Management of Chronic Knee Pain

Dr (Maj) Pankaj N SurangeMBBS, MD, FIPP(Hungary)

Director, Interventional Pain and Spine Centre, New DelhiChairman, WIP, India section

Cartilage• Forms the opposing articulating surface of Synovial joints

Low Friction Lubrication

Absorbs the

Mechanical Load

Painless smooth Movements

Collagen type -II

Proteoglycan

Hyaluronan(ECM)

Hyaluronan is an important component of articular cartilage, where it is present as a coat around each cell (chondrocyte). When aggrecan monomers bind to hyaluronan in the presence of link protein, large, highly negatively charged aggregates form. These aggregates imbibe water and are responsible for the resilience of cartilage (its resistance to compression).

• Articular Cartilage is Metabolically active but has limited capacity to replace damaged or lost cell

• Cartilage matrix surrounding a defect is antiadhesive- precursor cells are unable to attach themselves

• Being avascular---lacks the capacity to initiate cascade of cytokine production to attract repair cells

Injury and Repair

• Superficial Cartilage injuries –Do not heal because these lesion do not initiate inflammation.

• Deep cartilage and Subchondral bone injuries- hemorrhage, fibrin clot formation and inflammation---Repaired tissue is fibrocartilage

Pathophysiology –OA Knee

• Degenerative joint disease characterized by progressive loss of articular cartilage followed by attempted repair of articular cartilage, remodeling and sclerosis of subchondral bone and in many instances formation of subchondral bone cyst and osteophytes.

Subchondral bone responds with vascular invasion and increased cellularity, at areas of pressure

Loss of cartilage results in the loss of the joint space

Diagnosis

Clinical Radiological

Clinical Signs and Symptoms Pain

• Initially, it is typically aching in nature, related to joint use, and relieved by rest

MTF OA -anteromedial pain, mainly on walking.

PF OA causes localized anterior kneepain, worse on negotiating stairs/inclines, and a progressive aching on prolongedsitting that is relieved by standing and ‘stretching’ of the legs.

Posterior pain usually indicates a complicating popliteal cyst

As OA progresses, pain may become more persistent and

occur also at rest and at night.

Raised Intraosseous pressure secondary to venous obstruction

Bone marrow oedemaSynovitis

EnthesopathyBursitis

TendinitisLigamentous Strain

• Stiffness• from slowness of joint movement, to pain on initial

movement such as getting up from a chair• Early morning stifness with Synovitis or Enthesopathy

• Crepitus• May be palpable throughout the range of movement• In gross cases may be even audible

• Tenderness• Tenderness to palpation along the joint-line

(‘capsular/joint-line tenderness’) suggests a capsular/intracapsular origin of pain.

• Point tenderness away from the joint-line suggests a periarticular lesion;

inferior insertion of the medial collateral ligament.

• Deformity• Varus and Valgus Deformity• Popliteal cyst• Antalgic gait

• Swelling –Effusion• Patellar Displacement

Radiological Evaluation

• The plain radiograph remains a key investigation in the clinical management of OA. It is particularly useful for:

• diagnosis—showing characteristic structural changes typical of OA and• absence of features of alternative arthropathies (e.g., inflammatory

erosive disease);• assessment of the severity of structural change;• identification of associated chondrocalcinosis

• Limitations• The requirement of optimal views and techniques-Stress or loaded

views• insensitive for detection of early OA and minor progression of cartilage and bone change.• Plain radiographs are a static, not dynamic.

X-RayThe four main radiographic features of OA are joint-space

narrowing,subchondral sclerosis, subchondral cyst formation, and osteophyte

Postero-Anterior weight bearing views

Assessment of Joint Space, lateral subluxation and Varus/valgus deformity

Weight-bearing films in knee flexion

Demonstrate more narrowing than those in full extension, since the loadingis then on the part of the joint that is principally targeted by cartilage loss.

Lateral Radiograph

• marked loss of patellofemoral joint-space• femoral and superior patellar Osteophytes• anterior enthesophyte

Patellofemoral OA.

• Intercondylar Tibial or Femoral Central osteophytes

• Osteochondral Bodies

Skyline view

• complete joint-space loss• prominent grooving of the articular surfaces, • lateral patellar subluxation

doubtful JSN and possible osteophytic

lipping

definite osteophytes and possible

JSN

multiple osteophytes,definite JSN,

sclerosis, possible bony

deformity

large osteophytes, marked JSN,

severe sclerosisand definitely

bony deformity

MRI• Superficial cartilage loss even without narrowing• Bone marrow edema

• Three-dimension spoiled gradient recalled echo imaging with fat suppression (3D-SPGR) is the current standard for morphological imaging of cartilage

T2 mapping of articular cartilage

Management

Management of Osteoarthritis Knee-Non Pharmacological treatment

• Negative Approach• Exercises• Shock absorbing Insoles• Weight reduction • Patellar taping• Quadriceps Exercises

A high Q-angle causes the quadriceps to pull on the patella and leads to patellar tracking which is a predisposing factor for pain.

