Rheumatoid Arthritis Disease Presentation

Rheumatoid Arthritis a progressive inflammatory disorder characterized by polyarticular joint involvement and systemic manifestations.

1. RHEUMATOID ARTHRITIS and its Ayurvedic Management By Dr S G YADUNAND INTERN MIAMS MANIPAL

2. Autoimmune disease Lack of differentiation between self and non-self tissues

3. Olden days - Infectious diseases were causing devastating consequences Nowadays it’s Lifestyle diseases and Rheumatological Diseases Hetero- genous disease with variable severity, unpredictable course, and variable response to drug treatment. Under or Sub-optimum treatment – Progressive disability, Systemic complications, increased mortality due to cardiovascular and other systemic complications. INTRODUCTION

4. Progressive, Autoimmune, Chronic, Systemic, Inflammatory disease that clinically presents as Symmetric Polyarthritis that affecting small and large di-arthrodial joints of the extremities. CHRONIC DISEASE WITH ACUTE FLARES Can have articular and Extra-articular manifestations Female > Male 3:1 ( India – 5:1 ) (role of hormones) Age – any age, Typical peak of onset is 3 rd – 4th Decade Most common Inflammatory Arthritis Worldwide prevalence 1-3% population, India – 0.5 – 0.75% DEFINITION & EPIDEMIOLOGY

5. ACUTE (< 1week) CHRONIC (>weeks) Spondylo-arthropathies RA ( > 6weeks) Crystalline (Gout, Pseudo-gout) SLE Septic arthritis Tuberculosis Acute Rheumatic Fever (fleeting) Sarcoidosis How long?

6. FEVER, WEIGHT LOSS, etc RUBOR, CALOR, DOLOR, TUMOR, LOSS OF FUNCTION ESR and CRP increases Ferritin high, Thrombocytosis

7. With or Without Inflammation? NON-INFLAMMATORY INFLAMMATORY OA RA Fibromyalgia SLE Osteoporosis Seronegative Spondylo -arthritis Neuropathic Arthritis (Charcot) Gout Trauma, Metabolic Septic Arthritis

8. Asymmetric Symmetric OA RA PsA SLE Reactive arthritis PsA Crystalline arthritis (Gout, Pseudogout ) Scleroderma Septic, Lyme, Tuberculosis, Sarcoidosis Viral (Hep, Rubella, HIV) Depending on Symmetry of Involvement

9. How many Joints Involved? Mono articular Oligo arthritis Poly arthritis 1 joint 2-4 joints More than 5 joints Trauma Psoriatic arthritis RA Gout Enteropathic arthritis (IBD) SLE Osteoarthritis Reactive arthritis Septic arthritis Osteoarthritis Lyme disease

10. ETIOLOGY Idiopathic Genetic Markers – HLA-DR4 50-70% cases (not diagnostic) Hereditary – Increased incidence Environmental Triggers – tobacco, silica dust(miners), infections, etc. Citrullination , Carbamylation (Post Translational Modification) Hormonal variations

11. PATHOPHYSIOLOGY

12. AUTO-ANTIBODIES IN RA About 70-80% RA patients have auto-antibodies called as Rheumatoid Factor ( Sero -positive RA ). RA factors are antibodies that binds to Fc portion of own immunoglobulin G . The commonly mentioned rheumatoid factor is an IgM RF. (although other immunoglobulin types, including IgG and IgA, are rarely found) Anti-CCP antibodies are auto-antibodies produced by immune cells to fight against Cyclic Citrullinated Peptide. RA factor and anti-CCP is absent in some patients with clinically diagnosed Rheumatoid Arthritis ( Sero -negative RA –less common) Note: RA Factor could be positive in Viral Hepatitis, Sarcoidosis, Leprosy, Cirrhosis CCP antibodies are rarely found in other autoimmune conditions SLE, Sjorgen etc and in some infections like Tuberculosis.

13. PROGRESSIVE INTERMITTENT

14. Typical presentation is with Pain, Swelling, Stiffness (symmetric, bilateral) in smaller joints of hand and feet that improves with Activity. (as disease advances larger joints are affected) Inflammatory features include diurnal variation with symptoms that worsen after a period of inactivity JOINT STIFFNESS (morning stiffness) > 1 HOUR Associated with constitutional symptoms of Fatigue, Feverish , Anorexia, Weight loss and Muscle Wasting due to Inflammation (RA cachexia) Late stage or Poor Management – Extra-articular features SYMPTOMS

15. SKIN BLOOD VESSELS HEART, LUNGS, MUSCLES

16. JOINTS SYNDESMOLOGY FIBROUS None/Minimal Movement Syn -arthroses Sutures of skull FIBROCARTILAGENOUS Limited Movement Amphi -arthroses Intervertebral disc Costochondral junction Sacro-ilac joint Pubic symphysis SYNOVIAL Wide Movement Di-arthroses Most-extremities Atlanto -axial joint Tempero -mandibular joint Sterno -Clavicular Hip joint etc

