A SURVEY OF DIFFERENT
INFLAMMATORY ARTHRITIS
Dr.Rahul.R.Nair ,BAMS,MD(Ay)
Associate Professor & Head
Dept.of Roganidanam & Vikrtivijnanam
Ashtamgam Ayurveda Vidyapeedham
My humble welcome
JUVENILE IDIOPATHIC
ARTHRITIS
JIA – history findings
Most common chronic paediatric
rheumatologic disease
Arthritis for atleast 6 weeks before diagnosis
Insidious or abrupt onset
Morning stiffness and gel phenomenon,
arthralgia throughout the day
Limited ability to participate in physical education
Spiking fevers once or twice each day almost on
same time
Evanescent rash on trunks and extremities
Presence of a morning limp or abnormal joint
positioning
Physical examination
Arthritis – limitation of motion with pain,
erythema, swelling, warmth
Synovitis – increased joint volume, limitation
of range of motion in extremities, joint held
in comfortable position
Physical examination
Limbs will be held in flexion, soft swelling in
popliteal fossa
Obliteration of parapatellar fossae
Fingers may appear swollen
Hip held in flexion, abduction and external
rotation
Guarding may present
A suitable candidate
A child below 16 years of age,
with arthritis of atleast one joint
persisting for >6 weeks
Types of JIA
Systemic-onset juvenile idiopathic arthritis
Oligoarticular juvenile idiopathic arthritis
Polyarticular juvenile idiopathic arthritis
Psoriatic arthritis
Enthesitis-related arthritis
Undifferentiated arthritis
Systemic onset JIA – Still’s disease
Arthralgia
Myalgia
Evanescent salmon –pink macular rash, associated with
fever spikes
Hepato-splenomegaly
Axillary lymphadenopathy
Pleural or pericardial effusions
The rash
Pleural effusion B/L lung fields
Oligo articular JIA
4 or less than 4 joints affected
Large weightbearing joints like knee and ankles
affected
In asymmetrical arthritis, length dyscrepency seen
on progression
Extensor muscle atrophy
Anterior uveitis
Polyarticular JIA
5 or more joints are affected
Symmetrical involvement
Rheumatoid nodules are seen in RA +
Small joints of hand and weight bearing
joints affected
Psoriatic arthritis
Monoarticular arthritis
DIP joint involvement
Tenosynovitis
Nail involvement - pitting is the most common but
least specific finding
Disordered bone growth with resultant shortening
Sacroiliitis
Enthesis related arthritis
Paediatric spondyloarthropathy
Inflammation of enthesis
Pain,tenderness and swelling at enthesis
Mainly the finger joints
Sacroilitis only in the later stage
Diagnostic considerations
Arthritis and enthesitis co-exist
Presence of arthritis +/ or enthesitis with
two of the five below
Sacroiliac tenderness and/or inflammatory
lumbosacral pain
Positive human leukocyte antigen B27
(HLA-B27) test
continued
Onset of arthritis in a male 6 years old or older
Acute symptomatic anterior uveitis
Presence in a first-degree relative of ankylosing
spondylitis, enthesitis-related arthritis,
inflammatory bowel disease with sacroiliitis,
reactive arthritis, or acute anterior uveitis
Undifferentiated arthritis
If the symptoms NOT fitting into any
groups
OR
If it fits into more than one group
Investigations
No investigation is confirmatory
JIA is a clinical diagnosis
ESR and CRP may be elevated
Thrombocytosis, leucocytosis etc can be seen
ANA + points to uveitis
Complications
Macrophage Activating Syndrome
Cytokine storm is the pathogenic process
behind
Suspect MAS if
Falling ESR
Normalization or decrease in white blood cell (WBC)
count
Low platelets
Elevated liver enzymes
Increased ferritin
Increased triglycerides
Low fibrinogen
Erratic fevers
Hemorrhages (disseminated intravascular
coagulation–like pattern)
Prognosis
For oligoarthritis, it is good.
Condition may resolve on puberty
Polyarticular and systemic JIA ~ Still’s – bad
prognosis
JIA in adolescence
Uveitis
Persistence into adulthood ~ 50% cases
Reduced peak bone mass
Adult onset Still’s disease
Rare systemic inflammatory disorder
Intermittent fever, rash and arthralgia
Hepato-splenomegaly and lymphadenopathy
may be present.
Acute phase response with marked elevation of
ferritin.
