Arthritis

Examination

Osteoarthritis

The examination of osteoarthritis can be found on the page Ankle Osteoarthritis

Rheumatoid arthritis

The examination of rheumatoid arthritis can be found on the page Rheumatoid Arthritis

Medical Management

Osteoarthritis

There is no cure for osteoarthritis. There are several treatments that can be subdivided into pharmacological, non-pharmacological and surgical. The choice of treatment of ankle and foot OA depends on the severity of the disease. The main goals of OA management in the foot and ankle are, pain control, improvement in function and in quality of life. A number of different aspects like discomfort, comorbidity and radiologic damage also need to be considered. [60]

Pharmacological treatments

Analgesics

Simple painkillers like paracetamol or acetaminophen are usually enough to have a significant relief of symptoms, for patients with mild to moderate pain[60]

NSAID

NSAIDs are often used by patients with severe pain, where analgesics aren’t strong enough to relief symptoms [61]. Research shows improvements for short duration use. There is a lack of research in their long term use [60].

Opioids 

When NSAIDs do not offer enough relief, opioids are often used. Opioids are mostly taken by patients with moderate to severe pain. Some patients use simple analgesics in combination with a low dose opioid for a greater improvement in pain at rest as well as in motion[60].

Opioids decrease pain in the long term increasing quality of sleep and enjoyment of life. Common opioid side effects are present, but decrease as therapy continues[62].

Intra-articular injections

When simple analgesics have failed, injections are used in a hospital environment. Most of the time, hyaluronic acid is recommended if there is inadequate response to simple analgesics. Hyaluronic acid Is a natural component of synovial fluid. These gel-like fluid injections help to lubricate the joint and to act as a shock absorber for joint loads[61].Research indicates that there is an improvement in pain, but repeated injections in the same joint showed a decreased response[60]. It remains unclear, however, which dosage schedule should be used and which patients would benefit the most from it. Other research showed that there is a relief of pain, but more difficulty in walking on uneven surfaces, especially when compared with exercise therapy[63].

Surgical treatment

Osteotomy

Low tibial osteotomy (a change of alignment of the bone) is indicated for osteoarthritis in the ankle, more specifically for varus type osteoarthritis in a moderate stage[64].

Arthroscopy

There was no significant improvement in instability. But there was significant improvement in pain, swelling, stiffness, limp, and activity in the patients postoperatively compared with their preoperative status, but not with all patients however. Approximately one third of patients experienced no benefit from arthroscopic intervention[65].

Arthrodesis

The joint becomes fixed, so there no movement in the joint postoperatively. This method is used in end stage osteoarthritis, but research shows that arthroplasty offers better pain relief[66].

Arthroplasty

This method is used, like arthrodesis, in end stage osteoarthritis. This is a total replacement of the affected joint and the most effective of all medical interventions. The pain and disability of end stage osteoarthritis can be eliminated and restores patients to near normal function[67].

  

Rheumatoid arthritis

Pharmacological treatments

DMARD’s


DMARD’s are Disease-modifying antirheumatic drugs. Frequency of use ha increased over the years and enhanced the success of RA management[9].

Anti-TNF treatment 

The use of anti-TNF therapy on patients suffering from RA has accelerated ulcer healing [68]

The difference between DMARD combination treatments, including or excluding TNF inhibitors, is small however. Due to the huge cost differences, RA guidelines should recommend combination DMARD treatment before the initiation of TNF inhibitors[69].

Steroids

Choy et al. demonstrated that monthly injections of 120 mg intramuscular depomedrone in addition to a DMARD’s treatment showed only a transient clinical benefit. The value of steroids is still controversial. Previous studies found that steroids only provide short and medium term symptomatic improvements in RA. The level of steroid related adverse events such as diabetes, vertebral fractures and osteoporosis, exclude its use as a long term treatment strategy. Therefore, patients should not be given long term steroid treatment, but rather an alternative or additional DMARD’s treatment[70].


Haemophilic arthropathy

Pharmacological treatments

Narcotics

This is effective, but leads to dependence[41].

NSAIDs

NSAIDS act by inhibiting cyclooxygenase enzymes, which result in an analgesic and anti-inflammatory effect.
3 types: Aspirin, Traditional NSAIDS and Cox-2 inhibitors
Further evaluation of the safety and efficacy of drugs in patients with haemophilia is needed.[41].