17. RA OF UPPER EXTREMITIES Most commonly affects MCP, PIP, Wrists (DIP is usually spared) Flexor Tendon Synovitis ( most common cause for hand weakness) Dorsal Sublaxation of Ulna Carpel tunnel Syndrome or other entrapment syndromes may present. DIP MCP, PIP, WRIST OA RA Ps A SLE CPPD

18. Dorsal Sublaxation of Ulna at Distal radio-ulnar joint (may contribute rupture of extensor tendons)

19. Trigger Finger : due to inflammation within tendon sheath and nodule formation

20. Destruction of tendons, ligaments and joint capsules produce characteristic deformities.

21. dorsal subluxation of metacarpal heads, (2) boutonniere deformity, (3) swan neck deformity, (4) hitchhiker ’ s thumb, (5) ulnar deviation of fingers

22. 1) Swan Neck 2) Boutonniere Volar displacement of lateral bands Tear in lateral band

23. Z-thumb Ulnar Drift

24. MCP sublaxation

25. DEFORMITIES FOOT Cock-up Toe deformity Hammer Toe’s Rocker bottom deformity Baker’s cyst is a complication (may occur in combination with knee synovitis) RA OF LOWER EXTREMITIES RA involves – Mid-foot, MTP

26. Cock-up Toe Deformity Dorsal Sublaxation of MTP Joints – Cock-up Toe deformities leading to secondary bursae and callosities Loss of Longitudinal arch ( Flat foot ) due to rupture of tibialis posterior tendon

27. Baker’s Cyst/Popliteal Cyst (not specific to RA) Synovial fluid communicates with the cyst but is prevented from returning back to joint by a valve like mechanism Large effusion Rupture is often induced by flexion causing calf pain and swelling that may mimic DVT

28. Articular Findings of Chronic RA in my case study

29. RA OF ATLANTO-AXIAL JOINT C1-C2 Active long standing Sero -positive RA with extra-articular manifestations and any of the symptoms like: Recurrent occipital headache, Neck pain, Decreased neck ROM, Neurological deficits (weakness/paraesthesia) of upper extremities These are suggestive for RA of C1-C2 ( Thoraco -Lumbar and Sacro -Iliac is spared) Space between odontoid process from C2 and arch of the atlas exceeds more than 3 mm due to Inflammatory debris. potentially life threatening complication of Rheumatoid arthritis COMPLICATIONS OF C1-C2 Involvement in RA Compressive myelopathy Radiculopathy Neuropathy (entrapment syndromes) Acute sub-laxation of C1-C2

30. Sublaxation of C1-C2 Widening of space between Odontoid Process of Axis (C2) and Anterior arch of Atlas ANATOMY OF C1 C2

31. Investigations if you suspect Atlanto -Axial Sub-laxation X-Ray of C-Spine with flexion and extension views MRI – later or if neurological deficit noted during examination TREATMENT in c/o Cervical Spine Sub-laxation Surgery Stabilisation and Fixation NOTE: As the disease advances RA may effect larger joints like elbow, shoulders, knees, and ankles.

32. EXTRA-ARTICULAR MANIFESTATIONS IN RA Seen in long standing sero-positive RA Rheumatoid nodules Vasculitis Pulmonary complications Ocular involvement Kerato -conjunctivitis sicca Anaemia Osteopenia & Osteoporosis(#) Neurological Manifestations Cardiac involvement Peri / Myo /Endocarditis CAD MI Rare complications Nephrotic syndrome Risk of hematological malignancies

33. Rheumatoid Nodules RA nodules occur mostly in seropositive RA , Primarily effects extensor tendons of hands and later anywhere like Lung, Pericardium etc Consists of fibrous and inflammatory tissue

34. VASCULAR VASCULITIS PALMAR ERYTHEMA RAYNAUD’S PHENOMENON

35. PULMONARY COMPLICATIONS GROUND GLASS APPEARANCE HONEYCOMB APPEARANCE ENDOGENOUS TB

36. OCULAR KERATO-CONJUNCTIVITIS SICCA EPISCLERITIS

37. CRITERIA FOR DIAGNOSIS OF RA [ American College of Rheumatology 2010 ] Large joints = shoulders, elbows, hips, knees, ankles Small joints = metacarpophalangeal joints, proximal interphalangeal joints, metatarsophalangeal joints, thumb, wrists

38. LABORATORY FINDINGS ↑ erythrocyte sedimentation rate (ESR) ↑ C-reactive protein (CRP) ALP mild/moderately high (+) Rheumatoid factor (RF) 80% AMPA - (+) Anti-cyclic citrullinated peptide (anti-CCP) (70% RA) ANTI Nuclear Antibody (ANA) Antisreptolysin O (ASO) Low Hb , Thrombocytosis Albumin/Globulin ratio (reversal) Synovial fluid: Joint Aspiration turbid with many leukocytes Imaging – X ray, MRI (rare), Ultrasonography (erosions etc )

39. DIFFERENTIAL DIAGNOSIS Psoriatic Arthritis Spondylo -arthritis Reactive arthritis Gout OA IBS related arthritis Fibromyaligia Syphilitic Arthritis Tubercular Arthritis