Pharmacological treatment

• Pharmacologic recommendations for the initial management of knee OA1. Acetaminophen2. Oral NSAIDs3. Topical NSAIDs4. Tramadol

• Negative recommendations for knee OA– Chondroitin sulfate– Glucosamine– Topical capsaicin

Recommendations for Glucosamine and Chondroitin

• The largest and best-designed clinical trial is the Glucosamine/chondroitin Arthritis Intervention Trial (GAIT)

• Neither glucosamine hydrochloride nor chondroitin sulfate has been shown to be more efficacious than placebo for the treatment of OA Knee

• Three months of treatment is a sufficient period for the evaluation of efficacy; if there is no clinically significant decrease in symptoms by this time, the supplements should be discontinued. Furthermore, there is no evidence that these agents prevent osteoarthritis in healthy persons or in persons with knee pain but normal radiographs

• Hochberg MC. Nutritional supplements for knee osteoarthritis—Still no resolution. New England Journal of medicine 354:848-850, 2006.

• Sawitzke AD and others. The effect of glucosamine and/or chondroitin sulfate on the progression of knee osteoarthritis: A report from the Glucosamine/chondroitin Arthritis Intervention Trial. Arthritis & Rheumatism 58:3183-3191, 2008.

• Reichenbach S, and others. Meta-analysis: chondroitin for osteoarthritis of the knee or hip. Annals of Internal Medicine 146:580-590, 2007.

It is uncertain whether these compounds are absorbed intact, whether they are metabolized to any degree, and what role they actually play in vivo. Currently, there remains no theoretical or empirical evidence to support the original supposition that these compounds provide substrate for articular cartilage repair.

Recommendations for Glucosamine and Chondroitin

August 2014

• Knee Aspiration-ASAP

• Popliteal cyst Aspiration

• Intra-articular Corticosteroids

• Acute exacerbation of pain• Signs of inflammation

Joint Irrigation

• Removal of particulate debris from the joint space- loose bodies of cartilage and bone, calcium crystals

• Mobilizing phlogistic materials -degradative enzymes, cytokines from the joint.

• Aspiration or Injection• USG Guided Vs. Fluoroscopic Guided Vs. Blind

Viscosupplements

• High mw HA is viscoelastic

• Because of its HA content, joint fluid acts as a viscous lubricant during slow movement of the joint, as in walking, and as an elastic shock absorber during rapid movement, as in running.

• Synovial fluid HA lubricates the soft tissue and provides a surface layer on the articular cartilage.

• Other effects• it inhibits PGE-2 synthesis induced by interleukin-1• protects against proteoglycan (PG) depletion, and cytotoxicity

induced by oxygen-derived free radicals• suppresses cartilage matrix degradation by fibronectin fragmentsand• reduces leukocyte adherence, proliferation,migration, and

phagocytosis.3

• Altman, R.D., Hochberg, M.C., Moskowitz, R.W., and Schnitzer, T.J. (2000).Recommendations for the medical management of osteoarthritis of the hip and knee. Arthritis Rheum 43:1905–15.

The American College of Rheumatology Guidelines for the Medical Management of Osteoarthritis recommend the use of IA HA injections for treatment of joint pain in patients with knee OA who have failed to respond adequately to conservative non-pharmacologic therapy and simple analgesics.

Viscosupplement-Evidence

Viscosupplement-Evidence

Clin Orthop Relat Res. 2007 Feb;455:113-22.Viscosupplementation for knee osteoarthritis: a systematic review.Divine JG, Zazulak BT, Hewett TE.

systematic review of the five published meta-analyses, which include single- or double-blinded randomized trials performed at one center or multiple centerstrials…all come to a similar conclusion that when the strictest quality tools and interpretation of heterogeneity are used, Level I evidence demonstrates that the use of HA in patients with OA results in modest improvement in pain.

• Ann Intern Med. 2012 Aug 7;157(3):180-91. doi: 10.7326/0003-4819-157-3-201208070-00473.

• Viscosupplementation for osteoarthritis of the knee: a systematic review and meta-analysis.

• In patients with knee osteoarthritis, viscosupplementation is associated with a small and clinically irrelevant benefit and an increased risk for serious adverse events.

Viscosupplement-Evidence

• Viscosupplementation with hyaluronic acid in the treatment for cartilage lesions: a review of current evidence and future directions

• European Journal of Orthopaedic Surgery & Traumatology;Feb2013, Vol. 23 Issue 2, p119

• With a very solid safety profile, viscosupplementation with hyaluronic acid (HA) derivatives has become an excellent modality for treating diseased articular cartilage. Recent literature supports the use of HA not only in the management of the pain associated with osteoarthritis but also as a disease-modifying agent as well.

Viscosupplement-Evidence

• Further studies have started to define exciting new roles for Viscosupplementation in the treatment for acute injuries to the joint microenvironment.

Viscosupplement-Evidence

Platelet rich plasma

• Platelets are crucial for tissue repair and vascular remodelling. The first stage of normal wound healing, immediately following injury or insult, is inflammation, where activated platelets adhere to the site of injury releasing growth factors .

• Platelet-rich plasma injections aim to promote cartilage repair and relieve osteoarthritic symptoms, potentially delaying the need for joint replacement surgery. Platelets produce growth factors that are thought to stimulate chondrocyte proliferation, leading to cartilage repair.