Steroid-/ hyaluronic acid-injections

Both injections decrease pain [41]

Surgical treatments

Synovectomy

Excision of the friable synovium. This approach is frequently used to reduce pain in patients who experience recurrent haemarthrosis. This can be achieved by direct surgical excision or arthroscopic synovectomy. Another way is to inject a radioactive or chemical agent which causes fibrosis of sclerosis of the synovium. If there are several advanced changes in the joint, a joint arthroplasty may be considered[41].

Joint arthroplasty

Patients with haemophilia who develop severe arthropathy may experience relentless pain, loss of motion and functional disability. If conservative management fails (analgesics, orthotics and physical therapy) these patients may benefit from total joint replacement[41].


Diabetic foot arthropathy

A multidisciplinary approach is recommended for the management of Charcot foot.[19]

Pharmacological treatments

Biphosphonates

There is currently little evidence to support the use of bisphosphonates as part of the routine management of patients with diabetes complicated by acute Charcot neuropathic osteoarthropathy[71][20][43] but some authors found that bisphosphonates may improve the healing of Charcot foot by reducing skin temperature and the disease activity of Charcot foot. Bisphosphonates should be used in addition to standard interventions to control the position and shape of the foot[16].

Anti-TNF treatment

It is plausible to suggest the use of anti-TNF biological therapies for controlling Charcot neuropathic osteoarthropathy based on the excessive bone resorption due to circulating osteoclast precursors and serum levels of TNF-a[17].

Surgical treatments

Surgery

Surgery should be avoided during the active inflammatory stage because of the perceived risk of wound infection[43].A patient only becomes a candidate for surgical treatment after the failure of conservative management[20].
Specific methods for the surgical treatment of Charcot neuropathic osteoarthropathy to save the extremity or delay major amputation are still being developed. Below the knee amputation is the preferred option. [20].

Magnetic therapy treatment

Significant reduction in the amount of deformity and reduced healing time to consolidation after receiving magnetic therapy treatment[19].

Gout

Pharmacotherapy

Urate level

The goal of pharmacotherapy for gout is to maintain the serum urate level below 50–60 mg/L (300–360 moll/L). When urate levels fall below 50–60 mg/L, the urate crystals start to dissolve [32]. Currently used urate lowering medications include xanthine-oxidase inhibitors such as allopurinol, febuxostat, as well as available uricosuric agents. However, evidence comparing these agents remains low. Based on the reported data, febuxostat can play a major role in the treatment of hyperuricaemia and gout. Febuxostat is a suitable pharmacological option for first line treatment of gout, given its established efficacy and safety, documented in a high number of clinical studies and in daily practice[72]
During the first few months of urate-lowering therapy (ULT), an anti-inflammatory drug must be taken to also prevent the occurrence of gouty attacks[32]

NSAIDs

These are frequently used as first line therapies for acute gout. However, these agents may have serious side effects such as gastrointestinal toxicity, renal toxicity, or gastrointestinal bleeding[73]

Systemic corticosteroids

Systemic corticosteroids have also exhibited significant efficacy in patients with acute gout; intra-articular corticosteroids are frequently used in patients with monoarticular gout, particularly in patients who cannot receive oral therapy[73].

ACTH (Adrenocorticotropic hormone)

This is also quite useful in treating acute gout, particularly in those patients with renal and/or gastrointestinal contraindications to other therapies. Synthetic ACTH is effective partly via induction of adrenal glucocorticosteroids, and partly via rapid peripheral suppression of leukocyte activation by melatonin receptor 3 signalling[73]

Oral colchicine

In patients with contraindications or who cannot tolerate NSAIDs or systemic (either oral or parenteral) corticosteroids, oral colchicine is generally the next choice for primary therapy[73]
As the acute attack resolves, it is appropriate to use low doses of oral colchicine as an adjunct to NSAID, glucocorticosteroid, or ACTH treatment, and continuation of low dose oral colchicine can help to suppress rebound flares after treatment[73]

Psoriatic arthritis

Treatments such as oral disease modifying anti-rheumatic drugs and biologic therapy are effective, but have side effects which could limit their use in certain individuals[22]