40. RA vs OA OA Morning stiffness < 30 minutes, worse with activity Equal gender prevalence ↑ with Age Normal ESR Local symptoms ↑ in Obesity Hands, knees, hips, spine Asymmetrical Cartilage destruction, Osteophyte formation RA Morning stiffness > one hour, resolves with activity ↑ incidence females (3:1) ~ Age ↑ ESR Systemic symptoms ~ Obesity Wrists, hands, feet Symmetrical Cartilage and Bone destruction

41. GOALS OF TREATMENT Control disease activity and joint pain Maintain function in daily activities Slow destructive joint damage Achieve and maintain disease remission Improve or maintain functional status and quality of life

42. NSAID’s ( Analgesic and anti-inflammatory) Corticosteroids ( Suppress inflammatory response) DMARD’s ( halt the progression of RA) Non-biological DMARD’s Hydrochloroquinone , Methotrexate etc ( Sustained suppression of inflammation) Biological DMARD’s ( target pro-inflammatory cytokines or lymphocytes) Drug Targets: TNF α IL-1 IL-6 B cells PHARMACOLOGIC THERAPY

43. Rest Physical and occupational therapy Assistive devices Weight reduction Surgery NON-PHARMACOLOGIC

44. आमवातस्य निदानपूर्विका सम्प्राप्तिः अथामवातनिदानम् | विरुद्धाहारचेष्टस्य मन्दाग्नेर्निश्चलस्य च | स्निग्धं भुक्तवतो ह्यन्नं व्यायामं कुर्वतस्तथा ||१|| वायुना प्रेरितो ह्यामः श्लेष्मस्थानं प्रधावति | तेनात्यर्थं विदग्धोऽसौ धमनीः प्रतिपद्यते ||२|| वातपित्तकफैर्भूयो दूषितः सोऽन्नजो रसः | स्रोतांस्यभिष्यन्दयति नानावर्णोऽतिपिच्छिलः ||३|| जनयत्याशु दौर्बल्यं गौरवं हृदयस्य च | व्याधीनामाश्रयो ह्येष आमसञ्ज्ञोऽतिदारुणः ||४|| युगपत्कुपितावन्तस्त्रिकसन्धिप्रवेशकौ | स्तब्धं च कुरुतो गात्रमामवातः स उच्यते ||५|| Rhuematoid Arthritis can be co-related to Amavata in Ayurveda

45. आमवातस्य सामान्यलक्षणम् अङ्गमर्दोऽरुचिस्तृष्णा आलस्यं गौरवं ज्वरः | अपाकः शूनताऽङ्गानामामवातस्य लक्षणम् ||६||

46. आमवात चिकित्सा सूत्र ( चक्रदत्त २५/१-२ ) लङ्घनं स्वेदनं तिक्तं दीपनानि कटूनि च । विरेचनं स्नेहपानं बस्त्यश्च आम मारुते ॥ सैन्धवाद्ये अनुवास्य क्षार बस्ति प्रशस्यते । आमवाते पञ्चकोल सिद्धं पानान्नमिष्यते ॥ रूक्ष स्वेद: प्रकर्तव्यो वालुकपुतकैस्तथा ।

47. शोधन चिकित्सा IN AMAVATA विरेचन क्षार बस्ति वैतरण बस्ति

48. योगराज गुग्गुलु सिंहनाद गुग्गुलु बृहत् सिंहनाद गुग्गुलु अजमोददि वटकं चित्रकादि वटि रास्नादशमूला क्वाथ रास्ना पञ्चक क्वाथ रास्ना सप्तक क्वाथ शुंटी क्वाथ दशमूल क्वाथ हरीतकी चूर्ण नागर चूर्ण पञ्चकोल चूर्ण अमृतादि चूर्णं वैश्वानर चूर्णं षट्यादि चूर्णं एरण्ड तैल प्रयोग बृहत् सिन्धवाद्य तैलं नागर घृतं शुंटी घृतं हिङ्ग्वदि घृतं षट्यादि कल्क IMPORTANT YOGA’S

49. गोदन्ति भस्म आमवातरि रस मल्लसिन्दूर संजीवनी वटि अग्नितुण्डी वटि दशाङ्ग लेप हरिद्रा लेप निर्गुण्डी पत्र लेप जटामयादि लेप अमृत भल्लातक रसायन अश्वगन्द रसायन गोक्षुरादि अवलेह

50. पथ्य - अपथ्य पथ्य आहार वस्तुक शाक अरिष्ट पुनर्नव पटोल लशुन यव अन्न षष्टिक शालि तक्र अपथ्य विहार रूक्षण स्वेदनं लङ्घनं चङ्क्रमणं मृदु व्यायाम उष्ण वस्त्र आहार दधि मत्स्य गुड क्षीरं विरुद्ध आहार विहार पूर्व वायु वेग अवरोध निशा जागरण शीत जल स्नान अतिव्यवाय

51. THANK YOU