RF and ANA negative
FELTY’S SYNDROME
A potentially serious condition
Associated with seropositive RA
Described in 1924
1-3% of all patients with RA
Female> Male
Classical triad
Rheumatoid arthritis
Splenomegaly
Granulocytopenia
Death may happen due to infections
An eye to pathology
Abnormal splenic sequestration of
granulocytes
Destruction
Antibodies against granulocytes
Risk factors
RF positivity in high titers
Long-standing disease
Aggressive and erosive synovitis
Human leukocyte antigen (HLA)-DR4 positivity
and DR4 homozygosity
Extra-articular RA manifestations
Major clinical features
Splenomegaly
Keratoconjunctivitis sicca
Lymphadenopathy
Vasculitis
Leg ulcers
Weight loss
Recurrent infections
Skin pigmentation
Nodules
Laboratory findings
Normochromic normocytic anaemia
Neutropenia
Thrombocytopenia
Impaired T and B cell immunity
Abnormal liver function
Laboratory findings
(WBC) count and differential
Anemia and thrombocytopenia may result from
hypersplenism.
high titers of rheumatoid factor
Antinuclear antibodies (ANAs)
antineutrophil cytoplasmic antibodies
PALINDROMIC RHEUMATISM
PALINDROMIC RHEUMATISM
A disease of unknown cause
Frequent acute attacks of inflammation in
joints
Happens at irregular intervals
PALINDROMIC RHEUMATISM
Happens to cease within hours to days
Most commonly affected – knee and finger
joints
Only systemic manifestation – fever.
PALINDROMIC RHEUMATISM
No permanent articular damage , even
after hundreds of attacks
May be a prodrome of RA
Can progress to RA, SLE
DD – acute gouty arthritis
SJOGREN’S SYNDROME
Chronic, slowly progressive, autoimmune
exocrinopathy
Lymphocytic infiltration of lacrimal and salivary
glands- dry eyes and xerostomia
Named after Swedish opthalmologist Henrick
Sjogren
He introduced the term ‘Keratoconjunctivits sicca’,
for dryness of eyes.
The pattern
On third of patients have systemic
manifestations
Small but significant number may develop
lymphoma.
Primary – presenting alone
Secondary – with other autoimmune
rheumatism
Two age peaks, first in twenties and then in
sixties
Female to male 9:1
Pathologic hallmarks
T and B Lymphocytic infiltration of salivary
glands and B lymphocytic hyperactivity.
T cells predominate in mild lesions, B cells
in more severe lesions
Ductal and acinar epithelial cells play a
significant role.
Signals for lymphocytic activation
Produce pro-inflammatory cytokines and
lympho-attractant chemokines
Express functional receptors for immunity
T and B Cells resist apoptosis
B Cell Activating Factor (BAFF) surge in
patients, which provides the anti apoptotic
effect.
Glandular epithelial cells produce BAFF,
mostly activated by a coxsackie virus
strains
Why diminished secretions?
Defect in cholinergic activity
Redistribution of water channel protein
aquaporin -5
Both leads to neuro epithelial dysfunction
and hence diminished glandular secretions.
Clinical manifestations
Diminished lachrimal and salivary gland
secretions
Primary Sjogren – slow and benign course
Genealised dryness to full blown disease –
8-10 years
Oral symptoms
Dry mouth ~ xerostomia
Difficulty to swallow dry foods
Difficulty to speak continuously
Recurrent dental caries
Burning sensation
On examination
Dry erythematous and sticky oral mucosa
Atrophied filiform papillae of tongue
Cloudy, in expressible saliva
Salivary gland enlargement ~ mostly in
primary sjogrens
Parotid enlargement
Diagnostic tests
Scialometry
Scialography
Scintigraphy with 99Tc
USG Salivary glands
MR Scialography
Confirmation
Biopsy of labial minor salivary glands
Focal lymphocytic infiltration
Ocular symptoms
Dry eyes - xeropthalmia
Sandy or gritty feeling inside eyelids
Burning sensation
Accumulation of secretions at inner canthi
Decreased tearing
Redness
Eye fatigue
Photosensitivity
Eye itch
Togetherly called keratoconjunctivitis sicca
Uveitis
Diagnostic test
Measurement of tear flow by Schirmer I test
Determination of tear composition
Slit lamp corneal and conjunctival
examination post rose bengal staining
reveals corneal ulcerations and attached
filaments of corneal epithelium.