Pharmacological treatments

Corticosteroids

Corticosteroids are used in psoriatic arthritis and in many other inflammatory arthropathies to provide immediate symptom relief. They can rapidly diminish the inflammatory response seen in these conditions, causing a reduction in swelling and stiffness in the joints. They can be given as an intramuscular injection for general widespread relief or directly injected into the affected joint for a more targeted response. Long term steroid use should be avoided due to the side effect profile which includes diabetes, hypertension, osteoporosis, and immunosuppression. There is also a risk of skin psoriasis flares after intramuscular injections. In most cases steroids are used for short term relief and occasionally as bridging therapy while establishing the patient on more long term immunosuppressants[22]

Disease‐modifying anti‐rheumatic agents or immunosuppressive drugs

Disease modifying anti-rheumatic drugs (DMARDs) are used in psoriatic arthritis as in other inflammatory conditions. They are a group of drugs which can help to reduce inflammation as well as to slow disease progression to prevent joint damage, as opposed to nonsteroidal anti-inflammatory drugs and steroids which treat the inflammation, but not the underlying cause. However, evidence behind their use in psoriatic arthritis is not as robust as in RA. Use of DMARDs is mostly based on a clinician’s experience rather than evidence. Methotrexate can cause improvement in both the skin and peripheral joints. Sulfasalazine is useful for peripheral arthropathy although only with weak evidence. Cyclosporine has beneficial effects on the skin. Small studies have shown that leflunomide has similar efficacy for use in psoriatic arthritis as compared with RA. The main side effect with DMARDs is their immunosuppression, which can expose the patient to potentially serious infections such as neutropenic sepsis[22]

Intra –articular injections: TNF-α blockers Biologic drugs that are aimed at blocking TNF-α have been effective therapies for such conditions[22]

Reactive arthritis

The treatment of reactive arthritis comprises of mainly non-steroidal anti-inflammatory drugs, intra-articular steroid injections, and physical treatment. [74]

Pharmacological treatments

NSAIDs

Non‐steroidal anti‐inflammatory drugs (NSAIDs) form the basis of pharmacological therapy. They should be used in proper dosage and not be stopped too early. During recovery, insufficient analgesia may lead to limited joint movement and prolong the rehabilitation, but their use should be reduced as appropriate to recovery and not used unnecessarily[24].

Corticosteroids

Corticosteroids are a potent group of drugs to be used in ReA. Intra‐articular application results most often in prompt relief of the joint inflammation. This is of great value for a young, active and employed person. The injection can be repeated a number of times, if necessary. However, this treatment is not applicable if a number of joints is involved. There is the risk of infectious complications and true septic arthritis as however. [24]
In severe cases and when several joints are involved, peroral corticosteroids are useful. They should be started in high dosage, e.g. prednisolone 30–40 mg/day, and tapered rapidly down according to relief of symptoms. The drug should then be continued for a brief period in low dose, and stopped gradually. Corticosteroids are, in a similar manner, also useful in the treatment of acute relapses. If the patient later suffers from chronic arthralgias, corticosteroids should be avoided[24]. Steroids are administered when inflammatory symptoms are resistant to NSAIDs[75].

Antibiotics

Antibiotics seem to be ineffective in postenteric reactive arthritis.  By the time the patient seeks help for joint inflammation, the initial infection has already passed and antibiotics are no longer effective[76].

Disease modifying anti‐rheumatic agents or immunosuppressive drugs

The value of disease modifying anti‐rheumatic agents or immunosuppressive drugs has not been established, although Mielants and Veys[77] suggest that ileocolonoscopy should be performed for patients with ReA more often than is currently customary.
Experiences with other DMARDs such as azathioprine, methotrexate and cyclosporin, have been sporadically reported and they can be used in patients that are unresponsive to the more usual medicaments[78].

Intra –articular injections

Intra-articular steroid injections can be used as treatment for reactive arthritis[74].

TNF-α blockers

In more aggressive cases, or when ReA evolves towards ankylosing spondylitis, TNF-α blockers could represent an effective choice[78].

