Hip Osteoarthritis: Difference between revisions

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Revision as of 19:11, 20 June 2021

This article is still missing information.
Hip osteoarthritis illustration.png
Hip Osteoarthritis
Epidemiology ~4% symptomatic OA, ~20% radiographic OA, in age >50.
Risk Factors FAI, DDH, age >60, family history
Clinical Features Posterior pain with squat, groin pain with abduction or adduction, abductor weakness, decreased ROM, scour test
Diagnosis Clinically in mild to moderate disease
Tests Plain radiograph, MRI, diagnostic intra-articular hip joint local anaesthetic injection
Treatment Exercise, weight loss, education, injections, surgery


Epidemiology

A US study of mostly Caucasian people aged over 50, the prevalence of radiographic hip OA was 19.6%, and the prevalence of symptomatic disease was 4.2%, with the prevalence increasing with higher age. The authors found a male predominance of symptomatic OA, especially in older individuals, unlike other studies which have tended to find a female predominance. There is generally a male predominance of radiographic OA.[1] A Japanese study found the prevalence of radiographic hip osteoarthritis to be 18.2% in men and 14.3% in women[2]

The prevalence of hip OA in patients with hip and/or groin pain presenting to primary care is 35%.[3]

Prevalence of Radiographic and Symptomatic Hip Osteoarthritis by Sex, Age[1]
Radiographic Hip OA (95% Cl) Symptomatic Hip OA (95% Cl)
Men (n=434) 24.7% (20.6%-28.7%) 5.2% (3.3%-7.8%)
Women (n=544) 13.6% (10.7%-16.5%) 3.0% (1.7%-4.8%)
Age 50-59 (n=390) 14.6% (11.1%-18.1%) 3.4% (1.8%-5.8%)
Age 60-69 (n=337) 16.6% (12.6%-20.6%) 2.7% (1.3%-5.1%)
Age 70-79 (n=197) 25.9% (19.8%-32.0%) 6.3% (3.3%-10.7%)
Age โ‰ฅ 80 (n=54) 31.5% (19.1%-43.9%) 7.4% (0.2%-17.9%)
Crude Prevalence 18.5% (16.1%-20.9%) 4.0% (2.8%-5.4%)
Age-standardized Prevalence 19.6% (16.7%-23.0%) 4.2% (2.9%-6.1%)

Aetiology

Femoroacetabular impingement (FAI) and the less common developmental dysplasia of the hip (DDH) are hip joint morphology abnormalities that are associated with early onset hip OA. However, FAI is also common in asymptomatic individuals.

Pathophysiology

There are several structures around the hip that are richly innervated by sensory nerve fibres. These include the periosteum, subchondral bone, synovium, and surrounding soft tissues. In the presence of Central Sensitisation there may be an additional central physiological process. Hip osteoarthritis can also lead to changes in gait which can lead to pain in the knees and lumbar spine.[3]

Higher bone density can drive knee osteoarthritis but not hip osteoarthritis

Clinical Features

History

The pain is often poorly localised. Patients can have pain over quite a large area including the front of the thighs, groin, lateral thighs, buttocks, and the posterior upper thighs. Patients with Central Sensitisation can have unusual distributions of pain at a surprising distance from the hip such as below the knee.

There is no clear association between pain levels and radiographic severity of hip osteoarthritis. Up to 40% of patients with hip osteoarthritis have no pain. Patients with higher pain levels showed differences in sensitisation as measured by quantitative sensory testing.[4]

None of the features on history are particularly helpful on their own for identifying hip OA. Medial thigh pain is highly suggestive of hip OA but is only present in 2.7% of patients. The presence of morning stiffness, pain on walking, and relief of pain on sitting all have positive likelihood ratios of <2.0, but their negative likelihood ratios are more helpful, i.e. the absence of these factors.[3]