Involvement of other areas
Decrease in mucous gland secretions of upper
and lower respiratory tree
Dry nose, throat and trachea (xerotrachea)
Esophageal mucosal atrophy
Atrophic gastritis
Subclinical pancreatitis
Dyspareunia, dry skin
Extraglandular features
Easy fatigability
Low grade fever
Raynaud’s phenomenon
Myalgia and arthralgia
Non erosive arthritis
Dry cough
Intestitial nephritis
Evolution into lymphoma
Later in the disease process
Persistent parotid gland enlargement
Purpura and leukopenia, cryoglobulinaemia
Low C4 Complemet levels
Ectopic germinal centres in salivary gland
biopsy
Extra glandular manifestations
Arthritis – Jaccoud arthropathy
Raynaud’s phenomenon
Lymphadenopathy
Lung involvement - small airway disease
Vasculitis- cutaneous palpable purpura
Extraglandular manifestations
Kidney involvement – glomerulonephritis
Liver involvement – primary biliary cirrhosis
Lymphoma
Peripheral neuropathy – polyneuropathy
sensory and motor
Jaccoud Arthropathy
Diagnostic serology
Antinuclear antibodies
Antibodies to Ro/SS-A antigens or
Antibodies to La/ SS-B antigens
Elevated ESR, Leucopenia, eosinophilia,
hypergammaglobulinemia
RA Factor positive
Anti alpha fodrin antibody ~ for juvenile
Secondary Sjogrens
Rheumatoid arthritis
SLE
Scleroderma
Mixed connective tissue disease
Primary biliary cirrhosis
Chronic active hepatitis
DDx
HIV – DILS (Diffuse Infiltrative
Lymphocytosis Syndrome)
Hepatitis C
Sicca symptoms will be due to medications,
depression, mucous membrane
pemphigoid, radiation to neck,
amyloidosis, sarcoidosis
AYURVEDIC APPROACH
The covered slides
Full of clinical information
Confusing classifications
Often the classifications are based on
molecular diagnosis and treated
accordingly
Missing the forest for the trees
Our approach
More wholistic
Based on evolving pathogenitic models
Diseased is having equal weightage with
disease
Treated accordingly
OUR DIAGNOSIS
LAKSHANA SAMASHTI
AABHYANTARA VIKRTI PARAMPARA
OUR CHAPTERS in SAMHITAAS
Not merely diseases, INSTEAD
They are progressively evolving pathogenic
models (aabhyantara vikrti parampara)
Hence, can accommodate any new disease.
The cikitsaa
Focus to interrupt the progression of
aabhyantara vikrti parampara
Considers nidaanatyaagam as the first step
Sustainable results are the main target
along with symptom redressal
The key focus
“Raktamaargam nihantyaasu
S’aakhaasandhishu maaruta
Nivishya anyonyam-aavaarya
Vedanaabhirharati asoon”
Vaatarakta nidaanam
Asrk pradooshanam
vidaahi-virudha aahaaram
vidhiheena swapna and jaagara
sukumaara – improper stress response
sedentary nature
trauma
Vaata pradooshanam
Anyonya -aavaranam
VAATAM
The Phenomenon of
Anyonya -Aavaranam
●
Exposure to Nidaana
Koshtam
The Pathologic Co-ordinates
Koshtam
S’aakha
Sandhi
Vaatam
Raktam
The Pathologic migration of anyonya aavrta
vaata and rakta through three rogamargaa
The cryptic players- P&K
“S’eetadou tatra pittena kaphe syandita
s’oshite”
The processes of syandanam and s’oshanam
Rakta dhatu harbours the vitiation of pitta
and kapha.
How joint deformity happens?
●
● Ushnam
●
● snigdham
PITTAM
Yakrt & Pleehaa – Still’s & Felty’s
Rakta vaha srotomuulam
The dushti of a dhaatu can progressively
affect the srotomuula.
Hepato-splenomegaly
Vataraktam spectrum
Main presentations are joint or soft tissue
oriented
Jaanu,jangha,uuru,kati,amsa,hasta,paada,
angasandhishu
Aabhyantara Vidradhi
Aabhyantara visarpam
Focus on
PK –Kardama visarpam
VP- Agni visarpam
S’opha spectrum
The involvement of raktam
Cases like SLE, wherein
The spectrum of vishama jwaram
Very important
The presence of leena dosham
Kaars’yam, vaivarnyam, jaadyam
Recollect the scenario in JIA – systemic
The spectrum of krimi
The role of krimi in onset
Creation of an atmosphere in the koshtam
which creates krimi
Intestinal microbiome in Kids are very
important
Role of mind
Sukumaranaam – improper response to
stressful situations
Palindromic rheumatism
The concepts of
Bhuutva bhuutva pranashyanti muhuraavirbhavanti
ca
Ksheena kshanaat kshaant poornah
Bhajate krchra saadhyatam
Asnuveeta muhu swaasthaym
Muhuraswaasthyam aavrte
How to approach in a patient
Examine the patient well
Perform needed investigations and arrive
at a clinical diagnosis
Elicit the sannikrshta and viprakrshta hetu
in detail
The utility of investigations
To monitor the aggressiveness of the
disease
To predict the progression of the disease
It shall not influence our disease
assessment.