Physical Therapy Management

Osteoarthritis

Non care management and care management have been tested. Non care management includes resting and relaxing, although rigorous evidence for its effectiveness has not proved conclusive. On the other hand, physical activity and/or exercise is generally adopted and recognised by health professionals and patients. Specific joints can be targeted to improve general mobility, function and the reduction of pain. More intensive exercise can strengthen muscles around the affected joint of the foot. A limited number of OA patients may have increased pain symptoms while exercising, but with an exercise program that is appropriately targeted and adjusted to the individual's pace, it should be possible for every OA patient to be active [79]. (LOE: 1A)

Non-pharmacological treatments

Aerobic exercise Guidelines were developed for training parameters in people with osteoarthritis pain.
  • 2-5 sessions a week
  • 20-30 minutes/session
  • Holding each contraction 1-6 seconds
  • Avoidance of high-impact exercises
  • Targets should be achievable for the patient
  • Other exercises (flexibility, postural balance, strength) may be incorporated to achieve specific goals based on the patient his individual assessments[79] (LOE: 1A)
Range of motion and flexibility exercise Joint motion and flexibility exercises of the periarticular tissues on a regular basis are important for cartilage nutrition and health, protection of joint structures from damaging impact loads and comfort in daily activities. Those exercises are routines of low-intensity, controlled movements that do not increase the pain in foot or ankle[80].(LOE: 2B)


Rheumatoid arthritis

Physical therapy

Exercise therapy Education is key to patients adhering to their training program even when supervision is withdrawn, as the gains in muscle mass and strength dependent function diminish when the training stops. [63].(LOE: 1A)
Consistency is also key to reduce the rate of damage in the foot joints[63].
Patients with RA who participate in long term high intensity weight bearing exercise classes develop less radiological joint damage in the feet in comparison with patients participating in the more standard physical therapy protocols[63].
Resistance exercise therapy is safe and offers a clinically significant amelioration of functional capacity and disability. Further RCT’s are required to determine whether supervised exercises are clinically relevant[13].(LOE: 1A)
The maintenance of long-term positive effects gained from resistance exercise has not been extensively evaluated, and remains controversial, yet it is crucial for long-term benefits that after the intervention of a structured physical activity program is maintained, because the effects of detraining occur rapidly[13][13].
A 3 year follow up after completing a high-intensity progressive resistance training program [81]. (LOE: 2B)

Custom made foot orthoses

(Orthotic) Insoles and specialised shoes Cho et al suggest that the use of insoles combined with prescribed forefoot rocketed shoes with a wide toebox resulted in a significant reduction in foot pain and dysfunction in patients with rheumatoid foot problems, although custom made insoles showed no differences in terms of the anatomical location of foot pathology[82].(LOE: 1B)


The use of orthotic insoles is common in patients with RA and often part of an early conservative treatment which is strongly recommended to protect the rheumatoid foot from potentially destructive processes[83](LOE: 3A)[84](LOE: 2B).
Orthotic insoles can decrease foot pain and reduce disability[84][85],(LOE: 2B) but are not sufficient to correct gait.

Foot Orthoses Conceição et al. found pain improvements due to foot orthoses, but no effect on disability[86](LOE: 1B)


Haemophilic arthropathy

Physiotherapy is an integral component in haemophilic foot and ankle arthropathy. Physiotherapy can be used at the acute and chronic stages or after surgery. To prevent the progression of haemophilic arthropathy, regular exercise (30 min at least three time/week) are recommended[41](LOE: 1B), to reduce bleeding, pain and improve articular mobility of the ankle[87].(LOE: 2B)

Physical therapy

Therapy goals -restoration/maintenance of ROM
-muscle strengthening
-pain management
-improved balance/coordination/ proprioception[41].(LOE: 1B)
Varied therapy -passive mobilisations
-passive/active stretching (specifically: the anterior and posterior tibialis, peroneal, gastrocnemius and soleus muscles)
-proprioception exercises
-active exercises of strength with exercise bands
-joint stabilisation exercises[87].(LOE: 2B)


Custom made foot orthoses

Orthopaedic insoles(OI) and shoes(OS) Lobet et al. demonstrated that foot orthoses may have beneficial effects on ankle joints in hemophilic arthropathy. OI and OS provided significant pain relief, functional improvement and improved comfort in more than half of patients, with minimal side effects[88].(LOE: 1B)
OI/OS combined with physiotherapy Combined physiotherapy and OI/OS results in excellent patient satisfaction scores and significant pain reduction[88].