Historical factors and likelihood of hip osteoarthritis.[3]
Feature on History Sensitivity Specificity LR+ (95% CI) LR- (95% CI)
Family history of OA 34% 84% 2.1
(1.2-3.6)
0.79
(0.67-0.93)
Personal history of knee OA 33% 84% 2.1
(1.1-3.8)
0.80
(0.68-0.95)
Age > 60 96% 25% 1.5
(1.3-1.7)
0.11
(0.02-0.78]
Age < 50 91% 28% 1.3
(1.1-1.5)
0.32
(0.16-0.62)
Worst pain in medial thigh 12% 98% 7.8
(1.7-37)
0.89
(0.77-1.0)
Worst pain in buttock 12-67% 57-69% 0.38-2.0 0.38-0.76
Pain on climbing stairs or walking down slopes 68% 68% 2.1
(1.6-2.8)
0.47
(0.35-0.63)
Morning stiffness <60 min 56-91% 41-67% 1.5-1.7 0.22-0.65
Pain on initial steps after rest 92% 26% 1.2
(1.1-1.4)
0.31
(0.08-1.2)
Pain on walking 80-97% 12-34% 1.1-1.2 0.25-0.58
Pain relieved by sitting 92% 33% 1.4
(0.2-1.6)
0.24
(0.06-0.92)

Examination

Main article: Hip Examination

Physical examination findings are in general more useful than historical features for identifying hip OA. Posterior hip pain is the test with the highest likelihood ratio, but some patients may not be very excited about trying this. Groin pain on hip abduction or adduction, abductor weakness, decreased hip adduction, and decreased hip internal rotation are all findings with positive likelihood ratios above 3. For identifying those who do not have hip OA, normal hip passive adduction or abduction are the most helpful.[3]

Extension is examined with the patient prone and lifting the leg off the table. Flexion is examined with the patient supine, and the examiner lifts the knee to the abdomen. In this position the foot can be kept in the same position, and the knee moved towards the midline, causing internal rotation. The hip can then be moved away from the midline, which causes external rotation. Adduction and abduction are assessed by putting the feet together. The foot is then moved across or away from the midline respectively. Normal ranges of motion are below. Goniometers are sometimes used, but usually estimates are sufficient. The examiner should compare range to the other side, but keeping in mind that osteoarthritis is often bilateral.[3]

Normal range of motion of the hip joint
Passive Movement Normal ROM
Flexion 0 - 140ยฐ
Internal rotation 0 - 30ยฐ
External rotation 0 - 40ยฐ
Abduction 0 - 50ยฐ
Adduction 0 - 30ยฐ
Extension 0 - 20ยฐ
Examination findings and likelihood of hip osteoarthritis[3]
Feature on Exam Sensitivity Specificity LR+ (95% CI) LR-(95% CI)
Abductor weakness 44 90 4.5

(2.4-8.4)

0.62

(0.43-0.88)

Limp 85 43 1.5

(1.2-1.9)

0.35

(0.20-0.61)

Inguinal ligament tenderness 60 75 2.4

(1.6-3.8)

0.53

(0.33-0.87)

Tensor fascia lata tenderness 40 80 2.0

(1.1-3.4)

0.75

(0.54-1.1)

Squat causing posterior pain 24 96 6.1

(1.3-29)

0.79

(0.62-1.0)

Groin pain on abduction or adduction 33 94 5.7

(1.6-20)

0.71

(0.52-0.97)

Scour test 62 74 2.4

(1.4-4.3)

0.51

(0.29-0.90)

Pain on hip adduction 68-80 46-54 1.5 - 1.5 0.43-0.59
Pain on hip internal rotation 82-88 38-39 1.4 - 1.4 0.31-0.45
Restricted movement in 3 planes NA NA 4.4

(2.4-8.3)

NA
Restricted movement in 2 planes NA NA 1.5

(0.90-2.6)

NA
Restricted movement in 1 plane NA NA 1.3

(0.85-2.0)

NA
Restricted movement in 0 planes NA NA 0.91

(0.78-1.1)

NA
Decreased hip adduction 80 81 4.2

(3.0-6.0)

0.25

(0.11-0.54)

Decreased hip internal rotation 66 79 3.2

(1.7-6.0)

0.43

(0.31-0.60)

Decreased hip range of movement 75 74 2.9

(2.1-4.0)

0.34

(0.25-0.47)

Decreased hip extension 76 68 2.4

(1.8-3.2)

0.35

(0.17-0.71)

Decreased hip external rotation 76 64 2.1

(1.6-2.8)

0.37

(0.19-0.76)

Decreased hip abduction 88 46 1.6

(1.3-2.1)

0.26

(0.09-0.77)

Combinations of findings have also been studied.