• Platelet-rich plasma injections for osteoarthritis of the knee» NICE interventional procedure guidance 491

guidance.nice.org.uk/ipg491-2014

Prolotherapy

• Prolotherapy stimulates local healing of chronically injured extra- and intra-articular tissue.

• Every 2-4 weeks for 3-6 months

Genicular Branch Neurotomy

Radiofrequency treatment relieves chronic knee osteoarthritis pain: a double-blind randomized controlled trial. Pain. 2011 Mar;152(3):481-7

Volume of evidence is great but quality of evidence is

poor

Epidemiology

• Prevalance• Common worldwide• 2-5% adult US population• 35-50 yrs

• Gender • Women > Men

Pathophysiology

• Central Pain Mechanism

• Central sensitization- generalized heightened pain sensitivity of FM patients

In Fibromyalgia there is increased activation of second order neurons in the spinal cord• There are two types of second order neurons:– Nociceptive specific neurons– Wide dynamic range neurons

Central sensitization of nociceptive neurons leads to nociceptive nerve impulses being perceived as morepainful (hyperalgesia)

• Central sensitization of wide dynamic range neurons leads to nonnociceptive nerve impulses being perceived as painful (allodynia)

An Official Diagnosis• Chronic Rheumatism• Fibrositis• Multiache Syndrome• Psychological Pain- “all in your head”

AMA recognized FMS as a TRUE ILLNESS- 1987

WHO -1993

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Myofacial Pain Syndrome

• Myofascial pain syndrome is a chronic local/ regional musculo-skeletal pain disorder that may involve either a single muscle or a muscle group.

• No systemic features usually.

• The pain may be of a burning, stabbing, aching or nagging quality.

• Presence of trigger points in muscle belly.

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Myofacial Trigger points

Trigger points are usually associated with a taut band, a ropey thickening of the muscle tissue. Trigger point, when pressed upon, will cause the pain to be felt elsewhere. This is what is considered "referred pain".

Electron microscopy confirmed these to be contracted sarcomere

Recent research

• Neurogenic Mediators at motor End Plate

Injured muscles

Local ischemia

Activate muscle receptors

Triggers the release of CGRP from muscle pain fibres

Increased motor endplate activity

Staud RPathogenesis of chronic muscle pain.Best Pract Res Clin Rheumatol.2007;21,3:581-596

Central sensitization

• Referred muscle pain is frequently hyperalgesic in nature

• Arendt-Nielsen L, Svensson P. Referred muscle pain: Basic and clinical findings. Clin J Pain. 2001; 17:11-19.

• Bennett R. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 2007; 21,3:427-445.

Clinical conditions that result from central sensitization:

• Hyperpathia • Allodynia • Hyperalgesia• Neuropathic Pain

MPS FMS• Local/ regional musculo-

skeletal pain disorder that may involve either a single muscle or a muscle group.

• Trigger points at ms belly.

• Usually no systemic symptoms.

• More common in males & curable.

• No genetic predisposition.

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Systemic illness with widespread muscle pain.

Tender points at Ms. -Tendon junction.

Other systemic symptoms exists.

More common in females & seldom curable.

Genetic predisposition.

Clinical Presentation

FMS

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Pieces to the Puzzle

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Fibromyalgia

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Clinical Presentation

MPS

• Pain- poorly localized, regional , aching

• Weakness and Fatigue

• Numbness, paresthesias

• Varying level of disability

• Autonomic dysfunction

Trigger points and Referral pattern

Iliopsoas

Longissimus

Quadratus

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Trigger points and Referral pattern

Sternomastoid

Trapezius

Levator Scapula

Splenius capitiswww.ipscindia.com

classification

Primary

Concomittant

mildmoderatesevere

Diagnosis

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Diagnosis• Clinical

• No characteristic Lab findings.

• Demonstrable biochemical abnormalities- Research Laboratory

• Substance P in CSF is three times higher in FMS.

• Low serotonin levels in platelets & CNS.• Low levels of ATP in RBC and trigger points. • Dysfunction of the HPA axis. • Low growth hormone.• Nerve growth factor was 4 times higher in

CSF.

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f- MRI

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Diagnostic Criteria

• Gowers (1904) -Diffuse pain as Fibrositis.– Histopathologicaly could not be proven.

• Hench (1976)- First clinical definition– Pain– No physiological explanation

• Smythe (1979)– Tender points

• Yunus (1981)- Develop critera– Diffuse pain > 3 months duration– Lack of other obvious cause

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ACR Criteria (1990)• Widespread pain – 3 months

duration• Tenderness 11/18 tender points

Specificity-81%Sensitivity- 88%

Tender points = ESR

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Symptom Intensity scale score -2010“No Tender Points”

www.ipscindia.comWolfe F, Rasker JJ. The Symptom Intensity Scale, fibromyalgia, and the meaning of fibromyalgia-like symptoms. J

Rheumatol 2006; 33:2291–2299

Symptom Intensity scale score

• Simple way to measure overall health

• Severity

• Can detect FMS in patients with other disease

• Uncovers comorbid depression

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