Diabetic foot arthropathy

The treatment of Charcot neuroarthropathy is mostly conservative[20].(LOE: 1A) The first step in the management Charcot foot is to offload the affected extremity, prevent further collapse and deformity and protect the opposite foot. This can be done using a castor splint immobilisation to promote healing of the joint during the active stage of the disease[89](LOE: 1B)[20][43].(LOE: 1B)

Non-pharmacological treatments

Total contact cast The use of a total contact cast in an early stage of Charcot foot is also recommended[90](LOE: 2B) It should be changed 3 days after initial application and then every week.
The period of fixation depends on the reduction in oedema and a drop in skin temperature below 2°C compared to the contralateral leg. The usage of a wheelchair as a preventive means against overloading the other extremity can be considered[20](LOE: 1A)

CROW

CROW.jpg

Figure 10

Alternatively, it is also possible to use Charcot Restraint Orthotic Walker (CROW).
Kalish et al[89] (LOE: 1B)suggest that the use of accommodative footwear is essential for the long term effective management of Charcot foot.


Gout

A patient with a history of gout, hyperuricemia, and/or a septic joint presentation should be referred for medical evaluation before treatment. [29](LOE: 1B)

During acute exacerbations, the focus should be on reinforcement of the management programme and splinting, orthotics, or other assistive devices to protect the affected joint(s). During the inter-critical phases, maintaining ROM, strength, and function is essential and a suitable exercise routine should be designed along with advice on keeping weight under control. [29] (LOE: 1B)

Non-pharmacological treatments

Cryotherapy Cryotherapy, may be a useful adjunct to treatment of acute gouty arthritis, reducing pain.[91] (LOE: 1B)
Acupuncture The effectiveness of acupuncture as a complementary therapy may be effective for gouty arthritis patients, decreasing uric acid levels in some patients and the VAS score. [92] (LOE: 1A)


Psoriatic arthritis

The physical therapy management of psoriatic arthritis can be found on the page Psoriatic Arthritis.

Reactive arthritis

An exercise regime that includes regular aerobic activity as well as exercises to promote joint ROM and muscle strengthening should be followed. Strengthening should target muscles surrounding the affected joints. A brief period of non-weight bearing may be advised to decrease inflammation and limit pressure on the inflamed joints.  


Immobilisation and inactivity are discouraged as they can lead to decreased range of motion, contractures, joint stiffness, decreased muscle strength and decreased flexibility, as well as overall decreased cardiovascular fitness, which can cause a cascade effect on other body systems. [93](LOE: 1A)


Physical therapy

Therapy goals -pain relief

-improved activities of daily living

-reduce joint swelling

-prevention of joint damage and disability. [93]

Aerobic exercise Aerobic exercise should include low impact activities, such as swimming, walking or cycling, depending on the patient's cardiovascular level. [93]
Range of motion and flexibility exercise Stretching and ROM exercises should be completed to prevent muscle atrophy, especially if several joints are involved[25][24](LOE: 1A)to avoid stiffness and deformities and to promote mobility and strength[94](LOE: 4)[95]. (LOE: 1A)


Custom made foot orthoses

Orthopaedic insoles(OI) and shoes(OS) If enthesitis is present, heel support and orthosis can be considered to decrease pain and improve mobility[24](LOE: 1A)[96](LOE: 1B)[25](LOE: 1A)

Key Research

Osteoarthritis

D.M. Reid, C.G. Miller (eds.), Clinical Trials in Rheumatoid Arthritis and Osteoarthritis, Springer-Verlag London Limited 2008, 325p.

Witteveen, Angelique GH, Cheriel J. Hofstad, and Gino MMJ Kerkhoffs. "Hyaluronic acid and other conservative treatment options for osteoarthritis of the ankle." The Cochrane Library (2015).

Roth, Sanford H., et al. "Around-the-clock, controlled-release oxycodone therapy for osteoarthritis-related pain: placebo-controlled trial and long-term evaluation." Archives of Internal Medicine 160.6 (2000): 853-860.

Karatosun, V., et al. "Intra-articular hyaluronic acid compared to exercise therapy in osteoarthritis of the ankle. A prospective randomized trial with long-term follow-up." Clinical and experimental rheumatology 26.2 (2008): 288.

Rheumatoid arthritis

Conceição, Cristiano Sena da, et al. "Systematic review and meta-analysis of effects of foot orthoses on pain and disability in rheumatoid arthritis patients." Disability and rehabilitation 37.14 (2015): 1209-1213.

Mejjad, Othmane, et al. "Foot orthotics decrease pain but do not improve gait in rheumatoid arthritis patients." Joint Bone Spine 71.6 (2004): 542-545.