Combination of findings for identifying hip osteoarthritis[3]
Findings Number of findings LR+ (95% CI)
  • Age > 60
  • Inguinal ligament tenderness
  • Decreased external rotation
  • Deccreased internal rotation
  • Decreased adduction
  • Bony restriction using passive hip movement
  • Hip abductor weakness
5 or more 35 (13-95)
4 2.0 (0.88-4.3)
3 or fewer 0.05 (0.01-0.32)
  • Age > 60
  • Pain lasting longer than 3 months
  • Groin tenderness
  • Decreased external rotation
  • Absence of pain aggravation by sitting
4 or more 4.9 (2.8-8.7)
2-3 0.72 (0.57-0.93)
0 or 1 0.24 (0.09-0.64)

Imaging

Plain radiographs can demonstrate joint space narrowing, osteophytes, subchondral sclerosis, and subchondral cysts. They may also show alternative causes for pain such as pelvic bone tumours.

Laboratory Tests

Depending on the clinical context, rheumatological blood tests may need to be performed.

Diagnosis

The diagnosis can be made clinically in those with mild to moderate symptoms, with examination findings being more useful than historical factors. In those with more severe symptoms then plain radiographs are performed. If the radiographs are normal then there should be a search for other causes of pain.

Plain radiographs are cheap, however because most patients with radiographic OA have asymptomatic disease, there is a risk of incorrectly attributing the pain to osteoarthritis, and subsequently having incorrect treatment. Therefore it is as important as ever to consider the pre-test probability, and consider other diagnoses.

A commonly performed procedure in Musculoskeletal Medicine in New Zealand is the diagnostic intra-articular hip joint injection. Under either ultrasound or fluoroscopic guidance, local anaesthetic is infiltrated into the hip joint. An appreciable reduction in pain post-procedure is consistent with nociception arising from the hip joint.

Differential Diagnosis

Hip Pain Differential Diagnosis

Treatment

Research into hip OA has lagged far behind knee OA, and treatment recommendations for hip OA are often extrapolated from knee OA.

Non-pharmacological

Education, exercise, and weight loss are the mainstays of non-pharmacological management of hip and knee osteoarthritis. However long-term compliance is generally challenging.[5]

Some exercise options include aerobic exercise, flexibility exercises, strengthening exercises, water-based exercises, and tai chi. Exercise results in a modest reduction in pain (8 points more than control in a 0-100 scale) and improvement of function (7 points more than control in a 24 point scale).[6] Water-based exercises may be helpful for those with particularly severe symptoms that limit engagement with land-based exercises.

There may be a limited role for physiotherapy over home-exercises, as well as for manual therapy.[7]

The recommendation for weight loss has been extrapolated from knee osteoarthritis and the fact that obesity is a known risk factor for hip osteoarthritis.[8] There are no data on weight loss specifically for reducing symptoms of hip osteoarthritis.\

Medication

NSAIDs are effective for managing hip osteoarthritis, with greater effect with higher doses. Diclofenac 150mg/day is the most effective NSAID available.[9] However, the safety profile needs to be considered for the patient in question, and the lowest dose and shortest duration possible should be used in those with considerable symptoms and poor response to nonpharmacological treatments.

There is no evidence to support single-agent paracetamol.[9]

In a landmark study, opioids were not superior to treatment with nonopioid medications in a study of patients with severe chronic back pain, hip OA, or knee OA.[10] Due to both poor efficacy and safety concerns, opioids should not generally be used for hip osteoarthritis.

Injections

Main article: Hip Joint Injection

Hip joint steroid injections have a moderate short term effect for up to 8 weeks, and are generally well tolerated. The quality of the evidence however is generally poor.[11] The author is more likely to offer a steroid injection if there is a hip joint effusion. Injections can be done under ultrasound or fluoroscopic guidance.

There is limited evidence to support the use of platelet-rich plasma injections. In recalcitrant disease with the next step being surgery, the author will offer PRP injections into both the hip joint and gluteal tendons, but appreciating that the evidence is poor.