Eliciting nidanam
The stepping stone of management
Food pattern ~ quantity, quality, timing
Exercise pattern~ pre and post onset
Stress pattern ~ how the stress is dealt
The three factors
Aatanka samutpathi
Pattern of onset and progression of disease
Kaala prakarsham
Chronicity
Vedanaa samuchraayam
Exacerbating factors
OUR DIAGNOSIS
LAKSHANA SAMASHTI
AABHYANTARA VIKRTI PARAMPARA
The sampraapti
A Comparison
The roads The Roga Maargaa
The quality of roads The Rogibala
The detours of roads The associated spread
The wayside enjoyments The nidaana factors which
change the course
The entire trip story
Sampraapti
Identify
The dosha predominanace
The involved dhaatu and srotas
The strength of interaction between them
The vyaadhi avastha
The agni and koshta patterns
The rogi bala
The Core Principle
The symptom management shall not be our
exclusive target
Management of the entire sampraapti shall
be our exclusive target
MANAGEMENT
Approach
Vedana shamanam
Reduction of the raktadushti
Curtailing the aavaranam
Shophaharam
Prevention of further deformities
Shamana oushadhies
Phase I
Deepanam,
Paacanam,
Srotorodha haram
Vaata anulomanam
Raktadushtiharam
Phase II
Aavaranaharam
Balyam
Srotomoola- samrakshanam
Initial phase
Amrtotharam kashayam
Paacanaamrtam kashayam
Manjishtaadi kashayam
Kulakaadi kashayam
Shadamgam kashayam
Punarnavaadi kashayam
Ardhavilwam kashayam
Satata jwara naashana kashayam
Middle phase
Raasna pancakam
Rasna saptakam
Rasnairandaadi
Middle phase
Tiktakam kashayam
Traayantyaadi kashayam
Amrtavrshapatolaadi kashayam
Mahamanjishtaadi kashayam
Later phases
Kokilaaksham kashayam
Shatavarichinnaruhaadi kashayam
Vaashagudoochyaadi kashayam – in
hepato splenomegaly
Guggulutiktakam kashayam
In JIA
Krimihara oushadhies in the first phase
Nirgundyadi kashayam
Vizhalveradi kashayam
Vidangatanduladi kashayam
Rajanyaadi chuurnam
Amrtaguggulu
Kaishoraguggulu
Vettumaran gutika for pain relief
Ksheerabala 101
Chyavanapraasham
Pippali vardhamanam
gudaardrakam
The use of das’amoolam as paana jalam
The use of pancamoolam as gruel
The use of drakshadi lehyam
In paandu / Hb fall
Associated with severe inflammation
Amrta ayo lepam with milk
Associated with swelling and DoE
Punarnava ayo lepam
Procedures
Dhanyamla dhara and other mild swedanam
Lepanam
Ardhamaatrika vasti
Vaitarana vasti-dhaanyaamla vaitaranam
Ksheeravasti
Maadhutailikam
For virecanam and anulomanam
To regulate the P-K Axis
Trvrt lehyam
Kalyana gulam
Avipathi chuurnam
Eranda tailam saksheeram
External applications
Lepanam
With jatamayadi
Gudoocipatraadi
Grhadhoomaadi
Tailam
Murivenna
Chinchaadi tailam
Prabhanjana vimardanam
Pinda tailam
Aranaaladi tailam
Madhuyashtyaadi tailam
The role of raktamokshanam
Very essential
Acute pain relief
Jalaouka is having excellent transient
results
In ladies
Check for saama pittam from heart burn
and PV White discharge
Gudoochyaadi ks + gudooci satwam
Shatavari gulam
Perimenopausal syndrome
Shatavari gulam + Kukutandatwak
bhasmam
Associated advises
Avoid late night dinner
Avoid noon scalp bath and hot water scalp bath
Proper rest and sleep
Avoid pickles, curd and fried foods
Spicy foods and red meat
Loosening exercises
Wear chappal indoors
Avoid direct exposure to A/C and fan
Take home message
Focus on cikitsaa sthaanam
Identify clinical situations
Be a prayoga catura
Sir William Osler
Dedicated to
Late Prof.Dr.Prakash Sir
My Humble Pranaams