Baillet, Athan, et al. "Efficacy of resistance exercises in rheumatoid arthritis: meta-analysis of randomized controlled trials." Rheumatology 51.3 (2012): 519-527.

Rongen‐van Dartel, S. A. A., et al. "Effect of Aerobic Exercise Training on Fatigue in Rheumatoid Arthritis: A Meta‐Analysis." Arthritis care & research67.8 (2015): 1054-1062. A Meta-Analysis, Arthritis Care & Research, Vol. 67, No. 8, August 2015, pp 1054–1062.

Carroll, Matthew, et al. "Gait characteristics associated with the foot and ankle in inflammatory arthritis: a systematic review and meta-analysis." BMC musculoskeletal disorders 16.1 (2015): 1.

Graudal, Niels, et al. "Combination Therapy With and Without Tumor Necrosis Factor Inhibitors in Rheumatoid Arthritis: A Meta‐Analysis of Randomized Trials." Arthritis care & research 67.11 (2015): 1487-1495.

Diabetic foot arthropathy

Kalish, Jeffrey, and Allen Hamdan. "Management of diabetic foot problems." Journal of vascular surgery 51.2 (2010): 476-486.

Varma, Ajit Kumar. "Charcot neuroarthropathy of the foot and ankle: a review." The journal of foot and ankle surgery 52.6 (2013): 740-749.

Smith, Caroline, Saravana Kumar, and Ryan Causby. "The effectiveness of non‐surgical interventions in the treatment of Charcot foot." International Journal of Evidence‐Based Healthcare 5.4 (2007): 437-449.

Kucera, Tomas, Haroun Hassan Shaikh, and Pavel Sponer. "Charcot Neuropathic Arthropathy of the Foot: A Literature Review and Single-Center Experience." Journal of Diabetes Research 2016 (2016).

Richard, J-L., M. Almasri, and S. Schuldiner. "Treatment of acute Charcot foot with bisphosphonates: a systematic review of the literature." Diabetologia 55.5 (2012): 1258-1264.

Gout

Min, Z., and M. Junwu. "Research progress in the genetics of hyperuricaemia and gout." Yi chuan= Hereditas/Zhongguo yi chuan xue hui bian ji 38.4 (2016): 300-313.

Harris, MARK D., LORI B. Siegel, and JEFFREY A. Alloway. "Gout and hyperuricemia." American family physician 59.4 (1999): 925-934.

Owens, D., B. Whelan, and G. McCarthy. "A survey of the management of gout in primary care." Irish medical journal 101.5 (2008): 147-149.

Borghi, C., and F. Perez-Ruiz. "Urate lowering therapies in the treatment of gout: a systematic review and meta-analysis." European review for medical and pharmacological sciences 20.5 (2016): 983-992.

Cronstein, Bruce N., and Robert Terkeltaub. "The inflammatory process of gout and its treatment." Arthritis Research & Therapy 8.1 (2006): 1.

Schlesinger, Naomi, et al. "Local ice therapy during bouts of acute gouty arthritis." The Journal of rheumatology 29.2 (2002): 331-334.

Lee, Won Bock, et al. "Acupuncture for gouty arthritis: a concise report of a systematic and meta-analysis approach." Rheumatology 52.7 (2013): 1225-1232.

Psoriatic arthritis

Amherd‐Hoekstra, Anne, et al. "Psoriatic arthritis: a review." JDDG: Journal der Deutschen Dermatologischen Gesellschaft 8.5 (2010): 332-339.

Reactive arthritis

Olivieri I, Barozzi L, Padula A. Enthesiopathy: clinical manifestations, imaging and treatment. Baillieres Clin Rheumatol 1998;12(4).

Kim, Paul S., Thomas L. Klausmeier, and Donald P. Orr. "Reactive arthritis: a review." Journal of Adolescent Health 44.4 (2009): 309-315.

Silman, Alan J., and Marc C. Hochberg. Epidemiology of the rheumatic diseases. No. Ed. 2. Oxford University Press, 2001.

Clinical Bottom Line

Ankle and foot arthropathies covers all joint disease types of the foot and ankle. Physical therapy can be effective in all cases of ankle and foot arthropathies, but an accurate differentail diagnosis is important so that the most appropriate management protocol is implemented for the specific disease.

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