Intra-articular hyaluronic acid injections are no more effective than placebo. The cost of one vial of hyaluronic acid in New Zealand is around $500, and so this treatment has extremely poor cost-effectiveness.[12][13]

Saline appears to be as effective as other options. One systematic review and meta-analysis evaluated saline, glucocorticoids, hyaluronic acid, and PRP, and found that all (except HA+PRP) led to a clinically important improvement in pain.[14]

Surgery

Total hip joint replacement is usually effective for reducing pain. However 10% of patients have chronic postsurgical pain, and preoperative central sensitisation has been thought to be a risk factor for this.[4]

Prognosis

A minority have clear cut clinical and radiological recovery, especially with marked osteophytosis and concentric disease. Superolateral migration of the femoral head is correlated with more rapid osteoarthritis progression, also with atrophic bone response

Resources

References

  1. โ†‘ 1.0 1.1 Kim et al.. Prevalence of radiographic and symptomatic hip osteoarthritis in an urban United States community: the Framingham osteoarthritis study. Arthritis & rheumatology (Hoboken, N.J.) 2014. 66:3013-7. PMID: 25103598. DOI. Full Text.
  2. โ†‘ Iidaka et al.. Prevalence of radiographic hip osteoarthritis and its association with hip pain in Japanese men and women: the ROAD study. Osteoarthritis and cartilage 2016. 24:117-23. PMID: 26241774. DOI.
  3. โ†‘ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Metcalfe et al.. Does This Patient Have Hip Osteoarthritis?: The Rational Clinical Examination Systematic Review. JAMA 2019. 322:2323-2333. PMID: 31846019. DOI. Full Text.
  4. โ†‘ 4.0 4.1 Hattori T, Shimo K, Niwa Y, Tokiwa Y, Matsubara T. Association of Chronic Pain with Radiologic Severity and Central Sensitization in Hip Osteoarthritis Patients. J Pain Res. 2021;14:1153-1160 DOI
  5. โ†‘ Gay et al.. Educating patients about the benefits of physical activity and exercise for their hip and knee osteoarthritis. Systematic literature review. Annals of physical and rehabilitation medicine 2016. 59:174-183. PMID: 27053003. DOI.
  6. โ†‘ Fransen et al.. Exercise for osteoarthritis of the hip. The Cochrane database of systematic reviews 2014. CD007912. PMID: 24756895. DOI.
  7. โ†‘ Bennell et al.. Physical therapies in the management of osteoarthritis: current state of the evidence. Current opinion in rheumatology 2015. 27:304-11. PMID: 25775185. DOI.
  8. โ†‘ Jiang et al.. The relationship between body mass index and hip osteoarthritis: a systematic review and meta-analysis. Joint bone spine 2011. 78:150-5. PMID: 20580591. DOI.
  9. โ†‘ 9.0 9.1 da Costa et al.. Effectiveness of non-steroidal anti-inflammatory drugs for the treatment of pain in knee and hip osteoarthritis: a network meta-analysis. Lancet (London, England) 2017. 390:e21-e33. PMID: 28699595. DOI.
  10. โ†‘ Krebs et al.. Effect of Opioid vs Nonopioid Medications on Pain-Related Function in Patients With Chronic Back Pain or Hip or Knee Osteoarthritis Pain: The SPACE Randomized Clinical Trial. JAMA 2018. 319:872-882. PMID: 29509867. DOI. Full Text.
  11. โ†‘ McCabe et al.. The efficacy of intra-articular steroids in hip osteoarthritis: a systematic review. Osteoarthritis and cartilage 2016. 24:1509-17. PMID: 27143362. DOI.
  12. โ†‘ Brander et al.. Evaluating the use of intra-articular injections as a treatment for painful hip osteoarthritis: a randomized, double-blind, multicenter, parallel-group study comparing a single 6-mL injection of hylan G-F 20 with saline. Osteoarthritis and cartilage 2019. 27:59-70. PMID: 30223023. DOI.
  13. โ†‘ Wu et al.. Efficacy of intra-articular hyaluronic acid injections in hip osteoarthritis: a meta-analysis of randomized controlled trials. Oncotarget 2017. 8:86865-86876. PMID: 29156841. DOI. Full Text.
  14. โ†‘ Gazendam et al.. Intra-articular saline injection is as effective as corticosteroids, platelet-rich plasma and hyaluronic acid for hip osteoarthritis pain: a systematic review and network meta-analysis of randomised controlled trials. British journal of sports medicine 2021. 55:256-261. PMID: 32829298. DOI.

Literature Review